Chapter 9 Muscle - Los Angeles Mission College



Chapter 9 Muscle

Functions of Skeletal Muscle

* movement

* maintain posture

* stabilize joints

* heat production

Gross anatomy

* muscle cell = muscle fiber many myofibrils

* myofibrils cylindrical units within each cell contain sarcomeres

* fascicle = bundle many cells

* muscle many fascicles

microanatomy

* sarcolemma cell membrane

* T tubules run deep into SR

* sarcoplasmic reticulum stores Ca++

* surrounds myofibrils

* terminal cisternae

* sarcoplasm = cytoplasm

* glycogen

* myoglobin

* sarcomere unit of contraction

sarcomere

* unit of contraction

* many along length of myofibril - “striations”

* Z disc ends of sarcomere

* A band (dark) myosin and overlapping actin

* I band (light) non-overlapping actin

* contractile proteins actin ; myosin

contractile proteins

* thick filament myosin

* tail shaft

* heads 2 binding sites for actin

* thin filament

* actin helical chain of actin molecules myosin binding sites

* tropomyosin covers actin – myosin binding sites

* troponin binds tropomyosin to actin has Ca++ binding sites

Contraction of Sarcomere

* sarcomere gets shorter ; not the filaments

* Sliding Filament Model

* actin and myosin slide past each other

* Z discs get closer = sarcomere shortens

Ca stimulates filament sliding

* Ca++ binds to troponin

* troponin changes shape

* pulls tropomyosin off the actin

* exposes actin

* actin and myosin bind

Who does what to who ?

* myosin vs ADP

* w/ ADP myosin extended

* w/o ADP myosin bends

* actin vs ATP

* ATP knocks actin off myosin

* Actin knocks ADP off myosin

* Ca actin and myosin bind

put it together

* resting myosin extended w/ ADP

* stimulus Ca

* cross bridge formation myosin and actin bind actin knocks off ADP

* power stroke w/o ADP, myosin bends myosin bend pulls actin

* detachment ATP binds to myosin head breaks bond with actin

* “cocking” of myosin heads ATP ( ADP + P ADP extends myosin

* repeats

* some myosin always in contact with actin

* cycle repeats several times – pulling actin further

* 1 power stroke shortens muscle about 1%

* muscles shorten ~ 30 – 35 % of their resting length

* continues as long as Ca++ and ATP present

Neuromuscular junction

* = motor neuron + muscle fiber

* control cell = neuron axon terminal

* neurotransmitter acetylcholine (Ach)

* transport synapse

* target cell (post-synaptic cell) muscle

* motor end plate sarcolemma at synapse

* receptors for Ach

* action potential sarcolemma

Neuromuscular excitation

* GOAL: sarcomere contraction

* Muscle vs Nerve :

* NT depolarizes target cell

* effect of action potential:

* target cell = nerve NT release

* target cell = muscle Ca from sarcoplasmic reticulum

Sarcolemma

* polarized + outside / - inside

* Na channels

* chemically-gated at motor end plate

* voltage-gated sarcolemma, T-tubules

* receptors for Ach motor end plate only

Sarcolemma acts like an axon

* polarized at rest + outside / - inside Na / K

* Ach opens Na ligand-gated channel

* nature wants ?

* depolarization + in / - ouside

* Na+ inside opens voltage-gated Na channels

* action potential entire sarcolemma and T-tubules same as axon

action potential causes calcium release

* T-tubules next to terminal cisternae

* T tubules depolarize

* Na+ inside opens voltage gated Ca channels in SR

* sarcoplasmic reticulum releases Ca++

excitation-contraction coupling – short version

* neuron stim sarcolemma

* action potential

* Ca released

* sarcomere shortens

excitation-contraction coupling

* neuron depolarizes

* depolarization reaches axon terminal

* rush of Ca++ into axon terminal

* Ca++ causes release of Acetylcholine into synapse

* Ach binds with receptors on motor endplate

* Ach opens ligand-gated Na channels

* Na+ inside opens voltage-gated Na+

* action potential along sarcolemma and T-tubules

*

* Na+ inside causes sarcoplasmic reticulum to release Ca++

* Ca++ binds to troponin

* pulls tropomyosin off actin

* actin and myosin bind cross bridge

* myosin bends power stroke

* sarcomere shortens

How do you stop this darn thing?

* Acetylcholinesterase destroys Ach at motor end plate

* Na channels close

* sarcolemma repolarizes

* Na+ - K+ pump

* Ca++ pump Ca++ into SR via active transport

* troponin and tropomyosin cover actin

* ATP - detachment

* myosin extends

* sarcomere lengthens

ATP uses

* Na pump

* Ca pump

* break myosin and actin bond

Motor unit

* motor neuron + muscle cells it stimulates

* 1 neuron has several branches of its axon

* strength of contraction

* more motor units = stronger contraction of muscle

* recruitment

* control of movements

* small motor units (4-10) fine control fingers

* large motor units (100) poor control thigh

* alternation

one stimulus

* twitch = single contraction due to a single stimulus

* 3 parts:

* latent period time from excitation to contraction no change in myogram ~ 3 ms

* contraction begin contraction to max. force myogram increases ~ 10-100 ms

* relaxation myogram decreases ~ 10-100 ms sarcomere relaxes

myogram

* recording of muscle activity

* tension , not voltage

* muscles vary in speed and length of twitch size of motor unit

repeated stimuli

* graded response = varied strength of contraction

* number of motor units

* wave summation repeat stim w/o full relaxation

* 2nd twitch is a stronger contraction (summed)

* increased Ca++ available

* tetanus: smooth, sustained contraction normal muscle contraction

stronger stimuli

* motor unit summation = recruitment

* in vivo: more neurons

* lab: more electricity (mV)

* threshold stimulus

* minimum stim to cause contraction

* maximal stimulus

* strongest stim that increases force of contraction

* all motor units recruited

muscle tone

* muscle tone slight, constant contraction of all skeletal muscles

* posture

* stabilize joints

* heat production

treppe

* treppe “warming up”

* gradual increase strength of 1st few contractions

* increase Ca++ and enzyme activity

length - strength

* resting length vs strength

* ideal resting length

* 80 – 120 % of resting length

* too short

* sarcomeres already short

* too long

* actin and myosin too far away

force of muscle contraction

* affected by:

* recruitment

* size of muscle fibers

* wave summation (frequency)

* muscle length

types of muscle contraction

* muscle tension force

* load weight of object (bone)

* isometric contraction tension w/o movement

* isotonic contraction tension w/ movement

* concentric tension while shortening

* eccentric tension while lengthening

Energy production

* stored ATP 3 – 4 seconds

* creatine phosphate (CP) 10 – 15 sec

* creatine-P + ADP ( creatine + ATP CPK

* new ATP:

* glycolysis = anaerobic respiration

* fastest, but only 2 ATP made

* strenuous activity 30 – 40 sec

* when decreased O2 and blood flow

* lactic acid

* aerobic respiration = cell respiration

* glucose + O2 ( ATP + CO2 + H2O + heat

* 36 ATP made

* mild, or prolonged activity

fuel for ATP

* fatty acids main source at rest

* glycogen stored in muscle moderate to heavy exercise

* glucose blood minimal source in muscle

* pyruvic acid liver converted lactic acid replaces ATP after exercise

* oxygen myoglobin hemoglobin

effects of ATP use

* fatigue low ATP lactic acid - low pH inhibits enzymes inability to contract

* contractures lack ATP can’t detach cross-bridges decrease blood flow

* Oxygen debt replace O2 stored in myoglobin O2 for lactic acid ( pyruvic acid increased respiratory rate

* decreased pH CO2 , lactic acid

* increase body temp

types of skeletal muscle fibers

* slow oxidative fibers (type I)

* aerobic (cell respiration)

* myoglobin ; mitochondria (red)

* slow , prolonged contraction

* little fatigue

* fast glycolytic fibers (type II x)

* anaerobic

* little myoglobin or mitochondria (pale)

* fast contraction ; quick fatigue

* fast oxidative fibers (type II a) (pink)

* intermediate speed, strength, and fatigue

Exercise

* endurance exercise aerobic

* increase mitochondria , myoglobin , capillaries

* slow, oxidative fibers

* less fatigue

* no increase mass

* resistance exercise

* increase myofibrils , not # muscle cells = hypertrophy

* stores glycogen

* split ends theory

* atrophy

* disuse

* nerve damage

homeostatic responses to exercise

* vasodilation increase O2 , glucose remove CO2

* increase heart rate same

* increase respiration remove CO2 , raise pH remove heat repay oxygen debt

* acid-base mechanisms remove H+ , raise pH

* sweat decrease body heat

* thirst replace water loss

smooth muscle

* no sarcomeres

* network of sliding thick and thin filaments

* Ca++ stim sliding

* SR and caveoli (pouch of extracellular Ca++)

* gap junctions

* no fatigue slow contraction low ATP requirement

* neural stim acetylcholine norepinephrine α ß

* other controls hormones O2 , CO2 , pH histamine , paracrines

cardiac muscle

* see heart chapter

diseases

* Muscular Dystrophy

* myasthenia gravis

* atrophy

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