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Preeti RangarajApril 22, 2013Bio 473 Sec 10TA: Paige ChandlerThe Effect of Exercise on Cardiovascular and Respiratory PhysiologyIntroductionIn each situation the human body is confronted with, its response is always to strive to maintain stable internal environment, homeostasis, in order to ensure that all of its physiological functions can be executed effectively (Silverthorne). Exercise is an act that inherently forces the human body out of its normal comfort zone. In order to compensate for this change and maintain homeostasis, the body reacts in a number of different ways. Heart rate, carbon dioxide clearance, oxygen consumption, temperature, hemoglobin saturation and mean arterial pressure are all characteristics of the body that are changed by exercise, and that the body is required to regulate and maintain at specific ranges in order for the human body’s physiological processes to function in optimal capacity. During exercise, the body performs cell respiration at a higher rate due to an increased need for ATP. This can result in an increased need for oxygen to fuel this process, metabolic acidosis due to increased carbon dioxide production and increased oxygen consumption, as well as an increase in body temperature (Silverthorne). In order to compensate for these changes, the human body alters its heart rate, carbon dioxide clearance, oxygen consumption, temperature, hemoglobin saturation and mean arterial pressure.The purpose of this lab was to observe the effect that physical exercise can have on respiratory and cardiovascular physiology of the human body. This was accomplished through observing three different test subjects during rest, exercising them by requiring that they run on a treadmill until they reached a precalculated “exercise heart rate,” and then observing them during their recovery from this exercise. This information holds relevance for a number of different groups of people, including those with cardiac or respiratory health issues, doctors attempting to treat patients with these illnesses, companies attempting to create pharmaceuticals in order to minimize the risk associated with exercise for individuals with these conditions, and individuals with careers directly related to exercise and physical fitness such as personal trainers.It was hypothesized that in order to compensate for these changes, carbon dioxide clearance, oxygen consumption, heart rate, mean arterial pressure and temperature would increase during exercise in order to compensate for the aforementioned increased CO2 levels and increased O2 requirement, while hemoglobin saturation would decrease during exercise in order to facilitate the distribution of more oxygen to various organs through the bloodstream. During the resting phase, heightened carbon dioxide clearance, heart rate, oxygen consumption, temperature, mean arterial pressure and hemoglobin saturation are expected to attempt to return their resting values, and to the condition they were in before exercise began. MethodsThe majority of this lab followed the protocol outlined in the “Exercise Physiology,” lab handout provided by John Waters, and lab TA Paige Chandler. For each subject, baseline oxygen consumption, temperature, hemoglobin saturation, and mean arterial pressure were taken (Waters). Our procedure differed from protocol at this point in that CO2 clearance was not measured, due to an inability for our lab section to obtain a capnometer. Each subject then ran on a treadmill until their measured heart rate came within range of their calculated “exercise heart rate,” at which point the treadmill speed was gradually brought to a stop. After the treadmill reached a stop, each subject was given a 6-minute resting period, during which measurements were taken twice more in order to collect “resting data points.” For the duration of the exercise period, measurements were taken at regular intervals as well, in order to collect “exercise data points”. An exercise heart rate was calculated prior to the exercise phase in order to ensure that the subject stopped running before they were at serious risk of cardiac arrest or another physically debilitating state. In order to collect the data, a multitude of different instruments were used. A treadmill was utilized to ensure that experimenters could control the level of exercise each subject was exposed to. A heart rate monitor was used to measure heart rate, a spirometer to measure the volume of air exhaled, and a skin thermometer to measure temperature. A pulse oximeter was used to measure the percent oxygen in the subject’s blood as well as to measure the subjects’ heart rate when they were at rest. A sphygmomanometer was used to measure systolic and diastolic blood pressures, after which the formula “Mean Arterial Pressure = (1/3 * systolic pressure)+(2/3 * diastolic pressure)” was used to calculate MAP. The oxygen analyzer was used to measure the oxygen concentration of air exhaled by the subjects. The formula (20.9%-%O2 of exhaled air)*tidal volume (l/breath)*respiratory rate (breaths/min) = O2 consumption was used to obtain this number. Had a capnometer been used to measure carbon dioxide production, the formula (%Co2 of exhaled air)* tidal volume*repiratory rate=CO2 clearance would have been used to obtain this number (Waters). This experiment’s method is unique in that it does not have a “control” subject. Instead, the values taken at resting points are used as control values, and the measurements taken during and after exercises are used as data points and compared to these “control” values (Waters). The subject exercised by running on a treadmill until their heart rate came close to the calculated exercise heart rate at which point they were required to slow down. Certain data points weren’t collected while the subject was exercising. Temperature, hemoglobin saturation and mean arterial pressure were only measured directly before exercise, and after exercise during the resting phase. These measurements were not taken during the exercise phase because they could not be taken while the subject was running, due to the nature of the equipment required to measure them. For example, a stethoscope could not be used along with a sphygmomanometer in order to measure blood pressure without the subject slowing down their running speed.ResultsFigure 1. Changes in Heart RateFigure one graphs the heart rate of each subject as measured for the duration of the experiment. The first 3 minutes account for the control values, the last 6 minutes account for the resting period, and the exercise phase accounts for all of the values measured between these two time intervals. The exercise phase lasted for a duration of 9 minutes for subjects 2 and 3, and a duration of 12 minutes for subject 1. For all three subjects, heart rate started at a base value, increased for the duration of the exercise period, and then attempted to return to the control value during the resting phase, ending at a value slightly higher than the initial control after a period of 6 minutes.Figure 2. Changes in Oxygen ConsumptionFigure 2 graphs the level of oxygen consumption measured in each subject for the duration of the experiment. The first 3 minutes account for the control values, the last 6 minutes account for the resting period, and the exercise phase accounts for all of the values measured between these two time intervals. The exercise phase lasted for a duration of 9 minutes for subjects 2 and 3, and a duration of 12 minutes for subject 1. For subjects 1 and 2, oxygen consumption steadily decreased from the beginning of the exercise phase through the recovery phase, with the final measured values significantly lower than the control values measured. For subject 3 however, oxygen consumption steadily increased from the control value during the exercise phase, and began to decrease and attempt to return to the control value during the recovery phase.Table 1. TemperatureTime (and activitySkin Temperature (C): Subject 1Skin Temperature (C): Subject 2Skin Temperature (C): Subject 30 min (Sitting)36.735.936.73 min (Sitting)36.735.936.5Directly after exercise36.733.9353 min (After recovery began)36.435.3336.86 min (After recovery)36.535.736.2Table 1 shows the subjects’ temperatures measured before and after exercise. For subjects 1 and 2, temperature remained relatively stable, decreasing slightly during the recovery phase as compared to the control phase. For subject 3, temperature decreased leading up to the exercise phase, appeared to increase during the exercise phase, and decreased once more during the recovery phase. Table 2. Hemoglobin SaturationTime (and activityHemoglobin Saturation (%): Subject 1Hemoglobin Saturation (%): Subject 2Hemoglobin Saturation (%): Subject 30 min (Sitting)9898973 min (Sitting)989898Directly after exercise9597973 min (After recovery began)9697986 min (After recovery)979898Table 2 shows the subjects’ % hemoglobin saturation, calculated before and after exercise. The hemoglobin saturation decreased after exercise for all 3 subjects, and returned to homeostasis during recovery. Subject 3 appeared to recover most quickly. Table 3. Mean Arterial PressureTime (and activityMean Arterial Pressure (mmHg): Subject 1Mean Arterial Pressure (mmHg): Subject 2Mean Arterial Pressure (mmHg): Subject 30 min (Sitting)9787953 min (Sitting)968795Directly after exercise1051001033 min (After recovery began)100951076 min (After recovery)9795103Table 3 displays the Mean Arterial Pressure in mmHg as calculated before and after exercise. For all 3 subjects, MAP increased during the exercise phase, and attempt to return to the control value during the recovery phase, ending at a value slightly higher than the recovery phase, with the exception of Subject 1, who managed to completely return to his control MAP.DiscussionThe obtained results do appear to support the predictions made in the hypothesis. As expected, oxygen consumption increased during exercise in order to fuel the increased rate of cellular respiration necessary to create ATP to fuel the body during exercise, trending upward for Subjects 1 and 2. While Subject 3’s oxygen consumption did not follow this pattern, this variation is likely due to sources of error in the experiment, which will be discussed shortly.In order to supply this increased need for oxygen, heart rate was also expected to increase during exercise, to increase cardiac output to the aforementioned increased oxygen requirement for cells. Once again, the hypothesis was proven correct, and heart rate for all three subjects increased during exercise. Increased cardiac output also led to the expected increase in Mean Arterial Pressure in all three subjects during exercise. During the post exercise recovery period all three of the aforementioned values, Mean Arterial Pressure, Oxygen consumption, and heart rate, behaved as expected, stopped increasing, and steadily attempted to return to their original homeostatic control values. It was also hypothesized that the human body’s elevated oxygen requirement during exercise meant that hemoglobin saturation rates would decrease, and that the hemoglobin would release oxygen in order for oxygen to be distributed throughout the bloodstream more efficiently. This proved to be true for all 3 subjects, as did the prediction that their hemoglobin saturation rates would return to homeostatic values during the recovery phase (Silverthrone). The last prediction made was that temperature would increase during the exercise phase due to the increased metabolic activity of the body, and then lower in an attempt to return to the control value during the recovery phase. This pattern was seen in all three subjects, though it was observed to the greatest extent in subject 3.Though a capnometer was unavailable for use during this lab, had one been available it would have been used to measure the amount of carbon dioxide exhaled by measuring exhaled tidal CO2 concentration. It is predicted that carbon dioxide concentration in exhaled air would have increased during exercise as a byproduct of the increased rate of cell respiration (Silverthorne).Though the data shows strong support for the hypothesis, there are slight discrepancies. These are likely to due to a number of minor sources of error present in the experiment. For example, the calculated exercise heart rate did not appear to be high enough to allow for the subject to run long enough to experience a significant measurable increase in temperature. The temperature changes experienced during the experiment were minor enough that homeostatic mechanisms were able to self regulate skin temperature rapidly enough to make up for any increase due to metabolic activity. In addition, this lab section was unable to obtain a capnometer to take CO2 measurements as recommended in the lab protocol. The instruments that we were able to use were also old, and might not have measured values as precisely as required. Unfamiliarity with the equipment on the part of the data collectors is also a factor that could have impacted the data. In order to minimize this error, it would be helpful to use instruments that are either newer, or calibrated in such a way that it is known that their measurements are precise and accurate, to ensure that a capnometer can be obtained before initiation of the experiment, and perhaps for the subject to run for a period slightly longer than solely up to the calculated exercise heart rate. In conclusion, the hypothesis was strongly supported by the data. Human exercise results in the body straining itself in an attempt to maintain homeostasis. Individuals participating in exercise, especially those with cardiac or respiratory conditions should pay heed to this knowledge when exercising, and exercise caution when pushing themselves at the gym or in other situations where they might be putting their bodies in physical strain.ReferencesSilverthorn, D.U. (2013). Human Physiology: An Integrated Approach (6th ed.). New York: Pearson Education Inc.Waters, J. (2013). Exercise Physiology. 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