Chapter 11 Lecture PowerPoint Muscular Tissue

Chapter 11 Lecture PowerPoint Muscular Tissue
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

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 skeletal muscle. Discuss the possible elastic functions of the connective tissue components of a muscle.

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

Skeletal Muscle Skeletal muscle—voluntary, striated muscle attached to one or more bones Striations—alternating light and dark transverse bands Results from an overlapping of internal contractile proteins Voluntary—usually subject to conscious control Muscle cell, muscle fiber (myofiber)—as long as 30 cm Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Nucleus Muscle fiber Endomysium Striations © Ed Reschke Figure 11.1

Skeletal Muscle Tendons are attachments between muscle and bone matrix
Endomysium: connective tissue around muscle cells Perimysium: connective tissue around muscle fascicles Epimysium: 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

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.

The Muscle Fiber Sarcolemma—plasma membrane of a muscle fiber
Sarcoplasm—cytoplasm of a muscle fiber Myofibrils—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

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

The Muscle Fiber Sarcoplasmic reticulum (SR)—smooth ER that forms a network around each myofibril: calcium reservoir Calcium activates the muscle contraction process Terminal cisternae—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

The Muscle Fiber Figure 11.2
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 T riad: T erminal cisternae T ransverse tubule Figure 11.2 Sarcolemma Myofibrils Sarcoplasm Myofilaments

Myofilaments Thick filaments—made of several hundred myosin molecules
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Head Tail (a) Myosin 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

Myofilaments Thin filaments Fibrous (F) actin: two intertwined strands
String of globular (G) actin subunits each with an active site that can bind to head of myosin molecule Tropomyosin molecules Each blocking six or seven active sites on G actin subunits Troponin 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

Myofilaments Elastic filaments
Titin (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

Myofilaments Figure 11.3b,c
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

Myofilaments Figure 11.3d Thick filament Thin filament Bare zone
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Thick filament Thin filament Bare zone Portion of a sarcomere showing the overlap of thick and thin filaments Figure 11.3d

Myofilaments At least seven other accessory proteins in or associated with thick or thin filaments Anchor the myofilaments, regulate length of myofilaments, keep alignment for optimal contractile effectiveness Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Endomysium Linking proteins Basal lamina Sarcolemma Dystrophin Thin filament Thick filament Figure 11.4

Myofilaments 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 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Endomysium Linking proteins Basal lamina Sarcolemma Dystrophin Thin filament Thick filament Figure 11.4

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 cardiac muscle 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 (b) Z disc Elastic filament Z disc Figure 11.5b

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 (b) Z disc Elastic filament Z disc Figure 11.5b

Striations Figure 11.5a Nucleus Sarcomere 5 M line 4 H band
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Nucleus Sarcomere 5 Z disc M line 4 H band Individual myofibrils 3 I band A band I band 2 1 (a) Visuals Unlimited Figure 11.5a

Striations Sarcomere—segment from Z disc to Z disc
Functional contractile unit of muscle fiber Muscle cells shorten because their individual sarcomeres 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

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.

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

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 motor neuron

Motor unit—one nerve fiber and all the muscle fibers innervated by it Muscle fibers of one motor unit Dispersed throughout the muscle Contract in unison Produce weak contraction over wide area Provides ability to sustain long-term contraction as motor units take turns contracting (postural control) Effective contraction usually requires the contraction of several motor units at once Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Spinal cord Motor neuron 1 Motor neuron 2 Neuromuscular junction Skeletal muscle fibers Figure 11.6

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

The Neuromuscular Junction
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

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

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

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

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 Nucleus Synaptic cleft ACh receptor Junctional folds Nucleus Mitochondria Figure 11.7b Sarcoplasm Myofilaments (b)

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

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

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)

Stimulated (active) muscle fiber or nerve cell (cont.) Action potential: 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

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

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

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.

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

Excitation Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Nerve signal Motor nerve fiber Ca2+ enters synaptic knob Sarcolemma Synaptic knob Synaptic 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 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)

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

Excitation–Contraction Coupling
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 11.9 (6, 7) Terminal cisterna of SR T tubule T tubule Sarcoplasmic reticulum Ca2+ Ca2+ 6 Action potentials propagated down T tubules 7 Calcium released from 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

Excitation–Contraction Coupling
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Active sites Troponin Ca2+ Tropomyosin Actin Thin filament Myosin Ca2+ 8 Binding of calcium to troponin 9 Shifting of tropomyosin; 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

Contraction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Myosin ATPase enzyme in myosin head hydrolyzes an ATP molecule Activates the head “cocking” it in an extended position ADP + Pi remain attached Head binds to actin active site forming a myosin–actin cross-bridge Troponin Tropomyosin ADP Pi Myosin 10 Hydrolysis of ATP to ADP + Pi; activation and cocking of myosin head Cross-bridge: Actin Myosin 11 Formation of myosin–actin cross-bridge Figure (10, 11)

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 Upon binding more ATP, myosin releases actin and process is repeated Each head performs five power strokes per second Each stroke utilizes one molecule of ATP ATP 13 Binding of new ATP; breaking of cross-bridge ADP ADP Pi Pi 12 Power stroke; sliding of thin filament over thick filament Figure (12, 13)

Relaxation Nerve stimulation and ACh release stop
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure (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

Relaxation Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Terminal cisterna of SR Ca2+ Ca2+ Figure (16) 16 Reabsorption of calcium ions by 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

Relaxation Ca+2 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 and contraction of antagonistic muscles Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Ca2+ ADP Pi Ca2+ 17 Loss of calcium ions from troponin Tropomyosin ATP 18 Return of tropomyosin to position blocking active sites of actin Figure (17, 18)

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

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

Length–Tension Relationship
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Optimum resting length (2.0–2.25µm) z z Overly contracted z z Overly stretched z z 1.0 Tension (g) generated upon stimulation 0.5 0.0 1.0 2.0 3.0 4.0 Sarcomere length (µm) before stimulation Figure 11.12

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

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.

Threshold, Latent Period, and Twitch
The response of a muscle to weak electrical stimulus seen in frog gastrocnemius—sciatic nerve preparation Myogram—a chart of the timing and strength of a muscle’s contraction Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Relaxation phase Contraction phase Muscle tension Latent period Time of stimulation Time Figure 11.13

Weak, subthreshold electrical stimulus causes no contraction Threshold—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 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Relaxation phase Contraction phase Muscle tension Latent period Time of stimulation Time Figure 11.13

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

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

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

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

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

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Stimulus voltage Threshold 1 2 3 4 5 6 7 8 9 Stimuli to nerve Proportion of nerve fibers excited Maximum contraction Tension Figure 11.14 1 2 3 4 5 6 7 8 9 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

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 (a) Stimuli 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

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

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 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

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

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

Isometric and Isotonic Contraction
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Figure 11.16 Muscle develops tension but does not shorten Muscle shortens, tension remains constant Muscle lengthens while maintaining 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

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

Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Muscle tension Muscle length Length or Tension Figure 11.17 Isometric phase Isotonic 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

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.

ATP Sources All muscle contraction depends on ATP
ATP supply depends on availability of: Oxygen Organic energy sources such as glucose and fatty acids

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

ATP Sources Figure 11.18 10 seconds 40 seconds Repayment of
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 10 seconds 40 seconds Repayment of oxygen debt Duration of exercise Mode of ATP synthesis Aerobic respiration using oxygen from myoglobin Phosphagen system Glycogen– lactic acid system (anaerobic fermentation) Aerobic respiration supported by cardiopulmonary function Figure 11.18

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

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

Immediate Energy Figure 11.19 ADP ADP Pi Myokinase AMP ATP Creatine
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. ADP ADP Pi Myokinase AMP ATP Creatine phosphate ADP Pi Figure 11.19 Creatine kinase Creatine 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

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

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

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

Fatigue and Endurance Muscle fatigue—progressive weakness 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

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

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

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

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

Oxygen Debt Cont. Serving the elevated metabolic rate
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

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

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

Ratio of different fiber types have genetic predisposition—born sprinter Muscles differ in fiber types: gastrocnemius is predominantly FG for quick movements (jumping) Soleus is predominantly SO used for endurance (jogging) Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. FG SO Dr. Gladden Willis/Visuals Unlimited, Inc. Figure 11.20

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

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

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

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

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 and Smooth Muscle
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.

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

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

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

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

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

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

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

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

Types of Smooth Muscle Multiunit smooth muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 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 Autonomic nerve fibers Synapses (a) Multiunit smooth muscle Figure 11.23a

Types of Smooth Muscle Single-unit 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 and 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 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autonomic nerve fibers Varicosities Gap junctions (b) Single-unit smooth muscle Figure 11.23b

Types of Smooth Muscle Figure 11.21 Autonomic nerve fiber Varicosities
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

Types of Smooth Muscle Figure 11.22 Mucosa: Epithelium Lamina propria
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

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

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

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

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

Calcium binds to calmodulin 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

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

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

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

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

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

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

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

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

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

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

Myasthenia Gravis Treatments Cont.
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

Myasthenia Gravis movement upon upward gaze Figure 11.25
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

Chapter 11 Lecture PowerPoint Muscular Tissue

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