BMSP 2135 Chapter 11
BMSP 2135 Chapter 11 2135 BMSP
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This 21 page Class Notes was uploaded by Marlena Trone on Tuesday October 11, 2016. The Class Notes belongs to 2135 BMSP at Virginia Polytechnic Institute and State University taught by in Fall 2016. Since its upload, it has received 3 views.
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Date Created: 10/11/16
CHAPTER 11: Muscle Tissue CHARACTERISTICS OF MUSCLE • responsiveness (excitability) ‾ Muscle and nerve cells have developed this property to the highest degree. ‾ When stimulated by chemical signals, stretch and other stimuli, muscle cells respond with electrical changes across the plasma membrane • Conductivity ‾ Local electrical change triggers a wave of excitation that travels rapidly along the cell and initiates process leading to contraction • Contractility ‾ Muscle cells are unique in their ability to shorten when stimulated ‾ Enables them to pull on bones and other organs to create movement • Extensibility ‾ Ability to stretch again between contractions ‾ Muscle cells can stretch up to three times their contracted length • Elasticity ‾ After a muscle cell is stretched and then released, it recoils to a shorter length ‾ If it wasn’t for this elastic recoil, resting muscles would be too slack TYPES OF MUSCLE TISSUE • Skeletal • Cardiac • Smooth MUSCLE FIBER • Muscle cells are called muscle fibers or myofibers • Myofibrils composed of myofilaments THICK FILAMENTS • About 15 nm in diameter • Made of the protein myosin • Myosin is shaped like a golf club • The heads on one half of the thick filament angle to the left and the heads on the other half angle to the right • The middle is a bare zone and has no heads. THIN FILAMENTS • 7 nm in diameter • Composed primarily of two intertwined strands of a protein called fibrous (F) actin. • A string of subunits called globular (G) actin attach to F actin ‾ Each G actin has an active site that can bind to the head of a myosin molecule • When a muscle fiber is relaxed, each tropomyosin blocks the active sites of six or seven G actins and prevents myosin from bnding to them • Each tropomyosin molecule has a smaller calciumbinding protein called troponin bound to it • Regulatory proteins • Contractile proteins • Accessory proteins ‾ Elastic filament (titin) – anchors thick filaments to Z disc ‾ Dystrophin ‾ At least 7 others ELASTIC MYOFILAMENTS • titin (connectin) – huge springy protein ‾ flank each thick filament and anchor it to the Z disc ‾ helps stabilize the thick filament ‾ center it between the thin filaments ‾ prevents over stretching DYSTROPHIN • Dystrophin: most clinically important ‾ links actin in outermost myofilaments to transmembrane proteins and eventually to fibrous endomysium surrounding the entire muscle cell ‾ transfers forces of muscle contraction to connective tissue around muscle cell ‾ genetic defects in dystrophin produce disabling disease muscular dystrophy MUSCULAR DYSTROPHY • muscular dystrophy: group of hereditary diseases in which skeletal muscles degenerate and weaken, and are replaced with fat and fibrous scar tissue • Duchenne muscular dystrophy is caused by a sexlinked recessive trait (1 of 3500 live born boys) ‾ most common form ‾ disease of male diagnosed between 2 and 10 years of age ‾ mutation in gene for muscle protein dystrophin • actin not linked to sarcolemma and cell membranes damaged during contraction, necrosis and scar tissue results ‾ rarely live past 20 years of age due to affects on respiratory and cardiac muscle – incurable STRIATIONS • striated muscle has d“A”rk A bands alternating with l“I”ghter I bands ‾ A stands for anisotropic and I for isotropic • In the middle of the A band, there is a lighter region called the H band, into which the thin filaments do not reach • In the middle of the H band, the thick filaments are linked to each other through a dark, transverse protein complex called the M line • Each light I band is bisected by a dark narrow Z disc (Z line), which provides anchorage for the thin and elastic filaments • Each segment of a myofibril from one Z disc to the next is called a sarcomere. HIERARCHY OF SKELETAL MUSCLE Largest to smallest component • Muscle • Fascicle • Muscle fiber • Myofibril • Sarcomere • Myofilaments SLIDINGFILAMENT THEORY • The actin (thin) filaments of muscle fibers slide past the myosin (thick) filaments during muscle contraction, while the two groups of filaments remain at relatively constant length NERVEMUSCLE RELATIONSHIP • Motor unit: consists of one motor neuron and all skeletal muscle fibers that it innervates. • average motor unit ‾ 200 muscle fibers per neuron • small motor units: fine degree of control ‾ 36 muscle fibers per neuron ‾ eye and hand muscles • large motor units: more strength than control ‾ 1000 muscle fibers per neuron ‾ gastrocnemius THE NEUROMUSCULAR JUNCTION • synapse: point where a nerve fiber meets its target cell • neuromuscular junction (NMJ): when target cell is a muscle fiber • Synaptic knob • Synaptic cleft • Synaptic vesicles – acetylcholine (ACh) • Ach receptors – (50 million) ‾ Junctional folds • Acetylcholinesterase (AChE) MYASTHENIA GRAVIS • autoimmune disease in which antibodies attack neuromuscular junctions and bind ACh receptors together in clusters ‾ disease of women between 20 and 40 ‾ muscle fibers then removes the clusters of receptors from the sarcolemma by endocytosis ‾ fiber becomes less and less sensitive to ACh ‾ effects usually first appear in facial muscles • drooping eyelids and double vision, difficulty swallowing, and weakness of the limbs • treatments ‾ cholinesterase inhibitors retard breakdown of ACh allowing it to stimulate the muscle longer ‾ immunosuppressive agents suppress the production of antibodies that destroy ACh receptors ‾ thymus removal (thymectomy) – helps to dampen the overactive immune response that causes myasthenia gravis ‾ plasmapheresis –technique to remove harmful antibodies from blood plasma NEUROMUSCULAR TOXINS • toxins that interfere with synaptic function ‾ can paralyze muscles • cholinesterase inhibitors – found in some pesticides ‾ bind to acetylcholinesterase and prevent it from degrading ACh ‾ spastic paralysis a state of continual contraction of the muscles ‾ possible suffocation • tetanus (lockjaw) is a form of spastic paralysis caused by toxin of Clostridium tetani ELECTRICALLY EXCITABLE CELLS • muscle fibers and neurons are electrically excitable cells ‾ their plasma membrane exhibits voltage changes in response to stimulation • voltage (electrical potential): a difference in electrical charge from one point to another • resting membrane potential: about 90mV • action potential: quick upanddown voltage shift from the negative RMP to a positive value, and back to the negative value again. ‾ action potential is a quickly fluctuating voltage seen in an active stimulated cell ‾ an action potential at one point on a plasma membrane causes another one to happen immediately in front of it, which triggers another one a little farther along and so forth MUSCLE CONTRACTION AND RELAXATION • four major phases of contraction and relaxation ‾ excitation • the process in which nerve action potentials lead to muscle action potentials ‾ excitationcontraction coupling • events that link the action potentials on the sarcolemma to activation of the myofilaments, thereby preparing them to contract ‾ contraction • step in which the muscle fiber develops tension and may shorten ‾ relaxation • when its work is done, a muscle fiber relaxes and returns to its resting length EXCITATION • nerve signal opens voltagegated calcium channels in synaptic knob • calcium stimulates exocytosis of ACh from synaptic vesicles • ACh released into synaptic cleft + + • Two Ach molecules bind to each receptor protein, opening Na and K channels. + + • Na enters shifting RMP goes from 90mV to +75mV, then K exits and RMP returns to 90mV quick voltage shift is called an endplate potential (EPP) • Voltage change (EPP) in endplate region opens nearby voltagegated channels producing an action potential that spreads over muscle surface. EXCITATIONCONTRACTION COUPLING • Action potential spreads down into T tubules • Opens voltagegated ion channels in T tubules and Ca channels in SR • Ca enters the cytosol • Calcium binds to troponin in thin filament • Troponintropomyosin complex changes shape and exposes active sites on actin CONTRACTION • Myosin ATPase enzyme in myosin head hydrolyzes an ATP molecule • Activates the head “cocking” it in extended position ‾ ADP + P remain attached • head binds to actin active site forming a myosin actin crossbridge • myosin head releases ADP and P, flexis pulling thin filament past thick power stroke • upon binding more ATP, myosin releases actin and process is repeated ‾ each head performs 5 power strokes per second ‾ each stroke utilizes one molecule of ATP RELAXATION • nerve stimulation and Ach release stop • AChE breaks down Ach and fragments reabsorbed into synaptic knob • Stimulation by Ach stops • Ca pumped back into SR by active transport. Ca binds to calsequestrin while in storage in SR • ATP is needed for muscle relaxation as well as muscle contraction • Ca removed from troponin is pumped back into SR • tropomyosin reblocks the active sites • muscle fiber ceases to produce or maintain tension • muscle fiber returns to its resting length ‾ due to recoil of elastic components & contraction of antagonistic muscles RIGOR MORTIS • rigor mortis: hardening of muscles and stiffening of body beginning 3 to 4 hours after death ‾ deteriorating sarcoplasmic reticulum releases Ca +2 ‾ deteriorating sarcolemma allows Ca to enter cytosol ‾ Ca activates myosinactin crossbridging ‾ muscle contracts, but can not relax. • muscle relaxation requires ATP, and ATP production is no longer produced after death ‾ fibers remain contracted until myofilaments begins to decay • rigor mortis peaks about 12 hours after death, then diminishes over the next 48 to 60 hours BEHAVIOR OF WHOLE MUSCLES • myogram: a chart of the timing and strength of a muscle’s contraction • threshold: the minimum voltage necessary to generate an action potential in the muscle fiber and produce a contraction ‾ twitch – a quick cycle of contraction when stimulus is at threshold or higher ‾ a weak, subthreshold electrical stimulus causes no contraction PHASES OF A TWITCH CONTRACTION • latent period: 2 millisecond delay between the onset of stimulus and onset of twitch response ‾ time required for excitation, excitationcontraction coupling and tensing of elastic components of the muscle ‾ internal tension: force generated during latent period and no shortening of the muscle occurs • contraction phase: phase in which filaments slide and the muscle shortens ‾ once elastic components are taut, muscle begins to produce external tension – in muscle that moves a load ‾ shortlived phase +2 • relaxation phase: SR quickly reabsorbs Ca , myosin releases the thin filaments and tension declines ‾ muscle returns to resting length ‾ entire twitch lasts from 7 to 100 millisecond CONTRACTION STRENGTH OF TWITCHES Twitches vary in strength depending upon: • stimulus frequency: stimuli arriving closer together produce stronger twitches • how stretched muscle was before it was stimulated • temperature of the muscles: warmedup muscle contracts more strongly – enzymes work more quickly • lower than normal pH of sarcoplasm weakens the contraction fatigue • state of hydration of muscle affects overlap of thick & thin filaments – Increasing the voltage above threshold does not increase twitch strength in a muscle fiber INCREASING THE VOLTAGE • Increasing the voltage above threshold will NOT produce a stronger twitch in a muscle cell • Increasing the voltage applied to a whole muscle will increase the strength of contraction RECRUITMENT • Higher voltage applied to a whole muscle will lead to a stronger contraction • Recruitment of muscle fibers INCREASING THE FREQUENCY OF STIMULATION • Twitches – <10 stimuli/sec • Incomplete tetanus – 2040 stimuli/sec – Incomplete relaxation between stimuli – Temporal summation – Wave summation • Complete tetanus – 4050 stimuli/sec – Smooth, prolonged contraction – Rarely occurs in the body • Smooth contractions due to multiple motor units contracting at different times ISOMETRIC CONTRACTION • isometric muscle contraction – muscle is producing internal tension while an external resistance causes it to stay the same length – can be a prelude to movement when tension is absorbed by elastic component of muscle – important in postural muscle function • isotonic muscle contraction – muscle changes in length with no change in tension – concentric contraction – muscle shortens while maintains tension – eccentric contraction – muscle lengthens as it maintains tension ISOMETRIC AND ISOTONIC PHASES OF CONTRACTION • at the beginning of contraction – isometric phase – muscle tension rises but muscle does not shorten • when tension overcomes resistance of the load – tension levels off • muscle begins to shorten and move the load – isotonic phase MUSCLE METABOLISM • all muscle contraction depends on ATP • ATP supply depends on availability of: – organic energy sources such as glucose and fatty acids – oxygen • two main pathways of ATP synthesis – anaerobic fermentation • enables cells to produce ATP if oxygen is unavailable • yields little ATP and toxic lactic acid, a major factor in muscle fatigue – aerobic respiration • produces far more ATP • less toxic end products (CO a2d water) • requires a continual supply of oxygen IMMEDIATE ENERGY NEEDS • short, intense exercise (100 m dash) – muscles meet most of ATP demand by borrowing phosphate groups (P) from i other molecules and transferring them to ADP • two enzyme systems control these phosphate transfers – myokinase – transfers P fromione ADP to another converting the latter to ATP – creatine kinase – obtains P from a phosphatestorage molecule creatine phosphate i (CP) • fastacting system that helps maintain the ATP level while other ATP generating mechanisms are being activated • phosphagen system – ATP and CP collectively – provides nearly all energy used for short bursts of intense activity • one minute of brisk walking • 6 seconds of sprinting or fast swimming • important in activities requiring brief but maximum effort – football, baseball, and weight lifting PHOSPHAGEN SYSTEM • Creatine kinase adds phosphate to creatine and forms creatine phosphate • Myokinase adds phosphate to ADP and forms ATP SHORTTERM ENERGY NEEDS • as the phosphagen system is exhausted • muscles shift to anaerobic fermentation – muscles obtain glucose from blood and their own stored glycogen – if oxygen is unavailable, glycolysis can generate a net gain of 2 ATP for every glucose molecule consumed – converts glucose to lactic acid • glycogenlactic acid system – the pathway from glycogen to lactic acid • produces enough ATP for 30 – 40 seconds of maximum activity LONGTERM ENERGY NEEDS • after 40 seconds or so, the respiratory and cardiovascular systems “catch up” and deliver oxygen to the muscles fast enough for aerobic respiration to meet most of the ATP demands • aerobic respiration produces 36 ATP per glucose – efficient means of meeting the ATP demands of prolonged exercise – oxygen consumption levels off after 3 to 4 minutes to a steady state in which aerobic ATP production keeps pace with demand – For about 30 minutes energy comes equally from glucose and fatty acids – After 30 minutes depletion of glucose causes fatty acids to become the primary fuel FATIGUE AND ENDURANCE • Muscle fatigue: progressive weakness from prolonged use of muscles • Fatigue in highintensity exercise is thought to result from: – Potassium accumulation in the T tubules reduces excitability – Excess ADP and P slow irossbridge movements, inhibit calcium release and decrease force production in myofibrils – (Possibly a drop in pH, but lactic acid does not seem to accumulate in the muscle cell) • Fatigue in lowintensity (long duration) exercise is thought to result from: – Fuel depletion as glycogen and glucose levels decline – Electrolyte loss through sweat can decrease muscle excitability – Central fatigue when fewer motor signals are issued from brain • Brain cells inhibited by exercising muscles’ release of ammonia • Psychological will to persevere—not well understood ENDURANCE • Endurance: the ability to maintain highintensity exercise for more than 4 to 5 minutes – determined in large part by one’s maximum oxygen uptake – maximum oxygen uptake (VO max) – t2e point at which the rate of oxygen consumption reaches a plateau and does not increase further with an added workload • proportional to body size • peaks at around age 20 • usually greater in males than females • can be twice as great in trained endurance athletes as in untrained person – results in twice the ATP production EXCESS POSTEXERCISE OXYGEN CONSUMPTION (EPOC) • EPOC meets a metabolic demand known as oxygen debt • Needed for the following purposes: – To aerobically replenish ATP (some of which helps regenerate CP stores) – To replace oxygen reserves on myoglobin – To provide oxygen to liver that is busy disposing of lactic acid – To provide oxygen to many cells that have elevated metabolic rates after exercise • EPOC can be six times basal consumption and last an hour PHYSIOLOGICAL CLASSES OF MUSCLE FIBERS • There are different types of muscle fibers – Slow oxidative – Fast glycolytic • slow oxidative (SO), slowtwitch, red, or type I fibers – adapted for aerobic respiration and fatigue resistance • soleus of calf and postural muscles of the back – abundant mitochondria, myoglobin and capillaries deep red color – relative long twitch lasting about 100 msec • fast glycolytic (FG), fasttwitch, white, or type II fibers – fibers are well adapted for quick responses, but not for fatigue resistance • extrinsic eye muscles, gastrocnemius and biceps brachii – rich in enzymes of phosphagen and glycogenlactic acid systems – poor in mitochondria, myoglobin, and blood capillaries which gives pale appearance • ratio of different fiber types have genetic predisposition – muscles differ in fiber types gastrocnemius is predominantly FG for quick movements (jumping) – soleus is predominantly SO used for endurance (jogging) STRENGTH AND CONDITIONING • muscular strength depends on: – primarily on muscle size • a muscle can exert a tension of 3 or 4 kg / cm of crosssectional area – fascicle arrangement • pennate are stronger than parallel, and parallel stronger than circular – size of motor units • larger the motor unit the stronger the contraction – multiple motor unit summation – recruitment • when stronger contraction is required, the nervous system activates more motor units • muscular strength depends on: – temporal summation • nerve impulses usually arrive at a muscle in a series of closely spaced action potentials • the greater the frequency of stimulation, the more strongly a muscle contracts – length – tension relationship • a muscle resting at optimal length is prepared to contract more forcefully than a muscle that is excessively contracted or stretched – fatigue • fatigued muscles contract more weakly than rested muscles • resistance training (weight lifting) – contraction of a muscles against a load that resists movement – a few minutes of resistance exercise a few times a week is enough to stimulate muscle growth – growth is from cellular enlargement hypertrophy – muscle fibers synthesize more myofilaments and myofibrils and grow thicker • endurance training (aerobic exercise) – improves fatigue resistant muscles – slow twitch fibers produce more mitochondria, glycogen, and acquire a greater density of blood capillaries – improves skeletal strength – increases the red blood cell count and oxygen transport capacity of the blood – enhances the function of the cardiovascular, respiratory, and nervous systems CARDIAC MUSCLE • characteristics of cardiac muscle cells – striated like skeletal muscle, but myocytes (cardiocytes) are shorter and thicker – damaged cardiac muscle cells repair by fibrosis • a little mitosis observed following heart attacks, but not in significant amounts to regenerate functional muscle – each myocyte is joined to several others at the uneven, notched linkages – intercalated discs • appear as thick dark lines in stained tissue sections • electrical gap junctions allow each myocyte to directly stimulate its neighbors • mechanical junctions that keep the myocytes from pulling apart – autorhythmic: can contract without nervous stimulation • contains a builtin pacemaker that rhythmically sets off a wave of electrical excitation • wave travels through the muscle and triggers contraction of heart chambers – autonomic nervous system sends nerve fibers to the heart • can increase or decrease heart rate and contraction strength – very slow twitches does not exhibit quick twitches like skeletal muscle • maintains tension for about 200 to 250 msec, gives the heart time to expel blood – sarcoplasmic reticulum less developed, but T tubules are larger and admit supplemental Ca from the extracellular fluid – uses aerobic respiration almost exclusively • rich in myoglobin and glycogen • has especially large mitochondria – 25% of volume of cardiac muscle cell – 2% of skeletal muscle cell with smaller mitochondria – very adaptable with respect to fuel used – very vulnerable to interruptions of oxygen supply – highly fatigue resistant SMOOTH MUSCLE • composed of myocytes that have a fusiform shape • there is only one nucleus, located near the middle of the cell • no visible striations – reason for the name ‘smooth muscle’ – thick and thin filaments are present, but aligned differently • z discs are absent and replaced by dense bodies – well ordered array of protein masses in cytoplasm – protein plaques on the inner face of the plasma membrane • cytoplasm contains extensive cytoskeleton of intermediate filament – attach to the membrane plaques and dense bodies – provide mechanical linkages between the thin myofilaments and the plasma membrane • sarcoplasmic reticulum is scanty and there are no T tubules 2+ 2+ – Ca needed for muscle contraction comes from the ECF by way of Ca channels in the sarcolemma • some smooth muscles lack nerve supply, while others receive autonomic fibers (not somatic motor fibers as in skeletal muscle) • capable of mitosis and hyperplasia • injured smooth muscle regenerates well STIMULATION OF SMOOTH MUSCLE • smooth muscle is involuntary and can contract without nervous stimulation – can contract in response to chemical stimuli • hormones, carbon dioxide, low pH, and oxygen deficiency – in response to stretch • single unit smooth muscle in stomach and intestines has pacemaker cells that set off waves of contraction throughout the entire layer of muscle • most smooth muscle is innervated by autonomic nerve fibers – can trigger and modify contractions – stimulate smooth muscle with either acetylcholine or norepinephrine – can have contrasting effects • relax the smooth muscle of arteries • contract smooth muscles of the bronchioles 2 TYPES OF SMOOTH MUSCLE • Multiunit smooth muscle – Occurs in some of the largest arteries and pulmonary air passages, in piloerector muscles of hair follicle, and in the iris of the eye – Autonomic innervation similar to skeletal muscle • Terminal branches of a nerve fiber synapse with individual myocytes and form a motor unit • Each motor unit contracts independently of the others • Singleunit smooth muscle – More widespread – Occurs in most blood vessels, in the digestive, respiratory, urinary, and reproductive tracts also called visceral muscle • Often in two layers – Inner circular – Outer longitudinal – Myocytes of this cell type are electrically coupled to each other by gap junctions – They directly stimulate each other and a large number of cells contract as a single unit STRETCHING SMOOTH MUSCLE • stretch can open mechanicallygated calcium channels in the sarcolemma causing contraction – peristalsis: waves of contraction brought about by food distending the esophagus or feces distending the colon • propels contents along the organ • stressrelaxation response (receptive relaxation) helps hollow organs gradually fill (urinary bladder) – when stretched, tissue briefly contracts then relaxes – helps prevent emptying while filling CONTRACTION AND STRETCHING • skeletal muscle cannot contract forcefully if overstretched – smooth muscle can be anywhere from half to twice its resting length and still contract powerfully • smooth muscle contracts forcefully even when greatly stretched – allows hollow organs such as the stomach and bladder to fill and then expel their contents efficiently • plasticity: the ability to adjust its tension to the degree of stretch – a hollow organ such as the bladder can be greatly stretched yet not become flabby when it is empty • smooth muscle contracts forcefully even when greatly stretched beacuase: – there are no z discs, so thick filaments cannot butt against them and stop contraction – since the thick and thin filaments are not arranged in orderly sarcomeres, stretching does not cause a situation where there is too little overlap for cross bridges to form – the thick filaments of smooth muscle have myosin heads along their entire length, so crossbridges can form anywhere
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