Chapter 11 Lecture Outline Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 11-1

Chapter 11Lecture Outline

Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

11-1

Sarcoplasm

Sarcolemma

Openings intotransverse tubules

Sarcoplasmicreticulum

Mitochondria

Myofibrils

Myofilaments

A band

I band

Z disc

Nucleus

Triad:Terminal cisternaeT ransverse tubule

Musclefiber

11-2

Muscle Cells

• types and characteristics of muscular tissue• microscopic anatomy of skeletal muscle• nerve-muscle relationship• behavior of skeletal muscle fibers• behavior of whole muscles• muscle metabolism• cardiac and smooth muscle

Figure 11.2

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

11-3

Introduction to Muscle

• movement is a fundamental characteristic of all living things

• muscle cells are capable of converting the chemical energy of ATP into mechanical energy

• types of muscle

• physiology of skeletal muscle– basis of warm-up, quickness, strength,

endurance and fatigue

11-4

Characteristics of Muscle• responsiveness (excitability)

– to chemical signals, stretch and electrical changes across the plasma membrane

• conductivity

• contractility – ]

• extensibility – capable of being stretched between contractions

• elasticity – returns to its original resting length after being stretched

11-5

Skeletal Muscle

• skeletal muscle - voluntary, striated muscle attached to one or more bones

• striations -

• voluntary –

• muscle cell, muscle fiber, (myofiber) as long as 30 cm

Figure 11.1

Nucleus

Muscle fiber

Endomysium

Striations


© Ed Reschke

11-6

Connective Tissue Elements

• tendons are attachments between muscle and bone matrix– endomysium – connective tissue around muscle cells– perimysium – connective tissue around muscle fascicles– epimysium –

• 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• contribute to power output and muscle efficiency

Sarcoplasm

Sarcolemma

Openings intotransverse tubules


Mitochondria

Myofibrils

Myofilaments

A band

I band

Z disc

Nucleus

Triad:Terminal cisternaeTransverse tubule

Musclefiber

11-7

Structure of a Skeletal Muscle Fiber

Figure 11.2


11-8

The Muscle Fiber• sarcolemma – plasma membrane of a muscle fiber• sarcoplasm – cytoplasm of a muscle fiber• myofibrils – long protein bundles that occupies the main portion of the sarcoplasm

– glycogen – – myoglobin – red pigment – stores oxygen needed for muscle activity

• 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

• repair by fibrosis• mitochondria – packed in spaces between myofibrils• 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 muscle fiber from one side to the other

• T tubules –

11-9

Thick Myofilaments

• made of several hundred myosin molecules– shaped like a golf club

• two chains intertwined to form a shaft-like 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

Figure 11.3 a-b

(a) Myosin molecule

HeadTail

(b) Thick filament

Myosin head


11-10

Thin Myofilaments• 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

• troponin molecule - small, calcium-binding protein on each

(c) Thin filament

Troponin complex G actinTropomyosin


Figure 11.3c

11-11

Elastic Myofilaments

• titin (connectin) – huge springy protein– flank each thick filament and anchor it to the

Z disc– helps stabilize the thick filament

11-12

Regulatory and Contractile Proteins

• contractile proteins - myosin and actin

• regulatory proteins - tropomyosin and troponin – like a switch that determine 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

(b) Thick filament

Myosin head

(c) Thin filament

Troponin complex G actinTropomyosin


Figure 11.3 b-c

11-13

Overlap of Thick and Thin FilamentsCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

(d) Portion of a sarcomere showing the overlap of thick and thin filaments

Bare zone

Thin filament

Thick filament

Figure 11.3d

11-14

Accessory Proteins• at least seven other accessory

proteins in or associated with thick or thin filaments– anchor the myofilaments, regulate

length of myofilaments, alignment of myofilaments for maximum effectiveness

• dystrophin – most clinically important– links actin in outermost

myofilaments to transmembrane proteins and eventually to fibrous endomysium surrounding the entire muscle cell

Figure 11.4


Thick filament

Thin filament

Dystrophin

Sarcolemma

Basal lamina

Linking proteins

Endomysium

11-15

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

– A band – dark – A stands for anisotropic• part of A band where thick and thin filaments overlap is especially dark• H band in the middle of A band – just thick filaments• M line is in the middle of the H band

– I band –

– z disc – provides anchorage for thin filaments and elastic filaments• bisects I band


Sarcomere

I band I band A band

H band

Thick filament

TitinThin filamentElastic filament

(b) Z discZ disc

M line

Figure 11.5b

Striations and Sarcomeres

• sarcomere – functional contractile unit of the muscle fiber– muscle shortens because individual sarcomeres shorten

– pulls z discs closer to each other 11-16

Figure 11.5a


Ind

ivid

ual

myo

fib

rils

12

34

5

Sarcomere

I band I bandA band

H band

M line

(a)

Z disc

Nucleus

Visuals Unlimited

11-17

Sarcomeres• sarcomere - segment from Z disc to Z disc

• muscle cells shorten because their individual sarcomeres shorten

• neither thick nor thin filaments change length during shortening

• during shortening dystrophin & linking proteins also pull on extracellular proteins– transfers pull to extracellular tissue

11-18

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 –

• somatic motor neurons – nerve cells whose cell bodies are in the brainstem and spinal cord that serve skeletal muscles

• somatic motor fibers

11-19

Motor Units• motor unit –

• 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

• average motor unit – • small motor units -

• large motor units – more strength than control– powerful contractions supplied by large

motor units – gastrocnemius – 1000 muscle fibers per neuron

– many muscle fibers per motor unit

Figure 11.6

Spinal cord

Neuromuscularjunction

Skeletalmusclefibers

Motorneuron 1

Motorneuron 2


11-20

The Neuromuscular Junction • synapse –

• 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

11-21

Components of Neuromuscular Junction• synaptic knob - swollen end of nerve fiber

– contains synaptic vesicles filled with acetylcholine (ACh)

• synaptic cleft -

• Schwann cell• synaptic vesicles undergo exocytosis releasing ACh into synaptic cleft

• 50 million ACh receptors – proteins incorporated into muscle cell plasma membrane

• 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

11-22

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

(b)

Myelin

Motor nerve fiber

Schwann cell

Basal lamina

Synaptic knob

Synaptic vesicles(containing ACh)

Sarcolemma

Junctional folds

ACh receptor

Myofilaments

Nucleus

Synaptic cleft Nucleus

Sarcoplasm

Mitochondria

Figure 11.7b

11-23

Neuromuscular Junction - LM

Figure 11.7a


Neuromuscularjunction

Motor nervefibers

Muscle fibers

(a) 100 µmVictor B. Eichler

11-24

Neuromuscular Toxins• 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 of 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

• flaccid paralysis –

• 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

11-25

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• 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

• voltage (electrical potential) –• resting membrane potential – about -90mV

– maintained by sodium-potassium pump

11-26

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)– 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 alittle farther along and so forth

11-27

Muscle Contraction & Relaxation• four major phases of contraction and relaxation

– excitation•

– excitation-contraction coupling

– contraction• step in which the muscle fiber develops tension and may

shorten

– relaxation

11-28

Excitation of a Muscle FiberCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Arrival of nerve signal1 Acetylcholine (ACh) release2

3 4

Opening of voltage-regulated ion gates;creation of action potentials

5

K+

K+

Na+

Na+

Sarcolemma

Sarcolemma

Sarcolemma

AChreceptors

ACh receptor

ACh

Plasmamembraneof synapticknob

Nerve signal

ACh

Voltage-regulatedion gates

ACh

Motornervefiber

Ca2+ enterssynaptic knob

Synapticknob

Binding of ACh to receptor Opening of ligand-regulated ion gate;creation of end–plate potential

Figure 11.8

Synapticvesicles

Synapticcleft

11-29

Excitation (steps 1 and 2)

• nerve signal opens voltage-gated calcium channels in synaptic knob • calcium stimulates exocytosis of ACh from synaptic vesicles• ACh released into synaptic cleft

Figure 11.8 (1-2)


Arrival of nerve signal1 Acetylcholine (ACh) release2

Motornervefiber

Sarcolemma Synapticknob

Synapticvesicles

AChreceptors

Nerve signal

ACh

Ca2+ enterssynaptic knob

Synapticcleft

11-30

Excitation (steps 3 and 4)

• two ACh molecules bind to each receptor protein, opening Na+ and K+ channels.

Figure 11.8 (3-4)


Binding of ACh to receptor3

Sarcolemma

ACh receptor

AChACh


Opening of ligand-regulated ion gate;creation of end–plate potential

4

K+

Na+

11-31

Excitation (step 5)

• voltage change (EPP) in end-plate region opens nearby voltage-gated channels producing an action potential that spreads over muscle surface.


Opening of voltage-regulated ion gates;creation of action potentials

5

K+

Na+

Sarcolemma

Plasmamembraneof synapticknob

Voltage-regulatedion gates

Figure 11.8 (5)

11-32

Excitation-Contraction Coupling in Skeletal Muscle

Figure 11.9 (6-9)6 7

8 Shifting of tropomyosin;exposure of active siteson actin

9

Ca2+

Ca2+

Ca2+

Ca2+

T tubule

T tubule

TroponinTropomyosin Actin

Active sites

Myosin

Thin filament


Action potentials propagateddown T tubules

Binding of calciumto troponin

Calcium released fromterminal cisternae

Terminalcisternaof SR


11-33

Excitation-Contraction Coupling (steps 6 and 7)

• 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

Action potentials propagateddown T tubules

6 Calcium released fromterminal cisternae

7

Ca2+

T tubule

T tubuleTerminalcisternaof SR


Ca2+

Figure 11.9 (6-7)


11-34

• troponin-tropomyosin complex changes shape and exposes active sites on actin

Figure 11.9 (8-9)

8 Shifting of tropomyosin;exposure of active siteson actin

9

Active sites

MyosinCa2+

Ca2+Troponin

Tropomyosin Actin Thin filament

Binding of calciumto troponin


Excitation-Contraction Coupling (steps 8 and 9)

11-35

Contraction (steps 10 and 11)• 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

Figure 11.10 (10-11)


Tropomyosin

Formation of myosin–actin cross-bridge11

Hydrolysis of ATP to ADP + Pi;activation and cocking of myosin head

10

ADP

Pi

Myosin

Cross-bridge:ActinMyosin

Troponin

11-36

Contraction (steps 12 and 13)

• myosin head releasesADP and Pi, flexes pullingthin filament past thick - power stroke

• upon binding more ATP, myosin releases actin and process is repeated– each head performs 5 power

strokes per second– each stroke utilizes one

molecule of ATPPower stroke; sliding of thinfilament over thick filament

12

Binding of new ATP;breaking of cross-bridge

13

ATP

Pi

ADP

Pi

ADP


Figure 11.10 (12-13)

11-37

Relaxation (steps 14 and 15)

• nerve stimulation & ACh release stop• AChE breaks down ACh & fragments reabsorbed into synaptic

knob


AChE

Cessation of nervous stimulationand ACh release

14ACh breakdown byacetylcholinesterase (AChE)

15

ACh

Figure 11.11 (14-15)

11-38

Relaxation (step 16)

• .

Figure 11.11 (16)


Ca2+

Ca2+

Reabsorption of calcium ions bysarcoplasmic reticulum

16

Terminal cisternaof SR

11-39

Relaxation (steps 17 and 18)

• 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 & contraction of antagonistic muscles

Figure 11.11 (17-18)

Ca2+

Ca2+

Loss of calcium ions from troponin17

ADPPi

Return of tropomyosin to positionblocking active sites of actin

18

Tropomyosin

ATP


11-40

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

• muscle relaxation requires ATP, and ATP production is no longer produced after death– fibers remain contracted until myofilaments begins to

decay

11-41

Length-Tension Relationship• 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 can’t slide

• if too stretched before stimulated, a weak contraction

• 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

11-42

Length-Tension Relationship

Figure 11.12


0.0

0.5

1.0

Ten

sio

n (

g)

gen

erat

edu

po

n s

tim

ula

tio

n

1.0 2.0 3.0 4.0

Overly contractedOverly stretched

Optimum resting length(2.0–2.25µm)

z z

z

z z

z

Sarcomere length (µm) before stimulation

11-43

Behavior of Whole Muscles • 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

• weak, subthreshold electrical stimulus causes no contraction

• threshold -

Figure 11.13


Contractionphase

Relaxationphase

Time

Latentperiod

Time ofstimulation

Mu

scle

ten

sio

n

11-44

Phases of a Twitch Contraction• latent period - 2 msec delay between the onset of

stimulus and onset of twitch response– time required for excitation, excitation-contraction coupling and

tensing of elastic components of the muscle– internal tension –

• 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

• relaxation phase - SR quickly reabsorbs Ca+2, myosin releases the thin filaments and tension declines– muscle returns to resting length – entire twitch lasts from 7 to 100 msec

11-45

Contraction Strength of Twitches• at subthreshold stimulus – no contraction at all

• at threshold intensity and above -

• 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 the contraction - fatigue• state of hydration of muscle affects overlap of thick & thin filaments

• muscles need to be able to contract with variable strengths for different tasks

11-46

Recruitment and Stimulus Intensity

• 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


1 2 3 4 5 6 7 8 9

1 2 3 4 5 6 7 8 9

Threshold

Sti

mu

lus

volt

age

Stimuli to nerve

Te

ns

ion

Proportion of nerve fibers excited

Responses of muscle

Maximum contraction

Figure 11.14

11-47

Twitch Strength & Stimulus Frequency

• when stimulus intensity (voltage) remains constant twitch strength can vary with the stimulus frequency

• 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 Ca+2 it released– Ca+2 concentration in the cytosol rises higher and higher with each stimulus causing

subsequent twitches to be stronger– heat released by each twitch cause muscle enzymes such as myosin ATPase to

work more efficiently and produce stronger twitches as muscle warms up


Twitch

Muscle twitches

Stimuli(a)


(b)

Treppe

Figure 11.15a,b

11-48

Incomplete and Complete Tetanus

• 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

Figure 11.15c,d

Incomplete tetanus

(c)

Complete tetanus

Fatigue

(d)

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

11-49

Incomplete and Complete Tetanus

• 40-50 stimuli per second produces complete tetanus– muscle has no time to relax at all 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

Figure 11.15c,d

Incomplete tetanus Complete tetanus

Fatigue

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

(c) (d)

11-50

• isometric muscle contraction

• isotonic muscle contraction– muscle changes in length with no change in tension– concentric contraction – muscle shortens while maintains tension– eccentric contraction – muscle lengthens as it maintains tension


Muscle shortens,tension remainsconstant

Movement

Movement

Muscle developstension but doesnot shorten

No movement

Muscle lengthenswhile maintainingtension

(a) Isometric contraction (b) Isotonic concentric contraction (c) Isotonic eccentric contraction

Isometric and Isotonic Contractions

Figure 11.16

11-51

Isometric and Isotonic Phases of Contraction

• at the beginning of contraction – isometric phase– muscle tension rises but muscle does not shorten

• when tension overcomes resistance of the load– tension levels off

• muscle begins to shorten and move the load – isotonic phase


Muscletension

Musclelength

Isometricphase

Isotonicphase

Time

Len

gth

or

Ten

sio

n

Figure 11.17

11-52

Muscle Metabolism• all muscle contraction depends on ATP

• ATP supply depends on availability of:– oxygen– organic energy sources such as glucose and fatty acids

• two main pathways of ATP synthesis

– aerobic respiration

11-53

Modes of ATP Synthesis During Exercise

Figure 11.18


Aerobic respirationusing oxygen frommyoglobin

Glycogen–lactic acidsystem(anaerobicfermentation)

Phosphagensystem

Duration of exercise

0 10 seconds 40 seconds

Aerobicrespirationsupported bycardiopulmonaryfunction

Repayment ofoxygen debt

Mode of ATP synthesis

11-54

Immediate Energy Needs

• 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

– provides nearly all energy used for short bursts of intense activity• one minute of brisk walking• 6 seconds of sprinting or fast swimming• important in activities requiring brief but maximum effort

– football, baseball, and weight lifting

11-55

Creatinephosphate

Creatine

Creatinekinase

Myokinase

Pi

ATP

ATP

ADP ADP

ADP

AMP

Pi

Figure 11.19

Immediate Energy NeedsCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

11-56

Short-Term Energy Needs• 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 –

11-57

Long-Term Energy Needs

• after 40 seconds or so, the respiratory and cardiovascular systems “catch up” and deliver oxygen to the muscles fast enough for aerobic respiration to meet most of the ATP demands

• aerobic respiration produces 36 ATP per glucose– efficient means of meeting the ATP demands of prolonged exercise

– 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

– 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

11-58

Fatigue• muscle fatigue - progressive weakness and loss of contractility from

prolonged use of the muscles– repeated squeezing of rubber ball– holding text book out level to the floor

• causes of muscle fatigue– 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

– 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

11-59

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 – 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

11-60

Oxygen Debt• heavy breathing continues after strenuous exercise

– excess post-exercise oxygen consumption (EPOC) – the difference between the resting rate of oxygen consumption and the elevated rate following exercise.

– typically about 11 liters extra is needed after strenuous exercise– repaying the oxygen debt

• 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

– 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• 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

11-61

Beating Muscle Fatigue• Taking oral creatine increases level of creatine

phosphate in muscle tissue and increases speed of ATP regeneration– useful in burst type exercises – weight-lifting– risks are not well known

• muscle cramping, electrolyte imbalances, dehydration, water retention, stroke

• kidney disease from overloading kidney with metabolite creatinine

• carbohydrate loading –

11-62

Physiological Classes of Muscle Fibers• slow oxidative (SO), slow-twitch, red, or type I fibers

– abundant mitochondria, myoglobin and capillaries - deep red color• adapted for aerobic respiration and fatigue resistance

• 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 & reabsorbs Ca+2 quickly so contractions are quicker (7.5 msec/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)

11-63

FG and SO Muscle Fibers

Figure 11.20


FG

SO

11-64

Strength and Conditioning• muscles can generate more tension than the bones and tendons can

withstand

• muscular strength depends on:– primarily on muscle size

• a muscle can exert a tension of 3 or 4 kg / cm2 of cross-sectional area– fascicle arrangement

– size of motor units

– 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– 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

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Strength and Conditioning• resistance training (weight lifting)

– 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

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Cardiac Muscle

• limited to the heart where it functions to pump blood

• required 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

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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

– sarcoplasmic reticulum less developed, but T tubules are larger and admit supplemental Ca2+ from the extracellular fluid

– damaged cardiac muscle cells repair by fibrosis

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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 – because of its ability to contract rhythmically and independently

– 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 msec

– uses aerobic respiration almost exclusively• rich in myoglobin and glycogen• has especially large mitochondria

– very adaptable with respect to fuel used

– very vulnerable to interruptions of oxygen supply

– highly fatigue resistant

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Smooth Muscle• composed of myocytes that have a fusiform shape• there is only one nucleus, located near the middle of the cell• no visible striations

– reason for the name ‘smooth muscle’– thick and thin filaments are present, but 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

• cytoplasm contains extensive cytoskeleton of intermediate filament– attach to the membrane plaques and dense bodies– provide mechanical linkages between the thin myofilaments and the plasma membrane

• sarcoplasmic reticulum is scanty and there are no T tubules• 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

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2 Types of Smooth Muscle

• multiunit smooth muscle

– occurs in some of the largest arteries and pulmonary air passages, in piloerector muscles of hair follicle, and in the iris of the eye

– autonomic innervation similar to skeletal muscle

• terminal branches of a nerve fiber synapse with individual myocytes and form a motor unit

• each motor unit contracts independently of the others


Synapses

Autonomicnerve fibers

(a) Multiunit smooth muscle

Figure 11.21a

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2 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

– 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

Figure 11.21b


Varicosities

Gap junctions

Autonomicnerve fibers

(b) Single-unit smooth muscle

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Layers of Visceral Muscle

Epithelium

Mucosa:

Muscularis externa:

Lamina propria

Muscularismucosae

Circular layer

Longitudinallayer

Figure 11.22


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Stimulation of Smooth Muscle• smooth muscle is involuntary and can contract without nervous

stimulation– can contract in response to chemical stimuli

• hormones, carbon dioxide, low pH, and oxygen deficiency• in response to stretch• single unit smooth muscle in stomach and intestines has that set off waves

of contraction throughout the entire layer of muscle

• most smooth muscle is innervated by autonomic nerve fibers

• in single unit smooth, each autonomic nerve fibers has up to 20,000 beadlike swelling 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

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Stimulation of Smooth Muscle

Figure 11.23

Synapticvesicle

Mitochondrion

Autonomicnerve fiber

Varicosities

Single-unitsmooth muscle


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Contraction and Relaxation• contraction is triggered by Ca+2, energized by ATP, and

achieved by sliding thin past thick filaments

• contraction begins in response to Ca+2 that enters the cell from ECF, a little internally from sarcoplasmic reticulum

• calcium binds to calmodulin on thick filaments– activates myosin light-chain kinase – adds phosphate to

regulatory protein on myosin head– and 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

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• contraction and relaxation very slow in comparison to skeletal muscle– latent period in skeletal 2 msec, smooth muscle 50 - 100 msec– tension peaks at about 500 msec (0.5 sec)– declines over a period of 1 – 2 seconds– slows myosin ATPase enzyme and slow pumps that remove Ca+2

– Ca+2 binds to calmodulin instead of troponin

• 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

Contraction and Relaxation

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Contraction of Smooth MuscleCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Dense body

Intermediate filamentsof cytoskeleton

Actin filaments

(b) Contracted smooth muscle cells

(a) Relaxed smooth muscle cells

Plaque

Myosin

Figure 11.24

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Stretching Smooth Muscle

• 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)

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• skeletal muscle cannot contract forcefully if overstretched

• smooth muscle contracts forcefully even when greatly stretched

• 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

• plasticity – the ability to adjust its tension to the degree of stretch

Contraction and Stretching

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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 3500 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 results

– rarely live past 20 years of age due to affects on respiratory and cardiac muscle – incurable

• 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

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Myasthenia Gravis• autoimmune disease in which antibodies attack neuromuscular

junctions and bind ACh receptors together in clusters– disease of women between 20 and 40– muscle fibers then removes the clusters of receptors from the sarcolemma by

endocytosis– fiber becomes less and less sensitive to ACh– effects usually first appear in facial muscles

• drooping eyelids and double vision, difficulty swallowing, and weakness of the limbs

– strabismus –

• 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

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Myasthenia Gravis

drooping eyelids and weakness of muscles of eye movement

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