McMaster University
PHYSICAL ACTIVITY AND VASCULAR HEALTH IN ADULTS WITH CPRELATIONSHIPS BETWEEN MOTOR CLASSIFICATION, PHYSICAL ACTIVITY AND CARDIOVASCULAR HEALTH IN ADULTS WITH CEREBRAL PALSYByPATRICK MCPHEE, BSc.A Thesis Submitted to the School of Graduate Studies in Partial Fulfillment of the Requirements forthe Degree Masters of Science in KinesiologyMcMaster University MASTER OF SCIENCE (2014)Hamilton, Ontario (Kinesiology)TITLE: Relationships between motor classification, physical activity and cardiovascular health in adults with cerebral palsy AUTHOR: Patrick McPhee, BSc. (McMaster University)SUPERVISOR: Dr. Maureen MacDonaldSUPERVISORY COMMITTEE:Dr. Brian TimmonsDr. Jan Willem GorterNUMBER OF PAGES: xv, 110ABSTRACTCerebral palsy (CP) is a disability that impacts a person throughout their lifespan and may place adults with the condition at an increased risk of physical inactivity and cardiovascular disease. Cardiovascular structure and function in adults with CP has not been comprehensively investigated previously. In the current cross-sectional, observational study, endothelial function, carotid distensibility, and arterial stiffness were assessed using flow-mediated dilation (FMD), B-mode ultrasound, and pulse wave velocity (PWV), respectively, in forty adults with CP (age 33.7 ± 12.7 years). The study sample was separated based on whether subjects were community ambulant or community non-ambulant using the Gross Motor Function Classification System (GMFCS). Those in GMFCS I-II were labeled community ambulant (age 31.7 ± 10.4 years) while those in GMFCS III-V were community non-ambulant (age 34.8 ± 13.6 years). Resting arterial stiffness was examined through assessment of central and upper and lower limb peripheral PWV (cPWV, uPWV, lPWV). Carotid intima-media thickness (IMT), a measure of vascular structure, was also quantified using B-mode ultrasound images and a semi-automated edge detection software program. cPWV was calculated using the distance (carotid to femoral using the subtraction method) and time delay between the foot of the carotid waveform and the foot of the femoral waveform. uPWV was calculated from the carotid to radial artery distance (subtracting the distance from the carotid to sternal notch from the carotid to radial distance) and the time delay between the arrival of the foot of each corresponding waveform. lPWV was calculated from the femoral to posterior tibialis artery using the distance between each site and time delay between the arrival of the foot of each corresponding waveform. Physical activity (PA) levels were assessed using Actigraph accelerometry with cut points that had been previously determined in normal adults. Cardiometabolic markers of fasting serum interleukin-6, insulin, glucose, and a lipid panel were analyzed. The non-ambulant group had an increased uPWV (10.2 m/s ± 1.9) compared to the ambulant group (8.28 m/s ± 1.6) (p<0.01) despite no differences in cPWV or lPWV. There were no group differences (p>0.05) in absolute, relative or normalized FMD responses. Both groups also had similar values of carotid IMT and carotid distensibility. No group differences were found in any of the cardiometabolic or inflammatory markers. Moderate-to-vigorous PA (MVPA) levels were greater in the ambulant group (2.4 mins ± 2.1 per hour) compared to the non-ambulant group (0.3 mins ± 0.6 per hour) (p<0.01). Furthermore, sedentary time was greater in the non-ambulant group (57.8 mins ± 1.9 per hour) compared to the ambulant group (51.6 mins ± 4.7 per hour) (p<0.01). Despite differences in PA levels, MVPA was not a significant independent predictor of vascular or metabolic health in this cohort of adults with CP. However, GMFCS level was predictive of both uPWV and resting heart rate. Future research should include adults with CP who are older in age to gain further insight into the potential consequences of an activity-limited lifestyle (specifically in the non-ambulant group) on cardiovascular and metabolic health in this clinical population.ACKNOWLEDGMENTSI would like to thank my supervisor, Dr. Maureen MacDonald for her guidance, knowledge and support over the past two years. Although you were “across the pond” last year, you were always quick to respond to emails and meet through Skype whenever needed. Your edits of manuscripts, abstracts, and thesis documents have allowed me to enhance my skills in research writing – something that I lacked confidence in when starting my masters degree. I would like to thank the members of my committee, Dr. Timmons and Dr. Gorter for their insight and research expertise with this project. I would also like to thank Dr. Bentley and the staff at the Comprehensive Spasticity Management Program for assisting with participant recruitment. All of you have made this research project a positive learning experience.I would like to thank the members of the Vascular Dynamics Laboratory for their assistance with data collection and offering to go for much needed “coffee breaks” throughout long days of data analysis. I grew up playing competitive hockey and was excited when I was able to work in such a team oriented research setting. I would also like to acknowledge the adults with cerebral palsy who participated in this project. You truly made this research a rewarding experience. It was an honour to learn that you were so grateful that this research was being conducted in such an understudied clinical population. Finally, I would like to thank my family, friends, and significant other, Vanessa. The continued support through my educational journey helps to remind me that there is a light at the end of the tunnel – and that all of this hard work is worth it. TABLE OF CONTENTSTitle Page . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iiDescriptive Note . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iiiAbstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ivAcknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .viTable of Contents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . viiList of Appendices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xList of Tables . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xiList of Figures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiiList of Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .xivCHAPTER 1: Literature ReviewIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .11.1 - Vascular Markers of CVD Risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.1.1 Arterial System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21.1.2 Arterial Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .31.1.3 Carotid Intima-Media Thickness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .31.1.4 Arterial Stiffness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51.1.5 Further Causes of Increasing Arterial Stiffness . . . . . . . . . . . . . . . . . . . . . . .61.1.6 Non-Invasive Determination of Arterial Stiffness . . . . . . . . . . . . . . . . . . . . .71.1.7 Measuring PWV . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .81.1.8 Exercise and Arterial Stiffness . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .91.1.9 Arterial Compliance and Distensibility . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111.1.10 Measurement of Carotid Compliance and Distensibility . . . . . . . . . . . . . .121.1.11 Vascular Endothelium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131.1.12 Endothelial Function/Dysfunction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .141.1.13 Measurement of Endothelial Function – Flow-Mediated Vasodilation . . 151.1.14 Endothelial Function and Exercise . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161.2 - Other CVD Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .171.2.1 Physical Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .171.2.2 Insulin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191.2.3 Glucose . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211.2.4 Interleukin-6 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221.2.5 Lipids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231.3 - Cerebral Palsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 251.3.1 Cerebral Palsy and Physical Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271.3.2 Secondary Complications in Adults with Cerebral Palsy . . . . . . . . . . . . . .291.3.3 Physical Activity and Cardiovascular Health in Adulthood . . . . . . . . . . . .321.4 – Purpose and Hypothesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .331.5 – References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34CHAPTER 2: Relationships Between Motor Classification, Physical Activity and Cardiovascular Health in Adults with Cerebral Palsy2.1 - Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .452.2 - Methods . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 482.2.1 Participants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .482.2.2 Study Design . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492.2.3 Activity Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492.2.4 Anthropometric Measurements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .502.2.5 Blood Draw . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .512.2.6 Resting Heart Rate and Blood Pressure . . . . . . . . . . . . . . . . . . . . . . . . . . 522.2.7 Vascular Measures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 522.2.8 Statistical Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 582.3 – Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 592.3.1 Participant Characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 592.3.2 Physical Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 592.3.3 Vascular Indices . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .602.3.4 Cardiometabolic Blood Markers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 612.3.5 Multiple Linear Regression Coefficients . . . . . . . . . . . . . . . . . . . . . . . . .612.4 – Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 752.4.1 Limitations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 822.4.2 Future Directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 832.4.3 Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 832.5 – References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85LIST OF APPENDICESAppendix A:GMFCS description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90Appendix B:Participant Consent Form . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .91Appendix C:Data Collection Sheet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .97Appendix D:Raw Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99LIST OF TABLESTables from Chapter 2: Relationships between motor classification, physical activity and cardiovascular health in adults with cerebral palsyTable 1Subject Characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63Table 2Group comparisons of daily and hourly physical activity levels . . . . . . . 63Table 3Group comparisons of FMD response, carotid distensibility and IMT, central, lower, and upper PWV . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .64Table 4Group comparisons of glucose, insulin, HOMA-IR, IL-6, and lipid concentrations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .64Table 5Backward multiple linear regression . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65Table 6Forward multiple linear regression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .69LIST OF FIGURESFigures from Chapter 1: Literature ReviewFigure 1Measurement of central PWV . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .8Figures from Chapter 2: Relationships between motor classification, physical activity and cardiovascular health in adults with cerebral palsyFigure 1A) Group comparison of accelerometer wear time per day . . . . . . . . . . 70B) Group comparison of minutes of MVPA per day . . . . . . . . . . . . . . . 70C) Group comparison of minutes of MVPA per hour . . . . . . . . . . . . . . .70D) Group comparison of sedentary time per hour . . . . . . . . . . . . . . . . . .70Figure 2Group comparison of upper PWV . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .71Figure 3A) GMFCS as an independent predictor of HR . . . . . . . . . . . . . . . . . . . .72B) GMFCS as an independent predictor of uPWV . . . . . . . . . . . . . . . . . 72Figure 4A) Age as an independent predictor of SBP . . . . . . . . . . . . . . . . . . . . . . 73B) Age as an independent predictor of MAP . . . . . . . . . . . . . . . . . . . . . .73C) Age as an independent predictor of cPWV . . . . . . . . . . . . . . . . . . . . .73D) Age as an independent predictor of IMT . . . . . . . . . . . . . . . . . . . . . . 73E) Age as an independent predictor of distensibility . . . . . . . . . . . . . . . .73Figure 5A) Waist circumference as an independent predictor of HDL-C . . . . . . 74B) Waist circumference as an independent predictor of LDL-C . . . . . . .74C) Waist circumference as an independent predictor of triglycerides . . .74D) Waist circumference as an independent predictor of TC/HDL-C . . . .74E) Waist circumference as an independent predictor of IL-6 . . . . . . . . . .74F) Waist circumference as an independent predictor of HOMA-IR . . . . .74LIST OF ALL ABBREVIATIONS AND SYMBOLSBMIBody mass indexcIMTCarotid intima-media thicknessCPCerebral PalsyCRPC-reactive proteinCVDCardiovascular diseaseDBPDiastolic blood pressureFMDFlow-mediated vasodilationGMFCSGross motor function classification systemHDLHigh-density lipoproteinLDLLow-density lipoproteinLVLeft ventricleMIMyocardial infarctionMVPAModerate-to-vigorous physical activityNONitric OxideNOSNitric oxide synthasePAPhysical activityPPPulse pressurePTTPulse transit timePWVPulse wave velocitySBP Systolic blood pressureTC/HDL-CTotal cholesterol to HDL cholesterol ratioWCWaist circumferenceCHAPTER 1LITERATURE REVIEWIntroductionCardiovascular disease (CVD) is a disorder of the heart and blood vessels and includes diseases such as coronary heart disease, cerebrovascular disease, and peripheral artery disease. 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0098-7484 (Linking)</isbn><accession-num>8667564</accession-num><urls><related-urls><url>;[4].Aerobic exercise can improve many of the classical risk factors that are associated with elevated CVD such as body fatness, insulin resistance, and blood pressure, however the dose response curve for the relationship between exercise and each risk factor varies PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5GZXJyZWlyYTwvQXV0aG9yPjxZZWFyPjIwMDY8L1llYXI+
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ADDIN EN.CITE.DATA [5]. It is estimated that up to 30-40% of the CVD risk reduction associated with increased activity is not explained by traditional risk factors ADDIN EN.CITE <EndNote><Cite><Author>Mora</Author><Year>2007</Year><RecNum>3510</RecNum><DisplayText>[6, 7]</DisplayText><record><rec-number>3510</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3510</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Mora, Samia</author><author>Cook, Nancy</author><author>Buring, Julie E</author><author>Ridker, Paul M</author><author>Lee, I-Min</author></authors></contributors><titles><title>Physical activity and reduced risk of cardiovascular events potential mediating mechanisms</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>2110-2118</pages><volume>116</volume><number>19</number><dates><year>2007</year></dates><isbn>0009-7322</isbn><urls></urls></record></Cite><Cite><Author>Green</Author><Year>2008</Year><RecNum>3512</RecNum><record><rec-number>3512</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3512</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Green, Daniel J</author><author>O'Driscoll, Gerry</author><author>Joyner, Michael J</author><author>Cable, Nigel T</author></authors></contributors><titles><title>Exercise and cardiovascular risk reduction: time to update the rationale for exercise?</title><secondary-title>Journal of Applied Physiology</secondary-title></titles><periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></periodical><pages>766-768</pages><volume>105</volume><number>2</number><dates><year>2008</year></dates><isbn>8750-7587</isbn><urls></urls></record></Cite></EndNote>[6, 7]. Structural and functional adaptations to the vascular wall associated with exercise, such as decreased wall thickness, increased elastin content and the attenuation of collagen progression within the arterial wall and changes in endothelial function may also be involved in exercise related CVD risk reduction ADDIN EN.CITE <EndNote><Cite><Author>tanaka</Author><Year>2005</Year><RecNum>3267</RecNum><DisplayText>[8]</DisplayText><record><rec-number>3267</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3267</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Tanaka, H. and Safar ME</author></authors></contributors><titles><title>Influence of lifestyle modification on arterial stiffness and wave reflections</title><secondary-title>American Journal of Hypertension</secondary-title></titles><periodical><full-title>American Journal of Hypertension</full-title></periodical><pages>137-144</pages><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[8]. Cerebral palsy (CP) is a cause of disability that impacts a person across their lifespan and may consequently limit the amount of PA that this population can endure ADDIN EN.CITE <EndNote><Cite><Author>Svien</Author><Year>2008</Year><RecNum>3341</RecNum><DisplayText>[9]</DisplayText><record><rec-number>3341</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3341</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Svien, L. R., Berg, P., Stephenson, C.</author></authors></contributors><titles><title>Issues in aging with cerebral palsy</title><secondary-title>Topics in Geriatric Rehabilitation</secondary-title></titles><periodical><full-title>Topics in Geriatric Rehabilitation</full-title></periodical><pages>26-40</pages><volume>24</volume><number>1</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[9]. Particularly, adults with CP are likely not engaging in sufficient PA to produce improvements in fitness required to experience positive health benefits PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5UaG9ycGU8L0F1dGhvcj48WWVhcj4yMDA5PC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [10]. Regarding causes of mortality, many more deaths have been attributed to diseases of the respiratory and circulatory system in adults with CP aged 20-50, compared to the general population, and these are typically more pronounced in the more severely affected PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IZW1taW5nPC9BdXRob3I+PFllYXI+MjAwNjwvWWVhcj48
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ADDIN EN.CITE.DATA [11]. Perhaps the lack of PA in these individuals living with a disability may be compromising their cardiovascular health. In addition to the potential predictive benefit of indices of vascular health, other emerging risk markers such as PA levels and biomarkers of inflammation and metabolism may provide useful information about CVD risk in special populations at elevated risk.1.1 VASCULAR MARKERS OF CVD RISK1.1.1Arterial systemThe systemic arterial system serves to disperse blood at high pressures to peripheral vascular sites at rates required to meet tissue metabolic requirements PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5OaWNob2xzPC9BdXRob3I+PFllYXI+MjAwODwvWWVhcj48
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ADDIN EN.CITE.DATA [12]. The arterial system can essentially be separated into 3 anatomical regions with each having a distinct and individual function: (1) The large elastic arteries (aorta, iliac, carotid) serve as a buffering reservoir to transform pulsatile blood flow into continuous flow in order to perfuse the smaller arteries, arterioles, and capillaries. To do this, these elastic arteries passively expand and thereby store the blood ejected from the left ventricle (LV) during systole, and recoil to propel the blood away from the heart during diastole; (2) The muscular peripheral arteries modify the speed of travel of pressure and flow waves along their length by altering their smooth muscle tone. These peripheral arteries also determine when reflected pressure waves arrive back at the heart based on both bifurcation sites and impedance; and (3) The arterioles, by modifying their diameter, alter peripheral resistance and aid in the maintenance of mean arterial blood pressure in the face of increased or decreased flow PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5OaWNob2xzPC9BdXRob3I+PFllYXI+MjAwODwvWWVhcj48
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ADDIN EN.CITE.DATA [12].1.1.2Arterial anatomyAn artery can be described as a viscoelastic tube in which the diameter fluctuates with a pulsating pressure that is created by the oscillating flow generated through the cardiac cycle ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3223</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3223</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3223</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13]. The predominant structural materials of the arterial wall are collagen and elastin. The arterial wall is divided into three distinct regions: the intima, media, and adventitia. The intima consists of the vascular endothelium and a thin layer of elastin and collagen that anchors the intima to the internal elastic lamina; which separates the intima from the media layer. The media is the determinant of the mechanical properties of a blood vessel and is comprised of smooth muscle cells that run parallel to elastin fibers. The outer layer of the vascular wall, the adventitia, is mainly formed from collagen and elastin and merges with the surrounding connective tissue. The distribution of elastin and collagen is significantly different between the central and peripheral arteries. In the proximal aorta, elastin dominates, whereas in the distal peripheral arteries collagen is more pronounced ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13].1.1.3Carotid intima-media thicknessCarotid intima-media thickness (cIMT) is an index of arterial structure and represents a composite of intima and medial wall thickness ADDIN EN.CITE <EndNote><Cite><Author>Bots</Author><Year>2002</Year><RecNum>3275</RecNum><DisplayText>[14]</DisplayText><record><rec-number>3275</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3275</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bots, M. L., Dijk, J.M., Oren, A., Grobbee, D.E.</author></authors></contributors><titles><title>Carotid intima-media thickness, arterial stiffness and risk of cardiovascular disease: current evidence</title><secondary-title>Journal of Hypertension</secondary-title></titles><periodical><full-title>Journal of Hypertension</full-title></periodical><pages>2317-2325</pages><volume>20</volume><number>12</number><dates><year>2002</year></dates><urls></urls></record></Cite></EndNote>[14]. Increases in cIMT have been shown to correlate to atherosclerosis in the coronary arteries PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5WYXNhbmthcmkgVDwvQXV0aG9yPjxZZWFyPjIwMDE8L1ll
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ADDIN EN.CITE.DATA [15-17] and peripheral arteries. The presence of a traditional CVD risk factor(s) is positively associated with an increased cIMT ADDIN EN.CITE <EndNote><Cite><Author>Bots ML</Author><Year>1998</Year><RecNum>3281</RecNum><DisplayText>[18]</DisplayText><record><rec-number>3281</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3281</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bots ML, Iglesias del Sol A, Grobbee DE.</author></authors></contributors><titles><title>Carotid intima-media thickness measurements in observational and intervention studies</title><secondary-title>Curr Res Vasc Dis</secondary-title></titles><periodical><full-title>Curr Res Vasc Dis</full-title></periodical><pages>274-283</pages><volume>3</volume><dates><year>1998</year></dates><urls></urls></record></Cite></EndNote>[18]. A study conducted in middle-aged Finnish men reported that an increase of 0.1mm in far wall cIMT was associated with an 11% increased risk of myocardial infarction (MI) ADDIN EN.CITE <EndNote><Cite><Author>Salonen</Author><Year>1991</Year><RecNum>3282</RecNum><DisplayText>[19]</DisplayText><record><rec-number>3282</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3282</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Salonen, J. T.</author><author>Salonen, R.</author></authors></contributors><auth-address>Department of Community Health and General Practice, University of Kuopio, Finland.</auth-address><titles><title>Ultrasonographically assessed carotid morphology and the risk of coronary heart disease</title><secondary-title>Arterioscler Thromb</secondary-title><alt-title>Arteriosclerosis and thrombosis : a journal of vascular biology / American Heart Association</alt-title></titles><pages>1245-9</pages><volume>11</volume><number>5</number><keywords><keyword>Adult</keyword><keyword>Arteriosclerosis/complications/*ultrasonography</keyword><keyword>Carotid Artery Diseases/complications/*ultrasonography</keyword><keyword>Confidence Intervals</keyword><keyword>Coronary Disease/*etiology</keyword><keyword>Follow-Up Studies</keyword><keyword>Humans</keyword><keyword>Longitudinal Studies</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Prospective Studies</keyword><keyword>Risk Factors</keyword></keywords><dates><year>1991</year><pub-dates><date>Sep-Oct</date></pub-dates></dates><isbn>1049-8834 (Print)
1049-8834 (Linking)</isbn><accession-num>1911709</accession-num><urls><related-urls><url>;[19]. Furthermore, a cIMT greater than 0.82mm increases the risk of MI, stroke, and peripheral arterial disease ADDIN EN.CITE <EndNote><Cite><Author>O'Leary DH</Author><Year>1999</Year><RecNum>3283</RecNum><DisplayText>[20]</DisplayText><record><rec-number>3283</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3283</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Leary DH, Polak JF, Kronmal RA, Burke GL, Wolfson Jr SK</author></authors></contributors><titles><title>Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. Cardiovascular Health Study Collaborative Research Group.</title><secondary-title>N Engl J Med</secondary-title></titles><periodical><full-title>N Engl J Med</full-title></periodical><pages>14-22</pages><volume>340</volume><dates><year>1999</year></dates><urls></urls></record></Cite></EndNote>[20]. With regards to traditional CVD risk factors, obesity was the strongest predictor of cIMT in healthy and non-healthy individuals (mean age 34 years) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5CZXJuaTwvQXV0aG9yPjxZZWFyPjIwMTE8L1llYXI+PFJl
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ADDIN EN.CITE.DATA [22]. As cIMT is an independent predictor of incidental stroke, the literature has shown that increases in PA can attenuate the progression of stroke. However, it is uncertain as to whether this is a direct effect of a reduction in cIMT. Tanaka and colleagues showed that there was no difference in cIMT between healthy sedentary and endurance trained individuals within the same age group. Furthermore, 3 months of an exercise intervention did not reduce cIMT in the sedentary group PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5UYW5ha2E8L0F1dGhvcj48WWVhcj4yMDAyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [23]. Perhaps exercise mediates its prevention of stroke through other avenues apart from reductions in cIMT.CIMT is measured from B-mode ultrasound images of the arterial far wall that include two detectable lines representing the boundaries of the lumen-intima interface and the media-adventitia interface ADDIN EN.CITE <EndNote><Cite><Author>Pignoli</Author><Year>1986</Year><RecNum>3288</RecNum><DisplayText>[24]</DisplayText><record><rec-number>3288</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3288</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Pignoli, P.</author><author>Tremoli, E.</author><author>Poli, A.</author><author>Oreste, P.</author><author>Paoletti, R.</author></authors></contributors><titles><title>Intimal plus medial thickness of the arterial wall: a direct measurement with ultrasound imaging</title><secondary-title>Circulation</secondary-title><alt-title>Circulation</alt-title></titles><periodical><full-title>Circulation</full-title></periodical><alt-periodical><full-title>Circulation</full-title></alt-periodical><pages>1399-406</pages><volume>74</volume><number>6</number><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Aorta, Abdominal/*pathology</keyword><keyword>Arteriosclerosis/diagnosis/pathology</keyword><keyword>Carotid Arteries/*pathology</keyword><keyword>Evaluation Studies as Topic</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>*Ultrasonography/instrumentation/methods</keyword></keywords><dates><year>1986</year><pub-dates><date>Dec</date></pub-dates></dates><isbn>0009-7322 (Print)
0009-7322 (Linking)</isbn><accession-num>3536154</accession-num><urls><related-urls><url>;[24]. Reproducibility of cIMT measurements has improved over the years, with measurement error decreasing from 25-40% to a current level of 10-20% ADDIN EN.CITE <EndNote><Cite><Author>Bots</Author><Year>1997</Year><RecNum>3289</RecNum><DisplayText>[25]</DisplayText><record><rec-number>3289</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3289</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bots, M. L.</author><author>Hoes, A. W.</author><author>Koudstaal, P. J.</author><author>Hofman, A.</author><author>Grobbee, D. E.</author></authors></contributors><auth-address>Department of Epidemiology and Biostatistics, Erasmus University Medical School, Rotterdam, Netherlands.</auth-address><titles><title>Common carotid intima-media thickness and risk of stroke and myocardial infarction: the Rotterdam Study</title><secondary-title>Circulation</secondary-title><alt-title>Circulation</alt-title></titles><periodical><full-title>Circulation</full-title></periodical><alt-periodical><full-title>Circulation</full-title></alt-periodical><pages>1432-7</pages><volume>96</volume><number>5</number><keywords><keyword>Aged</keyword><keyword>Carotid Artery, Common/*ultrasonography</keyword><keyword>Case-Control Studies</keyword><keyword>*Cerebrovascular Disorders/epidemiology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>*Myocardial Infarction/epidemiology</keyword><keyword>Prospective Studies</keyword><keyword>Risk Factors</keyword><keyword>Tunica Intima/*ultrasonography</keyword><keyword>Tunica Media/*ultrasonography</keyword></keywords><dates><year>1997</year><pub-dates><date>Sep 2</date></pub-dates></dates><isbn>0009-7322 (Print)
0009-7322 (Linking)</isbn><accession-num>9315528</accession-num><urls><related-urls><url>;[25]. 1.1.4Arterial stiffnessMeasures of arterial stiffness predict the inherent ability of an artery to expand and contract with cardiac contraction and relaxation ADDIN EN.CITE <EndNote><Cite><Author>Bergel</Author><Year>1960</Year><RecNum>3242</RecNum><DisplayText>[26-28]</DisplayText><record><rec-number>3242</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3242</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bergel, B.H.</author></authors></contributors><titles><title>The static elastic properties of the arterial wall</title><secondary-title>J Physiol</secondary-title></titles><periodical><full-title>J Physiol</full-title></periodical><pages>445-457</pages><volume>156</volume><dates><year>1960</year></dates><urls></urls></record></Cite><Cite><Author>Dobrin</Author><Year>1978</Year><RecNum>3243</RecNum><record><rec-number>3243</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3243</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Dobrin, P.B.</author></authors></contributors><titles><title>Mechanical properties of arteries</title><secondary-title>Physiol Rev</secondary-title></titles><periodical><full-title>Physiol Rev</full-title></periodical><pages>397-460</pages><volume>58</volume><dates><year>1978</year></dates><urls></urls></record></Cite><Cite><Author>Grainfield</Author><Year>1964</Year><RecNum>3246</RecNum><record><rec-number>3246</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3246</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Grainfield, J.C., Tindall, G.T., Dillon, M.L.</author></authors></contributors><titles><title>Mechanics of the human carotid artery in vivo</title><secondary-title>Circ Res</secondary-title></titles><periodical><full-title>Circ Res</full-title></periodical><pages>240-246</pages><volume>15</volume><dates><year>1964</year></dates><urls></urls></record></Cite></EndNote>[26-28]. Arterial stiffness is determined by structural and functional components that relate to the intrinsic structural properties of the artery ADDIN EN.CITE <EndNote><Cite><Author>Bergel</Author><Year>1960</Year><RecNum>3242</RecNum><DisplayText>[26, 27]</DisplayText><record><rec-number>3242</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3242</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bergel, B.H.</author></authors></contributors><titles><title>The static elastic properties of the arterial wall</title><secondary-title>J Physiol</secondary-title></titles><periodical><full-title>J Physiol</full-title></periodical><pages>445-457</pages><volume>156</volume><dates><year>1960</year></dates><urls></urls></record></Cite><Cite><Author>Dobrin</Author><Year>1978</Year><RecNum>3243</RecNum><record><rec-number>3243</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3243</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Dobrin, P.B.</author></authors></contributors><titles><title>Mechanical properties of arteries</title><secondary-title>Physiol Rev</secondary-title></titles><periodical><full-title>Physiol Rev</full-title></periodical><pages>397-460</pages><volume>58</volume><dates><year>1978</year></dates><urls></urls></record></Cite></EndNote>[26, 27]. The elastic properties of an artery are the qualities that enable the artery to be stretched while retaining its ability to return to the original form when the pressure (or stressor) is removed ADDIN EN.CITE <EndNote><Cite><Author>Grainfield</Author><Year>1964</Year><RecNum>3246</RecNum><DisplayText>[28]</DisplayText><record><rec-number>3246</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3246</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Grainfield, J.C., Tindall, G.T., Dillon, M.L.</author></authors></contributors><titles><title>Mechanics of the human carotid artery in vivo</title><secondary-title>Circ Res</secondary-title></titles><periodical><full-title>Circ Res</full-title></periodical><pages>240-246</pages><volume>15</volume><dates><year>1964</year></dates><urls></urls></record></Cite></EndNote>[28]. The endothelium, elastin fibers, and smooth muscle are all contributors to arterial stiffness ADDIN EN.CITE <EndNote><Cite><Author>Grainfield</Author><Year>1964</Year><RecNum>3246</RecNum><DisplayText>[28]</DisplayText><record><rec-number>3246</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3246</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Grainfield, J.C., Tindall, G.T., Dillon, M.L.</author></authors></contributors><titles><title>Mechanics of the human carotid artery in vivo</title><secondary-title>Circ Res</secondary-title></titles><periodical><full-title>Circ Res</full-title></periodical><pages>240-246</pages><volume>15</volume><dates><year>1964</year></dates><urls></urls></record></Cite></EndNote>[28]. At low and normal pressures, the elastin fibers in the arterial wall bear most of the stress whereas at increased pressure (> 200mmHg) collagen fibers are involved in the mediation of stiffness and protect against arterial rupture ADDIN EN.CITE <EndNote><Cite><Author>O'Rourke</Author><Year>1982</Year><RecNum>3247</RecNum><DisplayText>[29]</DisplayText><record><rec-number>3247</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3247</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Rourke, M. F.</author></authors></contributors><auth-address>Edinburgh, Scotland: Churchill Livingstone</auth-address><titles><title>Arterial function in health and disease</title></titles><dates><year>1982</year></dates><urls></urls></record></Cite></EndNote>[29]. Differences in the ratio of elastin to collagen in the arterial wall can affect stiffness as the lower the ratio, the stiffer the artery ADDIN EN.CITE <EndNote><Cite><Author>D.A.</Author><Year>1974</Year><RecNum>3248</RecNum><DisplayText>[30]</DisplayText><record><rec-number>3248</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3248</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>McDonald D.A.</author></authors></contributors><auth-address>Baltimore, MD: Williams & Wilkins</auth-address><titles><title>Blood flow in arteries</title></titles><dates><year>1974</year></dates><urls></urls></record></Cite></EndNote>[30]. Elevated smooth muscle tone increases arterial stiffness as a result of increased alpha-adrenergic receptors promoting smooth muscle contraction through increased sympathetic activation ADDIN EN.CITE <EndNote><Cite><Author>Bevan</Author><Year>1991</Year><RecNum>3249</RecNum><DisplayText>[31]</DisplayText><record><rec-number>3249</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3249</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bevan, J. A.</author><author>Laher, I.</author></authors></contributors><auth-address>Vermont Center for Vascular Research, University of Vermont College of Medicine, Burlington 05405.</auth-address><titles><title>Pressure and flow-dependent vascular tone</title><secondary-title>FASEB J</secondary-title><alt-title>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</alt-title></titles><periodical><full-title>FASEB J</full-title></periodical><pages>2267-73</pages><volume>5</volume><number>9</number><keywords><keyword>Animals</keyword><keyword>Blood Flow Velocity</keyword><keyword>*Blood Pressure</keyword><keyword>Humans</keyword><keyword>*Muscle Tonus</keyword><keyword>Muscle, Smooth, Vascular/*physiology</keyword><keyword>*Vascular Resistance</keyword></keywords><dates><year>1991</year><pub-dates><date>Jun</date></pub-dates></dates><isbn>0892-6638 (Print)
0892-6638 (Linking)</isbn><accession-num>1860618</accession-num><urls><related-urls><url>;[31]. It has been shown that arteries become stiffer with increasing age and cardiovascular related diseases such as hypertension, diabetes, and atherosclerosis ADDIN EN.CITE <EndNote><Cite><Author>Safar</Author><Year>2011</Year><RecNum>3250</RecNum><DisplayText>[32]</DisplayText><record><rec-number>3250</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3250</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Safar, M.E., Blacher, J., Jankowski, P.</author></authors></contributors><titles><title>Arterial stiffness, pulse pressure, and cardiovascular disease - is it possible to break the vicious circle?</title><secondary-title>Atherosclerosis</secondary-title></titles><periodical><full-title>Atherosclerosis</full-title></periodical><pages>263-271</pages><volume>218</volume><dates><year>2011</year></dates><urls></urls></record></Cite></EndNote>[32]. Structural changes that contribute to increased arterial stiffness include fragmentation of elastin, increased deposition of collagen, arterial calcification, inflammation, and cross-linking of collagen molecules PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Ib3BlPC9BdXRob3I+PFllYXI+MjAwNzwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [35]. These increases in pressure lead to the development of cardiovascular complications and events, including stroke and MI ADDIN EN.CITE <EndNote><Cite><Author>Laurent</Author><Year>2005</Year><RecNum>3252</RecNum><DisplayText>[34]</DisplayText><record><rec-number>3252</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3252</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laurent, S.</author><author>Boutouyrie, P.</author><author>Lacolley, P.</author></authors></contributors><auth-address>Department of Pharmacology and INSERM EMI 107, Hopital Europeen Georges Pompidou, Paris, France. stephane.laurent@egp.ap-hop-paris.fr</auth-address><titles><title>Structural and genetic bases of arterial stiffness</title><secondary-title>Hypertension</secondary-title><alt-title>Hypertension</alt-title></titles><periodical><full-title>Hypertension</full-title></periodical><alt-periodical><full-title>Hypertension</full-title></alt-periodical><pages>1050-5</pages><volume>45</volume><number>6</number><keywords><keyword>Animals</keyword><keyword>Arteries/*pathology/*physiopathology</keyword><keyword>Compliance</keyword><keyword>Gene Expression</keyword><keyword>Gene Expression Profiling</keyword><keyword>Humans</keyword><keyword>Hypertension/physiopathology</keyword><keyword>Vascular Diseases/*genetics/physiopathology/therapy</keyword></keywords><dates><year>2005</year><pub-dates><date>Jun</date></pub-dates></dates><isbn>1524-4563 (Electronic)
0194-911X (Linking)</isbn><accession-num>15851625</accession-num><urls><related-urls><url>;[34].Increases in arterial stiffness cause a premature return of the reflected wave in late systole, resulting in increases in PP and thus systolic blood pressure (SBP) ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13] which is also referred to as augmentation index. Elevations in SBP increase the afterload on the LV, as the LV must now contract harder to overcome the increased central PP. With the LV subsequently working harder, arterial stiffness is thus associated with LV hypertrophy, a known risk factor for coronary events in normotensive and hypertensive patients ADDIN EN.CITE <EndNote><Cite><Author>Boutouyrie</Author><Year>1995</Year><RecNum>3489</RecNum><DisplayText>[36]</DisplayText><record><rec-number>3489</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3489</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Boutouyrie, Pierre</author><author>Laurent, Stéphane</author><author>Girerd, Xavier</author><author>Benetos, Athanase</author><author>Lacolley, Patrick</author><author>Abergel, Eric</author><author>Safar, Michel</author></authors></contributors><titles><title>Common carotid artery stiffness and patterns of left ventricular hypertrophy in hypertensive patients</title><secondary-title>Hypertension</secondary-title></titles><periodical><full-title>Hypertension</full-title></periodical><pages>651-659</pages><volume>25</volume><number>4</number><dates><year>1995</year></dates><isbn>0194-911X</isbn><urls></urls></record></Cite></EndNote>[36].1.1.5Further causes of increasing arterial stiffnessThe literature has documented aging as being the most important cause of arterial stiffness, with underlying hypertension as an accelerate of the aging process ADDIN EN.CITE <EndNote><Cite><Author>O'Rourke</Author><Year>1999</Year><RecNum>3253</RecNum><DisplayText>[37]</DisplayText><record><rec-number>3253</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3253</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Rourke, M.F.</author></authors></contributors><titles><title>Isolated systolic hypertension, pulse pressure, and arterial stiffness as risk factors for cardiovascular disease</title><secondary-title>Current Hypertension Reports</secondary-title></titles><periodical><full-title>Current Hypertension Reports</full-title><abbr-1>Curr Hypertens Rep</abbr-1></periodical><pages>204-211</pages><volume>3</volume><dates><year>1999</year></dates><urls></urls></record></Cite></EndNote>[37]. There is a near twofold increase in aortic pulse wave velocity (PWV) between age 20 and 80. These changes are not nearly as pronounced in the muscular arteries as these vessels are initially less distensible, and experience a more continuous pattern of flow as opposed to the pulsatile flow to which larger central elastic arteries are exposed ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13]. Fragmentation of the aortic elastic medial lamella can be attributed to the fatiguing effects of pulsatile stress acting over billions of heart cycles ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13]. PP can be defined as the difference between SBP and diastolic blood pressure (DBP). With aging, there is anincreased PP for a given stroke volume, and this is resultant of increased stiffness and an earlier arrival of the reflective wave, increasing SBP and lowering DBP, which inhibits perfusion, increases myocardial oxygen demand, and causes a mismatch between myocardial demand and supply. An increased resting heart rate likely promotes arterial stiffening through exposing the vessel wall to greater cyclic stress ADDIN EN.CITE <EndNote><Cite><Author>Vaitkevicius</Author><Year>1993</Year><RecNum>3255</RecNum><DisplayText>[38]</DisplayText><record><rec-number>3255</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3255</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Vaitkevicius, P. V.</author><author>Fleg, J. L.</author><author>Engel, J. H.</author><author>O'Connor, F. C.</author><author>Wright, J. G.</author><author>Lakatta, L. E.</author><author>Yin, F. C.</author><author>Lakatta, E. G.</author></authors></contributors><auth-address>Division of Geriatric Medicine, University of Maryland School of Medicine.</auth-address><titles><title>Effects of age and aerobic capacity on arterial stiffness in healthy adults</title><secondary-title>Circulation</secondary-title><alt-title>Circulation</alt-title></titles><periodical><full-title>Circulation</full-title></periodical><alt-periodical><full-title>Circulation</full-title></alt-periodical><pages>1456-62</pages><volume>88</volume><number>4 Pt 1</number><keywords><keyword>Aging/*physiology</keyword><keyword>Exercise</keyword><keyword>Exercise Test</keyword><keyword>Exercise Tolerance/*physiology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Longitudinal Studies</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Oxygen Consumption/physiology</keyword><keyword>Physical Education and Training</keyword><keyword>Physical Endurance/physiology</keyword><keyword>Pulse/physiology</keyword><keyword>Regression Analysis</keyword><keyword>Running/physiology</keyword><keyword>Vascular Resistance/*physiology</keyword></keywords><dates><year>1993</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>0009-7322 (Print)
0009-7322 (Linking)</isbn><accession-num>8403292</accession-num><urls><related-urls><url>;[38]. Hypertension accelerates the age associated arterial stiffening process through increasing the stretch of the artery that in turn transfers stress to the less extensible collagenous components of the wall, and renders the stretched artery as stiff ADDIN EN.CITE <EndNote><Cite><Author>Safar ME</Author><Year>1998</Year><RecNum>3254</RecNum><DisplayText>[39]</DisplayText><record><rec-number>3254</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3254</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Safar ME, London GM, Brunner H, et al.</author></authors></contributors><titles><title>Third workshop on structure and function of large arteries: part 1 [editorial]</title><secondary-title>Hypertension</secondary-title></titles><periodical><full-title>Hypertension</full-title></periodical><pages>155</pages><volume>32</volume><dates><year>1998</year></dates><urls></urls></record></Cite></EndNote>[39].1.1.6Non-invasive determination of arterial stiffnessRegional and local arterial stiffness can be determined directly and non-invasively at various sites along the arterial tree. The measurement of PWV is deemed as the most simple, robust, and reproducible arterial stiffness measurement method, and for those reasons, carotid-femoral PWV has been labeled as the “gold-standard” for determining arterial stiffness ADDIN EN.CITE <EndNote><Cite><Author>Laurent</Author><Year>2006</Year><RecNum>3256</RecNum><DisplayText>[40]</DisplayText><record><rec-number>3256</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3256</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laurent, S., Cockcroft, J., Van Bortel, L., et al.</author></authors></contributors><titles><title>Expert consensus document on arterial stiffness: methodological issues and clinical application</title><secondary-title>European Heart Journal</secondary-title></titles><periodical><full-title>European Heart Journal</full-title></periodical><pages>2588-2605</pages><volume>27</volume><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>[40]. Carotid-femoral PWV has been used extensively in epidemiological studies to demonstrate the predictive value of aortic stiffness for cardiovascular events ADDIN EN.CITE <EndNote><Cite><Author>Laurent</Author><Year>2006</Year><RecNum>3256</RecNum><DisplayText>[40]</DisplayText><record><rec-number>3256</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3256</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laurent, S., Cockcroft, J., Van Bortel, L., et al.</author></authors></contributors><titles><title>Expert consensus document on arterial stiffness: methodological issues and clinical application</title><secondary-title>European Heart Journal</secondary-title></titles><periodical><full-title>European Heart Journal</full-title></periodical><pages>2588-2605</pages><volume>27</volume><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>[40]. On the contrary, PWV measured outside the central column at the upper (carotid-radial PWV) or lower limb (femoral-tibial PWV) has shown little predictive value for future cardiovascular events ADDIN EN.CITE <EndNote><Cite><Author>Pannier B</Author><Year>2005</Year><RecNum>3257</RecNum><DisplayText>[41]</DisplayText><record><rec-number>3257</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3257</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Pannier B, Guerin AP, Marchais SJ, Safar ME, London G.</author></authors></contributors><titles><title>Stiffness of capacitive and conduit arteries: prognostic signficance for end-stage renal disease patients</title><secondary-title>Hypertension</secondary-title></titles><periodical><full-title>Hypertension</full-title></periodical><pages>592-596</pages><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[41] but still represents a valid assessment of regional stiffness ADDIN EN.CITE <EndNote><Cite><Author>McLeod AL</Author><Year>2004</Year><RecNum>3258</RecNum><DisplayText>[42]</DisplayText><record><rec-number>3258</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3258</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>McLeod AL, Uren NG, Wilkinson IB, et al.</author></authors></contributors><titles><title>Non-invasive measures of pulse wave velocity correlate with coronary artery plaque load in humans</title><secondary-title>Journal of Hypertension</secondary-title></titles><periodical><full-title>Journal of Hypertension</full-title></periodical><dates><year>2004</year></dates><urls></urls></record></Cite></EndNote>[42]. In addition to PWV, arterial stiffness can be assessed through arterial compliance and distensibility as well as augmentation index. Arterial compliance and distensibility may reflect functional changes to the arterial wall that precede structural changes PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IYWx1c2thPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48
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ADDIN EN.CITE.DATA [43]. Furthermore, augmentation index, defined as the proportion of central PP due to the late systolic peak, has been shown to be positively correlated with central PWV in clinical populations (r=0.29 p<0.005) ADDIN EN.CITE <EndNote><Cite><Author>Brown</Author><Year>1999</Year><RecNum>3491</RecNum><DisplayText>[44]</DisplayText><record><rec-number>3491</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3491</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Brown, MJ</author></authors></contributors><titles><title>Similarities and differences between augmentation index and pulse wave velocity in the assessment of arterial stiffness</title><secondary-title>Qjm</secondary-title></titles><periodical><full-title>Qjm</full-title></periodical><pages>595-600</pages><volume>92</volume><number>10</number><dates><year>1999</year></dates><isbn>1460-2725</isbn><urls></urls></record></Cite></EndNote>[44].1.1.7Measuring PWVPWV is routinely measured using the foot-to-foot velocity method from peripheral pressure waveforms [16]. These waveforms are usually obtained at the sites of the right common carotid artery and the right common femoral artery. The foot of the wave is defined at the end of the diastolic phase during the cardiac cycle, when the steep rise of the pressure wavefront begins (Fig. 1). The transit time (Δt) is the time of travel of the foot of the wave over a known distance ADDIN EN.CITE <EndNote><Cite><Author>Laurent</Author><Year>2006</Year><RecNum>3256</RecNum><DisplayText>[40]</DisplayText><record><rec-number>3256</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3256</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laurent, S., Cockcroft, J., Van Bortel, L., et al.</author></authors></contributors><titles><title>Expert consensus document on arterial stiffness: methodological issues and clinical application</title><secondary-title>European Heart Journal</secondary-title></titles><periodical><full-title>European Heart Journal</full-title></periodical><pages>2588-2605</pages><volume>27</volume><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>[40]. The time delay between the arrival of the wave from the carotid artery to the femoral artery is measured between the feet of the two waveforms (Fig. 1) ADDIN EN.CITE <EndNote><Cite><Author>Laurent</Author><Year>2006</Year><RecNum>3256</RecNum><DisplayText>[40]</DisplayText><record><rec-number>3256</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3256</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laurent, S., Cockcroft, J., Van Bortel, L., et al.</author></authors></contributors><titles><title>Expert consensus document on arterial stiffness: methodological issues and clinical application</title><secondary-title>European Heart Journal</secondary-title></titles><periodical><full-title>European Heart Journal</full-title></periodical><pages>2588-2605</pages><volume>27</volume><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>[40]. Pressure waves can also be recorded from different sites, Figure 1. Measurement of carotid-femoral PWV with the foot to foot method. and transit time calculated using an electrocardiogram. The distance covered by the waves is identified as the surface distance (D) between the two recording sites. It is critical for the distance component used in PWV calculations to be measured precisely as small inaccuracies can obscure the absolute value of PWV ADDIN EN.CITE <EndNote><Cite><Author>Chiu</Author><Year>1991</Year><RecNum>3259</RecNum><DisplayText>[45]</DisplayText><record><rec-number>3259</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3259</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Chiu, Y. C.</author><author>Arand, P. W.</author><author>Shroff, S. G.</author><author>Feldman, T.</author><author>Carroll, J. D.</author></authors></contributors><auth-address>Department of Medicine, University of Chicago Hospital, IL 60637.</auth-address><titles><title>Determination of pulse wave velocities with computerized algorithms</title><secondary-title>Am Heart J</secondary-title><alt-title>American heart journal</alt-title></titles><periodical><full-title>Am Heart J</full-title></periodical><alt-periodical><full-title>American Heart Journal</full-title></alt-periodical><pages>1460-70</pages><volume>121</volume><number>5</number><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>*Algorithms</keyword><keyword>Aorta, Abdominal/physiology</keyword><keyword>Aorta, Thoracic/physiology</keyword><keyword>Blood Flow Velocity/physiology</keyword><keyword>Blood Pressure/physiology</keyword><keyword>Cardiac Catheterization</keyword><keyword>Cardiomyopathy, Dilated/physiopathology</keyword><keyword>Coronary Disease/physiopathology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Pulsatile Flow/*physiology</keyword><keyword>Transducers, Pressure</keyword><keyword>Vascular Resistance/physiology</keyword></keywords><dates><year>1991</year><pub-dates><date>May</date></pub-dates></dates><isbn>0002-8703 (Print)
0002-8703 (Linking)</isbn><accession-num>2017978</accession-num><urls><related-urls><url>;[45] and the shorter the distance between two sites of interest, the greater the absolute error in determining the transit time. There are various measurement techniques that investigators have historically recommended, including the subtraction of the distance from the carotid location to the sternal notch from the distance between the sternal notch and the femoral site of measurement ADDIN EN.CITE <EndNote><Cite><Author>Van der Heijden-Spek</Author><Year>2000</Year><RecNum>3260</RecNum><DisplayText>[46]</DisplayText><record><rec-number>3260</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3260</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Van der Heijden-Spek, J.J., Staessen, J.A., Fagard, R.H., Hoeks, A.P., Boudier, H.A., Van Bortel, L.M.</author></authors></contributors><titles><title>Effect of age on brachial artery wall properties differs from the aorta and is gender dependent: a population study.</title><secondary-title>Hypertension</secondary-title></titles><periodical><full-title>Hypertension</full-title></periodical><pages>637-642</pages><volume>35</volume><dates><year>2000</year></dates><urls></urls></record></Cite></EndNote>[46]. The distance measurement procedure is unimportant provided that the study is interventional in nature with repeated measures using consistent and reproducible methods. However, when comparing various populations or performing a descriptive or observational study, it is critical that a consistent measuring technique be employed ADDIN EN.CITE <EndNote><Cite><Author>Laurent</Author><Year>2006</Year><RecNum>3256</RecNum><DisplayText>[40]</DisplayText><record><rec-number>3256</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3256</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laurent, S., Cockcroft, J., Van Bortel, L., et al.</author></authors></contributors><titles><title>Expert consensus document on arterial stiffness: methodological issues and clinical application</title><secondary-title>European Heart Journal</secondary-title></titles><periodical><full-title>European Heart Journal</full-title></periodical><pages>2588-2605</pages><volume>27</volume><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>[40]. 1.1.8Exercise and arterial stiffnessStudies have shown that both older men and postmenopausal women who performed endurance exercise training demonstrated lower levels of aortic PWV than their sedentary peers PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5WYWl0a2V2aWNpdXM8L0F1dGhvcj48WWVhcj4xOTkzPC9Z
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ADDIN EN.CITE.DATA [38, 47]. As the effects of exercise training were observed only on the central elastic arteries and not the peripheral muscular artery, mechanical or local factors may have interacted with structural or functional mechanisms to improve arterial compliance. When 3 months of endurance exercise were prescribed to postmenopausal women with elevated SBP, only small reductions of aortic PWV occurred, potentially due to the fact that arteries that have been exposed to chronically elevated blood pressure are less susceptible to exercise adaptations. Compared to adults that are recreationally active, clinically healthy young adult obese men (30 ± 8 yrs) have been shown to have increased aortic cross-sectional area and decreased aortic compliance ADDIN EN.CITE <EndNote><Cite><Author>Danias</Author><Year>2003</Year><RecNum>3269</RecNum><DisplayText>[48]</DisplayText><record><rec-number>3269</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3269</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Danias, P. G.</author><author>Tritos, N. A.</author><author>Stuber, M.</author><author>Botnar, R. M.</author><author>Kissinger, K. V.</author><author>Manning, W. J.</author></authors></contributors><auth-address>Cardiovascular, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. pdanias@caregroup.harvard.edu</auth-address><titles><title>Comparison of aortic elasticity determined by cardiovascular magnetic resonance imaging in obese versus lean adults</title><secondary-title>Am J Cardiol</secondary-title><alt-title>The American journal of cardiology</alt-title></titles><periodical><full-title>Am J Cardiol</full-title></periodical><alt-periodical><full-title>The American journal of cardiology</full-title></alt-periodical><pages>195-9</pages><volume>91</volume><number>2</number><keywords><keyword>Adult</keyword><keyword>Aorta, Abdominal/anatomy & histology/*physiology</keyword><keyword>Aorta, Thoracic/anatomy & histology/*physiology</keyword><keyword>Body Mass Index</keyword><keyword>Case-Control Studies</keyword><keyword>Cross-Sectional Studies</keyword><keyword>Elasticity</keyword><keyword>Humans</keyword><keyword>*Magnetic Resonance Imaging</keyword><keyword>Male</keyword><keyword>Obesity/pathology/*physiopathology</keyword></keywords><dates><year>2003</year><pub-dates><date>Jan 15</date></pub-dates></dates><isbn>0002-9149 (Print)
0002-9149 (Linking)</isbn><accession-num>12521634</accession-num><urls><related-urls><url>;[48]. Previous literature is not consistent with respect to the impact of obesity on arterial stiffness in adults; obese subjects are expected to have a larger stroke volume and cardiac output as a result of a larger body size, and this increased stroke volume could influence arterial compliance. However, in a study conducted by Danias et al., obese adults had elevated SBP which may be the underlying cause for decreased arterial compliance as the chronically elevated blood pressure could change the elastic lamella to more collagenous in nature. Lack of PA is the second leading behavioural cause of death in the USA, following only tobacco use ADDIN EN.CITE <EndNote><Cite><Author>Mokdad</Author><Year>2004</Year><RecNum>3270</RecNum><DisplayText>[49]</DisplayText><record><rec-number>3270</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3270</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Mokdad, A. H.</author><author>Marks, J. S.</author><author>Stroup, D. F.</author><author>Gerberding, J. L.</author></authors></contributors><auth-address>Division of Adult and Community Health, Centers for Disease Control and Prevention, Atlanta, Ga, USA. amokdad@</auth-address><titles><title>Actual causes of death in the United States, 2000</title><secondary-title>JAMA</secondary-title><alt-title>JAMA : the journal of the American Medical Association</alt-title></titles><alt-periodical><full-title>JAMA : the journal of the American Medical Association</full-title></alt-periodical><pages>1238-45</pages><volume>291</volume><number>10</number><keywords><keyword>Accidents, Traffic/mortality</keyword><keyword>Alcohol Drinking</keyword><keyword>Cause of Death/*trends</keyword><keyword>Communicable Diseases/mortality</keyword><keyword>Diet</keyword><keyword>Humans</keyword><keyword>Physical Fitness</keyword><keyword>Poisoning/mortality</keyword><keyword>Risk Factors</keyword><keyword>Sexual Behavior</keyword><keyword>Smoking/mortality</keyword><keyword>Substance-Related Disorders</keyword><keyword>United States/epidemiology</keyword><keyword>Wounds, Gunshot/mortality</keyword></keywords><dates><year>2004</year><pub-dates><date>Mar 10</date></pub-dates></dates><isbn>1538-3598 (Electronic)
0098-7484 (Linking)</isbn><accession-num>15010446</accession-num><urls><related-urls><url>;[49] and the aforementioned research has demonstrated some links between increases in PA and decreases in arterial stiffness. Despite these known benefits of PA, recent data have shown that moderate-to-vigorous PA (MVPA) levels decline from childhood to adulthood PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Ucm9pYW5vPC9BdXRob3I+PFllYXI+MjAwODwvWWVhcj48
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ADDIN EN.CITE.DATA [50], and that sedentary time may also be an important determinant of CVD risk independent of PA ADDIN EN.CITE <EndNote><Cite><Author>Warren</Author><Year>2010</Year><RecNum>3493</RecNum><DisplayText>[51, 52]</DisplayText><record><rec-number>3493</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3493</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Warren, Tatiana Y</author><author>Barry, Vaughn</author><author>Hooker, Steven P</author><author>Sui, Xuemei</author><author>Church, Timothy S</author><author>Blair, Steven N</author></authors></contributors><titles><title>Sedentary behaviors increase risk of cardiovascular disease mortality in men</title><secondary-title>Medicine and science in sports and exercise</secondary-title></titles><periodical><full-title>Medicine and Science in Sports and Exercise</full-title></periodical><pages>879</pages><volume>42</volume><number>5</number><dates><year>2010</year></dates><urls></urls></record></Cite><Cite><Author>Dunstan</Author><Year>2010</Year><RecNum>3495</RecNum><record><rec-number>3495</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3495</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Dunstan, DW</author><author>Barr, ELM</author><author>Healy, GN</author><author>Salmon, J</author><author>Shaw, JE</author><author>Balkau, Beverley</author><author>Magliano, DJ</author><author>Cameron, AJ</author><author>Zimmet, PZ</author><author>Owen, N</author></authors></contributors><titles><title>Television viewing time and mortality the australian diabetes, obesity and lifestyle study (AusDiab)</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>384-391</pages><volume>121</volume><number>3</number><dates><year>2010</year></dates><isbn>0009-7322</isbn><urls></urls></record></Cite></EndNote>[51, 52]. A recent study demonstrated that increased sitting time per weekend day, but not per weekday, was positively associated with elevated arterial stiffness, body fat, and resting heart rate in both males and females aged 31.4 ± 3.6 PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IdXluaDwvQXV0aG9yPjxZZWFyPjIwMTQ8L1llYXI+PFJl
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ADDIN EN.CITE.DATA [53]. Furthermore, the Canada Fitness Survey ADDIN EN.CITE <EndNote><Cite><Author>Katzmarzyk</Author><Year>2001</Year><RecNum>3272</RecNum><DisplayText>[54]</DisplayText><record><rec-number>3272</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3272</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Katzmarzyk, P. T.</author><author>Craig, C. L.</author><author>Bouchard, C.</author></authors></contributors><auth-address>School of Kinesiology and Health Science, York University, 4700 Keele St., Ontario, M3J 1P3, North York, Canada. katzmarz@yorku.ca</auth-address><titles><title>Original article underweight, overweight and obesity: relationships with mortality in the 13-year follow-up of the Canada Fitness Survey</title><secondary-title>J Clin Epidemiol</secondary-title><alt-title>Journal of clinical epidemiology</alt-title></titles><alt-periodical><full-title>Journal of Clinical Epidemiology</full-title></alt-periodical><pages>916-20</pages><volume>54</volume><number>9</number><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Canada/epidemiology</keyword><keyword>Female</keyword><keyword>*Health Surveys</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Obesity/etiology/*mortality</keyword><keyword>Proportional Hazards Models</keyword><keyword>Risk Factors</keyword><keyword>Sex Distribution</keyword></keywords><dates><year>2001</year><pub-dates><date>Sep</date></pub-dates></dates><isbn>0895-4356 (Print)
0895-4356 (Linking)</isbn><accession-num>11520651</accession-num><urls><related-urls><url>;[54] showed that adults aged 18-90 years had a hazard ratio of 1.54 for both CVD-related and all-cause mortality when greater than ? of their time was spent in the sedentary state. CVD-related mortality hazard ratio is nearly doubled when greater than 4h/day is spent watching TV. 1.1.9Arterial compliance and distensibilityArterial compliance can be defined as the absolute diameter change for a given pressure change at a controlled length ADDIN EN.CITE <EndNote><Cite><Author>O'Rourke</Author><Year>2002</Year><RecNum>3262</RecNum><DisplayText>[55]</DisplayText><record><rec-number>3262</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3262</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Rourke, M. F.</author><author>Staessen, J. A.</author><author>Vlachopoulos, C.</author><author>Duprez, D.</author><author>Plante, G. E.</author></authors></contributors><auth-address>St Vincent's Hospital/UNSW and St Vincent's Clinic, Sydney, Australia. m.orourke@unsw.edu.au</auth-address><titles><title>Clinical applications of arterial stiffness; definitions and reference values</title><secondary-title>Am J Hypertens</secondary-title><alt-title>American journal of hypertension</alt-title></titles><periodical><full-title>Am J Hypertens</full-title></periodical><alt-periodical><full-title>American Journal of Hypertension</full-title></alt-periodical><pages>426-44</pages><volume>15</volume><number>5</number><keywords><keyword>Arteries/*physiopathology</keyword><keyword>Elasticity</keyword><keyword>Humans</keyword><keyword>*Models, Cardiovascular</keyword><keyword>Reference Values</keyword><keyword>Terminology as Topic</keyword></keywords><dates><year>2002</year><pub-dates><date>May</date></pub-dates></dates><isbn>0895-7061 (Print)
0895-7061 (Linking)</isbn><accession-num>12022246</accession-num><urls><related-urls><url>;[55], while arterial distensibility is the relative diameter change for a given pressure change ADDIN EN.CITE <EndNote><Cite><Author>O'Rourke</Author><Year>2002</Year><RecNum>3262</RecNum><DisplayText>[55]</DisplayText><record><rec-number>3262</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3262</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Rourke, M. F.</author><author>Staessen, J. A.</author><author>Vlachopoulos, C.</author><author>Duprez, D.</author><author>Plante, G. E.</author></authors></contributors><auth-address>St Vincent's Hospital/UNSW and St Vincent's Clinic, Sydney, Australia. m.orourke@unsw.edu.au</auth-address><titles><title>Clinical applications of arterial stiffness; definitions and reference values</title><secondary-title>Am J Hypertens</secondary-title><alt-title>American journal of hypertension</alt-title></titles><periodical><full-title>Am J Hypertens</full-title></periodical><alt-periodical><full-title>American Journal of Hypertension</full-title></alt-periodical><pages>426-44</pages><volume>15</volume><number>5</number><keywords><keyword>Arteries/*physiopathology</keyword><keyword>Elasticity</keyword><keyword>Humans</keyword><keyword>*Models, Cardiovascular</keyword><keyword>Reference Values</keyword><keyword>Terminology as Topic</keyword></keywords><dates><year>2002</year><pub-dates><date>May</date></pub-dates></dates><isbn>0895-7061 (Print)
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ADDIN EN.CITE.DATA [43]. The age-associated changes in arterial compliance have been studied extensively PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5HYXJkbmVyPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48
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Tm90ZT5=
ADDIN EN.CITE PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5HYXJkbmVyPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48
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ADDIN EN.CITE.DATA [56, 57]. Arterial distensibility of the common carotid artery increases in children, adolescents, and young adults, plateaus near age 30, and begins to decline beyond 30 years of age in those who do not present with risk factors for CVD PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5HYXJkbmVyPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48
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ADDIN EN.CITE.DATA [59]. In fact, in younger adults, arterial compliance can be increased through PA interventions as brief as one week in duration [59]. These improvements in compliance are, however, likely due to acute residual effects from the preceding exercise bout and not from structural changes to the arteries PEVuZE5vdGU+PENpdGU+PEF1dGhvcj52YW4gZGUgTGFhcjwvQXV0aG9yPjxZZWFyPjIwMTE8L1ll
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ADDIN EN.CITE.DATA [59]. As arterial changes occur with advancing age PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5HYXJkbmVyPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48
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ADDIN EN.CITE PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5HYXJkbmVyPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48
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ADDIN EN.CITE.DATA [56], the acute effects of exercise in young adults are not necessarily similar in older adults. More recently, Nickel and colleagues showed that 30 mins of exercise at 50% of heart rate reserve in adults over the age of 60 (n=32) resulted in transient increases in carotid arterial compliance for up to 30 mins post exercise. This effect was diminished however after the 30 min mark PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5OaWNrZWw8L0F1dGhvcj48WWVhcj4yMDExPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [60]. The influence of inflammatory markers on arterial compliance has also been recently documented in young asymptomatic adults. It was discovered that increased levels of c-reactive protein (CRP), an indicator of systemic inflammation, were inversely correlated with large artery compliance ADDIN EN.CITE <EndNote><Cite><Author>Nakhai-Pour</Author><Year>2007</Year><RecNum>3295</RecNum><DisplayText>[61]</DisplayText><record><rec-number>3295</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3295</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nakhai-Pour HR, Grobbee DE, Bots ML, Muller M, van der Schouw YT</author></authors></contributors><titles><title>C-reactive protein and aortic stiffness and wave reflection in middle-aged and elderly men from the community</title><secondary-title>Journal of Human Hypertension</secondary-title></titles><periodical><full-title>Journal of Human Hypertension</full-title></periodical><pages>949-955</pages><volume>21</volume><dates><year>2007</year></dates><urls></urls></record></Cite></EndNote>[61]. However, this relationship was no longer significant after adjusting for age. Whether this response is evident in elderly, clinical, or less-functional patients warrants further investigation. The bioavailability of nitric oxide (NO) may also impact arterial stiffness as studies have shown that NO inhibition results in an increase in aortic PWV that was attributed to increases in blood pressure rather than a specific effect of nitric oxide synthase (NOS) inhibition on the elastic arterial wall ADDIN EN.CITE <EndNote><Cite><Author>Stewart</Author><Year>2003</Year><RecNum>3297</RecNum><DisplayText>[62]</DisplayText><record><rec-number>3297</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3297</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Stewart, A. D.</author><author>Millasseau, S. C.</author><author>Kearney, M. T.</author><author>Ritter, J. M.</author><author>Chowienczyk, P. J.</author></authors></contributors><auth-address>Department of Clinical Pharmacology, St Thomas' Hospital, King's College, London, UK.</auth-address><titles><title>Effects of inhibition of basal nitric oxide synthesis on carotid-femoral pulse wave velocity and augmentation index in humans</title><secondary-title>Hypertension</secondary-title><alt-title>Hypertension</alt-title></titles><periodical><full-title>Hypertension</full-title></periodical><alt-periodical><full-title>Hypertension</full-title></alt-periodical><pages>915-8</pages><volume>42</volume><number>5</number><keywords><keyword>Adult</keyword><keyword>Carotid Arteries/*physiology</keyword><keyword>Elasticity</keyword><keyword>Enzyme Inhibitors/pharmacology</keyword><keyword>Femoral Artery/*physiology</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Nitric Oxide/*antagonists & inhibitors/biosynthesis</keyword><keyword>Nitric Oxide Synthase/antagonists & inhibitors</keyword><keyword>Pulsatile Flow/drug effects</keyword><keyword>omega-N-Methylarginine/pharmacology</keyword></keywords><dates><year>2003</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>1524-4563 (Electronic)
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ADDIN EN.CITE.DATA [63]. It is possible that the lack of change in pulse pressure and the reduced smooth muscle content in the central elastic arteries were linked to the absence of reduced compliance with NOS inhibition in this young healthy population. 1.1.10Measurement of carotid compliance and distensibilityCompliance of the common carotid artery is often assessed as it is one of the main branches from the aorta and is thus indicative of central elastic stiffness and compliance ADDIN EN.CITE <EndNote><Cite><Author>tanaka</Author><Year>2005</Year><RecNum>3267</RecNum><DisplayText>[8, 64]</DisplayText><record><rec-number>3267</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3267</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Tanaka, H. and Safar ME</author></authors></contributors><titles><title>Influence of lifestyle modification on arterial stiffness and wave reflections</title><secondary-title>American Journal of Hypertension</secondary-title></titles><periodical><full-title>American Journal of Hypertension</full-title></periodical><pages>137-144</pages><dates><year>2005</year></dates><urls></urls></record></Cite><Cite><Author>Tanaka H</Author><Year>2000</Year><RecNum>3301</RecNum><record><rec-number>3301</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3301</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Tanaka H, Dinenno FA, Monahan KD, Clevenger CM, DeSouza CA, Seals DR. </author></authors></contributors><titles><title>Aging, habitual exercise, and dynamic arterial compliance</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>1270-1275</pages><volume>102</volume><dates><year>2000</year></dates><urls></urls></record></Cite></EndNote>[8, 64]. Direct assessment of common carotid compliance or distensibility can be conducted using combination of B-mode ultrasound imaging and applanation tonometry of the contralateral common carotid artery. Ultrasound images provide a distinct assessment of the change in lumen diameter throughout the cardiac cycle by quantifying the increase in arterial diameter that occurs during systole. The lumen diameter is dependent on the local distending arterial pressure, which is responsible for driving the change in diameter. Assessment of local blood pressure is commonly performed using a hand-held tonometer PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5TdWdhd2FyYTwvQXV0aG9yPjxZZWFyPjIwMTQ8L1llYXI+
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ADDIN EN.CITE.DATA [63] over the point of greatest pulsation of the common carotid artery. Carotid applanation tonometry has been validated against invasive blood pressure measurements, such as the invasive pressure measurement linked to catheterization ADDIN EN.CITE <EndNote><Cite><Author>Van Bortel</Author><Year>2001</Year><RecNum>3302</RecNum><DisplayText>[65]</DisplayText><record><rec-number>3302</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3302</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Van Bortel, L. M.</author><author>Balkestein, E. J.</author><author>van der Heijden-Spek, J. J.</author><author>Vanmolkot, F. H.</author><author>Staessen, J. A.</author><author>Kragten, J. A.</author><author>Vredeveld, J. W.</author><author>Safar, M. E.</author><author>Struijker Boudier, H. A.</author><author>Hoeks, A. P.</author></authors></contributors><auth-address>Department of Pharmacology, Maastricht University, The Netherlands. luc.vanbortel@rug.ac.be</auth-address><titles><title>Non-invasive assessment of local arterial pulse pressure: comparison of applanation tonometry and echo-tracking</title><secondary-title>J Hypertens</secondary-title><alt-title>Journal of hypertension</alt-title></titles><periodical><full-title>J Hypertens</full-title></periodical><alt-periodical><full-title>Journal of Hypertension</full-title></alt-periodical><pages>1037-44</pages><volume>19</volume><number>6</number><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Arteries/*physiology/*ultrasonography</keyword><keyword>Blood Pressure/*physiology</keyword><keyword>*Diagnostic Techniques, Cardiovascular</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Pulsatile Flow</keyword></keywords><dates><year>2001</year><pub-dates><date>Jun</date></pub-dates></dates><isbn>0263-6352 (Print)
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ADDIN EN.CITE.DATA [63]. Using several consecutive heart cycles, minimum and maximum carotid artery diameters are determined from the ultrasound images and the following equation is used to calculate distensibility ADDIN EN.CITE <EndNote><Cite><Author>O'Rourke</Author><Year>2002</Year><RecNum>3262</RecNum><DisplayText>[55]</DisplayText><record><rec-number>3262</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3262</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Rourke, M. F.</author><author>Staessen, J. A.</author><author>Vlachopoulos, C.</author><author>Duprez, D.</author><author>Plante, G. E.</author></authors></contributors><auth-address>St Vincent's Hospital/UNSW and St Vincent's Clinic, Sydney, Australia. m.orourke@unsw.edu.au</auth-address><titles><title>Clinical applications of arterial stiffness; definitions and reference values</title><secondary-title>Am J Hypertens</secondary-title><alt-title>American journal of hypertension</alt-title></titles><periodical><full-title>Am J Hypertens</full-title></periodical><alt-periodical><full-title>American Journal of Hypertension</full-title></alt-periodical><pages>426-44</pages><volume>15</volume><number>5</number><keywords><keyword>Arteries/*physiopathology</keyword><keyword>Elasticity</keyword><keyword>Humans</keyword><keyword>*Models, Cardiovascular</keyword><keyword>Reference Values</keyword><keyword>Terminology as Topic</keyword></keywords><dates><year>2002</year><pub-dates><date>May</date></pub-dates></dates><isbn>0895-7061 (Print)
0895-7061 (Linking)</isbn><accession-num>12022246</accession-num><urls><related-urls><url>;[55]:Distensibility=π (dmax2)2- π dmin22π(dmin2)2 x PPWhere dmax is the maximal lumen diameter, dmin is the minimum diameter, and PP is the carotid pulse pressure. PP is responsible for the change in artery cross sectional area.1.1.11Vascular endotheliumHistorically, the vascular endothelium was thought to be simply a passive lining of epithelial cells separating the vascular media layer from the flowing blood ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13]. It has since become apparent that the endothelium produces chemical substances that are designed to maintain homeostasis through elements that act on the intimal surface and on the vascular smooth muscle cells in the media ADDIN EN.CITE <EndNote><Cite><Author>Celermajer</Author><Year>1997</Year><RecNum>3395</RecNum><DisplayText>[66]</DisplayText><record><rec-number>3395</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3395</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Celermajer, David S</author></authors></contributors><titles><title>Endothelial dysfunction: does it matter? Is it reversible?</title><secondary-title>Journal of the American College of Cardiology</secondary-title></titles><periodical><full-title>Journal of the American College of Cardiology</full-title></periodical><pages>325-333</pages><volume>30</volume><number>2</number><dates><year>1997</year></dates><isbn>0735-1097</isbn><urls></urls></record></Cite></EndNote>[66]. In the endothelium, NO is produced from L-arginine through the activity of the enzyme NOS. Under normal resting conditions, NO is continually released from endothelial cells where it diffuses to the media layer and stimulates relaxation of smooth muscle cells and maintains vascular distensibility. Basal NO mediated vascular smooth muscle relaxation is most active in systemic arteries and less so in resistive arterioles ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13]. Endothelial shear stress and acetylcholine both stimulate the release of NO from the endothelium PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QeWtlPC9BdXRob3I+PFllYXI+MjAwNDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [67] and the magnitude of shear stress, inversely related to diameter, is commonly presented as systolic (peak), mean, or diastolic stress ADDIN EN.CITE <EndNote><Cite><Author>Dammers</Author><Year>2003</Year><RecNum>3398</RecNum><DisplayText>[68]</DisplayText><record><rec-number>3398</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3398</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Dammers, Ruben</author><author>Stifft, Frank</author><author>Tordoir, Jan HM</author><author>Hameleers, Jeroen MM</author><author>Hoeks, Arnold PG</author><author>Kitslaar, Peter JEHM</author></authors></contributors><titles><title>Shear stress depends on vascular territory: comparison between common carotid and brachial artery</title><secondary-title>Journal of Applied Physiology</secondary-title></titles><periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></periodical><pages>485-489</pages><volume>94</volume><number>2</number><dates><year>2003</year></dates><isbn>8750-7587</isbn><urls></urls></record></Cite></EndNote>[68]. To avoid errors in shear stress recording, velocity and diameter must be measured at the same location and during the same phase of the cardiac cycle ADDIN EN.CITE <EndNote><Cite><Author>O’Rourke</Author><Year>2004</Year><RecNum>3400</RecNum><DisplayText>[69]</DisplayText><record><rec-number>3400</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3400</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O’Rourke, Michael F</author><author>Nichols, Wilmer W</author></authors></contributors><titles><title>Shear stress and flow-mediated dilation</title><secondary-title>Hypertension</secondary-title></titles><periodical><full-title>Hypertension</full-title></periodical><pages>119-120</pages><volume>44</volume><number>2</number><dates><year>2004</year></dates><isbn>0194-911X</isbn><urls></urls></record></Cite></EndNote>[69].1.1.12Endothelial function/dysfunctionEndothelial function is optimal in the young and in those who are disease free and progressive deteriorations are observed with aging. Age-related decreases in endothelial function can be attributed to a thickening of the endothelial layer that is a result of endothelial cell hyperplasia and thickening of the lamina membrane that separates the intimal layer from the medial layer. Decreases in endothelial function may also be related to the degradation of the gaseous NO when required to travel a greater distance before reaching its activation site in the vascular smooth muscle ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[13]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[13]. These pathological processes are further expressed in atherosclerosis, when the distance between the endothelium and medial site is further increased by the deposition of atherosclerotic plaques. Endothelial dysfunction is prevalent in persons with risk factors for atherosclerosis, including hypertension, hypercholesterolemia, and obesity ADDIN EN.CITE <EndNote><Cite><Author>Celermajer</Author><Year>1997</Year><RecNum>3396</RecNum><DisplayText>[66, 70]</DisplayText><record><rec-number>3396</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3396</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Celermajer, David S</author></authors></contributors><titles><title>Endothelial dysfunction: does it matter? Is it reversible?</title><secondary-title>Journal of the American College of Cardiology</secondary-title></titles><periodical><full-title>Journal of the American College of Cardiology</full-title></periodical><pages>325-333</pages><volume>30</volume><number>2</number><dates><year>1997</year></dates><isbn>0735-1097</isbn><urls></urls></record></Cite><Cite><Author>Bonetti</Author><Year>2003</Year><RecNum>3402</RecNum><record><rec-number>3402</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3402</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bonetti, Piero O</author><author>Lerman, Lilach O</author><author>Lerman, Amir</author></authors></contributors><titles><title>Endothelial dysfunction a marker of atherosclerotic risk</title><secondary-title>Arteriosclerosis, thrombosis, and vascular biology</secondary-title></titles><periodical><full-title>Arteriosclerosis, Thrombosis, and Vascular Biology</full-title></periodical><pages>168-175</pages><volume>23</volume><number>2</number><dates><year>2003</year></dates><isbn>1079-5642</isbn><urls></urls></record></Cite></EndNote>[66, 70]. Impaired endothelial function is evident prior to the appearance of coronary atherosclerosis and has therefore been suggested as a valuable tool for early detection of CVD. Endothelial dysfunction is linked to the pathophysiology of atherosclerosis through the promotion of the adherence of monocytes and lipoproteins to the arterial wall, entry into the wall, and the inflammatory response and subsequent lipid deposition. Furthermore, studies have confirmed a distinct correlation between measurements of peripheral vascular endothelial dysfunction in the brachial artery and coronary atherosclerosis ADDIN EN.CITE <EndNote><Cite><Author>Anderson</Author><Year>1995</Year><RecNum>3404</RecNum><DisplayText>[66, 71]</DisplayText><record><rec-number>3404</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3404</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Anderson, Todd J</author><author>Uehata, Akimi</author><author>Gerhard, Marie D</author><author>Meredith, Ian T</author><author>Knab, Sarah</author><author>Delagrange, Danielle</author><author>Lieberman, Eric H</author><author>Ganz, Peter</author><author>Creager, Mark A</author><author>Yeung, Alan C</author></authors></contributors><titles><title>Close relation of endothelial function in the human coronary and peripheral circulations</title><secondary-title>Journal of the American College of Cardiology</secondary-title></titles><periodical><full-title>Journal of the American College of Cardiology</full-title></periodical><pages>1235-1241</pages><volume>26</volume><number>5</number><dates><year>1995</year></dates><isbn>0735-1097</isbn><urls></urls></record></Cite><Cite><Author>Celermajer</Author><Year>1997</Year><RecNum>3396</RecNum><record><rec-number>3396</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3396</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Celermajer, David S</author></authors></contributors><titles><title>Endothelial dysfunction: does it matter? Is it reversible?</title><secondary-title>Journal of the American College of Cardiology</secondary-title></titles><periodical><full-title>Journal of the American College of Cardiology</full-title></periodical><pages>325-333</pages><volume>30</volume><number>2</number><dates><year>1997</year></dates><isbn>0735-1097</isbn><urls></urls></record></Cite></EndNote>[66, 71]. 1.1.13Measurement of endothelial function – flow-mediated vasodilationThe flow-mediated vasodilation (FMD) assessment was originally introduced by Celermajer et al. in 1992. It has now become the most widely used method to measure endothelial function in humans. This technique requires the dual recording of brachial arterial diameter and blood velocity at baseline and during reactive hyperemia. To establish a flow stimulus in the brachial artery, a blood pressure cuff is placed distal to the antecubital fossa, and is inflated to at least 50 mmHg above systolic pressure to occlude arterial inflow for a standardized length of time, usually 5 minutes ADDIN EN.CITE <EndNote><Cite><Author>Pyke</Author><Year>2008</Year><RecNum>3232</RecNum><DisplayText>[72]</DisplayText><record><rec-number>3232</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3232</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Pyke, K. E.</author><author>Hartnett, J. A.</author><author>Tschakovsky, M. E.</author></authors></contributors><auth-address>Queen's University, Kingston, Ontario, Canada.</auth-address><titles><title>Are the dynamic response characteristics of brachial artery flow-mediated dilation sensitive to the magnitude of increase in shear stimulus?</title><secondary-title>J Appl Physiol (1985)</secondary-title><alt-title>Journal of applied physiology</alt-title></titles><periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></periodical><alt-periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></alt-periodical><pages>282-92</pages><volume>105</volume><number>1</number><keywords><keyword>Adult</keyword><keyword>Blood Pressure/physiology</keyword><keyword>Brachial Artery/anatomy & histology/*physiology/ultrasonography</keyword><keyword>Electrocardiography</keyword><keyword>Endothelium, Vascular/physiology</keyword><keyword>Forearm/physiology</keyword><keyword>Heart Rate/physiology</keyword><keyword>Hot Temperature</keyword><keyword>Humans</keyword><keyword>Laser-Doppler Flowmetry</keyword><keyword>Male</keyword><keyword>Pressure</keyword><keyword>Vasodilation/*physiology</keyword></keywords><dates><year>2008</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>8750-7587 (Print)
0161-7567 (Linking)</isbn><accession-num>18467554</accession-num><urls><related-urls><url>;[72]. Prior to cuff inflation, a baseline rest image and velocity signal are recorded using Duplex mode ultrasonography ADDIN EN.CITE <EndNote><Cite><Author>Pyke</Author><Year>2008</Year><RecNum>3232</RecNum><DisplayText>[72]</DisplayText><record><rec-number>3232</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3232</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Pyke, K. E.</author><author>Hartnett, J. A.</author><author>Tschakovsky, M. E.</author></authors></contributors><auth-address>Queen's University, Kingston, Ontario, Canada.</auth-address><titles><title>Are the dynamic response characteristics of brachial artery flow-mediated dilation sensitive to the magnitude of increase in shear stimulus?</title><secondary-title>J Appl Physiol (1985)</secondary-title><alt-title>Journal of applied physiology</alt-title></titles><periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></periodical><alt-periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></alt-periodical><pages>282-92</pages><volume>105</volume><number>1</number><keywords><keyword>Adult</keyword><keyword>Blood Pressure/physiology</keyword><keyword>Brachial Artery/anatomy & histology/*physiology/ultrasonography</keyword><keyword>Electrocardiography</keyword><keyword>Endothelium, Vascular/physiology</keyword><keyword>Forearm/physiology</keyword><keyword>Heart Rate/physiology</keyword><keyword>Hot Temperature</keyword><keyword>Humans</keyword><keyword>Laser-Doppler Flowmetry</keyword><keyword>Male</keyword><keyword>Pressure</keyword><keyword>Vasodilation/*physiology</keyword></keywords><dates><year>2008</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>8750-7587 (Print)
0161-7567 (Linking)</isbn><accession-num>18467554</accession-num><urls><related-urls><url>;[72]. Thereafter, arterial occlusion is created by cuff inflation to a supra-systolic pressure that results in ischemia and consequent dilation of downstream resistance vessels. After a 5 minute occlusion period, subsequent cuff deflation results in a brief high-flow state (reactive hyperemia) to provide blood to the dilated vessels. The resulting increase in shear stress in the conduit artery (brachial) supplying the ischemic downstream tissue causes the brachial artery to dilate ADDIN EN.CITE <EndNote><Cite><Author>Anderson</Author><Year>1989</Year><RecNum>3408</RecNum><DisplayText>[73]</DisplayText><record><rec-number>3408</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3408</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Anderson, Erling A</author><author>Mark, Allyn L</author></authors></contributors><titles><title>Flow-mediated and reflex changes in large peripheral artery tone in humans</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>93-100</pages><volume>79</volume><number>1</number><dates><year>1989</year></dates><isbn>0009-7322</isbn><urls></urls></record></Cite></EndNote>[73]. Provided that a positive linear relationship exists between relative FMD and shear rate, normalization of the data is possible PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QeWtlPC9BdXRob3I+PFllYXI+MjAwNDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [67]. Normalization facilitates comparison of endothelial dependent FMD responses between groups differing in baseline diameter. Furthermore, it is important to adhere to statistical assumptions when normalizing FMD. If the relationship between shear rate and FMD is weak then normalization should not be applied. When normalized, the FMD/shear rate ratio has been used to distinguish reduced endothelial function in a population with moderate risk for CVD from that of low risk PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QYWRpbGxhPC9BdXRob3I+PFllYXI+MjAwOTwvWWVhcj48
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ADDIN EN.CITE.DATA [74]. Regardless, the FMD measurement technique and resulting values need to be standardized before the method becomes a part of routine clinical evaluation of CVD risk PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Lb3JrbWF6PC9BdXRob3I+PFllYXI+MjAwODwvWWVhcj48
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ADDIN EN.CITE.DATA [75].1.1.14Endothelial function and exerciseThere is an inverse relationship between the level of PA and cardiovascular events ADDIN EN.CITE <EndNote><Cite><Author>Haskell</Author><Year>2007</Year><RecNum>3458</RecNum><DisplayText>[76]</DisplayText><record><rec-number>3458</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3458</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Haskell, William L</author><author>Lee, I-Min</author><author>Pate, Russell R</author><author>Powell, Kenneth E</author><author>Blair, Steven N</author><author>Franklin, Barry A</author><author>Macera, Caroline A</author><author>Heath, Gregory W</author><author>Thompson, Paul D</author><author>Bauman, Adrian</author></authors></contributors><titles><title>Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>1081</pages><volume>116</volume><number>9</number><dates><year>2007</year></dates><urls></urls></record></Cite></EndNote>[76]. Improved endothelial function that is seen with exercise is due to increased expression of the enzyme NOS in response to increased endothelial shear stress as a result of increased blood flow that occurs during exercise ADDIN EN.CITE <EndNote><Cite><Author>Vita</Author><Year>2000</Year><RecNum>3412</RecNum><DisplayText>[77]</DisplayText><record><rec-number>3412</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3412</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Vita, Joseph A</author><author>Keaney Jr, John F</author></authors></contributors><titles><title>Exercise--toning up the endothelium?</title><secondary-title>The New England journal of medicine</secondary-title></titles><periodical><full-title>The New England journal of medicine</full-title></periodical><pages>503</pages><volume>342</volume><number>7</number><dates><year>2000</year></dates><isbn>0028-4793</isbn><urls></urls></record></Cite></EndNote>[77]. Consistent with this, previously sedentary middle (27 ± 1 yrs) and older (58 ± 2 yrs) aged men completing a 3-month at home exercise intervention increased endothelium dependent dilation by 30% ADDIN EN.CITE <EndNote><Cite><Author>DeSouza</Author><Year>2000</Year><RecNum>3498</RecNum><DisplayText>[78]</DisplayText><record><rec-number>3498</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3498</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>DeSouza, Christopher A</author><author>Shapiro, Linda F</author><author>Clevenger, Christopher M</author><author>Dinenno, Frank A</author><author>Monahan, Kevin D</author><author>Tanaka, Hirofumi</author><author>Seals, Douglas R</author></authors></contributors><titles><title>Regular aerobic exercise prevents and restores age-related declines in endothelium-dependent vasodilation in healthy men</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>1351-1357</pages><volume>102</volume><number>12</number><dates><year>2000</year></dates><isbn>0009-7322</isbn><urls></urls></record></Cite></EndNote>[78]. In young healthy men (mean 20 yrs), 10 weeks of combined aerobic and anaerobic exercise training increased endothelial dependent dilation by 77% ADDIN EN.CITE <EndNote><Cite><Author>Clarkson</Author><Year>1999</Year><RecNum>3515</RecNum><DisplayText>[79]</DisplayText><record><rec-number>3515</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3515</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Clarkson, Peter</author><author>Montgomery, Hugh E</author><author>Mullen, Michael J</author><author>Donald, Ann E</author><author>Powe, Amanda J</author><author>Bull, Teresa</author><author>Jubb, Michael</author><author>Deanfield, John E</author></authors></contributors><titles><title>Exercise training enhances endothelial function in young men</title><secondary-title>Journal of the American College of Cardiology</secondary-title></titles><periodical><full-title>Journal of the American College of Cardiology</full-title></periodical><pages>1379-1385</pages><volume>33</volume><number>5</number><dates><year>1999</year></dates><isbn>0735-1097</isbn><urls></urls></record></Cite></EndNote>[79]. Contrary to this, brachial artery FMD was not changed when recreationally active young adults were instructed to reduce PA for 5 days ADDIN EN.CITE <EndNote><Cite><Author>Boyle</Author><Year>2013</Year><RecNum>3502</RecNum><DisplayText>[80]</DisplayText><record><rec-number>3502</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3502</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Boyle, Leryn J</author><author>Credeur, Daniel P</author><author>Jenkins, Nathan T</author><author>Padilla, Jaume</author><author>Leidy, Heather J</author><author>Thyfault, John P</author><author>Fadel, Paul J</author></authors></contributors><titles><title>Impact of reduced daily physical activity on conduit artery flow-mediated dilation and circulating endothelial microparticles</title><secondary-title>Journal of Applied Physiology</secondary-title></titles><periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></periodical><pages>1519-1525</pages><volume>115</volume><number>10</number><dates><year>2013</year></dates><isbn>8750-7587</isbn><urls></urls></record></Cite></EndNote>[80] suggesting that previously active individuals can maintain endothelial function in the face of a brief period of reduced activity. Therefore the literature suggests that PA does have a beneficial role in both increasing and maintaining endothelial function in young, middle and older aged healthy men. Similarly, it was shown that 4 weeks of PA improved endothelial function in patients with coronary artery disease through the enzyme NOS ADDIN EN.CITE <EndNote><Cite><Author>Hambrecht</Author><Year>2003</Year><RecNum>3517</RecNum><DisplayText>[81]</DisplayText><record><rec-number>3517</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3517</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hambrecht, R</author><author>Adams, V</author><author>Erbs, S</author><author>Linke, A</author><author>Kr?nkel, N</author><author>Shu, Y</author><author>Baither, Y</author><author>Gielen, S</author><author>Thiele, H</author><author>Gummert, JF</author></authors></contributors><titles><title>Regular physical activity improves endothelial function in patients with coronary artery disease by increasing phosphorylation of endothelial nitric oxide synthase</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>3152-3158</pages><volume>107</volume><number>25</number><dates><year>2003</year></dates><isbn>0009-7322</isbn><urls></urls></record></Cite></EndNote>[81]. In contrast, PA in healthy children restores seasonal decreases in endothelial function to normative values but does not increase above those levels ADDIN EN.CITE <EndNote><Cite><Author>Hopkins</Author><Year>2011</Year><RecNum>3500</RecNum><DisplayText>[82]</DisplayText><record><rec-number>3500</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3500</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hopkins, Nicola Dominique</author><author>Stratton, Gareth</author><author>Tinken, Toni M</author><author>Ridgers, Nicola D</author><author>Graves, Lee E</author><author>McWhannell, Nicola</author><author>Cable, N Tim</author><author>Green, Daniel J</author></authors></contributors><titles><title>Seasonal reduction in physical activity and flow-mediated dilation in children</title><secondary-title>Medicine and science in sports and exercise</secondary-title></titles><periodical><full-title>Medicine and Science in Sports and Exercise</full-title></periodical><pages>232</pages><volume>43</volume><number>2</number><dates><year>2011</year></dates><isbn>0195-9131</isbn><urls></urls></record></Cite></EndNote>[82]. Thus it seems that increasing PA enhances endothelial function in young, middle, older, and in individuals with increased CVD risk. 1.2 OTHER CVD RISK FACTORS1.2.1Physical activityThe accurate assessment of PA is essential when examining the association between PA and health related outcomes. Self reports of PA are susceptible to inaccuracy as they rely on an individual’s ability to recall on previous activities ADDIN EN.CITE <EndNote><Cite><Author>Oliver</Author><Year>2007</Year><RecNum>18</RecNum><DisplayText>[83]</DisplayText><record><rec-number>18</rec-number><foreign-keys><key app="EN" db-id="rz959pfebrtpsrewtfnx9vxfsx0w9550pp0w">18</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Oliver, M.</author><author>Schofield, G. M.</author><author>Kolt, G. S.</author></authors></contributors><auth-address>Centre for Physical Activity and Nutrition Research, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland, New Zealand. melody.oliver@aut.ac.nz</auth-address><titles><title>Physical activity in preschoolers: understanding prevalence and measurement issues</title><secondary-title>Sports Med</secondary-title><alt-title>Sports medicine</alt-title></titles><pages>1045-70</pages><volume>37</volume><number>12</number><keywords><keyword>Child, Preschool</keyword><keyword>Energy Metabolism/physiology</keyword><keyword>*Epidemiologic Methods</keyword><keyword>*Exercise</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword></keywords><dates><year>2007</year></dates><isbn>0112-1642 (Print)
0112-1642 (Linking)</isbn><accession-num>18027993</accession-num><urls><related-urls><url>;[83]. The development of devices for the measurement of PA has allowed researchers to more accurately measure the entire range of activity, from sedentary to very vigorous behavior, over a number of days. Accelerometry has been validated as an objective method of assessing PA, and has become a highly reproducible measure for quantifying PA ADDIN EN.CITE <EndNote><Cite><Author>Trost</Author><Year>2005</Year><RecNum>3214</RecNum><DisplayText>[84]</DisplayText><record><rec-number>3214</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3214</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Trost, S. G.</author><author>McIver, K. L.</author><author>Pate, R. R.</author></authors></contributors><auth-address>Community Health Institute, Kansas State University, Manhattan, KS 66506, USA. strost@ksu.edu</auth-address><titles><title>Conducting accelerometer-based activity assessments in field-based research</title><secondary-title>Med Sci Sports Exerc</secondary-title><alt-title>Medicine and science in sports and exercise</alt-title></titles><periodical><full-title>Medicine & Science in Sports & Exercise</full-title><abbr-1>Med Sci Sports Exerc</abbr-1></periodical><alt-periodical><full-title>Medicine and Science in Sports and Exercise</full-title></alt-periodical><pages>S531-43</pages><volume>37</volume><number>11 Suppl</number><keywords><keyword>*Acceleration</keyword><keyword>Automatic Data Processing</keyword><keyword>Ergometry/*instrumentation</keyword><keyword>Evidence-Based Medicine</keyword><keyword>Guidelines as Topic</keyword><keyword>Humans</keyword><keyword>Locomotion</keyword><keyword>Reproducibility of Results</keyword><keyword>*Research Design</keyword><keyword>United States</keyword></keywords><dates><year>2005</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>0195-9131 (Print)
0195-9131 (Linking)</isbn><accession-num>16294116</accession-num><urls><related-urls><url>;[84]. Accelerometers are devices that measure body movement in the form of acceleration which can then be used to estimate intensity of activity over a given time period ADDIN EN.CITE <EndNote><Cite><Author>Chen</Author><Year>2005</Year><RecNum>3273</RecNum><DisplayText>[85]</DisplayText><record><rec-number>3273</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3273</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Chen, K. Y.</author><author>Bassett, D. R., Jr.</author></authors></contributors><auth-address>Department of Medicine and Biomedical Engineering, Vanderbilt University, Nashville, TN 37232-2279, USA. kong.chen@vanderbilt.edu</auth-address><titles><title>The technology of accelerometry-based activity monitors: current and future</title><secondary-title>Med Sci Sports Exerc</secondary-title><alt-title>Medicine and science in sports and exercise</alt-title></titles><periodical><full-title>Medicine & Science in Sports & Exercise</full-title><abbr-1>Med Sci Sports Exerc</abbr-1></periodical><alt-periodical><full-title>Medicine and Science in Sports and Exercise</full-title></alt-periodical><pages>S490-500</pages><volume>37</volume><number>11 Suppl</number><keywords><keyword>*Acceleration</keyword><keyword>Diffusion of Innovation</keyword><keyword>*Equipment Design</keyword><keyword>Ergometry/*instrumentation</keyword><keyword>Humans</keyword><keyword>Locomotion</keyword><keyword>United States</keyword></keywords><dates><year>2005</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>0195-9131 (Print)
0195-9131 (Linking)</isbn><accession-num>16294112</accession-num><urls><related-urls><url>;[85]. Most accelerometers house one, or multiple, piezoelectric elements, and during acceleration, a seismic mass causes the element to experience deformation, which is recorded as a voltage and digitized to counts. Counts are then binned into select time periods, or epochs, to represent the count for that time period ADDIN EN.CITE <EndNote><Cite><Author>Chen</Author><Year>2005</Year><RecNum>3273</RecNum><DisplayText>[85]</DisplayText><record><rec-number>3273</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3273</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Chen, K. Y.</author><author>Bassett, D. R., Jr.</author></authors></contributors><auth-address>Department of Medicine and Biomedical Engineering, Vanderbilt University, Nashville, TN 37232-2279, USA. kong.chen@vanderbilt.edu</auth-address><titles><title>The technology of accelerometry-based activity monitors: current and future</title><secondary-title>Med Sci Sports Exerc</secondary-title><alt-title>Medicine and science in sports and exercise</alt-title></titles><periodical><full-title>Medicine & Science in Sports & Exercise</full-title><abbr-1>Med Sci Sports Exerc</abbr-1></periodical><alt-periodical><full-title>Medicine and Science in Sports and Exercise</full-title></alt-periodical><pages>S490-500</pages><volume>37</volume><number>11 Suppl</number><keywords><keyword>*Acceleration</keyword><keyword>Diffusion of Innovation</keyword><keyword>*Equipment Design</keyword><keyword>Ergometry/*instrumentation</keyword><keyword>Humans</keyword><keyword>Locomotion</keyword><keyword>United States</keyword></keywords><dates><year>2005</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>0195-9131 (Print)
0195-9131 (Linking)</isbn><accession-num>16294112</accession-num><urls><related-urls><url>;[85]. Choosing a short epoch is important if PA is sporadic and is accumulated in multiple short bouts. However, a disadvantage with shorter epochs is that their predictive physiological value in terms of risk reduction is relatively unknown. On the contrary, the main drawback of using a longer epoch is if a bout contains a mixture of activities at varying intensities, then the data will be averaged to reflect mean intensity. Initial observational studies in adults without diabetes (mean age 53.4) equipped with accelerometers have shown that device-measured increases in sedentary time is directly associated with elevations in a number of CV risk factors, specifically waist circumference (WC), blood glucose, insulin, and triglycerides ADDIN EN.CITE <EndNote><Cite><Author>Healy</Author><Year>2008</Year><RecNum>3274</RecNum><DisplayText>[86]</DisplayText><record><rec-number>3274</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3274</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Healy, G.N., Wijndaele, K., Dunstan, D.W., Shaw, J.E., Salmon, J., Zimmet, P.Z., Owen, N.</author></authors></contributors><titles><title>Objectively measured sedentary time, physical activtiy, and metabolic risk</title><secondary-title>Diabetes Care</secondary-title></titles><periodical><full-title>Diabetes Care</full-title></periodical><pages>369-371</pages><volume>31</volume><number>2</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[86]. These results have also been shown to be independent of MVPA levels. An interesting finding from this study was that adults who interrupted their sedentary bouts with more frequent ‘breaks’ had a better cardiovascular profile than those who endured in longer periods of sedentary time ADDIN EN.CITE <EndNote><Cite><Author>Healy</Author><Year>2008</Year><RecNum>3274</RecNum><DisplayText>[86]</DisplayText><record><rec-number>3274</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3274</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Healy, G.N., Wijndaele, K., Dunstan, D.W., Shaw, J.E., Salmon, J., Zimmet, P.Z., Owen, N.</author></authors></contributors><titles><title>Objectively measured sedentary time, physical activtiy, and metabolic risk</title><secondary-title>Diabetes Care</secondary-title></titles><periodical><full-title>Diabetes Care</full-title></periodical><pages>369-371</pages><volume>31</volume><number>2</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[86]. Interruptions in sedentary time being a transition from sedentary (<100 counts per minute (CPM)) to an active state (>100CPM) were deemed a ‘break’. The number of breaks was summed over valid days. The benefits of taking breaks were independent of time spent in MVPA. When looking at differences between breaks in sedentary time, the most significant findings were observed for WC. Of the 25% that took the most breaks, they had a 4.1cm smaller WC compared to the lowest group ADDIN EN.CITE <EndNote><Cite><Author>Healy</Author><Year>2008</Year><RecNum>3274</RecNum><DisplayText>[86]</DisplayText><record><rec-number>3274</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3274</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Healy, G.N., Wijndaele, K., Dunstan, D.W., Shaw, J.E., Salmon, J., Zimmet, P.Z., Owen, N.</author></authors></contributors><titles><title>Objectively measured sedentary time, physical activtiy, and metabolic risk</title><secondary-title>Diabetes Care</secondary-title></titles><periodical><full-title>Diabetes Care</full-title></periodical><pages>369-371</pages><volume>31</volume><number>2</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[86].1.2.2InsulinInsulin is a hormone that is produced by beta cells in the pancreas that influences the absorption of glucose by skeletal muscle and fat tissue cells from the blood ADDIN EN.CITE <EndNote><Cite><Author>Hsueh</Author><Year>1999</Year><RecNum>3303</RecNum><DisplayText>[87]</DisplayText><record><rec-number>3303</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3303</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hsueh, W. A.</author><author>Law, R. E.</author></authors></contributors><auth-address>Department of Medicine, University of California Los Angeles School of Medicine, USA.</auth-address><titles><title>Insulin signaling in the arterial wall</title><secondary-title>Am J Cardiol</secondary-title><alt-title>The American journal of cardiology</alt-title></titles><periodical><full-title>Am J Cardiol</full-title></periodical><alt-periodical><full-title>The American journal of cardiology</full-title></alt-periodical><pages>21J-24J</pages><volume>84</volume><number>1A</number><keywords><keyword>Animals</keyword><keyword>Arteries/metabolism/*physiopathology</keyword><keyword>Cell Movement/physiology</keyword><keyword>Endothelium, Vascular/metabolism/*physiopathology</keyword><keyword>Humans</keyword><keyword>Hypoglycemic Agents/metabolism/pharmacology</keyword><keyword>Insulin/metabolism/*physiology</keyword><keyword>Insulin Resistance/*physiology</keyword><keyword>*Signal Transduction/physiology</keyword><keyword>Thiazoles/metabolism/pharmacology</keyword><keyword>*Thiazolidinediones</keyword></keywords><dates><year>1999</year><pub-dates><date>Jul 8</date></pub-dates></dates><isbn>0002-9149 (Print)
0002-9149 (Linking)</isbn><accession-num>10418854</accession-num><urls><related-urls><url>;[87]. Increased levels of circulating insulin prevent the usage of triglycerides as an energy source by inhibiting the release of glucagon ADDIN EN.CITE <EndNote><Cite><Author>Hsueh</Author><Year>1999</Year><RecNum>3303</RecNum><DisplayText>[87]</DisplayText><record><rec-number>3303</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3303</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hsueh, W. A.</author><author>Law, R. E.</author></authors></contributors><auth-address>Department of Medicine, University of California Los Angeles School of Medicine, USA.</auth-address><titles><title>Insulin signaling in the arterial wall</title><secondary-title>Am J Cardiol</secondary-title><alt-title>The American journal of cardiology</alt-title></titles><periodical><full-title>Am J Cardiol</full-title></periodical><alt-periodical><full-title>The American journal of cardiology</full-title></alt-periodical><pages>21J-24J</pages><volume>84</volume><number>1A</number><keywords><keyword>Animals</keyword><keyword>Arteries/metabolism/*physiopathology</keyword><keyword>Cell Movement/physiology</keyword><keyword>Endothelium, Vascular/metabolism/*physiopathology</keyword><keyword>Humans</keyword><keyword>Hypoglycemic Agents/metabolism/pharmacology</keyword><keyword>Insulin/metabolism/*physiology</keyword><keyword>Insulin Resistance/*physiology</keyword><keyword>*Signal Transduction/physiology</keyword><keyword>Thiazoles/metabolism/pharmacology</keyword><keyword>*Thiazolidinediones</keyword></keywords><dates><year>1999</year><pub-dates><date>Jul 8</date></pub-dates></dates><isbn>0002-9149 (Print)
0002-9149 (Linking)</isbn><accession-num>10418854</accession-num><urls><related-urls><url>;[87]. Insulin resistance and hyperinsulinemia enhance alterations that can lead to the progression of atherosclerosis ADDIN EN.CITE <EndNote><Cite><Author>Laakso</Author><Year>1991</Year><RecNum>3506</RecNum><DisplayText>[88]</DisplayText><record><rec-number>3506</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3506</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laakso, Markku</author><author>Sarlund, Helena</author><author>Salonen, Riitta</author><author>Suhonen, Matti</author><author>Py?r?l?, K</author><author>Salonen, Jukka T</author><author>Karhap??, P</author></authors></contributors><titles><title>Asymptomatic atherosclerosis and insulin resistance</title><secondary-title>Arteriosclerosis, Thrombosis, and Vascular Biology</secondary-title></titles><periodical><full-title>Arteriosclerosis, Thrombosis, and Vascular Biology</full-title></periodical><pages>1068-1076</pages><volume>11</volume><number>4</number><dates><year>1991</year></dates><isbn>1079-5642</isbn><urls></urls></record></Cite></EndNote>[88]. Insulin also exhibits a protective effect on the vascular smooth muscle as insulin has been shown to stimulate endothelial cell production of NO ADDIN EN.CITE <EndNote><Cite><Author>AD</Author><Year>1999</Year><RecNum>3304</RecNum><DisplayText>[89]</DisplayText><record><rec-number>3304</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3304</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Baron AD</author></authors></contributors><titles><title>Vascular reactivity</title><secondary-title>Am J Cardiol</secondary-title></titles><periodical><full-title>Am J Cardiol</full-title></periodical><pages>25-27</pages><volume>84</volume><dates><year>1999</year></dates><urls></urls></record></Cite></EndNote>[89] through the phosphatidylinositol 3-kinase pathway ADDIN EN.CITE <EndNote><Cite><Author>Hsueh</Author><Year>1999</Year><RecNum>3303</RecNum><DisplayText>[87]</DisplayText><record><rec-number>3303</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3303</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hsueh, W. A.</author><author>Law, R. E.</author></authors></contributors><auth-address>Department of Medicine, University of California Los Angeles School of Medicine, USA.</auth-address><titles><title>Insulin signaling in the arterial wall</title><secondary-title>Am J Cardiol</secondary-title><alt-title>The American journal of cardiology</alt-title></titles><periodical><full-title>Am J Cardiol</full-title></periodical><alt-periodical><full-title>The American journal of cardiology</full-title></alt-periodical><pages>21J-24J</pages><volume>84</volume><number>1A</number><keywords><keyword>Animals</keyword><keyword>Arteries/metabolism/*physiopathology</keyword><keyword>Cell Movement/physiology</keyword><keyword>Endothelium, Vascular/metabolism/*physiopathology</keyword><keyword>Humans</keyword><keyword>Hypoglycemic Agents/metabolism/pharmacology</keyword><keyword>Insulin/metabolism/*physiology</keyword><keyword>Insulin Resistance/*physiology</keyword><keyword>*Signal Transduction/physiology</keyword><keyword>Thiazoles/metabolism/pharmacology</keyword><keyword>*Thiazolidinediones</keyword></keywords><dates><year>1999</year><pub-dates><date>Jul 8</date></pub-dates></dates><isbn>0002-9149 (Print)
0002-9149 (Linking)</isbn><accession-num>10418854</accession-num><urls><related-urls><url>;[87]. On the contrary, hyperinsulinemia promotes the effect of platelet-derived growth factor and other growth factors on vascular smooth muscle cells [63]. In this detrimental pathway, insulin acts through the mitogen-activated protein kinase pathway to indirectly produce vascular smooth muscle cell growth and plasminogen activator inhibitor-1; which attenuates fibrinolysis ADDIN EN.CITE <EndNote><Cite><Author>Anderson PW</Author><Year>1996</Year><RecNum>3305</RecNum><DisplayText>[90]</DisplayText><record><rec-number>3305</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3305</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Anderson PW, Zhang XY, Tian J, Correale JD, Xi XP, Yang D, Graf K, Law RE, Hsueh WA</author></authors></contributors><titles><title>Insulin and angiotensin II are additive in stimulating TGF-B1 and matrix mRNAs in mesangial cells</title><secondary-title>Kidney International</secondary-title></titles><periodical><full-title>Kidney International</full-title></periodical><pages>745-753</pages><volume>50</volume><dates><year>1996</year></dates><urls></urls></record></Cite></EndNote>[90] and subsequently results in the progression of arterial stiffness PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QYXJrPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [91]. Insulin also enhances cholesterol transport into arterial smooth muscle cells and increases lipid synthesis of these cells. Elevated plasma insulin concentrations enhance very-low-density lipoprotein synthesis. Progressive elimination of lipids from the very-low-density lipoprotein particle leads to an increased formation of low-density lipoprotein (LDL) in the arterial medial layer and increases endogenous lipid synthesis by these cells ADDIN EN.CITE <EndNote><Cite><Author>DeFronzo</Author><Year>1991</Year><RecNum>3307</RecNum><DisplayText>[92]</DisplayText><record><rec-number>3307</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3307</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>DeFronzo, R. A.</author><author>Ferrannini, E.</author></authors></contributors><auth-address>Department of Medicine, University of Texas Health Science Center, San Antonio 78284-7886.</auth-address><titles><title>Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease</title><secondary-title>Diabetes Care</secondary-title><alt-title>Diabetes care</alt-title></titles><periodical><full-title>Diabetes Care</full-title></periodical><alt-periodical><full-title>Diabetes Care</full-title></alt-periodical><pages>173-94</pages><volume>14</volume><number>3</number><keywords><keyword>Arteriosclerosis/*etiology/physiopathology</keyword><keyword>Diabetes Mellitus, Type 2/*etiology/physiopathology</keyword><keyword>Humans</keyword><keyword>Hyperlipidemias/*etiology/physiopathology</keyword><keyword>Hypertension/*etiology/physiopathology</keyword><keyword>Insulin Resistance/*physiology</keyword><keyword>Obesity/*etiology/physiopathology</keyword><keyword>Syndrome</keyword></keywords><dates><year>1991</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>0149-5992 (Print)
0149-5992 (Linking)</isbn><accession-num>2044434</accession-num><urls><related-urls><url>;[92]. Recently, studies have focused on the effects of weight loss, reduced WC, and insulin reduction in adults and youth to determine the effects on arterial stiffness PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IdWdoZXM8L0F1dGhvcj48WWVhcj4yMDEyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [93-96]. Body mass index (BMI) and WC were found to be correlated with each other and with steady-state plasma glucose concentrations in 330 non-diabetic adults. The more overweight or obese a person, the greater the degree of insulin resistance, which was independent of either index of adiposity (BMI or WC) ADDIN EN.CITE <EndNote><Cite><Author>Helke MF</Author><Year>2006</Year><RecNum>3311</RecNum><DisplayText>[96]</DisplayText><record><rec-number>3311</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3311</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Helke MF, Abbasi F, Reaven GM</author></authors></contributors><titles><title>Body mass index and waist circumference both contribute to differences in insulin-mediated glucose disposal in nondiabetic adults</title><secondary-title>THe American Journal of Clinical Nutrition</secondary-title></titles><periodical><full-title>THe American Journal of Clinical Nutrition</full-title></periodical><pages>47-51</pages><volume>83</volume><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>[96]. Weight loss ADDIN EN.CITE <EndNote><Cite><Author>Sutton-Tyrrell</Author><Year>2011</Year><RecNum>3312</RecNum><DisplayText>[97]</DisplayText><record><rec-number>3312</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3312</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Sutton-Tyrrell, K, Barinas-Mitchell K, Kinzel L, Woodard G, Lloyd K, Cooper J, Brooks M, Kriska A, Conroy M</author></authors></contributors><titles><title>The effects of a behavioural lifestyle and sodium intervention on aortic pulse wave velocity, a measure of vascular health: primary results of the SAVE clinical trial</title><secondary-title>American Heart Association Cardiovascular Disease Epidemiology and Prevention Scientific Sessions</secondary-title></titles><periodical><full-title>American Heart Association Cardiovascular Disease Epidemiology and Prevention Scientific Sessions</full-title></periodical><dates><year>2011</year></dates><urls></urls></record></Cite></EndNote>[97] and improved insulin sensitivity have been shown to be independently associated with improved aortic stiffness ADDIN EN.CITE <EndNote><Cite><Author>Dengo A</Author><Year>2010</Year><RecNum>3313</RecNum><DisplayText>[98]</DisplayText><record><rec-number>3313</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3313</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Dengo A, Dennis E, Orr J, Marinik E, Ehrlich E, Davy B, Davy K</author></authors></contributors><titles><title>Arterial destiffening with weight loss in overweight and obese middle-aged and older adults</title><secondary-title>Hypertension</secondary-title></titles><periodical><full-title>Hypertension</full-title></periodical><pages>885-861</pages><volume>55</volume><number>4</number><dates><year>2010</year></dates><urls></urls></record></Cite></EndNote>[98] but combined effects of weight loss and increased insulin sensitivity on aortic arterial stiffness have been poorly understood. In a large cohort of healthy men and women (n=339), with an average age of 37.9 years, decreases in brachial-ankle PWV were associated with reductions in weight and insulin levels that were independent of age, sex, race, smoking, status, and brachial blood pressure, following a 6 month interventional trial PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IdWdoZXM8L0F1dGhvcj48WWVhcj4yMDEyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [94]. However, results confirmed that a more adverse cardiovascular risk profile and stiffer arteries were found in young obese individuals presenting with insulin resistance. It has been suggested that a sex difference may exist with regards to insulin sensitivity. The female advantage in CVD risk refers to the approximately 10-year delay in the incidence of CVD in women compared with men ADDIN EN.CITE <EndNote><Cite><Author>Lerner</Author><Year>1986</Year><RecNum>3314</RecNum><DisplayText>[99]</DisplayText><record><rec-number>3314</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3314</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Lerner, D. J.</author><author>Kannel, W. B.</author></authors></contributors><titles><title>Patterns of coronary heart disease morbidity and mortality in the sexes: a 26-year follow-up of the Framingham population</title><secondary-title>Am Heart J</secondary-title><alt-title>American heart journal</alt-title></titles><periodical><full-title>Am Heart J</full-title></periodical><alt-periodical><full-title>American Heart Journal</full-title></alt-periodical><pages>383-90</pages><volume>111</volume><number>2</number><keywords><keyword>Adult</keyword><keyword>Age Factors</keyword><keyword>Aged</keyword><keyword>Angina Pectoris/epidemiology</keyword><keyword>Cholesterol, HDL/blood</keyword><keyword>Cholesterol, LDL/blood</keyword><keyword>Coronary Disease/*epidemiology/mortality</keyword><keyword>Death, Sudden/epidemiology</keyword><keyword>Diabetes Complications</keyword><keyword>Female</keyword><keyword>Follow-Up Studies</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Menopause</keyword><keyword>Middle Aged</keyword><keyword>Myocardial Infarction/epidemiology</keyword><keyword>Prospective Studies</keyword><keyword>Risk</keyword><keyword>Sex Factors</keyword><keyword>Smoking</keyword><keyword>Triglycerides/blood</keyword></keywords><dates><year>1986</year><pub-dates><date>Feb</date></pub-dates></dates><isbn>0002-8703 (Print)
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ADDIN EN.CITE.DATA [100]. 1.2.3GlucoseIn the postprandial state, skeletal muscle is the primary tissue responsible for insulin-dependent overall body glucose uptake ADDIN EN.CITE <EndNote><Cite><Author>Harris</Author><Year>1987</Year><RecNum>3316</RecNum><DisplayText>[101]</DisplayText><record><rec-number>3316</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3316</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Harris, M. I.</author><author>Hadden, W. C.</author><author>Knowler, W. C.</author><author>Bennett, P. H.</author></authors></contributors><titles><title>Prevalence of diabetes and impaired glucose tolerance and plasma glucose levels in U.S. population aged 20-74 yr</title><secondary-title>Diabetes</secondary-title><alt-title>Diabetes</alt-title></titles><periodical><full-title>Diabetes</full-title></periodical><alt-periodical><full-title>Diabetes</full-title></alt-periodical><pages>523-34</pages><volume>36</volume><number>4</number><keywords><keyword>Adult</keyword><keyword>African Americans</keyword><keyword>Age Factors</keyword><keyword>Aged</keyword><keyword>Blood Glucose/*analysis</keyword><keyword>Diabetes Mellitus/*epidemiology</keyword><keyword>European Continental Ancestry Group</keyword><keyword>Female</keyword><keyword>*Glucose Tolerance Test</keyword><keyword>Health Surveys</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Sex Factors</keyword><keyword>United States</keyword></keywords><dates><year>1987</year><pub-dates><date>Apr</date></pub-dates></dates><isbn>0012-1797 (Print)
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ADDIN EN.CITE.DATA [102] through the formation of advanced glycation end products in the arterial wall. Chronic hyperglycemia enhances the reaction between glucose and proteins and aids in the cross-linking of collagen. Hyperglycemia has further been shown to promote collagen deposition and tissue inflammation within the smooth muscle cells of the vasculature ADDIN EN.CITE <EndNote><Cite><Author>Monnier VM</Author><Year>2005</Year><RecNum>3318</RecNum><DisplayText>[103]</DisplayText><record><rec-number>3318</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3318</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Monnier VM, Sell DR, Genuth S</author></authors></contributors><titles><title>Glycation products as markers and predictors of the progression of diabetic complications</title><secondary-title>Ann N Y Acad Sci</secondary-title></titles><periodical><full-title>Ann N Y Acad Sci</full-title></periodical><pages>567-81</pages><volume>1043</volume><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[103]. Recently, researchers have shown that chronic hyperglycemia (as assessed using HbA1c) is strongly correlated with arterial stiffness independent of the artery wall thickness PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5SdWJpbjwvQXV0aG9yPjxZZWFyPjIwMTI8L1llYXI+PFJl
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ADDIN EN.CITE.DATA [104]. Finally, when comparing individuals with type-2 diabetes to those with impaired glucose metabolism and normal glucose metabolism, independent of age, sex and mean arterial pressure, researchers found that those with type-2 diabetes had increased arterial stiffness of carotid, femoral, and brachial arteries whereas those with impaired glucose metabolism had increased stiffness of the muscular arteries only PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IZW5yeTwvQXV0aG9yPjxZZWFyPjIwMDM8L1llYXI+PFJl
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ADDIN EN.CITE.DATA [105]. These findings suggest that the process of increasing arterial stiffness occurs prior to the onset of occult type-2 diabetes. Increases in fasting plasma glucose, even within normal ranges (<100mg/dL), have been associated with increased brachial-ankle PWV in 697 healthy adults without diabetes with an average age of 51.9 years PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5TaGluPC9BdXRob3I+PFllYXI+MjAxMTwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [106]. Although the aforementioned studies adjusted for age in their analyses, the average age of participants was approximately 50 years. When glucose intolerance and insulin resistance were examined in children, arterial stiffness examined using PWV was significantly higher in those with impaired glucose control. This relationship was, however, dependent on blood pressure, BMI, and intraventricular septal thickness PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5LaGFuPC9BdXRob3I+PFllYXI+MjAwNjwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [107], thus it seems that hyperglycemia is an independent predictor of arterial stiffening in older, but not younger individuals. 1.2.4Interleukin-6Interleukin (IL)-6 is a cytokine with a broad range of humoral and immune effects relating to inflammation, bacterial defense, and tissue injury ADDIN EN.CITE <EndNote><Cite><Author>Van Snick</Author><Year>1990</Year><RecNum>2946</RecNum><DisplayText>[108]</DisplayText><record><rec-number>2946</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">2946</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Van Snick, J.</author></authors></contributors><auth-address>Ludwig Institute for Cancer Research, Brussels Branch, Belgium.</auth-address><titles><title>Interleukin-6: an overview</title><secondary-title>Annu Rev Immunol</secondary-title><alt-title>Annual review of immunology</alt-title></titles><pages>253-78</pages><volume>8</volume><keywords><keyword>Amino Acid Sequence</keyword><keyword>Animals</keyword><keyword>Humans</keyword><keyword>*Interleukin-6/genetics/metabolism/physiology</keyword><keyword>Lymphocyte Activation</keyword><keyword>Lymphocytes/immunology</keyword><keyword>Molecular Sequence Data</keyword><keyword>Receptors, Immunologic/metabolism</keyword><keyword>Receptors, Interleukin-6</keyword></keywords><dates><year>1990</year></dates><isbn>0732-0582 (Print)
0732-0582 (Linking)</isbn><accession-num>2188664</accession-num><urls><related-urls><url>;[108]. IL-6 is produced in response to several factors, including infection, elevations in IL-1 and -2, and tumor necrosis factor ADDIN EN.CITE <EndNote><Cite><Author>Ng</Author><Year>1994</Year><RecNum>2950</RecNum><DisplayText>[109]</DisplayText><record><rec-number>2950</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">2950</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Ng, S. B.</author><author>Tan, Y. H.</author><author>Guy, G. R.</author></authors></contributors><auth-address>Institute of Molecular and Cell Biology, National University of Singapore, Republic of Singapore.</auth-address><titles><title>Differential induction of the interleukin-6 gene by tumor necrosis factor and interleukin-1</title><secondary-title>J Biol Chem</secondary-title><alt-title>The Journal of biological chemistry</alt-title></titles><pages>19021-7</pages><volume>269</volume><number>29</number><keywords><keyword>Dactinomycin/pharmacology</keyword><keyword>Dose-Response Relationship, Drug</keyword><keyword>Gene Expression Regulation/*drug effects</keyword><keyword>Genes</keyword><keyword>Humans</keyword><keyword>Interleukin-1/*administration & dosage</keyword><keyword>Interleukin-6/*genetics/metabolism</keyword><keyword>Interleukin-8/genetics</keyword><keyword>NF-kappa B/metabolism</keyword><keyword>RNA, Messenger/genetics/metabolism</keyword><keyword>Time Factors</keyword><keyword>Transcription, Genetic/drug effects</keyword><keyword>Tumor Necrosis Factor-alpha/*pharmacology</keyword></keywords><dates><year>1994</year><pub-dates><date>Jul 22</date></pub-dates></dates><isbn>0021-9258 (Print)
0021-9258 (Linking)</isbn><accession-num>8034659</accession-num><urls><related-urls><url>;[109]. IL-6 is also a primary determinant of the production of CRP from the liver ADDIN EN.CITE <EndNote><Cite><Author>Heinrich</Author><Year>1990</Year><RecNum>2949</RecNum><DisplayText>[110]</DisplayText><record><rec-number>2949</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">2949</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Heinrich, P. C.</author><author>Castell, J. V.</author><author>Andus, T.</author></authors></contributors><auth-address>Institut fur Biochemie der RWTH Aachen, Federal Republic of Germany.</auth-address><titles><title>Interleukin-6 and the acute phase response</title><secondary-title>Biochem J</secondary-title><alt-title>The Biochemical journal</alt-title></titles><pages>621-36</pages><volume>265</volume><number>3</number><keywords><keyword>Acute-Phase Proteins/metabolism</keyword><keyword>Acute-Phase Reaction/*metabolism</keyword><keyword>Animals</keyword><keyword>Base Sequence</keyword><keyword>Humans</keyword><keyword>Inflammation/*metabolism</keyword><keyword>Interleukin-6/biosynthesis/genetics/*physiology</keyword><keyword>Liver/metabolism</keyword><keyword>Molecular Sequence Data</keyword><keyword>Proteins/metabolism</keyword><keyword>Rats</keyword><keyword>Signal Transduction</keyword><keyword>Tumor Necrosis Factor-alpha/metabolism</keyword></keywords><dates><year>1990</year><pub-dates><date>Feb 1</date></pub-dates></dates><isbn>0264-6021 (Print)
0264-6021 (Linking)</isbn><accession-num>1689567</accession-num><urls><related-urls><url>;[110]. Elevated levels of IL-6 have been linked to the inflammatory processes that lead to atherosclerosis [84]. IL-6 can activate endothelial cells to express adhesion molecules, which mediate trans-endothelial migration of leukocytes resulting in fatty streaks and the formation of atherosclerotic plaques ADDIN EN.CITE <EndNote><Cite><Author>Rus</Author><Year>1996</Year><RecNum>2951</RecNum><DisplayText>[111]</DisplayText><record><rec-number>2951</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">2951</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Rus, H. G.</author><author>Vlaicu, R.</author><author>Niculescu, F.</author></authors></contributors><auth-address>Medical Clinic no. 1, 3-5, Cluj-Napoca, Romania.</auth-address><titles><title>Interleukin-6 and interleukin-8 protein and gene expression in human arterial atherosclerotic wall</title><secondary-title>Atherosclerosis</secondary-title><alt-title>Atherosclerosis</alt-title></titles><periodical><full-title>Atherosclerosis</full-title></periodical><alt-periodical><full-title>Atherosclerosis</full-title></alt-periodical><pages>263-71</pages><volume>127</volume><number>2</number><keywords><keyword>Aorta/metabolism/pathology</keyword><keyword>Arteriosclerosis/*metabolism/pathology</keyword><keyword>Cells, Cultured</keyword><keyword>DNA/biosynthesis</keyword><keyword>Endothelium, Vascular/*metabolism/pathology</keyword><keyword>Enzyme-Linked Immunosorbent Assay</keyword><keyword>Femoral Artery/metabolism/pathology</keyword><keyword>*Gene Expression</keyword><keyword>Humans</keyword><keyword>Immunohistochemistry</keyword><keyword>Interleukin-6/*biosynthesis/genetics</keyword><keyword>Interleukin-8/*biosynthesis/genetics</keyword><keyword>Middle Aged</keyword><keyword>Oligonucleotide Probes/chemistry</keyword><keyword>Protein-Serine-Threonine Kinases/metabolism</keyword><keyword>RNA/*analysis</keyword><keyword>Ribosomal Protein S6 Kinases</keyword></keywords><dates><year>1996</year><pub-dates><date>Dec 20</date></pub-dates></dates><isbn>0021-9150 (Print)
0021-9150 (Linking)</isbn><accession-num>9125317</accession-num><urls><related-urls><url>;[111]. Furthermore, IL-6 is produced in the adipose tissue in response to adipocytokines linking obesity to the state of chronic low-level inflammation as a potential trigger for cardiovascular and metabolic diseases ADDIN EN.CITE <EndNote><Cite><Author>Tilg</Author><Year>2006</Year><RecNum>3323</RecNum><DisplayText>[112]</DisplayText><record><rec-number>3323</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3323</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Tilg, H.</author><author>Moschen, A. R.</author></authors></contributors><auth-address>Christian Doppler Research Laboratory for Gut Inflammation and Department of Medicine, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria. herbert.tilg@uibk.ac.at</auth-address><titles><title>Adipocytokines: mediators linking adipose tissue, inflammation and immunity</title><secondary-title>Nat Rev Immunol</secondary-title><alt-title>Nature reviews. Immunology</alt-title></titles><periodical><full-title>Nat Rev Immunol</full-title></periodical><pages>772-83</pages><volume>6</volume><number>10</number><keywords><keyword>Adiponectin/immunology</keyword><keyword>Adipose Tissue/*immunology/metabolism</keyword><keyword>Animals</keyword><keyword>Cytokines/*immunology</keyword><keyword>Humans</keyword><keyword>*Immunity, Innate</keyword><keyword>Inflammation/*immunology</keyword><keyword>Leptin/immunology</keyword><keyword>Resistin/immunology</keyword><keyword>Signal Transduction/*immunology</keyword></keywords><dates><year>2006</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>1474-1733 (Print)
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ADDIN EN.CITE.DATA [113]. The progression of atherosclerosis in the presence of increased circulating levels of IL-6 has been linked to central arterial aging as a result of endothelial dysfunction and arterial stiffening PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5LYWxzPC9BdXRob3I+PFllYXI+MjAwODwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [114, 115]. As atherosclerosis is an inflammatory disease, the inflammatory response of the endothelium disrupts its membranous integrity and allows an influx of LDL and monocytes ADDIN EN.CITE <EndNote><Cite><Author>Schuett H</Author><Year>2009</Year><RecNum>3326</RecNum><DisplayText>[116]</DisplayText><record><rec-number>3326</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3326</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Schuett H, Luchtefeld M, Grothusen C, Grote K, Schieffer B</author></authors></contributors><titles><title>How much is too much? Interleukin-6 and its signalling in atherosclerosis</title><secondary-title>Throm Haemost</secondary-title></titles><periodical><full-title>Throm Haemost</full-title></periodical><volume>102</volume><number>215-222</number><dates><year>2009</year></dates><urls></urls></record></Cite></EndNote>[116]. LDL, upon oxidative or enzymatic modification, further promotes the inflammatory reaction in the evolving atherosclerotic plaque. Prolonged inflammation stimulates migration and proliferation of smooth muscle cells, which along with the accumulating macrophages, further release cytokines and growth factors ADDIN EN.CITE <EndNote><Cite><Author>Schuett H</Author><Year>2009</Year><RecNum>3326</RecNum><DisplayText>[116]</DisplayText><record><rec-number>3326</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3326</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Schuett H, Luchtefeld M, Grothusen C, Grote K, Schieffer B</author></authors></contributors><titles><title>How much is too much? Interleukin-6 and its signalling in atherosclerosis</title><secondary-title>Throm Haemost</secondary-title></titles><periodical><full-title>Throm Haemost</full-title></periodical><volume>102</volume><number>215-222</number><dates><year>2009</year></dates><urls></urls></record></Cite></EndNote>[116]. These processes result in a destructive remodeling of the vessel structure with the formation of a complex atherosclerotic lesion ADDIN EN.CITE <EndNote><Cite><Author>P</Author><Year>2002</Year><RecNum>3327</RecNum><DisplayText>[117]</DisplayText><record><rec-number>3327</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3327</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Libby P</author></authors></contributors><titles><title>Inflammation in atherosclerosis</title><secondary-title>Nature </secondary-title></titles><periodical><full-title>Nature</full-title></periodical><volume>420</volume><number>868-874</number><dates><year>2002</year></dates><urls></urls></record></Cite></EndNote>[117]. The presence of IL-6 and the associated relationship with endothelial dysfunction and arterial stiffness have been shown to be independent of other cardiovascular risk factors (blood pressure, low levels of high-density lipoprotein (HDL), fasting plasma glucose, WC, and serum triglycerides) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5XZWlzczwvQXV0aG9yPjxZZWFyPjIwMTM8L1llYXI+PFJl
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ADDIN EN.CITE.DATA [115]. 1.2.5LipidsHDL is a plasma lipoprotein that aids in reverse cholesterol transport, bringing cholesterol from peripheral cells to the hepatic system, where cholesterol is subsequently secreted into the bile ADDIN EN.CITE <EndNote><Cite><Author>JA</Author><Year>1973</Year><RecNum>3328</RecNum><DisplayText>[118]</DisplayText><record><rec-number>3328</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3328</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Glomset JA</author></authors></contributors><titles><title>The metabolic role of lecithin: cholesterol acyltransferase - perspectives from pathology</title><secondary-title>Adv Lipid Res</secondary-title></titles><periodical><full-title>Adv Lipid Res</full-title></periodical><volume>11</volume><number>1-65</number><dates><year>1973</year></dates><urls></urls></record></Cite></EndNote>[118]. HDL formation begins as a result of the liver and small intestine secreting apolipoprotein A-I. Apolipoprotein A-I circulates in the plasma acquiring cholesterol from peripheral cells PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Mb3dlbnN0ZWluPC9BdXRob3I+PFllYXI+MjAxMDwvWWVh
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ADDIN EN.CITE.DATA [119]. HDL levels have been shown to be inversely associated with coronary heart disease and for a 1% increase in HDL levels, coronary events decrease by approximately 2% ADDIN EN.CITE <EndNote><Cite><Author>Gordon T</Author><Year>1977</Year><RecNum>3330</RecNum><DisplayText>[120]</DisplayText><record><rec-number>3330</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3330</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Gordon T, Castelli WP, Hjortland MC, et al.</author></authors></contributors><titles><title>High density lipoprotein as a protective factor against coronary heart disease</title><secondary-title>Am J Med</secondary-title></titles><periodical><full-title>Am J Med</full-title></periodical><pages>707-714</pages><volume>62</volume><dates><year>1977</year></dates><urls></urls></record></Cite></EndNote>[120]. The major cardiovascular benefit of HDL is attributed to its role in transferring cholesterol, specifically LDL, from macrophages in atherosclerotic lesions to the liver [91]. HDL has also been shown to improve vascular function through the activation of endothelial NOS ADDIN EN.CITE <EndNote><Cite><Author>Yuhanna IS</Author><Year>2001</Year><RecNum>3331</RecNum><DisplayText>[121]</DisplayText><record><rec-number>3331</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3331</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Yuhanna IS, Zhu Y, Cox BE, et al.</author></authors></contributors><titles><title>High-density lipoprotien binding to scavenger receptor-BI activates endothelial nitric oxide synthase</title><secondary-title>Nat Med</secondary-title></titles><periodical><full-title>Nat Med</full-title></periodical><volume>7</volume><number>853-857</number><dates><year>2001</year></dates><urls></urls></record></Cite></EndNote>[121]. In persons with familial hypoalphalipoproteinemia, resulting in low-HDL levels, endothelial dysfunction is present [95]. Researchers found that by administering apolipoprotien A-I to 3 men and 6 women (42.9 ± 13.9 yrs) with familial hypoalphalipoproteinemia, previous blunted blood flow responses were returned to levels similar to healthy controls when challenged with a vasodilator (serotonin) ADDIN EN.CITE <EndNote><Cite><Author>Bosendial RJ</Author><Year>2003</Year><RecNum>3332</RecNum><DisplayText>[122]</DisplayText><record><rec-number>3332</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3332</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bosendial RJ, Hovingh KG, Levels HM, et al.</author></authors></contributors><titles><title>Restoration of endothelial function by increasing high-density lipoprotein in subjects with isolated low high-density lipoprotein</title><secondary-title>CIrculation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>2944-2948</pages><volume>107</volume><dates><year>2003</year></dates><urls></urls></record></Cite></EndNote>[122]. HDL has also been shown to inhibit vascular inflammation by decreasing the expression of E-selectin PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Db2NrZXJpbGw8L0F1dGhvcj48WWVhcj4xOTk5PC9ZZWFy
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ADDIN EN.CITE.DATA [123] and adhesion molecules such as vascular cell adhesion molecule ADDIN EN.CITE <EndNote><Cite><Author>Cockerill</Author><Year>1995</Year><RecNum>3334</RecNum><DisplayText>[124]</DisplayText><record><rec-number>3334</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3334</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Cockerill, G. W.</author><author>Rye, K. A.</author><author>Gamble, J. R.</author><author>Vadas, M. A.</author><author>Barter, P. J.</author></authors></contributors><auth-address>Hanson Center for Cancer Research, Department of Human Immunology, Adelaide, Australia.</auth-address><titles><title>High-density lipoproteins inhibit cytokine-induced expression of endothelial cell adhesion molecules</title><secondary-title>Arterioscler Thromb Vasc Biol</secondary-title><alt-title>Arteriosclerosis, thrombosis, and vascular biology</alt-title></titles><periodical><full-title>Arteriosclerosis, Thrombosis & Vascular Biology</full-title><abbr-1>Arterioscler Thromb Vasc Biol</abbr-1></periodical><alt-periodical><full-title>Arteriosclerosis, Thrombosis, and Vascular Biology</full-title></alt-periodical><pages>1987-94</pages><volume>15</volume><number>11</number><keywords><keyword>Cells, Cultured</keyword><keyword>Cytokines/*pharmacology</keyword><keyword>Dose-Response Relationship, Drug</keyword><keyword>Drug Interactions</keyword><keyword>E-Selectin/*biosynthesis</keyword><keyword>Endothelium, Vascular/*metabolism</keyword><keyword>Fibroblasts/metabolism</keyword><keyword>Humans</keyword><keyword>Intercellular Adhesion Molecule-1/*biosynthesis</keyword><keyword>Lipoproteins, HDL/*pharmacology</keyword><keyword>Vascular Cell Adhesion Molecule-1/*biosynthesis</keyword></keywords><dates><year>1995</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>1079-5642 (Print)
1079-5642 (Linking)</isbn><accession-num>7583580</accession-num><urls><related-urls><url>;[124]. Vascular inflammation begins when LDL is deposited into the arterial wall, resulting in endothelial cells to express selectins and adhesion molecules. This expression leads to leukocyte infiltration within the arterial wall, and oxidization of LDL macrophages into inflammatory foam cells, resulting in atherosclerosis ADDIN EN.CITE <EndNote><Cite><Author>Ley</Author><Year>2007</Year><RecNum>3335</RecNum><DisplayText>[125]</DisplayText><record><rec-number>3335</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3335</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Ley, K.</author><author>Laudanna, C.</author><author>Cybulsky, M. I.</author><author>Nourshargh, S.</author></authors></contributors><auth-address>Robert M. Berne Cardiovascular Research Center and Department of Biomedical Engineering, University of Virginia, Charlottesville, Virginia 22908, USA. klaus@</auth-address><titles><title>Getting to the site of inflammation: the leukocyte adhesion cascade updated</title><secondary-title>Nat Rev Immunol</secondary-title><alt-title>Nature reviews. Immunology</alt-title></titles><periodical><full-title>Nat Rev Immunol</full-title></periodical><pages>678-89</pages><volume>7</volume><number>9</number><keywords><keyword>Animals</keyword><keyword>Cell Adhesion/*immunology</keyword><keyword>Cell Movement</keyword><keyword>Endothelial Cells/immunology</keyword><keyword>Humans</keyword><keyword>Inflammation/*immunology</keyword><keyword>Integrins/metabolism</keyword><keyword>Leukocyte Rolling</keyword><keyword>Leukocytes/*immunology</keyword><keyword>Mice</keyword></keywords><dates><year>2007</year><pub-dates><date>Sep</date></pub-dates></dates><isbn>1474-1741 (Electronic)
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ADDIN EN.CITE.DATA [119]. Plaque accumulation is the underlying cause of atherosclerosis and arterial stiffening. LDL has also been shown to stimulate collagen synthesis in arterial smooth muscle cells PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5KaW1pPC9BdXRob3I+PFllYXI+MTk5NTwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [127], promotes intimal thickening, and impairs NO bioactivity PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5NYXR0aHlzPC9BdXRob3I+PFllYXI+MTk5NzwvWWVhcj48
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ADDIN EN.CITE.DATA [128]. From data derived in the Health, Aging and Body Composition (Health ABC) Study, it was determined that oxidated LDL levels were associated with increased arterial stiffness independent of traditional cardiovascular risk factors such as PA levels, blood pressure, and HDL cholesterol levels [102]. These risks were further exacerbated in those with LDL levels greater than 144 ± 33 mg/dL, in which they were at a 30-55% increased risk of having high arterial stiffness (>10.54m/s) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Ccmlua2xleTwvQXV0aG9yPjxZZWFyPjIwMDk8L1llYXI+
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ADDIN EN.CITE.DATA [130]. 1.3CEREBRAL PALSYCP is a cause of disability that impacts a person across their lifespan ADDIN EN.CITE <EndNote><Cite><Author>Svien</Author><Year>2008</Year><RecNum>3341</RecNum><DisplayText>[9]</DisplayText><record><rec-number>3341</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3341</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Svien, L. R., Berg, P., Stephenson, C.</author></authors></contributors><titles><title>Issues in aging with cerebral palsy</title><secondary-title>Topics in Geriatric Rehabilitation</secondary-title></titles><periodical><full-title>Topics in Geriatric Rehabilitation</full-title></periodical><pages>26-40</pages><volume>24</volume><number>1</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[9]. CP has a prevalence of 1.7 to 2.3 per 1000 live births PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5XaW50ZXI8L0F1dGhvcj48WWVhcj4yMDAyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [131, 132]. CP is a heterogeneous disorder that displays itself in numerous physiologic, neurologic, musculoskeletal, and psychosocial ways. Physiologic descriptors of CP are spastic, ataxic, dyskinetic, and mixed ADDIN EN.CITE <EndNote><Cite><Author>Blair</Author><Year>1985</Year><RecNum>3344</RecNum><DisplayText>[133]</DisplayText><record><rec-number>3344</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3344</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Blair, E.</author><author>Stanley, F.</author></authors></contributors><titles><title>Interobserver agreement in the classification of cerebral palsy</title><secondary-title>Dev Med Child Neurol</secondary-title><alt-title>Developmental medicine and child neurology</alt-title></titles><periodical><full-title>Dev Med Child Neurol</full-title><abbr-1>Developmental medicine and child neurology</abbr-1></periodical><alt-periodical><full-title>Dev Med Child Neurol</full-title><abbr-1>Developmental medicine and child neurology</abbr-1></alt-periodical><pages>615-22</pages><volume>27</volume><number>5</number><keywords><keyword>Age Factors</keyword><keyword>Cerebral Palsy/*classification/diagnosis/physiopathology</keyword><keyword>Child</keyword><keyword>Child, Preschool</keyword><keyword>Humans</keyword><keyword>Movement</keyword><keyword>Probability</keyword><keyword>Terminology as Topic</keyword></keywords><dates><year>1985</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>0012-1622 (Print)
0012-1622 (Linking)</isbn><accession-num>4065435</accession-num><urls><related-urls><url>;[133]. Bax originally defined CP in 1964 as a group of disorders in the development of posture and motor control, occurring as a result of a non-progressive lesion of the developing central nervous system ADDIN EN.CITE <EndNote><Cite><Author>MC</Author><Year>1964</Year><RecNum>3345</RecNum><DisplayText>[134]</DisplayText><record><rec-number>3345</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3345</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bax MC</author></authors></contributors><titles><title>Terminology and classification of cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>295-297</pages><volume>11</volume><dates><year>1964</year></dates><urls></urls></record></Cite></EndNote>[134]. This definition was later expanded and revised to encompass the secondary impairments that accompany CP: Cerebral palsy (CP) describes a group of permanent disorders of the development of movement and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain. The motor disturbances of cerebral palsy are often accompanied by disturbances of sensation, perception, cognition, communication, and behavior, by epilepsy, and by secondary musculoskeletal problems. PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Sb3NlbmJhdW08L0F1dGhvcj48WWVhcj4yMDA3PC9ZZWFy
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ADDIN EN.CITE.DATA [135]A five-level classification system was developed to classify the gross motor function, or control, of children with CP ADDIN EN.CITE <EndNote><Cite><Author>Palisano</Author><Year>2008</Year><RecNum>3347</RecNum><DisplayText>[136]</DisplayText><record><rec-number>3347</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3347</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Palisano, Robert J</author><author>Rosenbaum, Peter</author><author>Bartlett, Doreen</author><author>Livingston, Michael H</author></authors></contributors><titles><title>Content validity of the expanded and revised Gross Motor Function Classification System</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>744-750</pages><volume>50</volume><number>10</number><dates><year>2008</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[136]. This system, known as the Gross Motor Function Classification System (GMFCS), was derived to enhance communication among professionals and families with respect to determining a child’s needs, describing the development of children with CP, and generalizing the results of research into the outcome of treatment ADDIN EN.CITE <EndNote><Cite><Author>Palisano</Author><Year>1997</Year><RecNum>3349</RecNum><DisplayText>[137]</DisplayText><record><rec-number>3349</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3349</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Palisano, Robert</author><author>Rosenbaum, Peter</author><author>Walter, Stephen</author><author>Russell, Dianne</author><author>Wood, Ellen</author><author>Galuppi, Barbara</author></authors></contributors><titles><title>Development and reliability of a system to classify gross motor function in children with cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>214-223</pages><volume>39</volume><number>4</number><dates><year>1997</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[137]. The GMFCS reports the major functional characteristics of children with CP in each level within several age groups: birth to age 2, between ages 2 and 4, between ages 4 and 6, and between ages 6 and 12 years. Motor curves have been developed on the grounds of the five levels of function, demonstrating that individuals’ motor function generally remain stable over time ADDIN EN.CITE <EndNote><Cite><Author>Jahnsen</Author><Year>2006</Year><RecNum>3351</RecNum><DisplayText>[138]</DisplayText><record><rec-number>3351</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3351</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Jahnsen, Reidun</author><author>Aamodt, Geir</author><author>Rosenbaum, Peter</author></authors></contributors><titles><title>Gross Motor Function Classification System used in adults with cerebral palsy: agreement of self‐reported versus professional rating</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>734-738</pages><volume>48</volume><number>9</number><dates><year>2006</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[138]. Studies have reported good to excellent inter-rater reliability for the severity of gross motor function limitations using the GMFCS in children with CP ADDIN EN.CITE <EndNote><Cite><Author>Palisano</Author><Year>1997</Year><RecNum>3350</RecNum><DisplayText>[137, 139]</DisplayText><record><rec-number>3350</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3350</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Palisano, Robert</author><author>Rosenbaum, Peter</author><author>Walter, Stephen</author><author>Russell, Dianne</author><author>Wood, Ellen</author><author>Galuppi, Barbara</author></authors></contributors><titles><title>Development and reliability of a system to classify gross motor function in children with cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>214-223</pages><volume>39</volume><number>4</number><dates><year>1997</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite><Cite><Author>Wood</Author><Year>2000</Year><RecNum>3354</RecNum><record><rec-number>3354</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3354</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Wood, Ellen</author><author>Rosenbaum, Peter</author></authors></contributors><titles><title>The gross motor function classification system for cerebral palsy: a study of reliability and stability over time</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>292-296</pages><volume>42</volume><number>5</number><dates><year>2000</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[137, 139]. With respects to topographic distribution in children, Gorter et al. reported that those with hemi- and diplegia were most represented in GMFCS levels I, II and III, whereas those with tri- and quadriplegia were represented in GMFCS levels IV and V. Furthermore, with respect to type of motor impairments, 78% of the cohort was spastic and 33% of the spastic individuals were in GMFCS level I ADDIN EN.CITE <EndNote><Cite><Author>Gorter</Author><Year>2004</Year><RecNum>3356</RecNum><DisplayText>[140]</DisplayText><record><rec-number>3356</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3356</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Gorter, Jan Willem</author><author>Rosenbaum, Peter L</author><author>Hanna, Steven E</author><author>Palisano, Robert J</author><author>Bartlett, Doreen J</author><author>Russell, Dianne J</author><author>Walter, Stephen D</author><author>Raina, Parminder</author><author>Galuppi, Barbara E</author><author>Wood, MD</author></authors></contributors><titles><title>Limb distribution, motor impairment, and functional classification of cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>461-467</pages><volume>46</volume><number>7</number><dates><year>2004</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[140]. The relationship between limb distribution and GMFCS levels was stronger when two categories of limb distribution were used as opposed to four. Finally, the prevalence of CP recognizing motor function level is greatest in GMFCS level I (1.3/1000). Whereas levels II-V averaged 0.3/1000 births ADDIN EN.CITE <EndNote><Cite><Author>Westbom</Author><Year>2007</Year><RecNum>3414</RecNum><DisplayText>[141]</DisplayText><record><rec-number>3414</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3414</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Westbom, Lena</author><author>Hagglund, Gunnar</author><author>Nordmark, Eva</author></authors></contributors><titles><title>Cerebral palsy in a total population of 4–11 year olds in southern Sweden. Prevalence and distribution according to different CP classification systems</title><secondary-title>BMC pediatrics</secondary-title></titles><periodical><full-title>BMC Pediatrics</full-title><abbr-1>BMC Pediatr</abbr-1></periodical><pages>41</pages><volume>7</volume><number>1</number><dates><year>2007</year></dates><isbn>1471-2431</isbn><urls></urls></record></Cite></EndNote>[141]. Although CP is a condition that spans a lifetime, there is no defined systematic follow-up of adults with CP after the age of 18, and the literature is limited with regards to studies that have used the GMFCS in adults ADDIN EN.CITE <EndNote><Cite><Author>Sandstrom K</Author><Year>2004</Year><RecNum>3357</RecNum><DisplayText>[142]</DisplayText><record><rec-number>3357</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3357</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Sandstrom K, Alinder J, Oberg B.</author></authors></contributors><titles><title>Descriptions of functioning and health and relation to gross motor function classification in adults with cerebral palsy</title><secondary-title>Disability & Rehabilitation</secondary-title></titles><periodical><full-title>Disability & Rehabilitation</full-title><abbr-1>Disabil Rehabil</abbr-1></periodical><pages>1023-1031</pages><volume>26</volume><dates><year>2004</year></dates><urls></urls></record></Cite></EndNote>[142]. The intraclass correlation coefficient between professional rating and self-reported GMFCS levels is high (0.93) ADDIN EN.CITE <EndNote><Cite><Author>Jahnsen</Author><Year>2006</Year><RecNum>3352</RecNum><DisplayText>[138]</DisplayText><record><rec-number>3352</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3352</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Jahnsen, Reidun</author><author>Aamodt, Geir</author><author>Rosenbaum, Peter</author></authors></contributors><titles><title>Gross Motor Function Classification System used in adults with cerebral palsy: agreement of self‐reported versus professional rating</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>734-738</pages><volume>48</volume><number>9</number><dates><year>2006</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[138]. With regards to stability in GMFCS level as children with CP progress into their adult years, in a cohort of 62 adults with CP, 52% did not show any changes, whereas 40% showed a change in classification to a lower level of function in comparison to when they were 10 to 12 years ADDIN EN.CITE <EndNote><Cite><Author>Jahnsen</Author><Year>2006</Year><RecNum>3352</RecNum><DisplayText>[138]</DisplayText><record><rec-number>3352</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3352</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Jahnsen, Reidun</author><author>Aamodt, Geir</author><author>Rosenbaum, Peter</author></authors></contributors><titles><title>Gross Motor Function Classification System used in adults with cerebral palsy: agreement of self‐reported versus professional rating</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>734-738</pages><volume>48</volume><number>9</number><dates><year>2006</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[138]. The majority of participants described pain, exhaustion, and balance problems as the underlying reason to choose a wheelchair as the main mode of transportation, thus transposing them into a lower functioning level [124]. Therefore, based on the intraclass correlation coefficient, the GMFCS seems to be a strong tool for identifying the level of motor function in adults with CP. 1.3.1Cerebral palsy and physical activityThe majority of studies that have examined PA levels in the CP population have done so in cohorts of children PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5CZWxsPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [143-147]. PA levels and total energy expenditure have both been shown to be lower in children with CP who have moderate to high gross motor function compared to their typically developing peers [115-118]. Furthermore, PA levels of adolescents with CP were related to level of GMFCS and were inversely related to age PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5NYWhlcjwvQXV0aG9yPjxZZWFyPjIwMDc8L1llYXI+PFJl
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ADDIN EN.CITE.DATA [146]. Although total energy expenditure is similar between higher functioning children with CP and typically developing peers, the energy expenditure associated with walking is greater in children with CP that have lower PA levels PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5NYWx0YWlzPC9BdXRob3I+PFllYXI+MjAwNTwvWWVhcj48
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ADDIN EN.CITE PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5NYWx0YWlzPC9BdXRob3I+PFllYXI+MjAwNTwvWWVhcj48
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b3RlPgB=
ADDIN EN.CITE.DATA [148]. Ambulatory children with CP also have higher mean heart rate values at rest compared to their typically developing peers PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5LaG9sb2Q8L0F1dGhvcj48WWVhcj4yMDEzPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [145], while vigorous activity levels in ambulatory children with CP were lower than their typically developing peers. Despite these differences in activity levels, several indexes of vascular structure and function measures were not different between higher functioning adolescents with CP and their age matched healthy peers ADDIN EN.CITE <EndNote><Cite><Author>Martin</Author><Year>2012</Year><RecNum>3364</RecNum><DisplayText>[149]</DisplayText><record><rec-number>3364</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3364</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Martin, Audra A</author><author>Cotie, Lisa M</author><author>Timmons, Brian W</author><author>Gorter, Jan Willem</author><author>MacDonald, Maureen J</author></authors></contributors><titles><title>Arterial structure and function in ambulatory adolescents with cerebral palsy are not different from healthy controls</title><secondary-title>International journal of pediatrics</secondary-title></titles><periodical><full-title>International Journal of Pediatrics</full-title><abbr-1>Int J Pediatr</abbr-1></periodical><volume>2012</volume><dates><year>2012</year></dates><isbn>1687-9740</isbn><urls></urls></record></Cite></EndNote>[149]. These relationships have yet to be examined in the adult CP population.Although PA data in adults with CP is scarce, relationships similar to those observed in children with CP exist PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5OaWV1d2VuaHVpanNlbjwvQXV0aG9yPjxZZWFyPjIwMTE8
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ADDIN EN.CITE.DATA [151]. Physical strain also limits walking ability in adults with CP. Adults with CP with high physical strain, identified as the oxygen uptake while walking as a percentage of peak aerobic capacity, are likely to walk less in daily life PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5TbGFtYW48L0F1dGhvcj48WWVhcj4yMDEzPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [152]. This would imply that as gross motor function decreases, persons with CP would have lower walking/activity times, but greater energy expenditure during walking. Regardless of age, persons with CP are at an increased risk for increased levels of inactivity and low fitness, which can lead to secondary health complications. One exception to this trend has been noted, however, in that levels of daily PA in adults with CP that are high functioning are comparable to levels in healthy subjects. It should be emphasized that this study was conducted in a small cohort (n=16) with highest levels of motor functioning PEVuZE5vdGU+PENpdGU+PEF1dGhvcj52YW4gZGVyIFNsb3Q8L0F1dGhvcj48WWVhcj4yMDA3PC9Z
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ADDIN EN.CITE PEVuZE5vdGU+PENpdGU+PEF1dGhvcj52YW4gZGVyIFNsb3Q8L0F1dGhvcj48WWVhcj4yMDA3PC9Z
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ADDIN EN.CITE.DATA [153]. Persons with CP are also likely not to receive structural treatment to improve fitness and activity levels in their late adolescent years, which is precisely the period when adult PA patterns are developed PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5TbGFtYW48L0F1dGhvcj48WWVhcj4yMDEwPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [155]. The most recent literature has suggested that simply striving for increases in MVPA may not be enough. It may be of greater importance to replace sedentary behavior with light PA in adults with CP to put them at a lower risk for developing secondary complications, such as CVD PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5WZXJzY2h1cmVuPC9BdXRob3I+PFllYXI+MjAxNDwvWWVh
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ADDIN EN.CITE.DATA [156].1.3.2Secondary complications in adults with cerebral palsyPersons having a disability are at an increased risk of inactivity ADDIN EN.CITE <EndNote><Cite><Author>Hallum</Author><Year>1995</Year><RecNum>3508</RecNum><DisplayText>[157]</DisplayText><record><rec-number>3508</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3508</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hallum, Ann</author></authors></contributors><titles><title>Disability and the transition to adulthood: issues for the disabled child, the family, and the pediatrician</title><secondary-title>Current Problems in Pediatrics</secondary-title></titles><periodical><full-title>Current Problems in Pediatrics</full-title></periodical><pages>12-50</pages><volume>25</volume><number>1</number><dates><year>1995</year></dates><isbn>0045-9380</isbn><urls></urls></record></Cite></EndNote>[157]. For adults with CP, impaired function and poor health typically present common barriers to participation in PA. Adults with CP are likely not engaging in sufficient PA to produce the improvements in fitness required to experience positive health benefits PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5UaG9ycGU8L0F1dGhvcj48WWVhcj4yMDA5PC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [11, 160], those having the highest functioning levels with CP had a life expectancy that was only 5 years less than the normal population. Life expectancy becomes much more variable as the severity of CP increases ADDIN EN.CITE <EndNote><Cite><Author>Strauss</Author><Year>1998</Year><RecNum>3195</RecNum><DisplayText>[160]</DisplayText><record><rec-number>3195</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3195</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Strauss, D.</author><author>Shavelle, R.</author></authors></contributors><auth-address>Department of Statistics, University of California, Riverside 92521, USA.</auth-address><titles><title>Life expectancy of adults with cerebral palsy</title><secondary-title>Dev Med Child Neurol</secondary-title><alt-title>Developmental medicine and child neurology</alt-title></titles><periodical><full-title>Dev Med Child Neurol</full-title><abbr-1>Developmental medicine and child neurology</abbr-1></periodical><alt-periodical><full-title>Dev Med Child Neurol</full-title><abbr-1>Developmental medicine and child neurology</abbr-1></alt-periodical><pages>369-75</pages><volume>40</volume><number>6</number><keywords><keyword>Activities of Daily Living</keyword><keyword>Adolescent</keyword><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Cerebral Palsy/*mortality</keyword><keyword>Child</keyword><keyword>Female</keyword><keyword>Forecasting</keyword><keyword>Humans</keyword><keyword>*Life Expectancy</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Motor Skills</keyword><keyword>Risk Assessment</keyword></keywords><dates><year>1998</year><pub-dates><date>Jun</date></pub-dates></dates><isbn>0012-1622 (Print)
0012-1622 (Linking)</isbn><accession-num>9652777</accession-num><urls><related-urls><url> Technologies</remote-database-provider><language>English</language></record></Cite></EndNote>[160]. With respect to cause of death, many more deaths have been attributed to diseases of the respiratory and circulatory system in adults with CP aged 20-50, compared to the general population, and these are typically more pronounced in the more severely affected PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IZW1taW5nPC9BdXRob3I+PFllYXI+MjAwNjwvWWVhcj48
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Tm90ZT5=
ADDIN EN.CITE.DATA [11].Gaps in the literature are clearly evident with respect to respiratory and cardiovascular changes as persons with CP progress from adolescence into adulthood. Prior studies have focused on capturing the changes, if any, in gross motor function during this time frame PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5HYW5ub3R0aTwvQXV0aG9yPjxZZWFyPjIwMTA8L1llYXI+
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ADDIN EN.CITE.DATA [161, 162, 165]. What is even more interesting is that those who ambulate with difficulty at age 10 have a chance to improve through adolescence, whereas those with poorer function and/or using a wheelchair likely decline PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5EYXk8L0F1dGhvcj48WWVhcj4yMDA3PC9ZZWFyPjxSZWNO
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ADDIN EN.CITE.DATA [162]. In children, the ‘stable-limit’ model was adapted for those in GMFCS levels I and II, stating that motor development is accelerated up to age 5, and remains stable afterwards. The ‘peak and decline’ model showed a peak in development at age 7, which began to decline afterwards, and was highlighted in GMFCS level IV PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5TbWl0czwvQXV0aG9yPjxZZWFyPjIwMTM8L1llYXI+PFJl
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ADDIN EN.CITE.DATA [165]. Studies have shown that in the adult population, a third had deteriorated in motor function from adolescence to adulthood and this trend was evident in lower functioning individuals during their younger years ADDIN EN.CITE <EndNote><Cite><Author>Sandstrom K</Author><Year>2004</Year><RecNum>3357</RecNum><DisplayText>[142]</DisplayText><record><rec-number>3357</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3357</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Sandstrom K, Alinder J, Oberg B.</author></authors></contributors><titles><title>Descriptions of functioning and health and relation to gross motor function classification in adults with cerebral palsy</title><secondary-title>Disability & Rehabilitation</secondary-title></titles><periodical><full-title>Disability & Rehabilitation</full-title><abbr-1>Disabil Rehabil</abbr-1></periodical><pages>1023-1031</pages><volume>26</volume><dates><year>2004</year></dates><urls></urls></record></Cite></EndNote>[142]. Loss of motor function with aging in CP has been associated with weight increases PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5HYW5ub3R0aTwvQXV0aG9yPjxZZWFyPjIwMTA8L1llYXI+
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ADDIN EN.CITE.DATA [167]. Along with the motor impairments evident in adults with CP, high rates of sedentary time and diminished fitness have resulted in a comparison to individuals with a spinal cord injury ADDIN EN.CITE <EndNote><Cite><Author>Bauman</Author><Year>2009</Year><RecNum>3382</RecNum><DisplayText>[168]</DisplayText><record><rec-number>3382</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3382</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bauman, William A</author></authors></contributors><titles><title>The potential metabolic consequences of cerebral palsy: inferences from the general population and persons with spinal cord injury</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>64-78</pages><volume>51</volume><number>s4</number><dates><year>2009</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[168]; a population with enhanced sarcopenia, increased adiposity, insulin resistance, hyperlipidemia and CVD risk. However, in comparison to most traumatic SCI, individuals with CP have the added risk of muscle deterioration and metabolic dysregulation from birth. Mortality records have shown a nearly threefold greater death rate from coronary artery disease in adults with CP compared to the general population ADDIN EN.CITE <EndNote><Cite><Author>Strauss</Author><Year>1999</Year><RecNum>3384</RecNum><DisplayText>[169]</DisplayText><record><rec-number>3384</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3384</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Strauss, David</author><author>Cable, William</author><author>Shavelle, Robert</author></authors></contributors><titles><title>Causes of excess mortality in cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>580-585</pages><volume>41</volume><number>9</number><dates><year>1999</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[169]. Most of the research conducted has been observational and cross-sectional in nature, thus unable to track changes over time in outcome variables such as obesity, metabolic dysregulation, and CVD. The majority of these studies have looked at energy expenditure ADDIN EN.CITE <EndNote><Cite><Author>Dickerson</Author><Year>2003</Year><RecNum>3191</RecNum><DisplayText>[170]</DisplayText><record><rec-number>3191</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3191</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Dickerson, R. N.</author><author>Brown, R. O.</author><author>Hanna, D. L.</author><author>Williams, J. E.</author></authors></contributors><auth-address>Department of Pharmacy, University of Tennessee, Arlington, Tennessee 38163, USA. rdickerson@utmem.edu</auth-address><titles><title>Energy requirements of non-ambulatory, tube-fed adult patients with cerebral palsy and chronic hypothermia</title><secondary-title>Nutrition</secondary-title><alt-title>Nutrition</alt-title></titles><periodical><full-title>Nutrition</full-title><abbr-1>Nutrition</abbr-1></periodical><alt-periodical><full-title>Nutrition</full-title><abbr-1>Nutrition</abbr-1></alt-periodical><pages>741-6</pages><volume>19</volume><number>9</number><keywords><keyword>Adult</keyword><keyword>Basal Metabolism</keyword><keyword>Calorimetry, Indirect</keyword><keyword>Cerebral Palsy/complications/*metabolism</keyword><keyword>Disabled Persons</keyword><keyword>*Energy Intake</keyword><keyword>*Energy Metabolism</keyword><keyword>*Enteral Nutrition</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Hypothermia/complications/*metabolism</keyword><keyword>Male</keyword><keyword>Nutritional Requirements</keyword><keyword>Oxygen Consumption</keyword></keywords><dates><year>2003</year><pub-dates><date>Sep</date></pub-dates></dates><isbn>0899-9007 (Print)
0899-9007 (Linking)</isbn><accession-num>12921883</accession-num><urls><related-urls><url> Technologies</remote-database-provider><language>English</language></record></Cite></EndNote>[170], simple anthropometric measures PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5GZXJyYW5nPC9BdXRob3I+PFllYXI+MTk5MjwvWWVhcj48
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ADDIN EN.CITE.DATA [167]. These elevations in resting metabolic rate in non-ambulatory individuals with CP are unlikely sufficient to attenuate negative health impairments associated with their low activity levels and high sedentary behaviours. A recent study showed that increased sedentary behavior was associated with increased adiposity and intermuscular adipose tissue PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QZXRlcnNvbjwvQXV0aG9yPjxZZWFyPjIwMTI8L1llYXI+
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ADDIN EN.CITE.DATA [174]. Individuals with lower gross motor functioning, particularly GMFCS levels IV and V, have lower BMI compared to higher functioning individuals (GMFCS I-III) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QZXRlcnNvbjwvQXV0aG9yPjxZZWFyPjIwMTI8L1llYXI+
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ADDIN EN.CITE.DATA [172]. These conflicting anthropometric results indicate that BMI is likely not a valid predictor of cardiometabolic risk in the adult CP population. In support of this theory, it has been recently shown that higher body fat was the strongest predictor of 10-year CVD risk in a cohort of adults with CP PEVuZE5vdGU+PENpdGU+PEF1dGhvcj52YW4gZGVyIFNsb3Q8L0F1dGhvcj48WWVhcj4yMDEzPC9Z
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ADDIN EN.CITE.DATA [175].1.3.3Physical activity and cardiovascular health in adulthoodCP is a permanent disability that limits activity across the lifespan [115]. It has been identified that PA levels of persons with CP are related to the level of gross motor function and are inversely associated with age [131], thus potentially placing adults with CP who are lower functioning at an increased risk of CVD. The potential consequences of this reduced activity on specific parameters of arterial health and CVD risk in an adult population of CP patients have yet to be examined. To our knowledge, there is no previous published assessment of the potential impacts of this physical disability on levels of PA and vascular health in adults with CP. 1.4PURPOSE AND HYPOTHESISThe purposes of this study were to provide normative assessments of arterial structure (cIMT) and function (FMD, PWV, and carotid distensibility) and PA patterns in adults aged 18-75 with GMFCS levels I-V CP to determine if inactivity is predictive of compromised vascular health. We hypothesize that adults with CP who are of higher functioning (GMFCS I-II) will have increased levels of PA, increased endothelial function (FMD) and decreased arterial stiffness (distensibility and PWV) compared to those who are lower functioning (GMFCS III-V). 1.5REFERENCES ADDIN EN.REFLIST 1.Geneva, W.H.O., Global status report on noncommunicable disease 2010. 2011.2.Mathers, C.D. and D. Loncar, Projections of global mortality and burden of disease from 2002 to 2030. 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Gait Posture, 2010. 32(1): p. 46-52.162.Day, S.M., et al., Change in ambulatory ability of adolescents and young adults with cerebral palsy. Dev Med Child Neurol, 2007. 49(9): p. 647-53.163.Bottos, M., et al., Functional status of adults with cerebral palsy and implications for treatment of children. Dev Med Child Neurol, 2001. 43(8): p. 516-28.164.Sandstrom, K., J. Alinder, and B. Oberg, Descriptions of functioning and health and relations to a gross motor classification in adults with cerebral palsy. Disabil Rehabil, 2004. 26(17): p. 1023-31.165.Smits, D.W., et al., Longitudinal development of gross motor function among Dutch children and young adults with cerebral palsy: an investigation of motor growth curves. Dev Med Child Neurol, 2013. 55(4): p. 378-84.166.Blackman, J.A. and M.R. Conaway, Adolescents with cerebral palsy: transitioning to adult health care services. Clin Pediatr (Phila), 2014. 53(4): p. 356-63.167.Johnson, R.K., et al., Total energy expenditure in adults with cerebral palsy as assessed by doubly labeled water. J Am Diet Assoc, 1997. 97(9): p. 966-70.168.Bauman, W.A., The potential metabolic consequences of cerebral palsy: inferences from the general population and persons with spinal cord injury. Developmental Medicine & Child Neurology, 2009. 51(s4): p. 64-78.169.Strauss, D., W. Cable, and R. Shavelle, Causes of excess mortality in cerebral palsy. Developmental Medicine & Child Neurology, 1999. 41(9): p. 580-585.170.Dickerson, R.N., et al., Energy requirements of non-ambulatory, tube-fed adult patients with cerebral palsy and chronic hypothermia. Nutrition, 2003. 19(9): p. 741-6.171.Ferrang, T.M., R.K. Johnson, and M.S. Ferrara, Dietary and anthropometric assessment of adults with cerebral palsy. J Am Diet Assoc, 1992. 92(9): p. 1083-6.172.Peterson, M.D., H.J. Haapala, and E.A. Hurvitz, Predictors of cardiometabolic risk among adults with cerebral palsy. Arch Phys Med Rehabil, 2012. 93(5): p. 816-21.173.Johnson, R.K., et al., Athetosis increases resting metabolic rate in adults with cerebral palsy. J Am Diet Assoc, 1996. 96(2): p. 145-8.174.Peterson, M.D., et al., Secondary muscle pathology and metabolic dysregulation in adults with cerebral palsy. Am J Physiol Endocrinol Metab, 2012. 303(9): p. E1085-93.175.van der Slot, W.M., et al., Cardiovascular disease risk in adults with spastic bilateral cerebral palsy. J Rehabil Med, 2013. 45(9): p. 866-72.CHAPTER 2RELATIONSHIPS BETWEEN MOTOR CLASSIFICATION, PHYSICAL ACTIVITY AND CARDIOVASCULAR HEALTH IN ADULTS WITH CEREBRAL PALSY2.1INTRODUCTIONCerebral palsy (CP) is a disability that impacts a person throughout their lifespan ADDIN EN.CITE <EndNote><Cite><Author>Svien</Author><Year>2008</Year><RecNum>3417</RecNum><DisplayText>[1]</DisplayText><record><rec-number>3417</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3417</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Svien, L. R., Berg, P., Stephenson, C.</author></authors></contributors><titles><title>Issues in aging with cerebral palsy</title><secondary-title>Topics in Geriatric Rehabilitation</secondary-title></titles><periodical><full-title>Topics in Geriatric Rehabilitation</full-title></periodical><pages>26-40</pages><volume>24</volume><number>1</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[1] and limits activity as a result of disturbances that occurred during the development of the fetal or infant brain PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Sb3NlbmJhdW08L0F1dGhvcj48WWVhcj4yMDA3PC9ZZWFy
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ADDIN EN.CITE.DATA [2]. Despite the lifelong implications, there is no defined systematic follow-up of adults with CP after the age of 18 ADDIN EN.CITE <EndNote><Cite><Author>Sandstrom K</Author><Year>2004</Year><RecNum>3357</RecNum><DisplayText>[3]</DisplayText><record><rec-number>3357</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3357</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Sandstrom K, Alinder J, Oberg B.</author></authors></contributors><titles><title>Descriptions of functioning and health and relation to gross motor function classification in adults with cerebral palsy</title><secondary-title>Disability & Rehabilitation</secondary-title></titles><periodical><full-title>Disability & Rehabilitation</full-title><abbr-1>Disabil Rehabil</abbr-1></periodical><pages>1023-1031</pages><volume>26</volume><dates><year>2004</year></dates><urls></urls></record></Cite></EndNote>[3]. The Gross Motor Function Classification System (GMFCS) is a five-level classification system that was developed to classify gross motor function of children with CP ADDIN EN.CITE <EndNote><Cite><Author>Palisano</Author><Year>2008</Year><RecNum>3348</RecNum><DisplayText>[4]</DisplayText><record><rec-number>3348</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3348</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Palisano, Robert J</author><author>Rosenbaum, Peter</author><author>Bartlett, Doreen</author><author>Livingston, Michael H</author></authors></contributors><titles><title>Content validity of the expanded and revised Gross Motor Function Classification System</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>744-750</pages><volume>50</volume><number>10</number><dates><year>2008</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[4]. This scale has been adopted by the adult population, and studies have shown that 40% of adults with CP are in a lower GMFCS level compared to when they were children ADDIN EN.CITE <EndNote><Cite><Author>Jahnsen</Author><Year>2006</Year><RecNum>3352</RecNum><DisplayText>[5]</DisplayText><record><rec-number>3352</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3352</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Jahnsen, Reidun</author><author>Aamodt, Geir</author><author>Rosenbaum, Peter</author></authors></contributors><titles><title>Gross Motor Function Classification System used in adults with cerebral palsy: agreement of self‐reported versus professional rating</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>734-738</pages><volume>48</volume><number>9</number><dates><year>2006</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[5]. Reasons behind this decline in motor function may include the long-term impacts of pain, exhaustion, and balance problems. As such, adults with CP are less physically active than their healthy aged counterparts PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5DYXJsb248L0F1dGhvcj48WWVhcj4yMDEzPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [6, 7]. Lack of physical activity (PA) is the second leading behavioural cause of death in the USA, following only tobacco use ADDIN EN.CITE <EndNote><Cite><Author>Mokdad</Author><Year>2004</Year><RecNum>3270</RecNum><DisplayText>[8]</DisplayText><record><rec-number>3270</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3270</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Mokdad, A. H.</author><author>Marks, J. S.</author><author>Stroup, D. F.</author><author>Gerberding, J. L.</author></authors></contributors><auth-address>Division of Adult and Community Health, Centers for Disease Control and Prevention, Atlanta, Ga, USA. amokdad@</auth-address><titles><title>Actual causes of death in the United States, 2000</title><secondary-title>JAMA</secondary-title><alt-title>JAMA : the journal of the American Medical Association</alt-title></titles><alt-periodical><full-title>JAMA : the journal of the American Medical Association</full-title></alt-periodical><pages>1238-45</pages><volume>291</volume><number>10</number><keywords><keyword>Accidents, Traffic/mortality</keyword><keyword>Alcohol Drinking</keyword><keyword>Cause of Death/*trends</keyword><keyword>Communicable Diseases/mortality</keyword><keyword>Diet</keyword><keyword>Humans</keyword><keyword>Physical Fitness</keyword><keyword>Poisoning/mortality</keyword><keyword>Risk Factors</keyword><keyword>Sexual Behavior</keyword><keyword>Smoking/mortality</keyword><keyword>Substance-Related Disorders</keyword><keyword>United States/epidemiology</keyword><keyword>Wounds, Gunshot/mortality</keyword></keywords><dates><year>2004</year><pub-dates><date>Mar 10</date></pub-dates></dates><isbn>1538-3598 (Electronic)
0098-7484 (Linking)</isbn><accession-num>15010446</accession-num><urls><related-urls><url>;[8]. Lifelong decreases in PA could put adults with CP at an elevated risk of developing a variety of secondary complications, including cardiovascular disease (CVD) ADDIN EN.CITE <EndNote><Cite><Author>Blair</Author><Year>1996</Year><RecNum>3265</RecNum><DisplayText>[9]</DisplayText><record><rec-number>3265</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3265</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Blair, S. N.</author><author>Kampert, J. B.</author><author>Kohl, H. W., 3rd</author><author>Barlow, C. E.</author><author>Macera, C. A.</author><author>Paffenbarger, R. S., Jr.</author><author>Gibbons, L. W.</author></authors></contributors><auth-address>Cooper Institute for Aerobics Research, Dallas, Tex 75230, USA. steve0704@</auth-address><titles><title>Influences of cardiorespiratory fitness and other precursors on cardiovascular disease and all-cause mortality in men and women</title><secondary-title>JAMA</secondary-title><alt-title>JAMA : the journal of the American Medical Association</alt-title></titles><alt-periodical><full-title>JAMA : the journal of the American Medical Association</full-title></alt-periodical><pages>205-10</pages><volume>276</volume><number>3</number><keywords><keyword>Adult</keyword><keyword>Cardiovascular Diseases/*mortality</keyword><keyword>*Cause of Death</keyword><keyword>Confidence Intervals</keyword><keyword>Exercise Test</keyword><keyword>Female</keyword><keyword>Follow-Up Studies</keyword><keyword>Humans</keyword><keyword>Likelihood Functions</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Physical Examination</keyword><keyword>*Physical Fitness</keyword><keyword>Precipitating Factors</keyword><keyword>Proportional Hazards Models</keyword><keyword>Regression Analysis</keyword><keyword>Risk Factors</keyword></keywords><dates><year>1996</year><pub-dates><date>Jul 17</date></pub-dates></dates><isbn>0098-7484 (Print)
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ADDIN EN.CITE.DATA [10]. Furthermore, young adults with CP with moderate to high gross motor function typically participate in less than half the amount of PA of their able-bodied peers PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5DYXJsb248L0F1dGhvcj48WWVhcj4yMDEzPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [6]. Healthy adults over the age of 18 have been shown to be at an increased risk of CVD-related and all-cause mortality when greater than 75% of time is spent in the sedentary state ADDIN EN.CITE <EndNote><Cite><Author>Katzmarzyk</Author><Year>2001</Year><RecNum>3272</RecNum><DisplayText>[11]</DisplayText><record><rec-number>3272</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3272</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Katzmarzyk, P. T.</author><author>Craig, C. L.</author><author>Bouchard, C.</author></authors></contributors><auth-address>School of Kinesiology and Health Science, York University, 4700 Keele St., Ontario, M3J 1P3, North York, Canada. katzmarz@yorku.ca</auth-address><titles><title>Original article underweight, overweight and obesity: relationships with mortality in the 13-year follow-up of the Canada Fitness Survey</title><secondary-title>J Clin Epidemiol</secondary-title><alt-title>Journal of clinical epidemiology</alt-title></titles><alt-periodical><full-title>Journal of Clinical Epidemiology</full-title></alt-periodical><pages>916-20</pages><volume>54</volume><number>9</number><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Canada/epidemiology</keyword><keyword>Female</keyword><keyword>*Health Surveys</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Obesity/etiology/*mortality</keyword><keyword>Proportional Hazards Models</keyword><keyword>Risk Factors</keyword><keyword>Sex Distribution</keyword></keywords><dates><year>2001</year><pub-dates><date>Sep</date></pub-dates></dates><isbn>0895-4356 (Print)
0895-4356 (Linking)</isbn><accession-num>11520651</accession-num><urls><related-urls><url>;[11]. Sedentary time has been identified as being detrimentally associated with higher waist circumference (WC), hyperglycemia, and hyperinsulinemia ADDIN EN.CITE <EndNote><Cite><Author>Healy</Author><Year>2008</Year><RecNum>3274</RecNum><DisplayText>[12]</DisplayText><record><rec-number>3274</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3274</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Healy, G.N., Wijndaele, K., Dunstan, D.W., Shaw, J.E., Salmon, J., Zimmet, P.Z., Owen, N.</author></authors></contributors><titles><title>Objectively measured sedentary time, physical activtiy, and metabolic risk</title><secondary-title>Diabetes Care</secondary-title></titles><periodical><full-title>Diabetes Care</full-title></periodical><pages>369-371</pages><volume>31</volume><number>2</number><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[12]. Sedentary times in adults with CP have been reported to be twice the maximum recommended amount, therefore suggesting that this population may be at an increased risk for CVD PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5DYXJsb248L0F1dGhvcj48WWVhcj4yMDEzPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [13]. The potential consequences of this sedentary lifestyle on emerging CVD risk factors of arterial health and biomarkers of inflammation and metabolism in an adult population of individuals with CP have yet to be examined. Although some limited literature does exist on causes of mortality ADDIN EN.CITE <EndNote><Cite><Author>Strauss</Author><Year>1999</Year><RecNum>3385</RecNum><DisplayText>[31]</DisplayText><record><rec-number>3385</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3385</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Strauss, David</author><author>Cable, William</author><author>Shavelle, Robert</author></authors></contributors><titles><title>Causes of excess mortality in cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>580-585</pages><volume>41</volume><number>9</number><dates><year>1999</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[31], predictors of cardiometabolic risk PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QZXRlcnNvbjwvQXV0aG9yPjxZZWFyPjIwMTI8L1llYXI+
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ADDIN EN.CITE.DATA [33], to our knowledge, there is no assessment of the potential impacts of this physical disability on levels of PA, vascular and cardiometabolic health in adults with CP. Comprehensive assessment of traditional and novel CVD risk factors in adults with CP may help in the early detection of CVD and in the evaluation of interventions designed to combat CVD.It has been suggested in healthy populations that engaging in PA can increase elastin content and attenuate the progression of collagen within the arterial wall, thereby slowing the age-associated increase in arterial stiffness ADDIN EN.CITE <EndNote><Cite><Author>Tanaka</Author><Year>2005</Year><RecNum>3267</RecNum><DisplayText>[14]</DisplayText><record><rec-number>3267</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3267</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Tanaka, H. and Safar ME</author></authors></contributors><titles><title>Influence of lifestyle modification on arterial stiffness and wave reflections</title><secondary-title>American Journal of Hypertension</secondary-title></titles><periodical><full-title>American Journal of Hypertension</full-title></periodical><pages>137-144</pages><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[14]. Pulse wave velocity (PWV) is a robust and reproducible measure of arterial stiffness with increases in PWV being a subsequent marker of CVD risk ADDIN EN.CITE <EndNote><Cite><Author>Laurent</Author><Year>2006</Year><RecNum>3256</RecNum><DisplayText>[15]</DisplayText><record><rec-number>3256</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3256</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laurent, S., Cockcroft, J., Van Bortel, L., et al.</author></authors></contributors><titles><title>Expert consensus document on arterial stiffness: methodological issues and clinical application</title><secondary-title>European Heart Journal</secondary-title></titles><periodical><full-title>European Heart Journal</full-title></periodical><pages>2588-2605</pages><volume>27</volume><dates><year>2006</year></dates><urls></urls></record></Cite></EndNote>[15]. In adults, obesity, age, hypertension, hyperinsulinemia, and hyperglycemia have been shown to positively correlate with PWV, while increased levels of PA present with a negative relationship ADDIN EN.CITE <EndNote><Cite><Author>Seals DR</Author><Year>2008</Year><RecNum>3300</RecNum><DisplayText>[16]</DisplayText><record><rec-number>3300</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3300</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Seals DR, DeSouza CA, Donato AJ, Tanaka H</author></authors></contributors><titles><title>Habitual exercise and arterial aging</title><secondary-title>Journal of Applied Physiology</secondary-title></titles><periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></periodical><pages>1323-1332</pages><volume>105</volume><dates><year>2008</year></dates><urls></urls></record></Cite></EndNote>[16]. Carotid intima media thickness (cIMT) and distensibility are two additional indices of arterial health that assess structure and function, respectively. A cIMT greater than 0.82mm has been shown to increase the risk of myocardial infarction, stroke, and peripheral arterial disease in middle-aged men ADDIN EN.CITE <EndNote><Cite><Author>O'Leary DH</Author><Year>1999</Year><RecNum>3283</RecNum><DisplayText>[17]</DisplayText><record><rec-number>3283</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3283</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Leary DH, Polak JF, Kronmal RA, Burke GL, Wolfson Jr SK</author></authors></contributors><titles><title>Carotid-artery intima and media thickness as a risk factor for myocardial infarction and stroke in older adults. Cardiovascular Health Study Collaborative Research Group.</title><secondary-title>N Engl J Med</secondary-title></titles><periodical><full-title>N Engl J Med</full-title></periodical><pages>14-22</pages><volume>340</volume><dates><year>1999</year></dates><urls></urls></record></Cite></EndNote>[17]. The impact of PA on IMT has been controversial, with exercise training interventions longer than 3 months in duration required to elicit positive changes PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5UYW5ha2E8L0F1dGhvcj48WWVhcj4yMDAyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [19], inflammation ADDIN EN.CITE <EndNote><Cite><Author>Schuett H</Author><Year>2009</Year><RecNum>3326</RecNum><DisplayText>[20]</DisplayText><record><rec-number>3326</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3326</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Schuett H, Luchtefeld M, Grothusen C, Grote K, Schieffer B</author></authors></contributors><titles><title>How much is too much? Interleukin-6 and its signalling in atherosclerosis</title><secondary-title>Throm Haemost</secondary-title></titles><periodical><full-title>Throm Haemost</full-title></periodical><volume>102</volume><number>215-222</number><dates><year>2009</year></dates><urls></urls></record></Cite></EndNote>[20], and obesity PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IdWdoZXM8L0F1dGhvcj48WWVhcj4yMDEyPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [21].PA has also been shown to exhibit positive effects on the vascular endothelium as a result of elevated shear stress caused by increased blood flow that occurs during exercise ADDIN EN.CITE <EndNote><Cite><Author>Vita</Author><Year>2000</Year><RecNum>3413</RecNum><DisplayText>[22]</DisplayText><record><rec-number>3413</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3413</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Vita, Joseph A</author><author>Keaney Jr, John F</author></authors></contributors><titles><title>Exercise--toning up the endothelium?</title><secondary-title>The New England journal of medicine</secondary-title></titles><periodical><full-title>The New England journal of medicine</full-title></periodical><pages>503</pages><volume>342</volume><number>7</number><dates><year>2000</year></dates><isbn>0028-4793</isbn><urls></urls></record></Cite></EndNote>[22]. Endothelial dysfunction is present in individuals with risk factors for atherosclerosis, including those with hypertension, hypercholesterolemia, and obesity ADDIN EN.CITE <EndNote><Cite><Author>Celermajer</Author><Year>1997</Year><RecNum>3396</RecNum><DisplayText>[23, 24]</DisplayText><record><rec-number>3396</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3396</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Celermajer, David S</author></authors></contributors><titles><title>Endothelial dysfunction: does it matter? Is it reversible?</title><secondary-title>Journal of the American College of Cardiology</secondary-title></titles><periodical><full-title>Journal of the American College of Cardiology</full-title></periodical><pages>325-333</pages><volume>30</volume><number>2</number><dates><year>1997</year></dates><isbn>0735-1097</isbn><urls></urls></record></Cite><Cite><Author>Bonetti</Author><Year>2003</Year><RecNum>3403</RecNum><record><rec-number>3403</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3403</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bonetti, Piero O</author><author>Lerman, Lilach O</author><author>Lerman, Amir</author></authors></contributors><titles><title>Endothelial dysfunction a marker of atherosclerotic risk</title><secondary-title>Arteriosclerosis, thrombosis, and vascular biology</secondary-title></titles><periodical><full-title>Arteriosclerosis, Thrombosis, and Vascular Biology</full-title></periodical><pages>168-175</pages><volume>23</volume><number>2</number><dates><year>2003</year></dates><isbn>1079-5642</isbn><urls></urls></record></Cite></EndNote>[23, 24]. Impaired endothelial function is considered a precursor to coronary atherosclerosis [19]. Endothelial function is optimal in the young, and there is a progressive deterioration with aging ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[25]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[25]. Endothelial function is therefore an indicator of pre-clinical vascular disease and for adults with CP, may act as a signal for early changes in arterial function.The accumulation of certain metabolic markers has been shown to enhance CVD risk. Particularly, insulin resistance and hyperinsulinemia enhance alterations in the vasculature that can lead to the progression of atherosclerosis ADDIN EN.CITE <EndNote><Cite><Author>Laakso</Author><Year>1991</Year><RecNum>3506</RecNum><DisplayText>[26]</DisplayText><record><rec-number>3506</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3506</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Laakso, Markku</author><author>Sarlund, Helena</author><author>Salonen, Riitta</author><author>Suhonen, Matti</author><author>Py?r?l?, K</author><author>Salonen, Jukka T</author><author>Karhap??, P</author></authors></contributors><titles><title>Asymptomatic atherosclerosis and insulin resistance</title><secondary-title>Arteriosclerosis, Thrombosis, and Vascular Biology</secondary-title></titles><periodical><full-title>Arteriosclerosis, Thrombosis, and Vascular Biology</full-title></periodical><pages>1068-1076</pages><volume>11</volume><number>4</number><dates><year>1991</year></dates><isbn>1079-5642</isbn><urls></urls></record></Cite></EndNote>[26]. 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ADDIN EN.CITE.DATA [29] leading to the formation of atherosclerotic plaques ADDIN EN.CITE <EndNote><Cite><Author>Rus</Author><Year>1996</Year><RecNum>2951</RecNum><DisplayText>[30]</DisplayText><record><rec-number>2951</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">2951</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Rus, H. G.</author><author>Vlaicu, R.</author><author>Niculescu, F.</author></authors></contributors><auth-address>Medical Clinic no. 1, 3-5, Cluj-Napoca, Romania.</auth-address><titles><title>Interleukin-6 and interleukin-8 protein and gene expression in human arterial atherosclerotic wall</title><secondary-title>Atherosclerosis</secondary-title><alt-title>Atherosclerosis</alt-title></titles><periodical><full-title>Atherosclerosis</full-title></periodical><alt-periodical><full-title>Atherosclerosis</full-title></alt-periodical><pages>263-71</pages><volume>127</volume><number>2</number><keywords><keyword>Aorta/metabolism/pathology</keyword><keyword>Arteriosclerosis/*metabolism/pathology</keyword><keyword>Cells, Cultured</keyword><keyword>DNA/biosynthesis</keyword><keyword>Endothelium, Vascular/*metabolism/pathology</keyword><keyword>Enzyme-Linked Immunosorbent Assay</keyword><keyword>Femoral Artery/metabolism/pathology</keyword><keyword>*Gene Expression</keyword><keyword>Humans</keyword><keyword>Immunohistochemistry</keyword><keyword>Interleukin-6/*biosynthesis/genetics</keyword><keyword>Interleukin-8/*biosynthesis/genetics</keyword><keyword>Middle Aged</keyword><keyword>Oligonucleotide Probes/chemistry</keyword><keyword>Protein-Serine-Threonine Kinases/metabolism</keyword><keyword>RNA/*analysis</keyword><keyword>Ribosomal Protein S6 Kinases</keyword></keywords><dates><year>1996</year><pub-dates><date>Dec 20</date></pub-dates></dates><isbn>0021-9150 (Print)
0021-9150 (Linking)</isbn><accession-num>9125317</accession-num><urls><related-urls><url>;[30].The purpose of this study was to examine relationships between GMFCS levels, PA, arterial structure (cIMT) and function (flow-mediated dilation (FMD), PWV, and carotid distensibility) and cardiometabolic risk markers (lipids, glucose, IL-6) in adults aged 18-75 with GMFCS levels I-V CP to determine if inactivity is predictive of compromising vascular health. We hypothesized that adults with CP who are community ambulatory (GMFCS I-II) will have increased levels of PA, increased endothelial function, decreased arterial stiffness and decreased cardiometabolic risk compared to those who are non ambulatory (GMFCS III-V).2.2METHODS2.2.1ParticipantsForty adults with CP (mean age 33.7 ± 12.7 yrs) were recruited from across Ontario. Inclusion criteria consisted of a GMFCS ADDIN EN.CITE <EndNote><Cite><Author>Palisano</Author><Year>1997</Year><RecNum>3212</RecNum><DisplayText>[34]</DisplayText><record><rec-number>3212</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3212</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Palisano, R.</author><author>Rosenbaum, P.</author><author>Walter, S.</author><author>Russell, D.</author><author>Wood, E.</author><author>Galuppi, B.</author></authors></contributors><auth-address>Department of Physical Therapy, Allegheny University of the Health Sciences, Philadelphia, PA, USA.</auth-address><titles><title>Development and reliability of a system to classify gross motor function in children with cerebral palsy</title><secondary-title>Dev Med Child Neurol</secondary-title><alt-title>Developmental medicine and child neurology</alt-title></titles><periodical><full-title>Dev Med Child Neurol</full-title><abbr-1>Developmental medicine and child neurology</abbr-1></periodical><alt-periodical><full-title>Dev Med Child Neurol</full-title><abbr-1>Developmental medicine and child neurology</abbr-1></alt-periodical><pages>214-23</pages><volume>39</volume><number>4</number><keywords><keyword>Activities of Daily Living</keyword><keyword>Age Factors</keyword><keyword>Cerebral Palsy/*physiopathology</keyword><keyword>Child</keyword><keyword>Child, Preschool</keyword><keyword>Delphi Technique</keyword><keyword>Disabled Persons/*classification</keyword><keyword>Gait</keyword><keyword>Humans</keyword><keyword>Infant</keyword><keyword>Motor Skills/*classification</keyword><keyword>Observer Variation</keyword><keyword>Reproducibility of Results</keyword><keyword>Severity of Illness Index</keyword></keywords><dates><year>1997</year><pub-dates><date>Apr</date></pub-dates></dates><isbn>0012-1622 (Print)
0012-1622 (Linking)</isbn><accession-num>9183258</accession-num><urls><related-urls><url>;[34] level I-V, regardless of intellectual ability. All CP subjects were identified and segregated using the GMFCS (level I n=5, level II n=9, level III n=10, level IV n=9, level V n=7). The Hamilton Integrated Research Ethics Board granted study approval. Experimental procedures were thoroughly explained to participants and/or their guardians prior to obtaining written consent. 2.2.2Study designThis study employed a cross-sectional, observational design to characterize the specific measures of vascular structure and function, PA levels and blood markers specific to insulin, glucose, lipid panel (cholesterol), and inflammation. The eight-day study protocol required a single visit to the Vascular Dynamics Laboratory at McMaster University. On day one, a waist and wrist accelerometer with an accompanying logbook to record wear times were delivered personally or via courier to the participant’s place of residence. Participants were instructed to wear the accelerometer for seven consecutive days. On the eighth day the participants arrived at the Vascular Dynamics Laboratory and were assessed for basic anthropometry and vascular indices, and a blood sample was obtained. Vascular measures were collected in a quiet, temperature-controlled room (23.2 ± .9oC) with the participant in a supine position. All subjects were tested at least 12 hours postprandial. Subjects were also instructed to abstain from vigorous PA at least 12 hours prior to data collection ADDIN EN.CITE <EndNote><Cite><Author>Thijssen</Author><Year>2011</Year><RecNum>3213</RecNum><DisplayText>[35]</DisplayText><record><rec-number>3213</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3213</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Thijssen, D. H.</author><author>Black, M. A.</author><author>Pyke, K. E.</author><author>Padilla, J.</author><author>Atkinson, G.</author><author>Harris, R. A.</author><author>Parker, B.</author><author>Widlansky, M. E.</author><author>Tschakovsky, M. E.</author><author>Green, D. J.</author></authors></contributors><auth-address>Research Inst. for Sport and Exercise Science, Henry Cotton Campus, Liverpool John Moores Univ., 15-21 Webster St., Liverpool, L3 2ET, UK. d.thijssen@ljmu.ac.uk</auth-address><titles><title>Assessment of flow-mediated dilation in humans: a methodological and physiological guideline</title><secondary-title>Am J Physiol Heart Circ Physiol</secondary-title><alt-title>American journal of physiology. Heart and circulatory physiology</alt-title></titles><periodical><full-title>American Journal of Physiology - Heart & Circulatory Physiology</full-title><abbr-1>Am J Physiol Heart Circ Physiol</abbr-1></periodical><pages>H2-12</pages><volume>300</volume><number>1</number><keywords><keyword>Endothelium, Vascular/*physiology/ultrasonography</keyword><keyword>Hemodynamics/physiology</keyword><keyword>Humans</keyword><keyword>Vasodilation/*physiology</keyword></keywords><dates><year>2011</year><pub-dates><date>Jan</date></pub-dates></dates><isbn>1522-1539 (Electronic)
0363-6135 (Linking)</isbn><accession-num>20952670</accession-num><urls><related-urls><url>;[35].2.2.3Activity MeasuresObjective PA was measured using Actigraph GT3X accelerometers (Actigraph, Pensacola, FL, USA) located at the level of the wrist and hip for seven consecutive days. A seven-day period was selected to ensure that both measured activity and inactivity were representative of habitual levels ADDIN EN.CITE <EndNote><Cite><Author>Trost</Author><Year>2005</Year><RecNum>3214</RecNum><DisplayText>[36]</DisplayText><record><rec-number>3214</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3214</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Trost, S. G.</author><author>McIver, K. L.</author><author>Pate, R. R.</author></authors></contributors><auth-address>Community Health Institute, Kansas State University, Manhattan, KS 66506, USA. strost@ksu.edu</auth-address><titles><title>Conducting accelerometer-based activity assessments in field-based research</title><secondary-title>Med Sci Sports Exerc</secondary-title><alt-title>Medicine and science in sports and exercise</alt-title></titles><periodical><full-title>Medicine & Science in Sports & Exercise</full-title><abbr-1>Med Sci Sports Exerc</abbr-1></periodical><alt-periodical><full-title>Medicine and Science in Sports and Exercise</full-title></alt-periodical><pages>S531-43</pages><volume>37</volume><number>11 Suppl</number><keywords><keyword>*Acceleration</keyword><keyword>Automatic Data Processing</keyword><keyword>Ergometry/*instrumentation</keyword><keyword>Evidence-Based Medicine</keyword><keyword>Guidelines as Topic</keyword><keyword>Humans</keyword><keyword>Locomotion</keyword><keyword>Reproducibility of Results</keyword><keyword>*Research Design</keyword><keyword>United States</keyword></keywords><dates><year>2005</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>0195-9131 (Print)
0195-9131 (Linking)</isbn><accession-num>16294116</accession-num><urls><related-urls><url>;[36]. A sampling interval (epoch) of three seconds was used as previously outlined in healthy adults ADDIN EN.CITE <EndNote><Cite><Author>Freedson</Author><Year>1998</Year><RecNum>3215</RecNum><DisplayText>[37]</DisplayText><record><rec-number>3215</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3215</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Freedson, P. S.</author><author>Melanson, E.</author><author>Sirard, J.</author></authors></contributors><auth-address>University of Massachusetts, Department of Exercise Science, Amherst 01003, USA. psf@excsci.umass.edu</auth-address><titles><title>Calibration of the Computer Science and Applications, Inc. accelerometer</title><secondary-title>Med Sci Sports Exerc</secondary-title><alt-title>Medicine and science in sports and exercise</alt-title></titles><periodical><full-title>Medicine & Science in Sports & Exercise</full-title><abbr-1>Med Sci Sports Exerc</abbr-1></periodical><alt-periodical><full-title>Medicine and Science in Sports and Exercise</full-title></alt-periodical><pages>777-81</pages><volume>30</volume><number>5</number><keywords><keyword>Adult</keyword><keyword>Calibration</keyword><keyword>*Energy Metabolism</keyword><keyword>Exercise Test/standards</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>*Physical Fitness</keyword><keyword>Reference Values</keyword></keywords><dates><year>1998</year><pub-dates><date>May</date></pub-dates></dates><isbn>0195-9131 (Print)
0195-9131 (Linking)</isbn><accession-num>9588623</accession-num><urls><related-urls><url>;[37]. The waist accelerometer measured acceleration in three-axial planes and was secured at the participant’s right hip by an elastic belt. The wrist accelerometer was placed on the participant’s dominant arm and was secured using an adjustable velcro strap. The accelerometer units were worn during all waking hours and were only removed when sleeping or during any water activities such as bathing or swimming. Following the seven-day wear period, the accelerometer recordings were downloaded to a computer equipped with Actilife software (Actilife 6 Data Analysis Software, Pensacola, FL, USA). Accelerometer data were inspected to ensure that information recorded in the logbook corresponded with the accelerometer output. Any activity that was recorded during periods of non-wear time, defined by the participant in the logbook, was deleted ADDIN EN.CITE <EndNote><Cite><Author>Gorter</Author><Year>2012</Year><RecNum>3216</RecNum><DisplayText>[38]</DisplayText><record><rec-number>3216</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3216</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Gorter, J. W., Noorduyn, S.G., Obeid, J., Timmons, B.W.</author></authors></contributors><titles><title>Accelerometry: A feasible method to quantify physical activtiy in ambulatory and nonambulatory adolescents with cerebral palsy</title><secondary-title>International Journal of Pediatrics</secondary-title></titles><periodical><full-title>International Journal of Pediatrics</full-title><abbr-1>Int J Pediatr</abbr-1></periodical><pages>6</pages><dates><year>2012</year></dates><urls></urls></record></Cite></EndNote>[38]. Only participants with a minimum of 5 days of monitoring were included in the analyses. These criteria were selected based on the average allowable time previously used to estimate habitual PA in adults ADDIN EN.CITE <EndNote><Cite><Author>Trost</Author><Year>2005</Year><RecNum>3214</RecNum><DisplayText>[36]</DisplayText><record><rec-number>3214</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3214</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Trost, S. G.</author><author>McIver, K. L.</author><author>Pate, R. R.</author></authors></contributors><auth-address>Community Health Institute, Kansas State University, Manhattan, KS 66506, USA. strost@ksu.edu</auth-address><titles><title>Conducting accelerometer-based activity assessments in field-based research</title><secondary-title>Med Sci Sports Exerc</secondary-title><alt-title>Medicine and science in sports and exercise</alt-title></titles><periodical><full-title>Medicine & Science in Sports & Exercise</full-title><abbr-1>Med Sci Sports Exerc</abbr-1></periodical><alt-periodical><full-title>Medicine and Science in Sports and Exercise</full-title></alt-periodical><pages>S531-43</pages><volume>37</volume><number>11 Suppl</number><keywords><keyword>*Acceleration</keyword><keyword>Automatic Data Processing</keyword><keyword>Ergometry/*instrumentation</keyword><keyword>Evidence-Based Medicine</keyword><keyword>Guidelines as Topic</keyword><keyword>Humans</keyword><keyword>Locomotion</keyword><keyword>Reproducibility of Results</keyword><keyword>*Research Design</keyword><keyword>United States</keyword></keywords><dates><year>2005</year><pub-dates><date>Nov</date></pub-dates></dates><isbn>0195-9131 (Print)
0195-9131 (Linking)</isbn><accession-num>16294116</accession-num><urls><related-urls><url>;[36]. Activity outputs were analyzed by determining continuous activity at intensity levels of light, moderate, moderate to vigorous, and vigorous ADDIN EN.CITE <EndNote><Cite><Author>Freedson</Author><Year>1998</Year><RecNum>3215</RecNum><DisplayText>[37]</DisplayText><record><rec-number>3215</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3215</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Freedson, P. S.</author><author>Melanson, E.</author><author>Sirard, J.</author></authors></contributors><auth-address>University of Massachusetts, Department of Exercise Science, Amherst 01003, USA. psf@excsci.umass.edu</auth-address><titles><title>Calibration of the Computer Science and Applications, Inc. accelerometer</title><secondary-title>Med Sci Sports Exerc</secondary-title><alt-title>Medicine and science in sports and exercise</alt-title></titles><periodical><full-title>Medicine & Science in Sports & Exercise</full-title><abbr-1>Med Sci Sports Exerc</abbr-1></periodical><alt-periodical><full-title>Medicine and Science in Sports and Exercise</full-title></alt-periodical><pages>777-81</pages><volume>30</volume><number>5</number><keywords><keyword>Adult</keyword><keyword>Calibration</keyword><keyword>*Energy Metabolism</keyword><keyword>Exercise Test/standards</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>*Physical Fitness</keyword><keyword>Reference Values</keyword></keywords><dates><year>1998</year><pub-dates><date>May</date></pub-dates></dates><isbn>0195-9131 (Print)
0195-9131 (Linking)</isbn><accession-num>9588623</accession-num><urls><related-urls><url>;[37] PA using cut-off values for each respective intensity level as previously validated in adults. Observations of continuous epochs of “0” counts were considered sedentary time. 2.2.4Anthropometric measurementsSupine height (cm) was measured to the nearest .5cm without shoes and in light clothing. Body mass was measured to the nearest 0.1kg using a digital wheelchair scale (Detecto Scales, FHD Series, Webb City, Missouri, USA). For participants using either a manual or power wheelchair, weight of both the participant and wheelchair together were recorded, followed by weight of the wheelchair alone and subtracting the wheelchair’s mass to determine the participant’s weight. Body mass index (BMI) was determined by dividing the participant’s weight (kg) by their height (m2) ADDIN EN.CITE <EndNote><Cite><Author>Hildreth</Author><Year>1997</Year><RecNum>3218</RecNum><DisplayText>[39]</DisplayText><record><rec-number>3218</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3218</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Hildreth, H. G., Johnson, R.K., Goran, M.I., Contompasis, S.H.</author></authors></contributors><titles><title>Body composition in adults with cerebral palsy by dual energy X-ray absorptiometry, bioelectrial impedance analysis, and skinfold anthropometry compared with the 18O isotope-dilution technique</title><secondary-title>Am J Clin Nutr</secondary-title></titles><periodical><full-title>American Journal of Clinical Nutrition</full-title><abbr-1>Am J Clin Nutr</abbr-1></periodical><pages>1436-1442</pages><volume>66</volume><dates><year>1997</year></dates><urls></urls></record></Cite></EndNote>[39]. WC, an index of total abdominal fat, was measured to the nearest .5cm in the supine position at the border of the superior iliac crest on the right side of the body following the end of a normal expiration ADDIN EN.CITE <EndNote><Cite><Author>National Institutes of Health. National Heart</Author><Year>2000</Year><RecNum>3217</RecNum><DisplayText>[40]</DisplayText><record><rec-number>3217</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3217</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>National Institutes of Health. National Heart, Lung, and Blood Institute. North American Association for the Study of Obesity</author></authors></contributors><titles><title>The Practical Guide Identification, Evaluation, and Treatment of Overweight and Obesity in Adults</title></titles><dates><year>2000</year></dates><urls></urls></record></Cite></EndNote>[40].2.2.5Blood DrawFollowing at least 5 minutes of supine rest participants provided blood samples collected into four separate 4 mL red top (clot activator) tubes for serum analysis. Following blood sample collection, the tubes sat idle for 30 min before centrifugation to ensure adequate coagulation. The tubes were then centrifuged at 4000 rpm for 10 min at a temperature of 4oC and 4 mL of serum were aliquotted into 4 separate eppendorf tubes (1 mL per tube) and stored and frozen at -20oC. The samples were analyzed for lipids (cholesterol, HDL, LDL, TC/HDL, triglycerides), the inflammatory marker interleukin (IL)-6, glucose, and insulin, with the latter 2 variables used to calculate HOMA-IR – a marker of insulin resistance ADDIN EN.CITE <EndNote><Cite><Author>Matthews</Author><Year>1985</Year><RecNum>3220</RecNum><DisplayText>[41]</DisplayText><record><rec-number>3220</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3220</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Matthews, D. R.</author><author>Hosker, J. P.</author><author>Rudenski, A. S.</author><author>Naylor, B. A.</author><author>Treacher, D. F.</author><author>Turner, R. C.</author></authors></contributors><titles><title>Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man</title><secondary-title>Diabetologia</secondary-title><alt-title>Diabetologia</alt-title></titles><periodical><full-title>Diabetologia</full-title></periodical><alt-periodical><full-title>Diabetologia</full-title></alt-periodical><pages>412-9</pages><volume>28</volume><number>7</number><keywords><keyword>Adult</keyword><keyword>Blood Glucose/*metabolism</keyword><keyword>Computers</keyword><keyword>Diabetes Mellitus, Type 2/*diagnosis/physiopathology</keyword><keyword>Erythrocytes/metabolism</keyword><keyword>Fasting</keyword><keyword>Homeostasis</keyword><keyword>Humans</keyword><keyword>Insulin/*blood</keyword><keyword>*Insulin Resistance</keyword><keyword>Islets of Langerhans/*physiopathology</keyword><keyword>Middle Aged</keyword><keyword>Monocytes/metabolism</keyword><keyword>Receptor, Insulin/metabolism</keyword></keywords><dates><year>1985</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>0012-186X (Print)
0012-186X (Linking)</isbn><accession-num>3899825</accession-num><urls><related-urls><url>;[41]. Participant lipid labeled eppendorf tubes were sent to Hamilton Regional Laboratory Medicine Program – McMaster Medical Centre Campus for analysis of the previously mentioned markers. The analyte IL-6 was examined using a Quantikine High Sensitivity Human IL-6 ELISA kit (R&D Systems, Inc. Minneapolis, MN, USA). Insulin was examined using the ALPCO immunoassay ELISA kit for the determination of insulin in serum (ALPCO Diagnostics, Salem, NH, USA). Glucose was examined using the Glucose Hexokinase Reagent Set (Pointe Scientific, Inc. Canton, MI, USA). Insulin and glucose concentrations were factored to determine insulin resistance ADDIN EN.CITE <EndNote><Cite><Author>Matthews</Author><Year>1985</Year><RecNum>3220</RecNum><DisplayText>[41]</DisplayText><record><rec-number>3220</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3220</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Matthews, D. R.</author><author>Hosker, J. P.</author><author>Rudenski, A. S.</author><author>Naylor, B. A.</author><author>Treacher, D. F.</author><author>Turner, R. C.</author></authors></contributors><titles><title>Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man</title><secondary-title>Diabetologia</secondary-title><alt-title>Diabetologia</alt-title></titles><periodical><full-title>Diabetologia</full-title></periodical><alt-periodical><full-title>Diabetologia</full-title></alt-periodical><pages>412-9</pages><volume>28</volume><number>7</number><keywords><keyword>Adult</keyword><keyword>Blood Glucose/*metabolism</keyword><keyword>Computers</keyword><keyword>Diabetes Mellitus, Type 2/*diagnosis/physiopathology</keyword><keyword>Erythrocytes/metabolism</keyword><keyword>Fasting</keyword><keyword>Homeostasis</keyword><keyword>Humans</keyword><keyword>Insulin/*blood</keyword><keyword>*Insulin Resistance</keyword><keyword>Islets of Langerhans/*physiopathology</keyword><keyword>Middle Aged</keyword><keyword>Monocytes/metabolism</keyword><keyword>Receptor, Insulin/metabolism</keyword></keywords><dates><year>1985</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>0012-186X (Print)
0012-186X (Linking)</isbn><accession-num>3899825</accession-num><urls><related-urls><url>;[41].2.2.6Resting heart rate and blood pressureFollowing anthropometric measurements and blood sample collection, participants laid supine for an additional 10 minutes prior to vascular assessments ADDIN EN.CITE <EndNote><Cite><Author>Thijssen</Author><Year>2011</Year><RecNum>3213</RecNum><DisplayText>[35]</DisplayText><record><rec-number>3213</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3213</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Thijssen, D. H.</author><author>Black, M. A.</author><author>Pyke, K. E.</author><author>Padilla, J.</author><author>Atkinson, G.</author><author>Harris, R. A.</author><author>Parker, B.</author><author>Widlansky, M. E.</author><author>Tschakovsky, M. E.</author><author>Green, D. J.</author></authors></contributors><auth-address>Research Inst. for Sport and Exercise Science, Henry Cotton Campus, Liverpool John Moores Univ., 15-21 Webster St., Liverpool, L3 2ET, UK. d.thijssen@ljmu.ac.uk</auth-address><titles><title>Assessment of flow-mediated dilation in humans: a methodological and physiological guideline</title><secondary-title>Am J Physiol Heart Circ Physiol</secondary-title><alt-title>American journal of physiology. Heart and circulatory physiology</alt-title></titles><periodical><full-title>American Journal of Physiology - Heart & Circulatory Physiology</full-title><abbr-1>Am J Physiol Heart Circ Physiol</abbr-1></periodical><pages>H2-12</pages><volume>300</volume><number>1</number><keywords><keyword>Endothelium, Vascular/*physiology/ultrasonography</keyword><keyword>Hemodynamics/physiology</keyword><keyword>Humans</keyword><keyword>Vasodilation/*physiology</keyword></keywords><dates><year>2011</year><pub-dates><date>Jan</date></pub-dates></dates><isbn>1522-1539 (Electronic)
0363-6135 (Linking)</isbn><accession-num>20952670</accession-num><urls><related-urls><url>;[35]. Four measurements of supine brachial artery systolic (SBP), diastolic (DBP), and mean arterial pressures were obtained using an automated sphygmomanometer (Dinamap Pro 100, Critikon LCC, Tampa, Fla, USA). The first measurement was discarded for calibration purposes while the average of the remaining three measures were reported PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QaWNrZXJpbmc8L0F1dGhvcj48WWVhcj4yMDA1PC9ZZWFy
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ADDIN EN.CITE.DATA [42]. Continuous heart rate via a single-lead electrocardiograph and reconstructed brachial blood pressure measurements via an automated ‘finger cuff’ with oscillometric cuff calibration (Finometer MIDI, Finapres Medical Systems BV, Amsterdam, The Netherlands) were also obtained. All subsequent vascular assessment signals were acquired simultaneously using a commercially available data acquisition system (Powerlab model ML795; ADInstruments, Colorado Springs, CO, USA) and software program (Labchart 7; ADInstruments Inc., Colorado Springs, CO, USA).2.2.7Vascular measuresCarotid distensibility and intima-media thicknessCarotid distensibility measurements were acquired using a combination of high-resolution, two-dimensional, B-mode ultrasound images with a 10MHz probe (Vivid Q; GE Medical Systems, Horten, Norway) and simultaneous applanation tonometry (model SPT-301; Millar Instruments, Houston, TX, USA). With the participant in a supine position with their mandible elevated, digital images of the left common carotid artery in longitudinal orientation were acquired at a rate of 11 frames/second. A hand-held tonometer was placed over the point of greatest pulsation of the right common carotid artery and held in a fixed position for ten consecutive heart cycles to obtain continuous pressure waveforms. Applanation tonometry is sensitive to the pressure applied by the investigator and generates relative pressure values specific to the site of interest ADDIN EN.CITE <EndNote><Cite><Author>Rakobowchuk</Author><Year>2009</Year><RecNum>3222</RecNum><DisplayText>[43]</DisplayText><record><rec-number>3222</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3222</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Rakobowchuk, M.</author><author>Stuckey, M. I.</author><author>Millar, P. J.</author><author>Gurr, L.</author><author>Macdonald, M. J.</author></authors></contributors><auth-address>Department of Kinesiology, McMaster University, Hamilton, ON, Canada.</auth-address><titles><title>Effect of acute sprint interval exercise on central and peripheral artery distensibility in young healthy males</title><secondary-title>Eur J Appl Physiol</secondary-title><alt-title>European journal of applied physiology</alt-title></titles><periodical><full-title>European Journal of Applied Physiology</full-title><abbr-1>Eur J Appl Physiol</abbr-1></periodical><alt-periodical><full-title>European Journal of Applied Physiology</full-title><abbr-1>Eur J Appl Physiol</abbr-1></alt-periodical><pages>787-95</pages><volume>105</volume><number>5</number><keywords><keyword>Adult</keyword><keyword>Arteries/*physiology</keyword><keyword>Blood Flow Velocity</keyword><keyword>Exercise/*physiology</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Manometry</keyword><keyword>Oxygen Consumption</keyword><keyword>Physical Exertion</keyword><keyword>Vasodilation</keyword></keywords><dates><year>2009</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>1439-6327 (Electronic)
1439-6319 (Linking)</isbn><accession-num>19125283</accession-num><urls><related-urls><url>;[43]. To determine absolute carotid artery systolic blood pressures, the waveforms acquired using applanation tonometry were calibrated to the brachial artery blood pressures acquired simultaneously (Finometer MIDI, Finapres Medical Systems BV, Amsterdam, The Netherlands). When an individual is in a resting supine position, the diastolic and mean arterial pressures are assumed to be consistent in all conduit arteries ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3223</RecNum><DisplayText>[25]</DisplayText><record><rec-number>3223</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3223</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[25]. The brachial artery DBP and mean arterial pressure were equated to the minimum and mean pressures obtained from the right common carotid artery. Using this relationship, the carotid artery SBP was forecasted from the pressure waveforms ADDIN EN.CITE <EndNote><Cite><Author>Kelly</Author><Year>1992</Year><RecNum>3224</RecNum><DisplayText>[44]</DisplayText><record><rec-number>3224</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3224</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Kelly, R.</author><author>Fitchett, D.</author></authors></contributors><auth-address>Division of Cardiology, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.</auth-address><titles><title>Noninvasive determination of aortic input impedance and external left ventricular power output: a validation and repeatability study of a new technique</title><secondary-title>J Am Coll Cardiol</secondary-title><alt-title>Journal of the American College of Cardiology</alt-title></titles><periodical><full-title>J Am Coll Cardiol</full-title></periodical><alt-periodical><full-title>Journal of the American College of Cardiology</full-title></alt-periodical><pages>952-63</pages><volume>20</volume><number>4</number><keywords><keyword>Aorta/*physiology</keyword><keyword>Blood Flow Velocity/physiology</keyword><keyword>Blood Pressure Determination/*methods</keyword><keyword>Cardiac Catheterization</keyword><keyword>Doppler Effect</keyword><keyword>Echocardiography, Doppler/*methods</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Reproducibility of Results</keyword><keyword>Vascular Resistance/physiology</keyword><keyword>Ventricular Function, Left/*physiology</keyword></keywords><dates><year>1992</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>0735-1097 (Print)
0735-1097 (Linking)</isbn><accession-num>1527307</accession-num><urls><related-urls><url>;[44]. Ultrasound images were stored offline in Digital Image and Communications in Medicine (DICOM) format for later analysis using a semi-automated edge tracking system [AMS (Artery Measurement System) Image and Data Analysis; Gothenburg Sweden]. This software program was utilized to detect carotid artery lumen diameter within specific regions of interest according to contrasting brightness intensities between the lumen and the walls of the artery ADDIN EN.CITE <EndNote><Cite><Author>Woodman</Author><Year>2001</Year><RecNum>3225</RecNum><DisplayText>[45]</DisplayText><record><rec-number>3225</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3225</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Woodman, R.J., Playford, D.A., Watts, G.F., Cheetham, C., Reed, C., Taylor, R.R., Puddey, I.B., Beilin, L.J., Burke, V., Mori, T.A., Green, D.</author></authors></contributors><titles><title>Improved analysis of brachial artery ultrasound using a novel edge-detection software system</title><secondary-title>J Appl Physiol</secondary-title></titles><periodical><full-title>J Appl Physiol</full-title></periodical><pages>929-937</pages><volume>91</volume><dates><year>2001</year></dates><urls></urls></record></Cite></EndNote>[45]. After acquiring a region of interest, each frame was scanned to ensure proper placement of the measurement markers and make manual adjustments if necessary. In each frame, carotid artery minimum, mean and maximum lumen diameters were calculated from approximately 100 measurement markers within the region of interest. Distensibility was calculated using the following equation ADDIN EN.CITE <EndNote><Cite><Author>O'Rourke</Author><Year>2002</Year><RecNum>3226</RecNum><DisplayText>[46]</DisplayText><record><rec-number>3226</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3226</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Rourke, M. F.</author><author>Staessen, J. A.</author><author>Vlachopoulos, C.</author><author>Duprez, D.</author><author>Plante, G. E.</author></authors></contributors><auth-address>St Vincent's Hospital/UNSW and St Vincent's Clinic, Sydney, Australia. m.orourke@unsw.edu.au</auth-address><titles><title>Clinical applications of arterial stiffness; definitions and reference values</title><secondary-title>Am J Hypertens</secondary-title><alt-title>American journal of hypertension</alt-title></titles><periodical><full-title>Am J Hypertens</full-title></periodical><alt-periodical><full-title>American Journal of Hypertension</full-title></alt-periodical><pages>426-44</pages><volume>15</volume><number>5</number><keywords><keyword>Arteries/*physiopathology</keyword><keyword>Elasticity</keyword><keyword>Humans</keyword><keyword>*Models, Cardiovascular</keyword><keyword>Reference Values</keyword><keyword>Terminology as Topic</keyword></keywords><dates><year>2002</year><pub-dates><date>May</date></pub-dates></dates><isbn>0895-7061 (Print)
0895-7061 (Linking)</isbn><accession-num>12022246</accession-num><urls><related-urls><url>;[46]: Distensibility=π (dmax2)2- π dmin22π(dmin2)2 x PP (1)where dmax represents maximum diameter, dmin is the minimum diameter, and PP is the carotid pulse pressure (change in pressure from DBP to SBP). The mean carotid artery diameter was calculated using the average of all diameters acquired from all ten heart cycles. The same software program (AMS) and ultrasound images were used to calculate cIMT. Far-arterial wall IMT was calculated from the proximal aspect of the intima to the proximal interface of the adventitia using the average of the ten frames pertaining to the smallest arterial diameter (end-diastole).Pulse wave velocityMeasurements of resting pulse wave velocity PWV were acquired through simultaneous applanation tonometry and electrocardiography. Both central and peripheral PWV (cPWV, pPWV) were determined from 20 continuous heart cycles using the equation ADDIN EN.CITE <EndNote><Cite><Author>O'Rourke</Author><Year>2002</Year><RecNum>3226</RecNum><DisplayText>[46]</DisplayText><record><rec-number>3226</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3226</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>O'Rourke, M. F.</author><author>Staessen, J. A.</author><author>Vlachopoulos, C.</author><author>Duprez, D.</author><author>Plante, G. E.</author></authors></contributors><auth-address>St Vincent's Hospital/UNSW and St Vincent's Clinic, Sydney, Australia. m.orourke@unsw.edu.au</auth-address><titles><title>Clinical applications of arterial stiffness; definitions and reference values</title><secondary-title>Am J Hypertens</secondary-title><alt-title>American journal of hypertension</alt-title></titles><periodical><full-title>Am J Hypertens</full-title></periodical><alt-periodical><full-title>American Journal of Hypertension</full-title></alt-periodical><pages>426-44</pages><volume>15</volume><number>5</number><keywords><keyword>Arteries/*physiopathology</keyword><keyword>Elasticity</keyword><keyword>Humans</keyword><keyword>*Models, Cardiovascular</keyword><keyword>Reference Values</keyword><keyword>Terminology as Topic</keyword></keywords><dates><year>2002</year><pub-dates><date>May</date></pub-dates></dates><isbn>0895-7061 (Print)
0895-7061 (Linking)</isbn><accession-num>12022246</accession-num><urls><related-urls><url>;[46]: PWV=DΔt (2)Where D is the distance between measurement sites and Δt is the pulse transit time (PTT). Arterial pressure waveforms at the common carotid, femoral, radial, and posterior tibialis arteries were collected using simultaneous applanation tonometry on the right side of the body. Tonometry signals were bandpass-filtered (5-30 Hz) with the lower (≤5 Hz) and higher frequencies (≥30 Hz) withdrawn in order to correctly identify the foot of each waveform. The foot of each waveform was identified as the minimum value of the digitally filtered signal and corresponds to the end of diastole - when the steep rise in the wave occurs and appears as a sharp inflection of the original signal ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3223</RecNum><DisplayText>[25]</DisplayText><record><rec-number>3223</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3223</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[25]. Central PTT was determined as the time delay between the arrival of the common carotid pulse wave and the femoral artery pulse wave, with the path distance calculated by subtracting carotid to suprasternal notch distance from suprasternal notch to femoral distance ADDIN EN.CITE <EndNote><Cite><Author>Weber</Author><Year>2009</Year><RecNum>3227</RecNum><DisplayText>[47]</DisplayText><record><rec-number>3227</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3227</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Weber, T.</author><author>Ammer, M.</author><author>Rammer, M.</author><author>Adji, A.</author><author>O'Rourke, M. F.</author><author>Wassertheurer, S.</author><author>Rosenkranz, S.</author><author>Eber, B.</author></authors></contributors><auth-address>Cardiology Department, Klinikum Wels-Grieskirchen, Grieskirchnerstrasse 42, Wels 4600, Austria. thomas.weber3@liwest.at</auth-address><titles><title>Noninvasive determination of carotid-femoral pulse wave velocity depends critically on assessment of travel distance: a comparison with invasive measurement</title><secondary-title>J Hypertens</secondary-title><alt-title>Journal of hypertension</alt-title></titles><periodical><full-title>J Hypertens</full-title></periodical><alt-periodical><full-title>Journal of Hypertension</full-title></alt-periodical><pages>1624-30</pages><volume>27</volume><number>8</number><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Aged, 80 and over</keyword><keyword>*Blood Flow Velocity</keyword><keyword>Body Height</keyword><keyword>Carotid Arteries/*physiology</keyword><keyword>Female</keyword><keyword>Femoral Artery/*physiology</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>*Pulsatile Flow</keyword></keywords><dates><year>2009</year><pub-dates><date>Aug</date></pub-dates></dates><isbn>1473-5598 (Electronic)
0263-6352 (Linking)</isbn><accession-num>19531964</accession-num><urls><related-urls><url>;[47]. Peripheral PTT was determined as the time delay between the arrival of the femoral artery pulse wave and the posterior tibialis pulse wave ADDIN EN.CITE <EndNote><Cite><Author>Rakobowchuk</Author><Year>2009</Year><RecNum>3222</RecNum><DisplayText>[43]</DisplayText><record><rec-number>3222</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3222</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Rakobowchuk, M.</author><author>Stuckey, M. I.</author><author>Millar, P. J.</author><author>Gurr, L.</author><author>Macdonald, M. J.</author></authors></contributors><auth-address>Department of Kinesiology, McMaster University, Hamilton, ON, Canada.</auth-address><titles><title>Effect of acute sprint interval exercise on central and peripheral artery distensibility in young healthy males</title><secondary-title>Eur J Appl Physiol</secondary-title><alt-title>European journal of applied physiology</alt-title></titles><periodical><full-title>European Journal of Applied Physiology</full-title><abbr-1>Eur J Appl Physiol</abbr-1></periodical><alt-periodical><full-title>European Journal of Applied Physiology</full-title><abbr-1>Eur J Appl Physiol</abbr-1></alt-periodical><pages>787-95</pages><volume>105</volume><number>5</number><keywords><keyword>Adult</keyword><keyword>Arteries/*physiology</keyword><keyword>Blood Flow Velocity</keyword><keyword>Exercise/*physiology</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Manometry</keyword><keyword>Oxygen Consumption</keyword><keyword>Physical Exertion</keyword><keyword>Vasodilation</keyword></keywords><dates><year>2009</year><pub-dates><date>Mar</date></pub-dates></dates><isbn>1439-6327 (Electronic)
1439-6319 (Linking)</isbn><accession-num>19125283</accession-num><urls><related-urls><url>;[43]. Path length was measured as the distance between these two sites, for determining lower-limb pPWV. Upper-limb pPWV was determined by subtracting the carotid-suprasternal notch distance from the suprasternal-radial artery distance. The peripheral PTT was determined as the time delay between the arrival of the carotid artery pulse wave and the radial artery pulse wave. An anthropometric tape was used to measure the distances between superficial skin sites.Flow-mediated dilation assessmentWhile the participant was in the supine position, the left arm was positioned at an angle approximately 80o from the torso in order to obtain an optimal image of the brachial artery PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QeWtlPC9BdXRob3I+PFllYXI+MjAwNDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [48]. A sphygmomanometric cuff was placed on the left forearm, distal to the medial epicondyle and remained stationary during baseline data collection. Ultrasound images of the left brachial artery approximately 10cm above the antecubital fossa were collected using Duplex ultrasound for simultaneous acquisition of B-mode diameter and pulsed-wave Doppler velocity using a 10MHz linear array probe (Vivid Q; GE Medical Systems, Horten, Norway). All B-mode images were acquired at a rate of 7.7 frames/second. A baseline longitudinal image of the brachial artery was acquired for 30 sec. Prior to recording the baseline image, the brachial artery was imaged using high-resolution B-mode ultrasound to identify clear vascular boundaries. This was performed to permit distinction between the lumen and vessel walls of the artery ADDIN EN.CITE <EndNote><Cite><Author>Pignoli</Author><Year>1986</Year><RecNum>3229</RecNum><DisplayText>[49]</DisplayText><record><rec-number>3229</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3229</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Pignoli, P.</author><author>Tremoli, E.</author><author>Poli, A.</author><author>Oreste, P.</author><author>Paoletti, R.</author></authors></contributors><titles><title>Intimal plus medial thickness of the arterial wall: a direct measurement with ultrasound imaging</title><secondary-title>Circulation</secondary-title><alt-title>Circulation</alt-title></titles><periodical><full-title>Circulation</full-title></periodical><alt-periodical><full-title>Circulation</full-title></alt-periodical><pages>1399-406</pages><volume>74</volume><number>6</number><keywords><keyword>Adult</keyword><keyword>Aged</keyword><keyword>Aorta, Abdominal/*pathology</keyword><keyword>Arteriosclerosis/diagnosis/pathology</keyword><keyword>Carotid Arteries/*pathology</keyword><keyword>Evaluation Studies as Topic</keyword><keyword>Humans</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>*Ultrasonography/instrumentation/methods</keyword></keywords><dates><year>1986</year><pub-dates><date>Dec</date></pub-dates></dates><isbn>0009-7322 (Print)
0009-7322 (Linking)</isbn><accession-num>3536154</accession-num><urls><related-urls><url>;[49]. Modern Duplex ultrasound systems, such as was used in this study, incorporate a narrow Doppler beam aperture that can be steered 20-30o off center of the B-mode imaging beam. This ensures that measurable Doppler shifts are achievable at an angle less than 70o provided extensive flow calibrations have been undertaken ADDIN EN.CITE <EndNote><Cite><Author>Pyke</Author><Year>2008</Year><RecNum>3232</RecNum><DisplayText>[50]</DisplayText><record><rec-number>3232</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3232</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Pyke, K. E.</author><author>Hartnett, J. A.</author><author>Tschakovsky, M. E.</author></authors></contributors><auth-address>Queen's University, Kingston, Ontario, Canada.</auth-address><titles><title>Are the dynamic response characteristics of brachial artery flow-mediated dilation sensitive to the magnitude of increase in shear stimulus?</title><secondary-title>J Appl Physiol (1985)</secondary-title><alt-title>Journal of applied physiology</alt-title></titles><periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></periodical><alt-periodical><full-title>J Appl Physiol (1985)</full-title><abbr-1>Journal of applied physiology</abbr-1></alt-periodical><pages>282-92</pages><volume>105</volume><number>1</number><keywords><keyword>Adult</keyword><keyword>Blood Pressure/physiology</keyword><keyword>Brachial Artery/anatomy & histology/*physiology/ultrasonography</keyword><keyword>Electrocardiography</keyword><keyword>Endothelium, Vascular/physiology</keyword><keyword>Forearm/physiology</keyword><keyword>Heart Rate/physiology</keyword><keyword>Hot Temperature</keyword><keyword>Humans</keyword><keyword>Laser-Doppler Flowmetry</keyword><keyword>Male</keyword><keyword>Pressure</keyword><keyword>Vasodilation/*physiology</keyword></keywords><dates><year>2008</year><pub-dates><date>Jul</date></pub-dates></dates><isbn>8750-7587 (Print)
0161-7567 (Linking)</isbn><accession-num>18467554</accession-num><urls><related-urls><url>;[50]. The most consistent angle used in this study was of 68o. Upon ideal image detection, the gate width of the steer angle was adjusted accordingly to encompass the entire lumen while minimizing the wall noise of the vessel. To create a flow stimulus, the forearm cuff was instantaneously inflated to a suprasystolic pressure of 200mmHg to ensure arterial occlusion and ischemia of downstream tissue PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Db3JyZXR0aTwvQXV0aG9yPjxZZWFyPjIwMDI8L1llYXI+
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ADDIN EN.CITE.DATA [51]. A cuff occlusion time of 5 minutes performed distally to the ultrasound probe has been associated with a significant FMD response and variations to the duration, magnitude, and placement of the cuff will result in varying FMD responses due to dilators other than NO ADDIN EN.CITE <EndNote><Cite><Author>Doshi</Author><Year>2001</Year><RecNum>3234</RecNum><DisplayText>[52]</DisplayText><record><rec-number>3234</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3234</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Doshi, S.N., Naka, K.K, Payne, N., Jones, C.J., Ashton, M., Lewis, M.J., Goodfellow, J.</author></authors></contributors><titles><title>Flow-mediated dilation following wrist and upper arm occlusion in humans: the contribution of nitric oxide</title><secondary-title>Clin Sci (Lond)</secondary-title></titles><periodical><full-title>Clin Sci (Lond)</full-title></periodical><pages>629-635</pages><volume>101</volume><dates><year>2001</year></dates><urls></urls></record></Cite></EndNote>[52]. At the 4 minute time point of occlusion, a 30 sec image was recorded using Duplex ultrasound. At 5 minutes, the cuff was instantaneously deflated and Duplex images were recorded for 3 minutes to capture both hyperemic blood velocity and peak arterial diameter. The velocity signals were processed by an external spectral analysis system (Neurovision 500M, Multigon Ind; Yonkers NY) and an intensity-weighted calculated mean was outsourced to the Powerlab data acquisition system. The baseline, 4 minute, and post-occlusion images were stored offline as DICOM files. End-diastolic frames were extracted from each of the three images using a DICOM editing software program (Sante DICOM Editor 3.1.13, Santescroft, Athens, Greece). AMS was used to detect near and far wall adventitia within a specific region of interest for the end-diastolic frames as each time point. The peak dilation of the vessel at baseline and at 4 min was taken as an average of the frames recorded in their respective 30 sec image. To obtain the peak diameter after cuff release, 5-s time bins were calculated with the peak designated as the largest 5-s bin PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IYXJyaXM8L0F1dGhvcj48WWVhcj4yMDEwPC9ZZWFyPjxS
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ADDIN EN.CITE.DATA [53]. The absolute FMD (mm) and relative FMD (%FMD) were calculated as follows:Absolute FMD = Peak Diameter (mm) – Baseline Diameter (mm)Relative FMD = Absolute FMDBaseline Diameterx 100% (3)The magnitude of the shear rate stimulus is proportional to the relative FMD response PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QeWtlPC9BdXRob3I+PFllYXI+MjAwNDwvWWVhcj48UmVj
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ADDIN EN.CITE.DATA [48]. The following equation was used to calculate shear rate for each subject:Shear Rate = 8 x (VelocityDiameter) (4)Where velocity and diameter represent the mean velocity and internal arterial diameter for a specific frame. The area under the curve of the shear rate was calculated using the trapezoid rule to obtain the area under the curve up until peak diameter during cuff release (GraphPad PRISM version 5.0a. La Jolla, CA, USA). Relative FMD (%FMD) was normalized to the area under the entire shear rate curve to account for baseline diameter.NormalizedFMD=(%FMDSRAUC) (5)2.2.8Statistical analysisStatistical analysis was performed using SPSS software (SPSS 20. IBM, Armonk, NY, USA). All continuous variables were tested for normality using Shapiro-Wilks descriptive test. Data was originally separated into five groups based on the GMFCS. The GMFCS levels assess activity limitations pertaining to gross motor function with a five-level ordinal scale [1]. Individuals with GMFCS level I can typically walk without significant restrictions. Conversely, those with GMFCS level V are very restricted in their ability to function physically. The GMFCS has been validated as a reliable tool for use in the adult population with a strong inter-rater reliability PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5NY0Nvcm1pY2s8L0F1dGhvcj48WWVhcj4yMDA3PC9ZZWFy
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ADDIN EN.CITE.DATA [54, 55]. Differences in anthropometrics, vascular indices, activity levels, and metabolic markers were analyzed using one-way ANOVA with Tukey post hoc procedures. When performing one-way ANOVA, samples are more susceptible to unequal variances when the size of the population within each group is small or when sample sizes are unequal ADDIN EN.CITE <EndNote><Cite><Author>Field</Author><Year>2009</Year><RecNum>3236</RecNum><DisplayText>[56]</DisplayText><record><rec-number>3236</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3236</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Field, A</author></authors></contributors><titles><title>Discovering Statistics Using SPSS Third Edition</title></titles><dates><year>2009</year></dates><urls></urls></record></Cite></EndNote>[56]. Increasing the sample size within each group has been shown to mitigate the chance of committing a type I error. Data was collapsed into two groups based on whether participants were community ambulant or non-ambulant based on previous studies that have suggested those in GMFCS levels III-V prefer to use wheeled devices to move about in the community ADDIN EN.CITE <EndNote><Cite><Author>Palisano</Author><Year>2007</Year><RecNum>3450</RecNum><DisplayText>[57, 58]</DisplayText><record><rec-number>3450</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3450</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Palisano, Robert J</author><author>Copeland, Wendy P</author><author>Galuppi, Barbara E</author></authors></contributors><titles><title>Performance of physical activities by adolescents with cerebral palsy</title><secondary-title>Physical therapy</secondary-title></titles><periodical><full-title>Physical Therapy</full-title><abbr-1>Phys Ther</abbr-1></periodical><pages>77-87</pages><volume>87</volume><number>1</number><dates><year>2007</year></dates><isbn>0031-9023</isbn><urls></urls></record></Cite><Cite><Author>Palisano</Author><Year>2010</Year><RecNum>3452</RecNum><record><rec-number>3452</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3452</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Palisano, Robert J</author><author>Hanna, Steven E</author><author>Rosenbaum, Peter L</author><author>Tieman, Beth</author></authors></contributors><titles><title>Probability of walking, wheeled mobility, and assisted mobility in children and adolescents with cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>66-71</pages><volume>52</volume><number>1</number><dates><year>2010</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[57, 58]. Upon separation into two groups, data was reassessed for normality and independent t-tests were performed on the same variables. To determine the independent contribution of historical CVD risk attributes (age, WC, MVPA/hour) as well as the novelty of the CP population (GMFCS level) on these cardiovascular and cardiometabolic outcomes, separate multiple regression analyses were conducted for each dependent variable (i.e. each vascular and metabolic marker) using a backward regression model. Numeric coding was applied to the categorical variable GMFCS (GMFCS levels I-II=0 or GMFCS levels III-V=1). For each model, standardized regression coefficients were determined. Further, percent variance attributable to the main outcome within each model was tested using an analysis of variance to determine the significance of each model. If there was greater than one independent predictor for a particular model, a forward regression analysis was performed to determine which predictor represented the greatest variance. Data are reported as means SD. A minimum criterion alpha level of P≤0.05 was used to determine statistical significance. 2.3RESULTS2.3.1Participant CharacteristicsThe sample population, separated into two groups based on whether participants were community ambulant (GMFCS I-II) or non-ambulant (GMFCS III-V), were of similar age, body mass, WC, and BMI (Table 1). The ambulant group was taller than the non-ambulant group (p=0.013) (Table 1). There were no group differences between SBP, DBP or mean arterial pressure. The non-ambulant group had a higher resting, supine heart rate (p=0.05) (Table 1).2.3.2Physical ActivityThe total amount of minutes of wear time/day, moderate-to-vigorous physical activity (MVPA)/day, sedentary time/day, MVPA/hour, and sedentary time/hour are reported in Table 2. The ambulant participants wore the device for a greater duration per day compared to the non-ambulant group (p=0.033) (Fig. 1A). Furthermore, the ambulant group engaged in more MVPA/day (p=0.001) (Fig. 1B) and MVPA/hour (p=0.001) than the non-ambulant group (Fig. 1C). Sedentary time/day was not different between groups, however, after controlling for wear time, the non-ambulant group engaged in more sedentary time/hour than the ambulant group (p=0.001) (Fig. 1D).2.3.3Vascular IndicesThere were no differences in carotid artery distensibility or IMT between groups (Table 3). One non-ambulant CP participant was removed from these vascular assessments due to severe spasticity of the upper extremities resulting in inadequate ultrasound image quality. There were no group differences in central PWV (Table 3). Two ambulant and five non-ambulant participants were removed from the central and lower limb PWV analysis as a result of inadequate tonometry signals. No differences were observed in lower-limb PWV (Table 3), however upper-limb PWV was higher in the non-ambulant group indicative of an increase in arterial stiffness compared to the ambulant group (p=0.006) (Fig. 2). Two ambulant and three non-ambulant participants were removed from the upper-limb PWV analysis due to inadequate tonometry signals (Table 3).There were no between-group differences in pre-occlusion brachial artery diameter (mm) or peak brachial artery diameter (mm) achieved during reactive hyperemia (Table 3). Furthermore, there were no differences between groups in absolute FMD (mm), relative FMD (%), normalized FMD (%FMD/SRAUC), or SR stimulus (Table 3).2.3.4Cardiometabolic Blood MarkersThere were no between group differences for all metabolic markers assessed. Glucose (CV 8.8%), insulin (CV 8.2%), HOMA-IR, IL-6 (CV 9.0%) and lipid marker concentrations are reported in Table 4. Blood draws were not acquired on 1 ambulant and 7 non-ambulant participants for glucose, insulin, HOMA-IR and IL-6 due to contractures, spasticity, or vein size. An additional non-ambulant participant was not included in the lipid analysis (n=31) as a result of insufficient serum content to perform the assessment. Both group means were below the target HDL-C level of 1.30 mmol/L.2.3.5Multiple linear regression coefficientsFurther analysis was performed to determine if traditional risk factors (age and WC), as well as gross motor function classification and PA (MVPA/hour), were predictive of cardiovascular outcomes (Table 5). When controlling for age, WC, and time spent in MVPA/hour, GMFCS was an independent predictor of HR (β=.31; p=0.05) (Fig. 3A) and upper-limb PWV (β=.46; p=0.006) (Fig. 3B). When controlling for WC, MVPA/hour, and GMFCS, age was an independent predictor of SBP (β=.36; p=0.02) (Fig. 4A), mean arterial pressure (β=.42; p=0.007) (Fig. 4B), central PWV (β=.70; p=0.001) (Fig. 4C), IMT (β =.76; p=0.001) (Fig. 4D), and distensibility (β=-.38; p=0.02) (Fig. 4E). When controlling for age, GMFCS, and MVPA/hour, WC was an independent predictor of HDL-C (β=-.50; p=0.006) (Fig. 5A), LDL-C (β=.54; p=0.001) (Fig. 5B), triglycerides (β=.54; p=0.002) (Fig. 5C), TC/HDL-C ratio (β=.72; p=0.001) (Fig. 5D), IL-6 (β=.41; p=0.02) (Fig. 5E), and HOMA-IR (β=.40; p=0.025) (Fig. 5F). Finally, when controlling for age, GMFCS, and WC, MVPA/hour was an independent predictor of DBP, mean arterial pressure, triglyceride level, and HOMA-IR. However, when placed in a forward regression to determine which independent variable was the strongest predictor, MVPA/hour was not found to be a significant predictor of any outcome variable (Table 6).Table 1Subject CharacteristicsGMFCS I-II (n=14)GMFCS III-V (n=26)P ValueGender8/6 (M/F)13/13 (M/F)0.376Age, yrs31.7 ± 10.434.8 ± 13.60.464Height, m1.67 ± .101.57 ± .12*0.013Mass, kg69.7 ± 21.163.9 ± 24.30.461Resting HR, bpm71.9 ± 9.379.8 ± 13.4*0.050Resting Systolic BP, mmHg123.2 ± 9.9124.3 ± 19.00.848Resting Diastolic BP, mmHg73.1 ± 8.874.5 ± 9.00.648Resting MAP, mmHg ?91.9 ± 6.893.6 ± 11.40.676BMI, kg/m2 ?24.7 ± 5.925.5 ± 8.40.900WC, cm83.9 ± 17.485.9 ± 18.60.835Values are represented as means ± SD. HR, heart rate; BPM, beats per minute; BP, blood pressure; MAP, mean arterial pressure; BMI, body mass index; WC, waist circumference.? Logarithm transformation performed*p≤0.05Table 2Group comparisons of daily and hourly physical activity levelsGMFCS I-II (n=14)GMFCS III-V (n=26)P valueWear time/day, minψ736.2 ± 124.9648.8 ± 119.6*.033MVPA/day, min?29.6 ± 28.43.23 ± 6.54*.001Sedentary time/day, min?630.8 ± 111.6625.8 ± 122.6.861MVPA/hour, min?2.36 ± 2.130.32 ± 0.64*.001Sedentary time/hour, min?51.6 ± 4.7157.8 ± 1.94*.001Values are represented as means ± SD. MVPA, moderate to vigorous physical activity.Ψ Square transformation performed? Logarithm transformation performed?Mann-Whitney U test was performed on non-normally distributed data *p<0.05Table 3Group comparisons of FMD response, carotid distensibility and IMT, central, lower and upper PWVGMFCS I-II GMFCS III-V P ValuePre-occlusion diameter, mm3.60 ± .563.40 ± .580.3104min diameter, mm3.56 ± .563.37 ± .590.344RH peak diameter, mm3.90 ± .563.68 ± .530.248Absolute FMD, mm0.30 ± .130.28 ± .150.741Relative FMD (%FMD)?8.6 ± 4.38.9 ± 5.50.838Normalized (%FMD/SRAUC)?7.2e-4 ± 1.6e-32.5e-3 ± 7.8e-30.397Mean SR?34500 ± 1923031022 ± 295290.181Distensibility, mmHg-1?4.7e-3 ± 4.3e-33.4e-3 ± 1.4e-30.216IMT, mm.49 ± .10 .55 ± .170.189Central PWV (m/s)6.23 ± .506.69 ± 1.470.305Lower PWV (m/s)8.30 ± 1.498.37 ± 1.850.923Upper PWV (m/s)8.28 ± 1.6110.2 ± 1.92*0.006Values are represented as means ± SD. RH, reactive hyperemia; FMD, flow mediated dilation; SR, shear rate; SRAUC, shear rate area under the curve; IMT, intima media thickness; distensibility (GMFCS I-II n=14)(GMFCS III-V n=25). PWV, pulse wave velocity, central and lower (GMFCS I-II n=12)(GMFCS III-V n=21). Upper (GMFCS I-II n=12)(GMFCS III-V n=23).?Mann-Whitney U test was performed on non-normally distributed data? Logarithm transformation performed*p<0.05Table 4Group comparisons of glucose, insulin, HOMA-IR, IL-6, and lipid concentrationsGMFCS I-II GMFCS III-V P ValueGlucose, mg/dL99.14 ± 9.49101.10 ± 17.790.719Insulin, μIU/mL ?7.39 ± 4.6210.7 ± 16.00.910HOMA-IR, mass units ?1.77 ± 1.042.82 ± 4.400.652IL-6, pg/mL ?2.76 ± 2.872.04 ± 1.510.545Cholesterol, mmol/L4.98 ± .984.84 ± 1.080.714Triglycerides, mmol/L ?1.11 ± .551.23 ± .680.659HDL-C, mmol/L1.26 ± .231.15 ± .250.204LDL-C, mmol/L3.21 ± .843.13 ± .880.795TC/HDL-C ratio4.09 ± 1.24.36 ± 1.30.523Values are represented as means ± SD. HOMA-IR, Homeostasis model assessment insulin resistance; IL-6, Interleukin 6 (GMFCS I-II n=13)(GMFCS III-V n=19). HDL-C, high density lipoprotein cholesterol; LDL-C, low density lipoprotein cholesterol; TC/HDL-C, total cholesterol to high density lipoprotein cholesterol (GMFCSI-II n=13)(GMFCS III-V n=18).? Logarithm transformation performed? Mann-Whitney U test was performed on non-normally distributed dataTable 5Backward multiple linear regression Table 6Forward multiple linear regressionFigure 1 A.) Group comparison of accelerometer wear time per dayB.) Group comparison of minutes of MVPA per day C.) Group comparison of minutes of MVPA per hour D.) Group comparison of sedentary time per hourambulant n=14, non-ambulant n=26*p<0.05Figure 2. Group comparison of upper PWV; ambulant n=12, non-ambulant n=23*p<0.05Figure 3 A.) GMFCS as an independent predictor of heart rate; n=40B.) GMFCS as an independent predictor of upper-limb PWV; n=35Figure 4 A.) Age as an independent predictor of SBP; n=40B.) Age as an independent predictor of MAP; n=40C.) Age as an independent predictor of central PWV; n=32D.) Age as an independent predictor of IMT; n=39E.) Age as an independent predictor of distensibility; n=39Figure 5 A.) Waist circumference as an independent predictor of HDL-C; n=31B.) Waist circumference as an independent predictor of LDL-C; n=31C.) Waist circumference as an independent predictor of triglycerides; n=31 D.) Waist circumference as an independent predictor of TC/HDL-C; n=31 E.) Waist circumference as an independent predictor of IL-6; n=32 F.) Waist circumference as an independent predictor of HOMA-IR; n=322.4DISCUSSIONProlonged exposure to decreased PA levels in the general population is associated with impairments of vascular health and increased cardiovascular risk, and many individuals with CP may be in a lifelong state of physical limitation resulting in chronically decreased PA. The primary novel findings of this study were that clinically significant measures of vascular health and blood markers of cardiometabolic risk were not different between community ambulant (GMFCS I-II) and non-ambulant (GMFCS III-V) adults with CP. These lack of group differences in cardiovascular disease risk factors were observed in the face of the non-ambulant group spending significantly less time performing MVPA and having increased sedentary time per hour compared to the ambulant group. The present cross-sectional observational study is the first to characterize indices of vascular health in adults with CP (33.7 ± 12.5 yrs, min-max 18-75) across the complete range of the GMFCS scale (I-V). Previous research has shown that adults with CP have a near threefold increased death rate from coronary disease compared to the general population ADDIN EN.CITE <EndNote><Cite><Author>Strauss</Author><Year>1999</Year><RecNum>3453</RecNum><DisplayText>[31]</DisplayText><record><rec-number>3453</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3453</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Strauss, David</author><author>Cable, William</author><author>Shavelle, Robert</author></authors></contributors><titles><title>Causes of excess mortality in cerebral palsy</title><secondary-title>Developmental Medicine & Child Neurology</secondary-title></titles><periodical><full-title>Developmental Medicine & Child Neurology</full-title></periodical><pages>580-585</pages><volume>41</volume><number>9</number><dates><year>1999</year></dates><isbn>1469-8749</isbn><urls></urls></record></Cite></EndNote>[31]. 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ADDIN EN.CITE.DATA [14, 59, 60]. Current PA guidelines suggest 150 min of MVPA per week as the minimum to promote health benefits ADDIN EN.CITE <EndNote><Cite><Author>Haskell</Author><Year>2007</Year><RecNum>3457</RecNum><DisplayText>[61]</DisplayText><record><rec-number>3457</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3457</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Haskell, William L</author><author>Lee, I-Min</author><author>Pate, Russell R</author><author>Powell, Kenneth E</author><author>Blair, Steven N</author><author>Franklin, Barry A</author><author>Macera, Caroline A</author><author>Heath, Gregory W</author><author>Thompson, Paul D</author><author>Bauman, Adrian</author></authors></contributors><titles><title>Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>1081</pages><volume>116</volume><number>9</number><dates><year>2007</year></dates><urls></urls></record></Cite></EndNote>[61]. According to these guidelines, our sample of ambulatory adults with CP is achieving the minimum levels required for health benefits (mean 210 min/week) while the non-ambulatory participants are far below that level (23 min/week) and would be predicted to be at an elevated risk of CVD. MVPA levels and sedentary time per hour were different between the two groups, with the ambulatory group having increased MVPA and reduced sedentary time per hour. Lack of PA is the second leading behavioural cause of death in America ADDIN EN.CITE <EndNote><Cite><Author>Danias</Author><Year>2003</Year><RecNum>3482</RecNum><DisplayText>[62]</DisplayText><record><rec-number>3482</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3482</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Danias, P. G.</author><author>Tritos, N. A.</author><author>Stuber, M.</author><author>Botnar, R. M.</author><author>Kissinger, K. V.</author><author>Manning, W. J.</author></authors></contributors><auth-address>Cardiovascular, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. pdanias@caregroup.harvard.edu</auth-address><titles><title>Comparison of aortic elasticity determined by cardiovascular magnetic resonance imaging in obese versus lean adults</title><secondary-title>Am J Cardiol</secondary-title><alt-title>The American journal of cardiology</alt-title></titles><periodical><full-title>Am J Cardiol</full-title></periodical><alt-periodical><full-title>The American journal of cardiology</full-title></alt-periodical><pages>195-9</pages><volume>91</volume><number>2</number><keywords><keyword>Adult</keyword><keyword>Aorta, Abdominal/anatomy & histology/*physiology</keyword><keyword>Aorta, Thoracic/anatomy & histology/*physiology</keyword><keyword>Body Mass Index</keyword><keyword>Case-Control Studies</keyword><keyword>Cross-Sectional Studies</keyword><keyword>Elasticity</keyword><keyword>Humans</keyword><keyword>*Magnetic Resonance Imaging</keyword><keyword>Male</keyword><keyword>Obesity/pathology/*physiopathology</keyword></keywords><dates><year>2003</year><pub-dates><date>Jan 15</date></pub-dates></dates><isbn>0002-9149 (Print)
0002-9149 (Linking)</isbn><accession-num>12521634</accession-num><urls><related-urls><url>;[62]. It is apparent that PA levels decline from childhood into the adult years in the general population ADDIN EN.CITE <EndNote><Cite><Author>Mokdad</Author><Year>2004</Year><RecNum>3270</RecNum><DisplayText>[8]</DisplayText><record><rec-number>3270</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3270</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Mokdad, A. H.</author><author>Marks, J. S.</author><author>Stroup, D. F.</author><author>Gerberding, J. L.</author></authors></contributors><auth-address>Division of Adult and Community Health, Centers for Disease Control and Prevention, Atlanta, Ga, USA. amokdad@</auth-address><titles><title>Actual causes of death in the United States, 2000</title><secondary-title>JAMA</secondary-title><alt-title>JAMA : the journal of the American Medical Association</alt-title></titles><alt-periodical><full-title>JAMA : the journal of the American Medical Association</full-title></alt-periodical><pages>1238-45</pages><volume>291</volume><number>10</number><keywords><keyword>Accidents, Traffic/mortality</keyword><keyword>Alcohol Drinking</keyword><keyword>Cause of Death/*trends</keyword><keyword>Communicable Diseases/mortality</keyword><keyword>Diet</keyword><keyword>Humans</keyword><keyword>Physical Fitness</keyword><keyword>Poisoning/mortality</keyword><keyword>Risk Factors</keyword><keyword>Sexual Behavior</keyword><keyword>Smoking/mortality</keyword><keyword>Substance-Related Disorders</keyword><keyword>United States/epidemiology</keyword><keyword>Wounds, Gunshot/mortality</keyword></keywords><dates><year>2004</year><pub-dates><date>Mar 10</date></pub-dates></dates><isbn>1538-3598 (Electronic)
0098-7484 (Linking)</isbn><accession-num>15010446</accession-num><urls><related-urls><url>;[8], and this may be exacerbated in the CP population. Participants in the non-ambulatory group spent 96% of their time within an hour in the sedentary state. Sitting time has been shown to be positively associated with resting heart rate in a cohort with similar age to the present study. Average MVPA values in our ambulant group were 29.6 ± 28.4 min/day that would adhere to the required 150 minimum of MVPA suggested for health benefits in adults ADDIN EN.CITE <EndNote><Cite><Author>Haskell</Author><Year>2007</Year><RecNum>3458</RecNum><DisplayText>[61]</DisplayText><record><rec-number>3458</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3458</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Haskell, William L</author><author>Lee, I-Min</author><author>Pate, Russell R</author><author>Powell, Kenneth E</author><author>Blair, Steven N</author><author>Franklin, Barry A</author><author>Macera, Caroline A</author><author>Heath, Gregory W</author><author>Thompson, Paul D</author><author>Bauman, Adrian</author></authors></contributors><titles><title>Physical activity and public health: updated recommendation for adults from the American College of Sports Medicine and the American Heart Association</title><secondary-title>Circulation</secondary-title></titles><periodical><full-title>Circulation</full-title></periodical><pages>1081</pages><volume>116</volume><number>9</number><dates><year>2007</year></dates><urls></urls></record></Cite></EndNote>[61]. These values would appear to be larger than those reported from a Dutch cohort of ambulant CP subjects, in which they reported activity levels that were 85% of the able-bodied aged reference sample PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5OaWV1d2VuaHVpanNlbjwvQXV0aG9yPjxZZWFyPjIwMTE8
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ADDIN EN.CITE.DATA [7]. It should be noted, however, that time spent in the sedentary state may not represent inactivity for the CP population. Adults with CP may use increased intentional muscular activity to maintain a seated posture and the increased atypical muscle tone (i.e. spasticity) present in adults with CP likely elevates energy expenditure during sitting ADDIN EN.CITE <EndNote><Cite><Author>Verschuren</Author><Year>2014</Year><RecNum>3519</RecNum><DisplayText>[63]</DisplayText><record><rec-number>3519</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3519</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Verschuren, Olaf</author><author>Darrah, Johanna</author><author>Novak, Iona</author><author>Ketelaar, Marjolijn</author><author>Wiart, Lesley</author></authors></contributors><titles><title>Health-enhancing physical activity in children with cerebral palsy: more of the same is not enough</title><secondary-title>Physical therapy</secondary-title></titles><periodical><full-title>Physical Therapy</full-title><abbr-1>Phys Ther</abbr-1></periodical><pages>297-305</pages><volume>94</volume><number>2</number><dates><year>2014</year></dates><isbn>0031-9023</isbn><urls></urls></record></Cite></EndNote>[63]. Therefore, we cannot assume that persons with CP are ‘sedentary’ while sitting. There are three inherent factors within the definition of sedentary behaviour: (1) Posture (sitting or reclining); (2) Energy expenditure (≤ 1.5 metabolic equivalents); and (3) Muscular inactivity ADDIN EN.CITE <EndNote><Cite><Author>Verschuren</Author><Year>2014</Year><RecNum>3519</RecNum><DisplayText>[63]</DisplayText><record><rec-number>3519</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3519</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Verschuren, Olaf</author><author>Darrah, Johanna</author><author>Novak, Iona</author><author>Ketelaar, Marjolijn</author><author>Wiart, Lesley</author></authors></contributors><titles><title>Health-enhancing physical activity in children with cerebral palsy: more of the same is not enough</title><secondary-title>Physical therapy</secondary-title></titles><periodical><full-title>Physical Therapy</full-title><abbr-1>Phys Ther</abbr-1></periodical><pages>297-305</pages><volume>94</volume><number>2</number><dates><year>2014</year></dates><isbn>0031-9023</isbn><urls></urls></record></Cite></EndNote>[63]. Perhaps the muscular demands required for some individuals with CP to maintain their balance while sitting are large enough to label sitting as non-sedentary. This would suggest that the muscle activity elicited while sitting may provide enough cardiovascular benefit to note the lack of differences in endothelial function and central stiffness between the ambulant and non-ambulant groups in the present study. Future interventional studies in the CP population suggest replacing time spent in the sedentary state, or sitting, with standing exercises that require large muscle groups to remain under tension. With respect to body composition, men are at an increased risk for CVD if they present a WC greater than 102cm; women are at an increased risk if they have a WC greater than 88cm ADDIN EN.CITE <EndNote><Cite><Author>National Institutes of Health. National Heart</Author><Year>2000</Year><RecNum>2956</RecNum><DisplayText>[40]</DisplayText><record><rec-number>2956</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">2956</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>National Institutes of Health. National Heart, Lung, and Blood Institute. North American Association for the Study of Obesity</author></authors></contributors><titles><title>The Practical Guide Identification, Evaluation, and Treatment of Overweight and Obesity in Adults</title></titles><dates><year>2000</year></dates><urls></urls></record></Cite></EndNote>[40]. In the current study there was no difference in WC between the two groups. While the mean of each group was below the risk cut-off of 88cm, the standard deviations were quite large (Table 1). Individual data shows that 5 males (2 ambulant, 3 non-ambulant) and 7 females (2 ambulant, 5 non-ambulant) were at elevated risk of CVD based on their WC values. BMI has been scrutinized as a means of determining normal, obese, or overweight values in certain populations ADDIN EN.CITE <EndNote><Cite><Author>Fujimoto</Author><Year>1991</Year><RecNum>3462</RecNum><DisplayText>[64]</DisplayText><record><rec-number>3462</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3462</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Fujimoto, WY</author><author>Newell-Morris, LL</author><author>Grote, M</author><author>Bergstrom, RW</author><author>Shuman, WP</author></authors></contributors><titles><title>Visceral fat obesity and morbidity: NIDDM and atherogenic risk in Japanese American men and women</title><secondary-title>International journal of obesity</secondary-title></titles><periodical><full-title>International journal of obesity</full-title></periodical><dates><year>1991</year></dates><isbn>0307-0565</isbn><urls></urls></record></Cite></EndNote>[64]. For older individuals, WC assumes greater value for estimating risk of obesity-related diseases ADDIN EN.CITE <EndNote><Cite><Author>National Institutes of Health. National Heart</Author><Year>2000</Year><RecNum>2956</RecNum><DisplayText>[40]</DisplayText><record><rec-number>2956</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">2956</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>National Institutes of Health. National Heart, Lung, and Blood Institute. North American Association for the Study of Obesity</author></authors></contributors><titles><title>The Practical Guide Identification, Evaluation, and Treatment of Overweight and Obesity in Adults</title></titles><dates><year>2000</year></dates><urls></urls></record></Cite></EndNote>[40]. 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ADDIN EN.CITE.DATA [32]. Contrary to this, van der Slot et al. recently showed that WC was the strongest independent predictor of systematic coronary risk evaluation in adults with CP PEVuZE5vdGU+PENpdGU+PEF1dGhvcj52YW4gZGVyIFNsb3Q8L0F1dGhvcj48WWVhcj4yMDEzPC9Z
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ADDIN EN.CITE.DATA [33]. Regardless, according to BMI cut-offs 7 individuals were overweight (BMI 25.0–29.9), 4 were obese level I (BMI 30.0–34.9), 4 were obese level II (BMI 35.0–39.9), and 1 was extremely obese (BMI >40.0). In contrast, 9 participants were underweight (BMI <18.5) with 6 of those in the non-ambulant group. Peterson et al., also found that BMI was lowest in the adults with lower gross motor function (GMFCS IV-V) PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5QZXRlcnNvbjwvQXV0aG9yPjxZZWFyPjIwMTI8L1llYXI+
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ADDIN EN.CITE.DATA [32]. In our cohort, while both groups appeared healthy with respect to average resting systolic and diastolic blood pressures 6 participants had an SBP ≥140mmHg and 3 of those also had a DBP ≥90mmHg. In the current study, no significant differences were found between groups for central or lower-limb PWV and our values were comparable to reference values for the general population determined from 245 normotensive participants aged 30-39 years (PWV = 6.5 ± 1.4 m/s) ADDIN EN.CITE <EndNote><Cite><Author>Collaboration</Author><Year>2010</Year><RecNum>3466</RecNum><DisplayText>[65]</DisplayText><record><rec-number>3466</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3466</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Reference Values for Arterial Stiffness' Collaboration</author></authors></contributors><titles><title>Determinants of pulse wave velocity in healthy people and in the presence of cardiovascular risk factors:‘establishing normal and reference values’</title><secondary-title>European heart journal</secondary-title></titles><periodical><full-title>European Heart Journal</full-title></periodical><pages>2338-2350</pages><volume>31</volume><number>19</number><dates><year>2010</year></dates><isbn>0195-668X</isbn><urls></urls></record></Cite></EndNote>[65]. Although MVPA levels and sedentary time/hour were different between our groups, age was the only significant independent predictor of central PWV using multiple linear regression analysis. Perhaps the relatively young adult age of the participants explains the comparable stiffness values to reference values. Previous research has shown a negative relationship between PA levels and arterial stiffness in the adult population ADDIN EN.CITE <EndNote><Cite><Author>Vaitkevicius</Author><Year>1993</Year><RecNum>3255</RecNum><DisplayText>[66]</DisplayText><record><rec-number>3255</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3255</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Vaitkevicius, P. V.</author><author>Fleg, J. L.</author><author>Engel, J. H.</author><author>O'Connor, F. C.</author><author>Wright, J. G.</author><author>Lakatta, L. E.</author><author>Yin, F. C.</author><author>Lakatta, E. G.</author></authors></contributors><auth-address>Division of Geriatric Medicine, University of Maryland School of Medicine.</auth-address><titles><title>Effects of age and aerobic capacity on arterial stiffness in healthy adults</title><secondary-title>Circulation</secondary-title><alt-title>Circulation</alt-title></titles><periodical><full-title>Circulation</full-title></periodical><alt-periodical><full-title>Circulation</full-title></alt-periodical><pages>1456-62</pages><volume>88</volume><number>4 Pt 1</number><keywords><keyword>Aging/*physiology</keyword><keyword>Exercise</keyword><keyword>Exercise Test</keyword><keyword>Exercise Tolerance/*physiology</keyword><keyword>Female</keyword><keyword>Humans</keyword><keyword>Longitudinal Studies</keyword><keyword>Male</keyword><keyword>Middle Aged</keyword><keyword>Oxygen Consumption/physiology</keyword><keyword>Physical Education and Training</keyword><keyword>Physical Endurance/physiology</keyword><keyword>Pulse/physiology</keyword><keyword>Regression Analysis</keyword><keyword>Running/physiology</keyword><keyword>Vascular Resistance/*physiology</keyword></keywords><dates><year>1993</year><pub-dates><date>Oct</date></pub-dates></dates><isbn>0009-7322 (Print)
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ADDIN EN.CITE.DATA [67]. We did, however find that upper-limb arterial stiffness was increased in the non-ambulant group. Research has shown that exercise training interventions in older adults results in decreases in central arterial stiffness only with no changes observed in upper- or lower-limb PWV ADDIN EN.CITE <EndNote><Cite><Author>Tanaka</Author><Year>2005</Year><RecNum>3267</RecNum><DisplayText>[14]</DisplayText><record><rec-number>3267</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3267</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Tanaka, H. and Safar ME</author></authors></contributors><titles><title>Influence of lifestyle modification on arterial stiffness and wave reflections</title><secondary-title>American Journal of Hypertension</secondary-title></titles><periodical><full-title>American Journal of Hypertension</full-title></periodical><pages>137-144</pages><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[14]. It is difficult to speculate why the ambulant group, with higher MVPA levels, would have similar central PWV values but reduced upper PWV compared to the non-ambulant group. It has been shown in a sample of young females (18-30yrs) that increased muscle sympathetic nervous system activity was correlated with elevated inflammatory markers and peripheral arterial stiffness PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Ccmlua2xleTwvQXV0aG9yPjxZZWFyPjIwMDk8L1llYXI+
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ADDIN EN.CITE.DATA [68], however this theory is not supported by group differences in blood pressure indices. We also found that severity of gross motor function (GMFCS level) was the strongest independent predictor of upper limb stiffness in this cohort and this relationship was present after adjusting for age, MVPA per hour, and WC.Carotid distensibility is an estimate of local arterial elasticity and has been shown to increase in children, adolescents, and young adults, plateaus near age 30, and begins to decline thereafter PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5IYWx1c2thPC9BdXRob3I+PFllYXI+MjAxMDwvWWVhcj48
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ADDIN EN.CITE.DATA [69]. Perhaps the fact that both groups were relatively young, age associated decreases in distensibility may not be apparent. It is important to note, however, that age was the only significant independent predictor of distensibility, explaining 14.3% of the variance. There is an apparent progressive deterioration in endothelial function with aging that can be resultant of endothelial cell hyperplasia and atherosclerosis ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3240</RecNum><DisplayText>[25]</DisplayText><record><rec-number>3240</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3240</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[25]. In the present study, there was no difference between the two groups with respect to endothelial function. Improved endothelial function that is seen with exercise training is attributed to increased expression of the enzyme NOS in response to increased endothelial shear stress associated with exercise PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Lb3JrbWF6PC9BdXRob3I+PFllYXI+MjAwODwvWWVhcj48
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ADDIN EN.CITE.DATA [71]. It may be that endothelial function was maintained in the higher functioning GMFCS I-II who attained roughly 30 min of MVPA per day. In contrast it is difficult to explain why the lower functioning group maintained similar levels of endothelial function. Acetylcholine has been referenced as a stimulus for the release of NO from the endothelium, which would subsequently promote smooth muscle relaxation and vasodilation ADDIN EN.CITE <EndNote><Cite><Author>Celermajer</Author><Year>1997</Year><RecNum>3396</RecNum><DisplayText>[23]</DisplayText><record><rec-number>3396</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3396</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Celermajer, David S</author></authors></contributors><titles><title>Endothelial dysfunction: does it matter? Is it reversible?</title><secondary-title>Journal of the American College of Cardiology</secondary-title></titles><periodical><full-title>Journal of the American College of Cardiology</full-title></periodical><pages>325-333</pages><volume>30</volume><number>2</number><dates><year>1997</year></dates><isbn>0735-1097</isbn><urls></urls></record></Cite></EndNote>[23]. Research has shown that acetylcholine receptors are elevated in children with CP, in areas distal to the neuromuscular junction ADDIN EN.CITE <EndNote><Cite><Author>Theroux</Author><Year>2002</Year><RecNum>3475</RecNum><DisplayText>[72]</DisplayText><record><rec-number>3475</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3475</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Theroux, Mary C</author><author>Akins, Robert E</author><author>Barone, Carol</author><author>Boyce, Bobbie</author><author>Miller, Freeman</author><author>Dabney, Kirk W</author></authors></contributors><titles><title>Neuromuscular junctions in cerebral palsy: presence of extrajunctional acetylcholine receptors</title><secondary-title>Anesthesiology</secondary-title></titles><periodical><full-title>Anesthesiology</full-title></periodical><pages>330-335</pages><volume>96</volume><number>2</number><dates><year>2002</year></dates><isbn>0003-3022</isbn><urls></urls></record></Cite></EndNote>[72]. Muscanaric acetylcholine receptor levels have not been identified in the CP population, but this could possibly explain a preservation of endothelial function in the lower functioning group. Age has been previously identified as the strongest predictor of carotid IMT PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5TdTwvQXV0aG9yPjxZZWFyPjIwMTI8L1llYXI+PFJlY051
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ADDIN EN.CITE.DATA [18]. In agreement we did not observe group differences in IMT despite the higher functioning group being more physically active. It has also been identified that having a carotid IMT greater than 0.82mm increased the risk of myocardial infarction, stroke, and peripheral artery disease in a cohort of middle-aged Finnish men ADDIN EN.CITE <EndNote><Cite><Author>Bots ML</Author><Year>1998</Year><RecNum>3281</RecNum><DisplayText>[74]</DisplayText><record><rec-number>3281</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3281</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Bots ML, Iglesias del Sol A, Grobbee DE.</author></authors></contributors><titles><title>Carotid intima-media thickness measurements in observational and intervention studies</title><secondary-title>Curr Res Vasc Dis</secondary-title></titles><periodical><full-title>Curr Res Vasc Dis</full-title></periodical><pages>274-283</pages><volume>3</volume><dates><year>1998</year></dates><urls></urls></record></Cite></EndNote>[74]. Three subjects in the current study, all in the non-ambulant group, presented an IMT greater than 0.82mm. There were no group differences in lipid profiles between the two groups, nor were there differences in glucose, insulin, or IL-6 concentrations. Average cholesterol levels in both groups were below clinical minimum levels (<5.20 mmol/L), however, average HDL-C levels were below the target level of 1.30 mmol/L. Both groups were classified at low risk for CVD by having average LDL-C levels below 3.40 mmol/L and both groups were below the low risk level of 6.0 for TC/HDL-C ratio. In agreement with previous literature [12], when adjusted for age, GMFCS, and MVPA levels, participants with a higher WC were predictive of having higher LDL-C, triglyceride levels, TC/HDL-C ratio, IL-6 and lower HDL-C. There was no evidence for associations between MVPA levels and vascular or metabolic health. This absence of predictability may be a result of the relatively young age of the study sample and our small sample size. The inclusion of lower functioning persons produced broader ranges of MVPA levels, however, PA was overpowered by traditional predictors of vascular and metabolic markers such as age and WC in terms of predictive capacity in the regression analysis. Previous literature has documented that adults with CP are significantly shorter than healthy controls, likely due to reduced growth maturation seen in children with CP in that it persists to adulthood PEVuZE5vdGU+PENpdGU+PEF1dGhvcj5Kb2huc29uPC9BdXRob3I+PFllYXI+MTk5NjwvWWVhcj48
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ADDIN EN.CITE.DATA [75, 76]. Although previous studies examining stature did not separate participants using the GMFCS, those with the greatest impairments, evident through a specialized feeding apparatus, were shortest in height [76]. Our current results also suggest that adults with CP who are lower functioning tend to be shorter than their higher functioning peers. This shorter stature is likely resultant of the inability of contracted muscles to remain in parallel with bone growth, leading to joint deformities and reduced ambulation. We have demonstrated that although age was the strongest independent predictor for the majority of the vascular outcome variables, GMFCS showed a trend towards significance and may be a predictor in a larger and older cohort of adults with CP. Of particular interest would be further research in the non-ambulant group, who presented with elevated resting heart rate and upper limb arterial stiffness. A faster heart rate over time has been associated with an increased progression of collagen formation in the central arteries as a result of constant pressure loads ADDIN EN.CITE <EndNote><Cite><Author>Nichols</Author><Year>2005</Year><RecNum>3473</RecNum><DisplayText>[25]</DisplayText><record><rec-number>3473</rec-number><foreign-keys><key app="EN" db-id="rvvpx5vflaprexep5d0v5ppia2td052xddx5">3473</key></foreign-keys><ref-type name="Journal Article">17</ref-type><contributors><authors><author>Nichols, W.W., O'Rourke, M.F.</author></authors></contributors><titles><title>McDonald's Blood Flow in Arteries. Theoretical, experimental and clinical principles. Fifth Edition</title></titles><dates><year>2005</year></dates><urls></urls></record></Cite></EndNote>[25]. However, our postulation that increased acetylcholine receptors in those with CP may attenuate the progression of endothelial dysfunction as mediated through increased enzyme NOS activity and subsequent vasodilation and the predictive use of assessments of vascular health in adults with CP warrant further investigation. 2.4.1LimitationsAlthough the vascular health assessment methodology performed in the current study is relatively straightforward, limitations to the procedure vary and encompass both technical and interpretive challenges. Data are largely dependent on the quality of the ultrasound images and require a skilled operator and appropriate equipment and analysis software. The current results are limited to adults with CP across the entirety of the GMFCS scale. Specific technical difficulties that were incurred included contractures and spasms in the musculature of the imaged arm that may have hindered image quality and impacted on outcomes. Regarding measurement of PA, it is difficult to state whether the accelerometer captured true habitual PA, specifically in those whom were lower functioning. The accelerometers may not have been worn during transfer activities and were certainly not worn during water activities – two instances when activity may be greatest for persons who are lower functioning (i.e GMFCS V).2.4.2Future DirectionsDespite significant differences in MVPA levels and sedentary time/hour, there were no differences in central or lower-limb stiffness, brachial artery endothelial function, and cardiometabolic markers between groups, indicating a disconnect between levels of PA and vascular indices of health in this cohort of adults with CP. This disconnect may be due to the fact that the adult cohort studied was relatively young, and the effects of inactivity in the non-ambulant group may not compromise vascular health this early in life. Furthermore, we did not assess light PA in this study, which could possibly explain the preservation of endothelial function in the non-ambulant group. However, the fact that 96% of the time was spent in the sedentary state suggests that the non-ambulant group was performing very little, if any, activity while wearing the accelerometers. The long term preservation of sedentary behavior in the non-ambulant group may have deleterious consequences on vascular health in the later adult years and warrants further longitudinal investigation.2.4.3ConclusionIn agreement with the literature in the general population age was the strongest independent predictor for the majority of the vascular outcome variables in our cohort of adults with CP. However, the novel finding in this study was that GMFCS was an independent predictor of both uPWV and resting heart rate in this cohort of subjects. GMFCS may be a stronger independent predictor in larger, older cohorts of adults with CP, specifically in lower functioning individuals who experience minimal MVPA and increased sedentary time. It is important to highlight the establishment of techniques to assess arterial health in adults with CP, which is critically important for determining future cardiovascular risk in this clinical population. This study confirms the feasibility of using these vascular assessment techniques in this population and identifies the potential for future, longitudinal assessments of adults with CP across the entire GMFCS scale.2.5REFERENCES ADDIN EN.REFLIST 1.Svien, L.R., Berg, P., Stephenson, C., Issues in aging with cerebral palsy. Topics in Geriatric Rehabilitation, 2008. 24(1): p. 26-40.2.Rosenbaum, P., et al., A report: the definition and classification of cerebral palsy April 2006. 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J Am Diet Assoc, 1992. 92(9): p. 1083-6.APPENDIX A – GMFCS Self Report Questionnaire for Adults Aged 18 years andOlderPlease read the following and mark only one box beside the description that best represents your own movement abilities.I, ? Have difficulty sitting on my or his/her own and controlling my head and body posture in most positionsand have difficulty achieving any voluntary control of movementand need a specially adapted chair to sit comfortably and be transported anywhereand have to be lifted or hoisted by another person or special equipment to move? Can sit with some pelvic and trunk support but do not stand or walk without significant supportand therefore always rely/relies on wheelchair when outdoorsand can achieve self-mobility using a powered wheelchairand can crawl or roll to a limited extent to move around indoors ? Can stand on my own and walk if using a hand-held walking aid (such as a walker, rollator, crutches, canes, etc.)and find it difficult to climb stairs, or walk on uneven surfaces without supportand use a variety of means to move around depending on the circumstancesand prefer to use a wheelchair to travel quickly or over longer distances? Can walk on my own without any walking aids, but need/needs to hold the handrail when going up or down stairsand therefore walks in most settingsand often finds it difficult to walk on uneven surfaces, slopes or in crowdsand may occasionally prefer to use a walking aid (such as a cane or crutch) or a wheelchair to travel quickly or over longer distances? Can walk on my own without using walking aids, and can go up or down stairs without needing to hold the handrailand walk wherever they want to go (including uneven surfaces, slopes or in crowds)and can run and jump although their speed, balance, and coordination may be limitedAPPENDIX B – Letter of Information / ConsentA study of physical activity, cardiovascular health and obesity in adults with cerebral palsy aged 20-40Investigators: Principal Investigator:Dr. Jan Willem GorterDepartment of PediatricsMcMaster UniversityHamilton, Ontario, Canada(905) 521-2100 x 27855E-mail: gorter@mcmaster.caCo-Investigator(s):Dr. Brian TimmonsDepartment of PediatricsMcMaster University Hamilton, Ontario, Canada(905) 521-2100 ext. 77218E-mail: timmonbw@mcmaster.caDr. Maureen MacDonaldDepartment of KinesiologyMcMaster University (905) 525 9140 ext. 23580 E-mail: macdonmj@mcmaster.caDr. Todd BentleyDepartment of MedicineMcMaster University(905) 304-7950E-mail: msksportdoc@Why is this research being done?This research is being conducted as part of a larger study called the Stay-FIT research program, led by Dr. Jan Willem Gorter at the CanChild Centre for Childhood Disability Research at McMaster University. The goal of the Stay-FIT study is to understand and ultimately reduce the risk of cardiovascular disease in individuals with cerebral palsy (CP) and to develop community-based programs for youth with CP that promote physical activity and healthy living across the lifespan. Leading a physically inactive lifestyle can increase a person’s chance of developing cardiovascular disease and obesity. We know that the mobility limitations associated with CP have an impact on physical activity. Adolescents with CP are less physically active than their healthy peers. This may put adolescents at risk of developing cardiovascular disease and it has already been shown that obesity among children with CP has risen over the last decade. There is very little research, however, on the cardiovascular health of adults with CP. We therefore want to learn more about how the physical activity levels of adults with CP impact their health. We are particularly interested in measuring risk factors for cardiovascular disease and obesity.What is the purpose of this study?The results obtained in this study will provide some insight into the relationship between physical activity, cardiovascular health, and obesity in adults with CP aged 20-40 years who have varying degrees of mobility spanning all levels of the GMFCS spectrum (I-V). What will happen during this study?If you decide to volunteer to participate in this study, we will ask you to do the following things:Schedule 1 visit to the Department of Kinesiology at McMaster University. Before your scheduled visit we will give you a small pager-like device called an accelerometer to wear on your wrist and around your waist for 7 days prior to your visit. This device will automatically send us information on your physical activity levels throughout the week. We will also give you a logbook so that you can keep track of when you take off the accelerometer, for example, when you go to sleep at night. The accelerometer is to be returned at your visit.We will require you to have fasted for 12 hours prior to your arrival. Specific requirements can be found on the accompanying page “Participant Guidelines for Fasting.”At the visit, we will ask you to step on a scale to measure your weight. We will also measure your height and the size of your waist. Next, we will provide you with a short questionnaire that will ask you about the levels of fatigue you experience in a typical week.Following the questionnaire we will conduct an interview about the type, frequency, duration, and intensity of physical activity you do throughout the week. This interview will take about 20 to 25 minutes to complete. Then we will ask to take a blood sample from a vessel in your arm (located at the inside of the elbow) to measure the amount of lipids, insulin, Vitamin D, and glucose in your bloodstream. We will then measure the health of the main blood vessels in your neck and arm using a non-invasive ultrasound machine. These vascular health tests will require that you lie on a bed for about 20 minutes while the measurements are taken. What are the possible risks and discomforts?The risks involved in participating in this study are minimal. The ultrasound machine used to measure the health of your blood vessels is the same machine used on mothers to take pictures of their babies when they are pregnant. You will not feel any pain, however we will need to put some special jelly on your skin in order to take the pictures, which may feel cold at first. You may experience a small, pinching-type pain when the needle is inserted into your arm to draw your blood, but this should last no longer than a few seconds. You may experience discomfort during one of the vascular measurements, called a flow-mediated dilation (FMD) assessment. This test will require that we occlude the blood flow to your hand for five minutes using a blood pressure cuff on your forearm. You may feel a tingling sensation or no feeling at all during these five minutes, a sensation similar to when your hand or foot fall asleep. No permanent damage or pain will result from this and any discomfort will go away as soon as the five minutes is over. It is not likely that there will be any harms or discomforts associated with wearing the accelerometer around your waist and wrist. However, you may find it inconvenient at first. Remember that you will not be forced to do anything that makes you feel uncomfortable and you have the right to stop taking part in the study at any time. I describe below the steps I am taking to protect your privacy. Are there any benefits to doing this study? Although we cannot promise any personal benefits to you from your participation in this study, you will get the opportunity to learn more about the health of your blood vessels and your body composition. These measurements are important for your health and can be improved with physical activity. You will also be able to see for yourself how much physical activity you do in a typical week. By participating in this study, you will help us to understand the relationship between barriers to physical activity in cerebral palsy and risk for cardiovascular disease and obesity. We hope to use this information in order to create community-based programs for youth with CP that will promote the importance of physical activity and a healthy lifestyle and ultimately, prevent the risk of developing these diseases amongst individuals with CP later in life. Payment or Reimbursement We will reimburse you for any travel costs and parking expenses you may incur in getting to McMaster University. We will reimburse these expenses even if you decide that you no longer want to participate part-way through the study. Who will know what I said or did in the study?You are participating in this study confidentially. Your name will not be used, nor will there be any information published that would allow you to be identified. No one but Dr. Jan Willem Gorter, and the research assistants involved in the project will know whether you participated unless you choose to tell them.The information you provide will be kept in a locked desk/cabinet where only the investigators and research assistants will have access to it. Information kept on a computer will be protected by a password. Once the study has been completed, the data will be securely stored and will be destroyed after 10 years. If the results of the study are published, your identity will remain confidential. What if I change my mind about being in the study?It is your choice to be a part of this study or not. If you decide to participate, you have the right to stop (withdraw) at any time and for whatever reason, even after signing the consent form or part-way through the study. If you decide to withdraw, there will be no consequences to you whatsoever and no one will judge you. In cases of withdrawal, any data you have provided will be destroyed unless you indicate otherwise. If you do not feel comfortable doing something, you do not have to do it and will not be forced to, however please note that you can still be in the study if this is the case. How do I find out what was learned in this study?If you would like a brief summary of your results, please provide your preferred contact information at the end of this form and the results will be sent to you upon completion of the project. If I have any questions or concerns, whom can I call?If you have questions or need more information about the study itself, please do not hesitate to contact Dr. Jan Willem Gorter at (905) 521-2100 x 27855?or gorter@mcmaster.ca This study has been reviewed by the Hamilton Integrated Research Ethics Board (HIREB) and received ethics clearance.If you have concerns or questions about your rights as a participant or about the way the study is conducted, please contact: Office of the Chair of the HIREBTelephone: (905) 521-2100 ext. 42013CONSENTI have read the information presented in the information letter about a study being conducted by Dr. Jan Willem Gorter at McMaster University. I have had the opportunity to ask questions about my involvement in this study and to receive additional details I requested. I understand that if I agree to participate in this study, I may withdraw from the study at any time. I will be given a signed copy of this form. I agree to participate in the study.Date of Consent (MM/DD/YYYY):___________________________________________ Name of Participant (Printed): _______________________________________________Signature of Participant: ________________________________________________________________________Name of Person who obtained consent (Printed):_________________________________Signature of Person who obtained consent: ________________________________________________________________________Name of Primary Investigator (Printed): _______________________________________Signature of Primary Investigator: ________________________________________________________________________Please check one of the boxes below to indicate whether you would be willing to be contacted to participate in future research: Yes, I would be willing to be contacted to participate in future research. I prefer to be contacted through this email address: ________________________________________________________________________ I prefer to be contacted through this mailing address: ________________________________________________________________________ No, I do not wish to be contacted to participate in future research. Please check one of the boxes below to indicate whether and how (if applicable) you would like a brief summary of your results after the study is complete: Yes, I would like to receive a summary of the study’s results. I prefer it to be sent to this email address: ________________________________________________________________________ I prefer it to be sent to this mailing address: ________________________________________________________________________ No, I do not want to receive a summary of the study’s results. APPENDIX C – Data Collection FormAPPENDIX D – Raw Data ................
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