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Chapter 9 Muscle Functions of Skeletal Muscle • • • • movement maintain posture stabilize joints heat production Gross anatomy • • • muscle cell – = muscle fiber myofibrils fascicle many myofibrils cylindrical units within each cell contain sarcomeres = bundle many cells muscle many fascicles 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 Z disc - “striations” ends of sarcomere A band (dark) myosin and overlapping actin I band non-overlapping actin (light) 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 – neurotransmitter transport axon terminal acetylcholine (Ach) synapse • target cell – (post-synaptic cell) muscle motor end plate sarcolemma at synapse • receptors • action potential for Ach 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 • Na channels • – – + outside / - inside chemically-gated at motor end plate voltage-gated receptors sarcolemma, T-tubules for Ach motor end plate only Sarcolemma acts like an axon • polarized • Ach opens Na ligand-gated channel • • • – at rest + outside / - inside Na / K 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 sarcomere relaxes ~ 10-100 ms myogram • • • recording of muscle activity tension , not voltage muscles vary in speed and length of twitch size of motor unit repeated stimuli • graded response = • wave summation • – – – varied strength of contraction number of motor units 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 – – = in vivo: more neurons lab: more electricity (mV) recruitment 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 + 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 slow , prolonged contraction little fatigue (red) • • 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 • other controls α ß hormones O2 , CO2 , pH histamine , paracrines cardiac muscle • see heart chapter diseases • • • Muscular Dystrophy myasthenia gravis atrophy