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Download Ch 9 Muscle Physiology
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Ch 9 Muscle Physiology Functions of Skeletal Muscle • • • • movement maintain posture stabilize joints heat production Gross anatomy • • • • muscle many fascicles fascicle = bundle muscle cell = muscle fiber myofibrils many cells many myofibrils contractile tissue microanatomy • • • • sarcolemma – T tubules cell membrane run deep into SR stores Ca++ sarcoplasmic reticulum – – surrounds myofibrils terminal cisternae sarcoplasm – – = cytoplasm glycogen myoglobin sarcomere unit of contraction sarcomere • • • • • • unit of contraction many along length of myofibril - “striations” Z line ends of sarcomere A band (dark) myosin and overlapping actin I band non-overlapping actin (light) contractile proteins – – thin filament actin thick filament myosin contractile proteins • • thick filament – – tail shaft heads 2 binding sites for actin thin filament – – – myosin actin actin helical chain of actin molecules myosin binding sites tropomyosin covers actin – myosin binding sites troponin binds tropomyosin to actin Ca++ binding sites Contraction of Sarcomere • • • Sliding Filament Model actin and myosin slide past each other Z lines get closer = sarcomere shortens actin – myosin binding • • • • • ++ Ca binds to troponin troponin changes shape pulls tropomyosin off the actin binding sites exposed actin and myosin bind myosin and ATP • • w/ ATP – myosin extended ATP ADP + P w/o ADP + P myosin bends put it together • • • • resting myosin extended w/ ADP stimulus Ca cross bridge formation myosin and actin bind power stroke actin knocks off ADP myosin bends pulls actin • detachment ATP binds to myosin head breaks bond with actin • “cocking” of myosin heads ATP extends myosin ATP ADP + P energy used to bend head • repeats • • • • • some myosin always in contact with actin cycle repeats several times – so, no backward movement 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 excitation • • GOAL: release Ca from SR how? depolarize sarcolemma Neuromuscular junction • • • • motor neuron + muscle fiber axon terminal – – synaptic vesicles release neurotransmitter acetylcholine (Ach) synapse motor end plate – – receptors sarcolemma at synapse for Ach Acetylcholinesterase Sarcolemma • • • polarized + outside / - inside Na channels – – chemically gated at motor end plate voltage gated along sarcolemma receptors for Ach motor end plate only depolarization • • • polarized cell membrane – + out / - inside resting membrane potential (same as neuron) Ach opens Na channel (ligand gated) – nature wants ? depolarization + in / - ouside action potential • • • • depolarization + in / - ouside + + inside (Na ) opens adjacent Na channels – voltage gated this spreads along entire cell membrane all or none same for neurons and muscle fibers from depolarization to calcium • • • + Na rushes in thru sarcolemma and T tubules Na+ inside opens voltage gated Ca channels in SR sarcoplasmic reticulum releases Ca++ 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 causes Na channels to open Na+ rushes into muscle cell sarcolemma depolarizes cont. • • • • • • + Na rushes in thru sarcolemma and T tubules Na+ inside causes sarcoplasmic reticulum to release Ca ++ Ca++ binds to troponin pulls tropomyosin off actin actin and myosin bind sliding – – – – – actin knocks ADP + P off myosin myosin bends pulls actin closer ATP breaks myosin – actin bond myosin extends repeat How do you stop this darn thing? • • • Ca++ pulled back into SR via active transport – – troponin and tropomyosin cover actin sarcomere lengthens Acetylcholinesterase destroys Ach at motor end plate – Na channels close Na+ - K+ pump restores “polarized” sarcolemma 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 Motor unit • • • strength of contraction – more motor units = stronger contraction of muscle 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 sarcomere relaxes ~ 10-100 ms myogram • • recording of muscle activity muscles vary in speed and length of twitch size of motor unit repeated stimuli • • • graded response = varied strength of contraction – number of fibers contracting wave summation – – repeat stim w/o full relaxation nd 2 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 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 • “warming up” treppe – – 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 • glycolysis • aerobic respiration + ADP creatine + ATP = anaerobic respiration • fastest, but only 2 ATP made • strenuous activity 30 – 40 sec • when decreased O2 and blood flow • lactic acid = cell respiration • glucose + O2 ATP + CO2 • 36 ATP made • mild, or prolonged activity + H2O + heat fuel for ATP • • fatty acids main source at rest glycogen stored in muscle moderate to heavy exercise • glucose blood minimal source • pyruvic acid liver converted lactic acid replaces ATP after exercise • oxygen myoglobin blood 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 velocity of muscle contraction • • type of muscle fiber : – slow vs fast – oxidative aerobic pathway of ATP production cell respiration – glycolytic anaerobic pathway of ATP prod. glycolysis load speed of myosin ATPase increased weight slows the contraction Exercise • • • endurance exercise – – – – aerobic increase mitochondria , myoglobin , capillaries slow, oxidative fibers less fatigue no increase mass resistance exercise – – – increase myofibrils , not muscle cells stores glycogen split ends theory atrophy – – disuse nerve damage = hypertrophy effects of ATP use • fatigue low ATP lactic acid - low pH inhibits enzymes inability to contract • contractures lack ATP can’t detach cross-bridges • Oxygen debt replace O2 stored in myoglobin O2 used to replace ATP O2 for lactic acid pyruvic acid decreased pH CO2 , lactic acid • • • increase body temp ketones homeostatic responses to exercise • • • • • • vasodilation increase O2 , glucose remove CO2 increase heart rate same increase respiration remove CO2 , raise pH remove heat 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 self-excitatory no fatigue slow contraction low ATP requirement • neural stim acetylcholine norepinephrine • other controls α ß hormones O2 , CO2 , pH histamine , paracrines diseases • • • Muscular Dystrophy myasthenia gravis atrophy
