Lecture Powerpoint Muscular Tissue

Chapter 11 *Lecture PowerPoint Muscular Tissue *See separate FlexArt PowerPoint slides for all figures and tables preinserted into PowerPoint without notes. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Introduction • Movement is a fundamental characteristic of all living organisms • Three types of muscular tissue—skeletal, cardiac, and smooth • Important to understand muscle at the molecular, cellular, and tissue levels of organization 11-2 Types and Characteristics of Muscular Tissue • Expected Learning Outcomes – Describe the physiological properties that all muscle types have in common. – List the defining characteristics of <a href="/tags/Skeletal_muscle/" rel="tag">skeletal muscle</a>. – Discuss the possible elastic functions of the connective tissue components of a muscle. 11-3 Universal Characteristics of Muscle • Responsiveness (excitability) – To chemical signals, stretch, and electrical changes across the plasma membrane • Conductivity – Local electrical change triggers a wave of excitation that travels along the muscle fiber • Contractility – Shortens when stimulated • Extensibility – Capable of being stretched between contractions • Elasticity – Returns to its original resting length after being stretched 11-4 Skeletal Muscle • Skeletal muscle— voluntary, striated muscle attached to one or more bones Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. • Striations—alternating light and dark transverse Nucleus bands Muscle fiber – Results from an overlapping of internal <a href="/tags/Endomysium/" rel="tag">Endomysium</a> contractile proteins • Voluntary—usually Striations subject to conscious control © Ed Reschke • <a href="/tags/Muscle_cell/" rel="tag">Muscle cell</a>, muscle fiber Figure 11.1 (myofiber)—as long as 30 cm 11-5 Skeletal Muscle • Tendons are attachments between muscle and bone matrix – Endomysium: connective tissue around muscle cells – <a href="/tags/Perimysium/" rel="tag">Perimysium</a>: connective tissue around muscle fascicles – <a href="/tags/Epimysium/" rel="tag">Epimysium</a>: connective tissue surrounding entire muscle – Continuous with collagen fibers of tendons – In turn, with connective tissue of bone matrix • Collagen is somewhat extensible and elastic – Stretches slightly under tension and recoils when released • Resists excessive stretching and protects muscle from injury • Returns muscle to its resting length • Contributes to power output and muscle efficiency 11-6 Microscopic Anatomy of Skeletal Muscle • Expected Learning Outcomes – Describe the structural components of a muscle fiber. – Relate the striations of a muscle fiber to the overlapping arrangement of its protein filaments. – Name the major proteins of a muscle fiber and state the function of each. 11-7 The Muscle Fiber • <a href="/tags/Sarcolemma/" rel="tag">Sarcolemma</a>—plasma membrane of a muscle fiber • <a href="/tags/Sarcoplasm/" rel="tag">Sarcoplasm</a>—cytoplasm of a muscle fiber • <a href="/tags/Myofibril/" rel="tag">Myofibrils</a>—long protein bundles that occupy the main portion of the sarcoplasm – Glycogen: stored in abundance to provide energy with heightened exercise – Myoglobin: red pigment; stores oxygen needed for muscle activity 11-8 The Muscle Fiber • Multiple nuclei—flattened nuclei pressed against the inside of the sarcolemma – Myoblasts: stem cells that fuse to form each muscle fiber – Satellite cells: unspecialized myoblasts remaining between the muscle fiber and endomysium • May multiply and produce new muscle fibers to some degree • Mitochondria—packed into spaces between myofibrils 11-9 The Muscle Fiber • <a href="/tags/Sarcoplasmic_reticulum/" rel="tag">Sarcoplasmic reticulum</a> (SR)—smooth ER that forms a network around each <a href="/tags/Myofibril/" rel="tag">myofibril</a>: calcium reservoir – Calcium activates the <a href="/tags/Muscle_contraction/" rel="tag">muscle contraction</a> process • <a href="/tags/Terminal_cisternae/" rel="tag">Terminal cisternae</a>—dilated end-sacs of SR which cross the muscle fiber from one side to the other • T tubules—tubular infoldings of the sarcolemma which penetrate through the cell and emerge on the other side • Triad—a T tubule and two terminal cisterns 11-10 The Muscle Fiber Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Muscle fiber Nucleus A band I band Z disc Mitochondria Openings into transverse tubules Sarcoplasmic reticulum Triad: Terminal cisternae Transverse tubule Sarcolemma Myofibrils Sarcoplasm Figure 11.2 Myofilaments 11-11 <a href="/tags/Myofilament/" rel="tag">Myofilaments</a> Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Head Tail (a) <a href="/tags/Myosin/" rel="tag">Myosin</a> molecule Myosin head Figure 11.3a,b (b) Thick filament • Thick filaments—made of several hundred myosin molecules – Shaped like a golf club • Two chains intertwined to form a shaftlike tail • Double globular head – Heads directed outward in a helical array around the bundle • Heads on one half of the thick filament angle to the left • Heads on the other half angle to the right • Bare zone with no heads in the middle 11-12 Myofilaments • Thin filaments – Fibrous (F) <a href="/tags/Actin/" rel="tag">actin</a>: two intertwined strands • String of globular (G) actin subunits each with an active site that can bind to head of myosin molecule – <a href="/tags/Tropomyosin/" rel="tag">Tropomyosin</a> molecules • Each blocking six or seven active sites on G actin subunits – <a href="/tags/Troponin/" rel="tag">Troponin</a> molecule: small, calcium-binding protein on each tropomyosin molecule Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Tropomyosin Troponin complex G actin (c) Thin filament Figure 11.3c 11-13 Myofilaments • Elastic filaments – <a href="/tags/Titin/" rel="tag">Titin</a> (connectin): huge, springy protein – Flank each thick filament and anchor it to the Z disc – Help stabilize the thick filament – Center it between the thin filaments – Prevent overstretching 11-14 Myofilaments Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Myosin head (b) Thick filament Tropomyosin Troponin complex G actin Figure 11.3b,c (c) Thin filament • Contractile proteins—myosin and actin do the work • Regulatory proteins—tropomyosin and troponin – Like a switch that determines when the fiber can contract and when it cannot – Contraction activated by release of calcium into sarcoplasm and its binding to troponin – Troponin changes shape and moves tropomyosin off the active sites on actin 11-15 Myofilaments Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Thick filament Thin filament Bare zone (d) Portion of a <a href="/tags/Sarcomere/" rel="tag">sarcomere</a> showing the overlap of thick and thin filaments Figure 11.3d 11-16 Myofilaments • At least seven other Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. accessory proteins in or Endomysium associated with thick or thin Linking proteins filaments Basal lamina – Anchor the myofilaments, regulate length of Sarcolemma myofilaments, keep alignment for optimal contractile <a href="/tags/Dystrophin/" rel="tag">Dystrophin</a> effectiveness Thin filament Thick filament Figure 11.4 11-17 Myofilaments • Dystrophin—most clinically important Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. – Links actin in outermost Endomysium Linking proteins myofilaments to transmembrane proteins and eventually to Basal lamina fibrous endomysium surrounding the entire muscle Sarcolemma cell Dystrophin – Transfers forces of muscle Thin filament contraction to connective tissue around muscle cell Thick filament – Genetic defects in dystrophin produce disabling disease muscular dystrophy Figure 11.4 11-18 Striations • Myosin and actin are proteins that occur in all cells – Function in cellular motility, mitosis, transport of intracellular material • Organized in a precise way in skeletal and <a href="/tags/Cardiac_muscle/" rel="tag">cardiac muscle</a> Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Sarcomere I band A band I band H band Thick filament Thin filament M line Titin Elastic filament (b) Z disc Z disc Figure 11.5b 11-19 Striations – A band: dark; A stands for anisotropic • Part of A band where thick and thin filaments overlap is especially dark – H band: middle of A band; thick filaments only – M line: middle of H band – I band: alternating lighter band; I stands for isotropic • The way the bands reflect polarized light – Z disc: provides anchorage for thin filaments and elastic filaments • Bisects I band Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Sarcomere I band A band I band H band Thick filament Thin filament M line Titin Elastic filament (b) Z disc Z disc Figure 11.5b 11-20 Striations Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Nucleus Sarcomere 5Z disc M line 4H band 3I band I band A band 2Individual myofibrils Individual 1(a) Visuals Unlimited Figure 11.5a 11-21 Striations • Sarcomere—segment from Z disc to Z disc – Functional contractile unit of muscle fiber • Muscle cells shorten because their individual <a href="/tags/Sarcomere/" rel="tag">sarcomeres</a> shorten – Z disc (Z lines) are pulled closer together as thick and thin filaments slide past each other • Neither thick nor thin filaments change length during shortening – Only the amount of overlap changes • During shortening dystrophin and linking proteins also pull on extracellular proteins – Transfers pull to extracellular tissue 11-22 The Nerve—Muscle Relationship • Expected Learning Outcomes – Explain what a motor unit is and how it relates to muscle contraction. – Describe the structure of the junction where a nerve fiber meets a muscle fiber. – Explain why a cell has an electrical charge difference across its plasma membrane and, in general terms, how this relates to muscle contraction. 11-23 The Nerve—Muscle Relationship • Skeletal muscle never contracts unless stimulated by a nerve • If nerve connections are severed or poisoned, a muscle is paralyzed – Denervation atrophy: shrinkage of paralyzed muscle when connection not restored 11-24 Motor Neurons and Motor Units • Somatic motor neurons—nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles • Somatic motor fibers—their axons that lead to the skeletal muscle – Each nerve fiber branches out to a number of muscle fibers – Each muscle fiber is supplied by only one <a href="/tags/Motor_neuron/" rel="tag">motor neuron</a> 11-25 Motor Neurons and Motor Units • Motor unit—one nerve fiber Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. and all the muscle fibers Spinal cord innervated by it • Muscle fibers of one motor unit Motor neuron 1 – Dispersed throughout the Motor muscle neuron 2 – Contract in unison Neuromuscular – Produce weak contraction junction over wide area Skeletal muscle – Provides ability to sustain fibers long-term contraction as Figure 11.6 motor units take turns contracting (postural control) – Effective contraction usually requires the contraction of several motor units at once 11-26 Motor Neurons and Motor Units • Average motor unit—200 muscle fibers for each motor unit • Small motor units—fine degree of control – Three to six muscle fibers per neuron – Eye and hand muscles • Large motor units—more strength than control – Powerful contractions supplied by large motor units (e.g., gastrocnemius has 1,000 muscle fibers per neuron) – Many muscle fibers per motor unit 11-27 The <a href="/tags/Neuromuscular_junction/" rel="tag">Neuromuscular Junction</a> • Synapse—point where a nerve fiber meets its target cell • Neuromuscular junction (NMJ)—when target cell is a muscle fiber • Each terminal branch of the nerve fiber within the NMJ forms separate synapse with the muscle fiber • One nerve fiber stimulates the muscle fiber at several points within the NMJ 11-28 The Neuromuscular Junction • Synaptic knob—swollen end of nerve fiber – Contains synaptic vesicles filled with acetylcholine (ACh) • Synaptic cleft—tiny gap between synaptic knob and muscle sarcolemma • Schwann cell envelops and isolates all of the NMJ from surrounding tissue fluid • Synaptic vesicles undergo exocytosis releasing ACh into synaptic cleft 11-29 The Neuromuscular Junction • Synaptic vesicles undergo exocytosis releasing ACh into synaptic cleft • 50 million ACh receptors—proteins incorporated into muscle cell plasma membrane – Junctional folds of sarcolemma beneath synaptic knob • Increase surface area holding ACh receptors – Lack of receptors leads to paralysis in disease myasthenia gravis 11-30 The Neuromuscular Junction • Basal lamina—thin layer of collagen and glycoprotein separates Schwann cell and entire muscle cell from surrounding tissues – Contains acetylcholinesterase (AChE) that breaks down ACh after contraction causing relaxation 11-31 The Neuromuscular Junction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Motor nerve fiber Myelin Schwann cell Synaptic knob Basal lamina Synaptic vesicles (containing ACh) Sarcolemma Synaptic cleft Nucleus ACh receptor Junctional folds Nucleus Mitochondria Sarcoplasm Myofilaments Figure 11.7b (b) 11-32 The Neuromuscular Junction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Motor nerve fibers Neuromuscular junction Muscle fibers Figure 11.7a (a) 100 µm Victor B. Eichler 11-33 Electrically Excitable Cells • Muscle fibers and neurons are electrically excitable cells – Their plasma membrane exhibits voltage changes in response to stimulation • Electrophysiology—the study of the electrical activity of cells • Voltage (electrical potential)—a difference in electrical charge from one point to another • Resting membrane potential—about −90 mV – Maintained by sodium–potassium pump 11-34 Electrically Excitable Cells • In an unstimulated (resting) cell – There are more anions (negative ions) on the inside of the plasma membrane than on the outside – The plasma membrane is electrically polarized (charged) – There are excess sodium ions (Na+) in the extracellular fluid (ECF) – There are excess potassium ions (K+) in the intracellular fluid (ICF) – Also in the ICF, there are anions such as proteins, nucleic acids, and phosphates that cannot penetrate the plasma membrane – These anions make the inside of the plasma membrane negatively charged by comparison to its outer surface 11-35 Electrically Excitable Cells • Stimulated (active) muscle fiber or nerve cell – Ion gates open in the plasma membrane – Na+ instantly diffuses down its concentration gradient into the cell – These cations override the negative charges in the ICF – Depolarization: inside of the plasma membrane becomes briefly positive – Immediately, Na+ gates close and K+ gates open – K+ rushes out of cell – Repelled by the positive sodium charge and partly because of its concentration gradient – Loss of positive potassium ions turns the membrane negative again (repolarization) 11-36 Electrically Excitable Cells • Stimulated (active) muscle fiber or nerve cell (cont.) – <a href="/tags/Action_potential/" rel="tag">Action potential</a>: quick up-and-down voltage shift from the negative RMP to a positive value, and back to the negative value again – RMP is a stable voltage seen in a waiting muscle or nerve cell – 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 11-37 Neuromuscular Toxins and Paralysis • Toxins that interfere with synaptic function can paralyze the muscles • Some pesticides contain cholinesterase inhibitors – 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 Clostridium tetani – Glycine in the spinal cord normally stops motor neurons from producing unwanted muscle contractions – Tetanus toxin blocks glycine release in the spinal cord and causes overstimulation and spastic paralysis of the muscles 11-38 Neuromuscular Toxins and Paralysis • Flaccid paralysis—a state in which the muscles are limp and cannot contract – Curare: compete with ACh for receptor sites, but do not stimulate the muscles – Plant poison used by South American natives to poison blowgun darts • Botulism—type of food poisoning caused by a neuromuscular toxin secreted by the bacterium Clostridium botulinum – Blocks release of ACh causing flaccid paralysis – Botox cosmetic injections for wrinkle removal 11-39 Behavior of Skeletal Muscle Fibers • Expected Learning Outcomes – Explain how a nerve fiber stimulates a skeletal muscle fiber. – Explain how stimulation of a muscle fiber activates its contractile mechanism. – Explain the mechanism of muscle contraction. – Explain how a muscle fiber relaxes. – Explain why the force of a muscle contraction depends on sarcomere length prior to stimulation. 11-40 Behavior of Skeletal Muscle Fibers • Four major phases of contraction and relaxation – Excitation • The process in which nerve action potentials lead to muscle action potentials – Excitation–contraction 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 11-41 Excitation Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Nerve signal 2+ Motor Ca enters nerve synaptic knob fiber Sarcolemma Synaptic Synaptic knob vesicles ACh Synaptic cleft ACh receptors 1 Arrival of nerve signal 2 Acetylcholine (ACh) release Figure 11.8 (1, 2) • Nerve signal opens voltage-gated calcium channels in synaptic knob • Calcium stimulates exocytosis of ACh from synaptic vesicles 11-42 • ACh released into synaptic cleft Excitation Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. ACh ACh K+ ACh receptor Sarcolemma Na+ 3 Binding of ACh to receptor 4 Opening of ligand-regulated ion gate; creation of end-plate potential Figure 11.8 (3, 4) • Two ACh molecules bind to each receptor protein, opening Na+ and K+ channels • Na+ enters; shifting RMP goes from −90 mV to +75 mV, then K+ exits and RMP returns to −90 mV; quick voltage shift is called an end-plate potential (EPP) 11-43 Excitation Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. K+ Plasma membrane of synaptic knob Na+ Voltage-regulated ion gates Sarcolemma Figure 11.8 (5) 5 Opening of voltage-regulated ion gates; creation of action potentials • Voltage change (EPP) in end-plate region opens nearby voltage- gated channels producing an action potential that spreads over muscle surface 11-44 Excitation–Contraction Coupling Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 11.9 (6, 7) Terminal T tubule cisterna of SR T tubule Sarcoplasmic reticulum Ca2+ Ca2+ 6 Action potentials propagated 7 Calcium released from down T tubules terminal cisternae • Action potential spreads down into T tubules • Opens voltage-gated ion channels in T tubules and Ca+2 channels in SR • Ca+2 enters the cytosol 11-45 Excitation–Contraction Coupling Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Active sites 2+ Troponin Ca Tropomyosin Actin Thin filament Myosin Ca2+ 8 Binding of calcium 9 Shifting of tropomyosin; to troponin exposure of active sites on actin Figure 11.9 (8, 9) • Calcium binds to troponin in thin filaments • Troponin–tropomyosin complex changes shape and exposes active sites on actin 11-46 Contraction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. • Myosin ATPase enzyme in myosin Troponin Tropomyosin head hydrolyzes an ATP molecule ADP Pi • Activates the head Myosin ―cocking‖ it in an 10 Hydrolysis of ATP to ADP + Pi; activation and cocking of myosin head extended position – ADP + Pi remain attached Cross-bridge: Actin • Head binds to actin Myosin active site forming a 11 Formation of myosin–actin cross-bridge myosin–actin cross- bridge Figure 11.10 (10, 11) 11-47 Contraction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. • Myosin head releases ADP and Pi, flexes pulling thin filament past thick— power stroke ATP 13 Binding of new ATP; • Upon binding more ATP, breaking of cross-bridge myosin releases actin and process is repeated – Each head performs five ADPADP PPi i power strokes per second 12 Power stroke; sliding of thin – Each stroke utilizes one filament over thick filament molecule of ATP Figure 11.10 (12, 13) 11-48 Relaxation Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 11.11 (14, 15) AChE ACh 14 Cessation of nervous stimulation and ACh release 15 ACh breakdown by acetylcholinesterase (AChE) • Nerve stimulation and ACh release stop • AChE breaks down ACh and fragments reabsorbed into synaptic knob • Stimulation by ACh stops 11-49 Relaxation Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Terminal cisterna of SR Ca2+ Ca2+ 16 Reabsorption of calcium ions by Figure 11.11 (16) sarcoplasmic reticulum • Ca+2 pumped back into SR by active transport • Ca+2 binds to calsequestrin while in storage in SR • ATP is needed for muscle relaxation as well as muscle contraction 11-50 Relaxation • Ca+2 removed from troponin Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. is pumped back into SR Ca2+ • Tropomyosin reblocks the ADP P Ca2+ active sites i 17 Loss of calcium ions from troponin • Muscle fiber ceases to produce or maintain tension Tropomyosin • Muscle fiber returns to its resting length ATP – Due to recoil of elastic 18 Return of tropomyosin to position components and blocking active sites of actin contraction of antagonistic Figure 11.11 (17, 18) muscles 11-51 The Length–Tension Relationship and Muscle Tone • Length–tension relationship—the amount of tension generated by a muscle and the force of contraction depends on how stretched or contracted it was before it was stimulated • If overly contracted at rest, a weak contraction results – Thick filaments too close to Z discs and cannot slide • If too stretched before stimulated, a weak contraction results – Little overlap of thin and thick does not allow for very many cross-bridges to form 11-52 The Length–Tension Relationship and Muscle Tone • Optimum resting length produces greatest force when muscle contracts – Muscle tone: central nervous system continually monitors and adjusts the length of the resting muscle, and maintains a state of partial contraction called muscle tone – Maintains optimum length and makes the muscles ideally ready for action 11-53 Length–Tension Relationship Copyright © The McGraw-Hill Companies, Inc. 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Optimum resting length (2.0–2.25µm) z z Overly contracted z z Overly stretched z z 1.0 0.5 upon upon stimulation Tension (g) generated Tension 0.0 1.0 2.0 3.0 4.0 Sarcomere length (µm) before stimulation Figure 11.12 11-54 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+2 to enter cytosol – Ca+2 activates myosin-actin cross-bridging – Muscle contracts, but cannot relax • Muscle relaxation requires ATP, and ATP production is no longer produced after death – Fibers remain contracted until myofilaments begin to decay • Rigor mortis peaks about 12 hours after death, then diminishes over the next 48 to 60 hours 11-55 Behavior of Whole Muscles • Expected Learning Outcomes – Describe the stages of a muscle twitch. – Explain why muscle does not contract in an all-or- none manner. – Explain how successive muscle twitches can add up to produce stronger muscle contractions. – Distinguish between isometric and isotonic contraction. – Distinguish between concentric and eccentric contraction. 11-56 Threshold, Latent Period, and Twitch • The response of a muscle Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. to weak electrical stimulus Relaxation Contraction phase seen in frog phase gastrocnemius—sciatic Latent nerve preparation period Muscletension Time of • Myogram—a chart of the stimulation timing and strength of a Time muscle’s contraction Figure 11.13 11-57 Threshold, Latent Period, and Twitch • Weak, subthreshold electrical stimulus causes no Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. contraction Relaxation Contraction phase phase • Threshold—minimum Latent voltage necessary to period Muscletension generate an action potential in the muscle fiber and Time of stimulation produce a contraction Time – Twitch—a quick cycle of Figure 11.13 contraction when stimulus is at threshold or higher 11-58 Threshold, Latent Period, and Twitch • Latent period—2 ms delay between the onset of stimulus and the onset of twitch response – Time required for excitation, excitation–contraction 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 – Short-lived phase 11-59 Threshold, Latent Period, and Twitch • Relaxation phase—SR quickly reabsorbs Ca2+, myosin releases the thin filaments, and tension declines – Muscle returns to resting length – Entire twitch lasts from 7 to 100 ms 11-60 Contraction Strength of Twitches • At subthreshold stimulus—no contraction at all • At threshold intensity and above—a twitch is produced – Twitches caused by increased voltage are no stronger than those at threshold 11-61 Contraction Strength of Twitches • Not exactly true that muscle fiber obeys an all-or- none law—contracting to its maximum or not at all – Electrical excitation of a muscle follows all-or-none law – Not true that muscle fibers follow the all-or-none law – Twitches vary in strength depending upon: • Stimulus frequency—stimuli arriving closer together produce stronger twitches • Concentration of Ca+2 in sarcoplasm can vary the frequency 11-62 Contraction Strength of Twitches Cont. • How stretched muscle was before it was stimulated • Temperature of the muscles—warmed-up muscle contracts more strongly; enzymes work more quickly • Lower than normal pH of sarcoplasm weakens contraction— fatigue • State of hydration of muscle affects overlap of thick and thin filaments • Muscles need to be able to contract with variable strengths for different tasks 11-63 Contraction Strength of Twitches Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Threshold Stimulus voltage Stimulus1 2 3 4 5 6 7 8 9 Stimuli to nerve Proportion of nerve fibers excited Maximum contraction Tension1 2 3 4 5 6 7 8 9 Figure 11.14 Responses of muscle • Stimulating the nerve with higher and higher voltages produces stronger contractions – Higher voltages excite more and more nerve fibers in the motor nerve which stimulates more and more motor units to contract • Recruitment or multiple motor unit (MMU) summation—the process of bringing more motor units into play 11-64 Contraction Strength of Twitches Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Twitch Treppe Muscle twitches Stimuli (a) Figure 11.15a,b (b) • When stimulus intensity (voltage) remains constant twitch strength can vary with the stimulus frequency • Up to 10 stimuli per second – Each stimulus produces identical twitches and full recovery between twitches 11-65 Contraction Strength of Twitches • 10–20 stimuli per second produces treppe (staircase) phenomenon – Muscle still recovers fully between twitches, but each twitch develops more tension than the one before – Stimuli arrive so rapidly that the SR does not have time between stimuli to completely reabsorb all of the Ca2+ it released – Ca2+ concentration in the cytosol rises higher and higher with each stimulus causing subsequent twitches to be stronger – Heat released by each twitch causes muscle enzymes such as myosin ATPase to work more efficiently and produce stronger twitches as muscle warms up 11-66 Contraction Strength of Twitches Copyright © The McGraw-Hill Companies, Inc. 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Incomplete tetanus Complete tetanus Fatigue (c) (d) Figure 11.15c,d • 20–40 stimuli per second produces incomplete tetanus – Each new stimulus arrives before the previous twitch is over – New twitch ―rides piggy-back‖ on the previous one generating higher tension – Temporal summation: results from two stimuli arriving close together 11-67 Contraction Strength of Twitches Cont. – Wave summation: results from one wave of contraction added to another – Each twitch reaches a higher level of tension than the one before – Muscle relaxes only partially between stimuli – Produces a state of sustained fluttering contraction called incomplete tetanus 11-68 Contraction Strength of Twitches • 40–50 stimuli per second produces complete tetanus – Muscle has no time to relax between stimuli – Twitches fuse to a smooth, prolonged contraction called complete tetanus – A muscle in complete tetanus produces about four times the tension as a single twitch – Rarely occurs in the body, which rarely exceeds 25 stimuli per second – Smoothness of muscle contractions is because motor units function asynchronously • When one motor unit relaxes, another contracts and takes over so the muscle does not lose tension 11-69 Isometric and Isotonic Contraction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 11.16 Muscle develops Muscle shortens, Muscle lengthens tension but does tension remains while maintaining not shorten constant tension Movement No movement Movement (a) Isometric contraction (b) Isotonic concentric contraction (c) Isotonic eccentric contraction • Isometric muscle contraction – Muscle is producing internal tension while an external resistance causes it to stay the same length or become longer – Can be a prelude to movement when tension is absorbed by elastic component of muscle – Important in postural muscle function and antagonistic muscle joint stabilization 11-70 Isometric and Isotonic Contraction • Isotonic muscle contraction – Muscle changes in length with no change in tension – Concentric contraction: muscle shortens as it maintains tension – Eccentric contraction: muscle lengthens as it maintains tension 11-71 Isometric and Isotonic Contraction Copyright © The McGraw-Hill Companies, Inc. 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Muscle Muscle tension length Length or Tension or LengthIsometric Isotonic Figure 11.17 phase phase Time • 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 11-72 Muscle Metabolism • Expected Learning Outcomes – Explain how skeletal muscle meets its energy demands during rest and exercise. – Explain the basis of muscle fatigue and soreness. – Define oxygen debt and explain why extra oxygen is needed even after an exercise has ended. – Distinguish between two physiological types of muscle fibers, and explain their functional roles. – Discuss the factors that affect muscular strength. – Discuss the effects of resistance and endurance exercises on muscles. 11-73 ATP Sources • All muscle contraction depends on ATP • ATP supply depends on availability of: – Oxygen – Organic energy sources such as glucose and fatty acids 11-74 ATP Sources • Two main pathways of ATP synthesis – Anaerobic fermentation • Enables cells to produce ATP in the absence of oxygen • Yields little ATP and toxic lactic acid, a major factor in muscle fatigue – Aerobic respiration • Produces far more ATP • Less toxic end products (CO2 and water) • Requires a continual supply of oxygen 11-75 ATP Sources Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 0 10 seconds 40 seconds Repayment of Duration of exercise oxygen debt Mode of ATP synthesis Aerobic respiration Phosphagen Glycogen– Aerobic using oxygen from system lactic acid respiration myoglobin system supported by (anaerobic cardiopulmonary fermentation) function Figure 11.18 11-76 Immediate Energy • Short, intense exercise (100 m dash) – Oxygen need is briefly supplied by myoglobin for a limited amount of aerobic respiration at onset—rapidly depleted – Muscles meet most of ATP demand by borrowing phosphate groups (Pi) from other molecules and transferring them to ADP • Two enzyme systems control these phosphate transfers – Myokinase: transfers Pi from one ADP to another, converting the latter to ATP – Creatine kinase: obtains Pi from a phosphate-storage molecule creatine phosphate (CP) • Fast-acting system that helps maintain the ATP level while other ATP-generating mechanisms are being activated 11-77 Immediate Energy • Phosphagen system—ATP and CP collectively – Provides nearly all energy used for short bursts of intense activity • 1 minute of brisk walking • 6 seconds of sprinting or fast swimming • Important in activities requiring brief but maximum effort – Football, baseball, and weightlifting 11-78 Immediate Energy Copyright © The McGraw-Hill Companies, Inc. 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ADP ADP Pi Myokinase AMP ATP Creatine ADP phosphate Pi Figure 11.19 Creatine 11-79 Creatine kinase ATP Short-Term Energy • As the phosphagen system is exhausted muscles shift to anaerobic fermentation – Muscles obtain glucose from blood and their own stored glycogen – In the absence of oxygen, glycolysis can generate a net gain of 2 ATP for every glucose molecule consumed – Converts glucose to lactic acid • Glycogen–lactic acid system—the pathway from glycogen to lactic acid • Produces enough ATP for 30 to 40 seconds of maximum activity 11-80 Long-Term Energy • 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 11-81 Long-Term Energy • Aerobic respiration produces 36 ATP per glucose – Efficient means of meeting the ATP demands of prolonged exercise – One’s rate of oxygen consumption rises for 3 to 4 minutes and levels off to a steady state in which aerobic ATP production keeps pace with demand 11-82 Long-Term Energy Cont. – Little lactic acid accumulates under steady-state conditions – Depletion of glycogen and blood glucose, together with the loss of fluid and electrolytes through sweating, set limits on endurance and performance even when lactic acid does not 11-83 Fatigue and Endurance • Muscle fatigue—progressive <a href="/tags/Weakness/" rel="tag">weakness</a> and loss of contractility from prolonged use of the muscles – Repeated squeezing of rubber ball – Holding textbook out level to the floor • Fatigue is thought to result from: – ATP synthesis declines as glycogen is consumed – ATP shortage slows down the Na+–K+ pumps • Compromises their ability to maintain the resting membrane potential and excitability of the muscle fibers – Lactic acid lowers pH of sarcoplasm • Inhibits enzymes involved in contraction, ATP synthesis, and other aspects of muscle function 11-84 Fatigue and Endurance • Fatigue is thought to result from (cont.): – Release of K+ with each action potential causes the accumulation of extracellular K+ • Hyperpolarizes the cell and makes the muscle fiber less excitable – Motor nerve fibers use up their ACh • Less capable of stimulating muscle fibers—junctional fatigue – Central nervous system, where all motor commands originate, fatigues by unknown processes, so there is less signal output to the skeletal muscles 11-85 Fatigue and Endurance • Endurance—the ability to maintain high-intensity exercise for more than 4 to 5 minutes – Determined in large part by one’s maximum oxygen uptake (VO2max) – Maximum oxygen uptake: the 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 persons – Results in twice the ATP production 11-86 Beating Fatigue • Taking oral creatine increases level of creatine phosphate in <a href="/tags/Muscle_tissue/" rel="tag">muscle tissue</a> and increases speed of ATP regeneration – Useful in burst-type exercises: weightlifting – Risks are not well known • Muscle cramping, electrolyte imbalances, dehydration, water retention, stroke • Kidney disease from overloading kidney with metabolite creatinine • Carbohydrate loading—dietary regimen – Packs extra glycogen into muscle cells – Extra glycogen is hydrophilic and adds 2.7 g water per gram of glycogen • Athletes feel sense of heaviness outweighs benefits of extra available glycogen 11-87 Oxygen Debt • Heavy breathing continues after strenuous exercise – Excess postexercise oxygen consumption (EPOC): the difference between the resting rate of oxygen consumption and the elevated rate following exercise – Typically about 11 L extra is needed after strenuous exercise • Needed for the following purposes: – Replace oxygen reserves depleted in the first minute of exercise • Oxygen bound to myoglobin and blood hemoglobin, oxygen dissolved in blood plasma and other extracellular fluid, and oxygen in the air in the lungs 11-88 Oxygen Debt • Needed for the following purposes (cont.): – Replenishing the phosphagen system • Synthesizing ATP and using some of it to donate the phosphate groups back to creatine until resting levels of ATP and CP are restored – Oxidizing lactic acid • 80% of lactic acid produced by muscles enter bloodstream 11-89 Oxygen Debt Cont. • Reconverted to pyruvic acid in the kidneys, cardiac muscle, and especially the liver • Liver converts most of the pyruvic acid back to glucose to replenish the glycogen stores of the muscle – Serving the elevated metabolic rate • Occurs while the body temperature remains elevated by exercise and consumes more oxygen 11-90 Physiological Classes of Muscle Fibers • Slow oxidative (SO), slow-twitch, red, or type I fibers – Abundant mitochondria, myoglobin, capillaries: deep red color • Adapted for aerobic respiration and fatigue resistance – Relative long twitch lasting about 100 ms – Soleus of calf and postural muscles of the back 11-91 Physiological Classes of Muscle Fibers • Fast glycolytic (FG), fast-twitch, white, or type II fibers – Fibers are well adapted for quick responses, but not for fatigue resistance – Rich in enzymes of phosphagen and glycogen–lactic acid systems generate lactic acid, causing fatigue – Poor in mitochondria, myoglobin, and blood capillaries which gives pale appearance • SR releases and reabsorbs Ca2+ quickly so contractions are quicker (7.5 ms/twitch) – Extrinsic eye muscles, gastrocnemius, and biceps brachii 11-92 Physiological Classes of Muscle Fibers • Ratio of different fiber types have genetic predisposition— Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. born sprinter – Muscles differ in fiber types: gastrocnemius is FG predominantly FG for quick movements SO (jumping) – Soleus is predominantly Dr. Gladden Willis/Visuals Unlimited, Inc. SO used for endurance (jogging) Figure 11.20 11-93 Muscular Strength and Conditioning • Muscles can generate more tension than the bones and tendons can withstand • Muscular strength depends on: – Primarily muscle size • A muscle can exert a tension of 3 or 4 kg/cm2 of cross- sectional area – Fascicle arrangement • Pennate are stronger than parallel, and parallel stronger than circular – Size of motor units • The larger the motor unit the stronger the contraction 11-94 Muscular Strength and Conditioning • Muscular strength depends on (cont.) – Multiple motor unit summation: recruitment • When stronger contraction is required, the nervous system activates more motor units – 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 11-95 Muscular Strength and Conditioning Cont. – 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 11-96 Muscular Strength and Conditioning • Resistance training (weightlifting) – Contraction of a muscle 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 – Muscle fibers synthesize more myofilaments and myofibrils and grow thicker 11-97 Muscular Strength and Conditioning • 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 11-98 Cardiac and <a href="/tags/Smooth_muscle/" rel="tag">Smooth Muscle</a> • Expected Learning Outcomes – Describe the structural and physiological differences between cardiac muscle and skeletal muscle. – Explain why these differences are important to cardiac function. – Describe the structural and physiological differences between smooth muscle and skeletal muscle. – Relate the unique properties of smooth muscle to its locations and functions. 11-99 Cardiac Muscle • Limited to the heart where it functions to pump blood • Properties of cardiac muscle – Contraction with regular rhythm – Muscle cells of each chamber must contract in unison – Contractions must last long enough to expel blood – Must work in sleep or wakefulness, without fail, and without conscious attention – Must be highly resistant to fatigue 11-100 Cardiac Muscle • Characteristics of cardiac muscle cells – Striated like skeletal muscle, but myocytes (cardiocytes) are shorter and thicker – 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 11-101 Cardiac Muscle • Sarcoplasmic reticulum less developed, but T tubules are larger and admit supplemental Ca2+ from the extracellular fluid • Damaged cardiac muscle cells repair by fibrosis – A little mitosis observed following heart attacks – Not in significant amounts to regenerate functional muscle 11-102 Cardiac Muscle • Can contract without need for nervous stimulation – Contains a built-in pacemaker that rhythmically sets off a wave of electrical excitation – Wave travels through the muscle and triggers contraction of heart chambers – Autorhythmic: able to contract rhythmically and independently 11-103 Cardiac Muscle – Autonomic nervous system does send 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 ms • Gives the heart time to expel blood – 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 11-104 Smooth Muscle • Sarcoplasmic reticulum is scanty and there are no T tubules • Ca2+ needed for muscle contraction comes from the ECF by way of Ca2+ 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 11-105 Myocyte Structure • Myocytes 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 not aligned with each other • 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 11-106 Myocyte Structure • 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 11-107 Types of Smooth Muscle Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autonomic • Multiunit smooth muscle nerve fibers – Occurs in some of the largest arteries and pulmonary air passages, in piloerector muscles of hair follicle, and in the iris of the eye Synapses – 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 (a) Multiunit independently of the others smooth muscle Figure 11.23a 11-108 Types of Smooth Muscle • Single-unit smooth muscle Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. – More widespread Autonomic – Occurs in most blood nerve fibers vessels, in the digestive, respiratory, urinary, and reproductive tracts Varicosities – Also called visceral muscle • Often in two layers: inner circular and outer longitudinal – Myocytes of this cell type are electrically coupled to each Gap junctions other by gap junctions – They directly stimulate each other and a large number of cells contract as a single (b) Single-unit unit smooth muscle Figure 11.23b 11-109 Types of Smooth Muscle Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autonomic nerve fiber Varicosities Mitochondrion Synaptic vesicle Single-unit smooth muscle Figure 11.21 11-110 Types of Smooth Muscle Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 11.22 Mucosa: Epithelium Lamina propria Muscularis mucosae Muscularis externa: Circular layer Longitudinal layer 11-111 Excitation 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 11-112 Excitation of Smooth 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 11-113 Excitation of Smooth Muscle • In single-unit smooth, each autonomic nerve fiber has up to 20,000 beadlike swellings called varicosities – Each contains synaptic vesicles and a few mitochondria – Nerve fiber passes amid several myocytes and stimulates all of them at once when it releases its neurotransmitter • No motor end plates, but receptors scattered throughout the surface—diffuse junctions—no one-to-one relationship between nerve fiber and myocyte 11-114 Contraction and Relaxation • Contraction is triggered by Ca2+, energized by ATP, and achieved by sliding thin past thick filaments • Contraction begins in response to Ca2+ that enters the cell from ECF, a little internally from sarcoplasmic reticulum – Voltage, ligand, and mechanically gated (stretching) – Ca2+ channels open to allow Ca2+ to enter cell 11-115 Contraction and Relaxation • Calcium binds to <a href="/tags/Calmodulin/" rel="tag">calmodulin</a> on thick filaments – Activates myosin light-chain kinase; adds phosphate to regulatory protein on myosin head – Myosin ATPase, hydrolyzing ATP • Enables myosin similar power and recovery strokes like skeletal muscle 11-116 Contraction and Relaxation Cont. – Thick filaments pull on thin ones, thin ones pull on dense bodies and membrane plaques – Force is transferred to plasma membrane and entire cell shortens – Puckers and twists like someone wringing out a wet towel 11-117 Contraction and Relaxation • Contraction and relaxation very slow in comparison to skeletal muscle – Latent period in skeletal 2 ms, smooth muscle 50 to 100 ms – Tension peaks at about 500 ms (0.5 sec) – Declines over a period of 1 to 2 seconds – Slows myosin ATPase enzyme and pumps that remove Ca2+ – Ca2+ binds to calmodulin instead of troponin • Activates kinases and ATPases that hydrolyze ATP 11-118 Contraction and Relaxation • Latch-bridge mechanism is resistant to fatigue – Heads of myosin molecules do not detach from actin immediately – Do not consume any more ATP – Maintains tetanus tonic contraction (smooth muscle tone) • Arteries—vasomotor tone; intestinal tone – Makes most of its ATP aerobically 11-119 Smooth Muscle Contraction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Plaque Intermediate filaments of cytoskeleton Actin filaments Dense body Myosin (b) Contracted smooth muscle cells Figure 11.24a,b (a) Relaxed smooth muscle cells 11-120 Response to Stretch • Stretch can open mechanically gated 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 • Stress–relaxation response (receptive relaxation)— helps hollow organs gradually fill (urinary bladder) – When stretched, tissue briefly contracts then relaxes; helps prevent emptying while filling 11-121 Response to Stretch • Skeletal muscle cannot contract forcefully if overstretched • 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 11-122 Response to Stretch • Smooth muscle can be anywhere from half to twice its resting length and still contract powerfully • Three reasons – 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 cross-bridges can form anywhere 11-123 Response to Stretch • 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 empty 11-124 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 sex- linked recessive trait (1 of 3,500 live-born boys) – Most common form – Disease of males; 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 result – Rarely live past 20 years of age due to effects on respiratory and cardiac muscle; incurable 11-125 Muscular Dystrophy • Facioscapulohumeral MD―autosomal dominant trait affecting both sexes equally – Facial and shoulder muscles more than pelvic muscles • Limb-girdle dystrophy – Combination of several diseases of intermediate severity – Affects shoulder, arm, and pelvic muscles 11-126 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 remove 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 – Strabismus: inability to fixate on the same point with both eyes 11-127 Myasthenia Gravis Cont. • 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 11-128 Myasthenia Gravis Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 11.25 • Drooping eyelids and weakness of muscles of eye movement upon upward gaze 11-129

Lecture Powerpoint Muscular Tissue

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