Ch 09 Muslces and Muslce Tissue Gillette College

PowerPoint® Lecture Slidesprepared byBarbara Heard,Atlantic Cape Community College

C H A P T E R

© 2013 Pearson Education, Inc.© Annie Leibovitz/Contact Press Images

9

Muscles and Muscle Tissue:

© 2013 Pearson Education, Inc.

Muscle Tissue

• Nearly half of body's mass

• Transforms chemical energy (ATP) to directed mechanical energy exerts force

• Three types– Skeletal– Cardiac– Smooth

• Myo, mys, and sarco - prefixes for muscle


Types of Muscle Tissue

• Skeletal muscles – Organs attached to bones and skin

– Elongated cells called muscle fibers– Striated (striped) – Voluntary (i.e., conscious control)– Contract rapidly; tire easily; powerful– Require nervous system stimulation

Table 9.3



• Cardiac muscle– Only in heart; bulk of heart walls

– Striated– Can contract without nervous system

stimulation – Involuntary– More details in Chapter 18

Table 9.3



• Smooth muscle– In walls of hollow organs, e.g., stomach,

urinary bladder, and airways– Not striated– Can contract without nervous system

stimulation – Involuntary

Table 9.3


Special Characteristics of Muscle Tissue

• Excitability (responsiveness): ability to receive and respond to stimuli

• Contractility: ability to shorten forcibly when stimulated

• Extensibility: ability to be stretched

• Elasticity: ability to recoil to resting length


Muscle Functions

• Four important functions– Movement of bones or fluids (e.g., blood)

– Maintaining posture and body position – Stabilizing joints– Heat generation (especially skeletal muscle)

• Additional functions– Protects organs, forms valves, controls pupil

size, causes "goosebumps"


Skeletal Muscle

• Each muscle served by one artery, one nerve, and one or more veins– Enter/exit near central part and branch

through connective tissue sheaths– Every skeletal muscle fiber supplied by nerve

ending that controls its activity– Huge nutrient and oxygen need; generates

large amount of waste


Skeletal Muscle

• Connective tissue sheaths of skeletal muscle– Support cells; reinforce whole muscle– External to internal

• Epimysium: dense irregular connective tissue surrounding entire muscle; may blend with fascia

• Perimysium: fibrous connective tissue surrounding fascicles (groups of muscle fibers)

• Endomysium: fine areolar connective tissue surrounding each muscle fiber


Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.

Bone

Tendon

Epimysium Epimysium

Perimysium

Endomysium

Muscle fiberin middle of a fascicle

Blood vessel

Perimysiumwrapping a fascicleEndomysium(between individualmuscle fibers)

Musclefiber

Perimysium

Fascicle


Skeletal Muscle: Attachments

• Attach in at least two places– Insertion – movable bone

– Origin – immovable (less movable) bone

• Attachments direct or indirect– Direct—epimysium fused to periosteum of

bone or perichondrium of cartilage– Indirect—connective tissue wrappings extend

beyond muscle as ropelike tendon or sheetlike aponeurosis


Microscopic Anatomy of a Skeletal Muscle Fiber

• Long, cylindrical cell – 10 to 100 µm in diameter; up to 30 cm long

• Multiple peripheral nuclei

• Sarcolemma = plasma membrane

• Sarcoplasm = cytoplasm– Glycosomes for glycogen storage,

myoglobin for O2 storage

• Modified structures: myofibrils, sarcoplasmic reticulum, and T tubules


Myofibrils

• Densely packed, rodlike elements

• ~80% of cell volume

• Contain sarcomeres - contractile units – Sarcomeres contain myofilaments

• Exhibit striations - perfectly aligned repeating series of dark A bands and light I bands


Figure 9.2b Microscopic anatomy of a skeletal muscle fiber.

Diagram of part of a muscle fiber showingthe myofibrils. One myofibril extends from the cut end of the fiber.

Sarcolemma

Mitochondrion

MyofibrilNucleusLight

I bandDark

A band


Sarcomere

• Smallest contractile unit (functional unit) of muscle fiber

• Align along myofibril like boxcars of train

• Contains A band with ½ I band at each end

• Composed of thick and thin myofilaments made of contractile proteins


Figure 9.2c Microscopic anatomy of a skeletal muscle fiber.

Small part of onemyofibril enlarged to show the myofilamentsresponsible for thebanding pattern. Each sarcomere extends from one Z disc to the next.

Thin (actin)filament Z disc H zone Z disc

Thick (myosin)filament

I band A band I band M lineSarcomere


Figure 9.2d Microscopic anatomy of a skeletal muscle fiber.

Enlargement of one sarcomere (sectioned length-wise). Notice themyosin heads on the thick filaments.

Z discSarcomere

M line Z discThin (actin)filamentElastic (titin)filamentsThick(myosin)filament


Longitudinal section of filaments within onesarcomere of a myofibril

Thick filament

Thin filament

In the center of the sarcomere, the thick filamentslack myosin heads. Myosin heads are present onlyin areas of myosin-actin overlap.

Thick filament. Thin filamentEach thick filament consists of many myosin

molecules whose heads protrude at oppositeends of the filament.

A thin filament consists of two strands of actinsubunits twisted into a helix plus two types ofregulatory proteins (troponin and tropomyosin).

Portion of a thick filament Portion of a thin filament

Myosin head Tropomyosin Troponin Actin

Actin-binding sites

ATP-bindingsite

Heads Tail

Flexible hinge region

Myosin molecule

Actin subunits

Actin subunits

Active sitesfor myosinattachment

Figure 9.3 Composition of thick and thin filaments.


Figure 9.5 Relationship of the sarcoplasmic reticulum and T tubules to myofibrils of skeletal muscle.

Part of a skeletal muscle fiber (cell)

Myofibril

Sarcolemma

I band A band I band

Z disc H zone Z disc

Mline

Sarcolemma

Triad:• T tubule

• Terminal cisterns of the SR (2)

Tubules ofthe SRMyofibrils

Mitochondria


Sliding Filament Model of Contraction

• Generation of force

• Does not necessarily cause shortening of fiber

• Shortening occurs when tension generated by cross bridges on thin filaments exceeds forces opposing shortening



• In relaxed state, thin and thick filaments overlap only at ends of A band

• Sliding filament model of contraction– During contraction, thin filaments slide past

thick filaments actin and myosin overlap more

– Occurs when myosin heads bind to actin cross bridges



• Myosin heads bind to actin; sliding begins

• Cross bridges form and break several times, ratcheting thin filaments toward center of sarcomere– Causes shortening of muscle fiber– Pulls Z discs toward M line

• I bands shorten; Z discs closer; H zones disappear; A bands move closer (length stays same)


Figure 9.6 Sliding filament model of contraction. Slide 1Slide 1

Fully contracted sarcomere of a muscle fiber

1

2

Fully relaxed sarcomere of a muscle fiber

Z H Z

II A

Z Z

I IA


Figure 9.6 Sliding filament model of contraction. Slide 2

1 Fully relaxed sarcomere of a muscle fiber

Z H Z

II A



2 Fully contracted sarcomere of a muscle fiber

Z Z

II A



Fully contracted sarcomere of a muscle fiber

1

2

Fully relaxed sarcomere of a muscle fiber

Z H Z

II A

Z Z

I IA


The Nerve Stimulus and Events at the Neuromuscular Junction

• Skeletal muscles stimulated by somatic motor neurons

• Axons of motor neurons travel from central nervous system via nerves to skeletal muscle

• Each axon forms several branches as it enters muscle

• Each axon ending forms neuromuscular junction with single muscle fiber– Usually only one per muscle fiber


Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. Slide 1

Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal of neuromuscular junction

Sarcolemma ofthe muscle fiber

Synaptic vesiclecontaining ACh

Synaptic cleft

Junctionalfolds of sarcolemma

Sarcoplasm ofmuscle fiber

Postsynaptic membraneion channel opens;ions pass.

Ion channel closes;ions cannot pass.

Action potential arrives at axon terminal of motor neuron.

Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient.

Ca2+ entry causes ACh (aneurotransmitter) to be releasedby exocytosis.

ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma.

ACh binding opens ionchannels in the receptors thatallow simultaneous passage ofNa+ into the muscle fiber and K+

out of the muscle fiber. More Na+

ions enter than K+ ions exit,which produces a local changein the membrane potential calledthe end plate potential.

ACh effects are terminated byits breakdown in the synapticcleft by acetylcholinesterase anddiffusion away from the junction.

Axon terminalof motor neuron

Fusing synaptic vesicles

Degraded AChACh

Acetylcho-linesterase

ACh

4

3

2

1

5

6




Synaptic cleft


Fusing synaptic vesiclesa

ACh Junctionalfolds of sarcolemma


Action potential arrives at axon terminal of motor neuron.1




Synaptic cleft







1

2




Synaptic cleft








1

2

3




Synaptic cleft








ACh diffuses across the synaptic cleft and binds to its receptors onthe sarcolemma.

1

2

3

4




ACh binding opens ionchannels in the receptors thatallow simultaneous passage ofNa+ into the muscle fiber and K+out of the muscle fiber. More Na+ions enter than K+ ions exit,which produces a local changein the membrane potential calledthe end plate potential.

5




6

Degraded AChACh

Acetylcholinesterase




Actionpotential (AP)

Myelinated axonof motor neuron

Axon terminal of neuromuscular junction

Sarcolemma ofthe muscle fiber


Synaptic cleft

Junctionalfolds of sarcolemma







ACh diffuses across the synaptic cleft and binds to its receptors on the sarcolemma.

ACh binding opens ionchannels in the receptors thatallow simultaneous passage ofNa+ into the muscle fiber and K+

out of the muscle fiber. More Na+

ions enter than K+ ions exit,which produces a local changein the membrane potential calledthe end plate potential.



Fusing synaptic vesicles

Degraded AChACh

Acetylcho-linesterase

ACh

4

3

2

1

5

6


Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletalmuscle fiber.

Slide 1Open Na+

channel

Na+

Closed K+

channel

K+

Action potential

Axon terminal ofneuromuscularjunction

ACh-containingsynaptic vesicle

Ca2+

Ca2+

Synapticcleft

Wave ofdepolarization

An end plate potential is generated at theneuromuscular junction (see Figure 9.8).

Depolarization: Generating and propagating an actionpotential (AP). The local depolarization current spreads to adjacentareas of the sarcolemma. This opens voltage-gated sodium channelsthere, so Na+ enters following its electrochemical gradient and initiatesthe AP. The AP is propagated as its local depolarization wave spreads toadjacent areas of the sarcolemma, opening voltage-gated channels there.Again Na+ diffuses into the cell following its electrochemical gradient.

Repolarization: Restoring the sarcolemma to its initialpolarized state (negative inside, positive outside). Repolarizationoccurs as Na+ channels close (inactivate) and voltage-gated K+ channelsopen. Because K+ concentration is substantially higher inside the cellthan in the extracellular fluid, K+ diffuses rapidly out of the muscle fiber.

1

2

3

Closed Na+

channelOpen K+

channel

Na+

K+

– – – – – – – – – – – – – – – – – – – + + + +

– – – – + + + + + + + + + + + + + + + +

+ + + + + + + + + + + + + + + + + + + + + +

– – – – – – – – – – – – – – – – – – – – – –



Slide 2



Ca2+

Ca2+

Synapticcleft



1



Slide 3Open Na+

channel

Na+

Closed K+

channel

K+

Action potential



Ca2+

Ca2+

Synapticcleft




1

2

+ + + +

+ + + + + + + + + + + + + + + +

– – – – – – – – – – – – – – – – – – –

– – – –



Slide 4Open Na+

channel

Na+

Closed K+

channel

K+

Action potential



Ca2+

Ca2+

Synapticcleft




Repolarization: Restoring the sarcolemma to its initialpolarized state (negative inside, positive outside). Repolarizationoccurs as Na+ channels close (inactivate) and voltage-gated K+ channelsopen. Because K+ concentration is substantially higher inside the cellthan in the extracellular fluid, K+ diffuses rapidly out of the muscle fiber.

1

2

3

Closed Na+

channelOpen K+

channel

Na+

K+

+ + + +

+ + + + + + + + + + + + + + + +

+ + + + + + + + + + + + + + + + + + + + + +

– – – – – – – – – – – – – – – – – – –

– – – –

– – – – – – – – – – – – – – – – – – – – – –


Figure 9.10 Action potential tracing indicates changes in Na+ and K+ ion channels.

Mem

bran

e po

tent

ial (

mV

)

+30

0

–95

0 5 10 15 20

Depolarizationdue to Na+ entry

Na+ channelsclose, K+ channelsopen

Repolarizationdue to K+ exit

K+ channelsclosed

Na+

channelsopen

Time (ms)


Excitation-Contraction (E-C) Coupling

• Events that transmit AP along sarcolemma lead to sliding of myofilaments

• AP brief; ends before contraction– Causes rise in intracellular Ca2+ which

contraction

• Latent period– Time when E-C coupling events occur– Time between AP initiation and beginning of

contraction


Events of Excitation-Contraction (E-C) Coupling

• AP propagated along sarcomere to T tubules

• Voltage-sensitive proteins stimulate Ca2+ release from SR – Ca2+ necessary for contraction


Figure 9.11 Excitation-contraction (E-C) coupling is the sequence of events by which transmission of anaction potential along the sarcolemma leads to the sliding of myofilaments.

Slide 1

Setting the stageThe events at the neuromuscular junction (NMJ) set the stage for E-C coupling by providing excitation. Released acetylcholine binds to receptor proteins on the sarcolemma and triggers an action potential in a muscle fiber.

Synapticcleft

Axon terminal ofmotor neuron at NMJ

Action potentialis generated

ACh

Muscle fiber

T tubule

Terminal cisternof SR

Triad

One sarcomere

One myofibril

Sarcolemma

The action potential (AP) propagates along the sarcolemma and down theT tubules.

Calcium ions are released. Transmission of the AP along the T tubules of the triads causes the voltage-sensitive tubule proteins to change shape. This shape change opens the Ca2+ release channels in the terminal cisterns of the sarcoplasmic reticulum (SR), allowing Ca2+ to flow into the cytosol.

Steps in E-C Coupling:


Ca2+

releasechannel

Voltage-sensitivetubule protein

T tubuleSarcolemma 1

2

3

4

Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca2+ binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments.

Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over.

The aftermathWhen the muscle AP ceases, the voltage-sensitive tubule proteins return to their original shape, closing the Ca2+ release channels of the SR. Ca2+ levels in the sarcoplasm fall as Ca2+ is continually pumped back into the SR by active transport. Without Ca2+, the blocking action of tropomyosin is restored, myosin-actin interaction is inhibited, and relaxation occurs. Each time an AP arrives at the neuromuscular junction, the sequence of E-C coupling is repeated.

Myosincross bridge

Active sites exposed and ready for myosin binding

Myosin

Tropomyosinblocking active sites

Actin

Troponin



Slide 2


Synapticcleft


Action poten-tial is generated

Muscle fiber

T tubuleTerminal cisternof SR

Triad

One sarcomere

One myofibril

SarcolemmaACh



Slide 3





Ca2+

releasechannel


T tubule

Sarcolemma




Myosincross bridge


Myosin


Actin

Troponin

2

1

3

4



Slide 4




Ca2+ releasechannel


T tubule

Sarcolemma 1



Slide 5




Ca2+ releasechannel


T tubule

Sarcolemma

Calcium ions are released.

1

2



Slide 6

Myosin


Actin

Troponin

The aftermath



Slide 7



Myosin


Actin

Troponin

The aftermath

3



Slide 8



Myosincross bridge


Myosin


Actin

Troponin

The aftermath

3

4



A&P Flix™: Excitation-contraction coupling.

PLAYPLAY

Slide 9





Ca2+

releasechannel


T tubule

Sarcolemma




Myosincross bridge


Myosin


Actin

Troponin

2

1

3

4



Slide 10


Synapticcleft


Action potentialis generated

ACh

Muscle fiber

T tubule


Triad

One sarcomere

One myofibril

Sarcolemma





Ca2+

releasechannel


T tubuleSarcolemma 1

2

3

4




Myosincross bridge


Myosin


Actin

Troponin


Channels Involved in Initiating Muscle Contraction

• Nerve impulse reaches axon terminal voltage-gated calcium channels open ACh released to synaptic cleft

• ACh binds to its receptors on sarcolemma opens ligand-gated Na+ and K+ channels end plate potential

• Opens voltage-gated Na+ channels AP propagation

• Voltage-sensitive proteins in T tubules change shape SR releases Ca2+ to cytosol


Role of Calcium (Ca2+) in Contraction

• At low intracellular Ca2+ concentration– Tropomyosin blocks active sites on actin

– Myosin heads cannot attach to actin– Muscle fiber relaxed


Role of Calcium (Ca2+) in Contraction

• At higher intracellular Ca2+ concentrations– Ca2+ binds to troponin

• Troponin changes shape and moves tropomyosin away from myosin-binding sites

• Myosin heads bind to actin, causing sarcomere shortening and muscle contraction

– When nervous stimulation ceases, Ca2+ pumped back into SR and contraction ends


Cross Bridge Cycle

• Continues as long as Ca2+ signal and adequate ATP present

• Cross bridge formation—high-energy myosin head attaches to thin filament

• Working (power) stroke—myosin head pivots and pulls thin filament toward M line


Cross Bridge Cycle

• Cross bridge detachment—ATP attaches to myosin head and cross bridge detaches

• "Cocking" of myosin head—energy from hydrolysis of ATP cocks myosin head into high-energy state


Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filamentstoward the center of the sarcomere.

Slide 1

Actin Ca2+ Thin filament

Myosincross bridge Thick

filament

Myosin

ATPhydrolysis

In the absence of ATP, myosin heads will not detach, causing rigor mortis.

*This cycle will continue as long

as ATP is available and Ca2+ is

bound to troponin.

Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge.

Cocking of the myosin head. As ATP is hydrolyzed to ADP and Pi, the myosin head returns to its prestroke high-energy, or “cocked,” position. *

Cross bridge detachment. After ATP attaches to myosin, the link between myosin and actin weakens, and the myosin head detaches (the cross bridge “breaks”).

The power (working) stroke. ADP and Pi are released and the myosin head pivots and bends, changing to its bent low-energy state. As a result it pulls the actin filament toward the M line.

1

2

3

4



Slide 2

Actin Thin filament


filament

Myosin


1



Slide 3


2



Slide 4


3



Slide 5


4

ATPhydrolysis



bound to troponin.



Slide 6

A&P Flix™: The Cross Bridge Cycle

PLAYPLAY

Actin Ca2+ Thin filament


filament

Myosin

ATPhydrolysis

In the absence of ATP, myosin heads will not detach, causing rigor mortis.



bound to troponin.





1

2

3

4


Homeostatic Imbalance

• Rigor mortis– Cross bridge detachment requires ATP

– 3–4 hours after death muscles begin to stiffen with weak rigidity at 12 hours post mortem

• Dying cells take in calcium cross bridge formation

• No ATP generated to break cross bridges


Review Principles of Muscle Mechanics

• Same principles apply to contraction of single fiber and whole muscle

• Contraction produces muscle tension, force exerted on load or object to be moved


Review Principles of Muscle Mechanics

• Contraction may/may not shorten muscle– Isometric contraction: no shortening; muscle

tension increases but does not exceed load – Isotonic contraction: muscle shortens

because muscle tension exceeds load

• Force and duration of contraction vary in response to stimuli of different frequencies and intensities


Motor Unit: The Nerve-Muscle Functional Unit

• Each muscle served by at least one motor nerve– Motor nerve contains axons of up to hundreds

of motor neurons– Axons branch into terminals, each of which

NMJ with single muscle fiber

• Motor unit = motor neuron and all (four to several hundred) muscle fibers it supplies– Smaller number = fine control


Figure 9.13 A motor unit consists of one motor neuron and all the muscle fibers it innervates.

Spinal cord

Motorunit 1

Motorunit 2

Axon terminals atneuromuscular junctions

Branching axonto motor unit

Motor neuroncell body

Motor neuronaxon

Muscle

Musclefibers

Nerve

Branching axon terminals form neuromuscular junctions, one per muscle fiber (photomicro-

graph 330x). Axons of motor neurons extend from the spinal cord to the muscle. There each

axon divides into a number of axon terminals that form neuromuscular junctions with muscle fibers scattered throughout the muscle.


Motor Unit

• Muscle fibers from motor unit spread throughout muscle so single motor unit causes weak contraction of entire muscle

• Motor units in muscle usually contract asynchronously; helps prevent fatigue


Muscle Twitch

• Motor unit's response to single action potential of its motor neuron

• Simplest contraction observable in lab (recorded as myogram)


Muscle Twitch

• Three phases of muscle twitch– Latent period: events of excitation-

contraction coupling; no muscle tension– Period of contraction: cross bridge

formation; tension increases– Period of relaxation: Ca2+ reentry into SR;

tension declines to zero

• Muscle contracts faster than it relaxes


Figure 9.14a The muscle twitch.

Latentperiod

Period ofcontraction

Period ofrelaxation

Per

cent

age

ofm

axim

um t

ensi

on

Singlestimulus

Time (ms)140120100806040200

Myogram showing the three phases of an isometric twitch


Muscle Twitch Comparisons

• Different strength and duration of twitches due to variations in metabolic properties and enzymes between muscles

• Muscle twitch only in lab or neuromuscular problems; normal muscle contraction smooth


Figure 9.14b The muscle twitch.

Latent period

Extraocular muscle (lateral rectus)

Gastrocnemius

Soleus

Per

cent

age

ofm

axim

um t

ensi

on

Singlestimulus

Comparison of the relative duration of twitch responses of three muscles

160 200Time (ms)

12080400


Graded Muscle Responses

• Graded muscle responses– Varying strength of contraction for different

demands

• Required for proper control of skeletal movement

• Responses graded by1.Changing frequency of stimulation

2.Changing strength of stimulation


Response to Change in Stimulus Frequency

• Single stimulus results in single contractile response—muscle twitch


Figure 9.15a A muscle's response to changes in stimulation frequency.

Single stimulus single twitch

Contraction Maximal tension of a single twitch

Relaxation

Stimulus

300200100Time (ms)

A single stimulus is delivered. The muscle contracts and relaxes.

Ten

sion

0



• Wave (temporal) summation– Increased stimulus frequency (muscle does

not completely relax between stimuli) second contraction of greater force

• Additional Ca2+ release with second stimulus stimulates more shortening

• Produces smooth, continuous contractions

• Further increase in stimulus frequency → unfused (incomplete) tetanus


Figure 9.15b A muscle's response to changes in stimulation frequency.

Low stimulation frequency

unfused (incomplete) tetanus

Partial relaxation

Time (ms)

If another stimulus is applied before the muscle relaxescompletely, then more tension results. This is wave (or

temporal) summation and results in unfused (or incomplete) tetanus.

Ten

sion

300200100

0 Stimuli



• If stimuli are given quickly enough, muscle reaches maximal tension fused (complete) tetany results– Smooth, sustained contraction– No muscle relaxation muscle fatigue

• Muscle cannot contract; zero tension


Figure 9.15c A muscle's response to changes in stimulation frequency.

High stimulation frequency

fused (complete) tetanus

Stimuli

At higher stimulus frequencies, there is no relaxation at allbetween stimuli. This is fused (complete) tetanus.

Ten

sion

Time (ms)

0

300200100


Response to Change in Stimulus Strength

• Recruitment (multiple motor unit summation) controls force of contraction

• Subthreshold stimuli – no observable contractions

• Threshold stimulus: stimulus strength causing first observable muscle contraction

• Maximal stimulus – strongest stimulus that increases contractile force



• Muscle contracts more vigorously as stimulus strength increases above threshold

• Contraction force precisely controlled by recruitment – activates more and more muscle fibers

• Beyond maximal stimulus no increase in force of contraction


Figure 9.16 Relationship between stimulus intensity (graph at top) and muscle tension (tracing below).

Stimulus strength

Sti

mul

us v

olta

ge

Threshold stimulus

Maximalstimulus

109

87654321

Proportion of motor units excited

Strength of muscle contraction

Maximal contraction

Time (ms)

Ten

sion

Stimuli to nerve



• Recruitment works on size principle– Motor units with smallest muscle fibers

recruited first – Motor units with larger and larger fibers

recruited as stimulus intensity increases– Largest motor units activated only for most

powerful contractions


Figure 9.17 The size principle of recruitment.

Skeletalmuscle

fibers

Ten

sion

Motorunit 1

recruited(smallfibers)

Motorunit 2

recruited(medium

fibers)

Motorunit 3

recruited(large

fibers)

Time


Isotonic Contractions

• Muscle changes in length and moves load– Thin filaments slide

• Isotonic contractions either concentric or eccentric:– Concentric contractions—muscle shortens

and does work– Eccentric contractions—muscle generates

force as it lengthens


Isometric Contractions

• Load greater than tension muscle can develop

• Tension increases to muscle's capacity, but muscle neither shortens nor lengthens– Cross bridges generate force but do not move

actin filaments


Muscle Tone

• Constant, slightly contracted state of all muscles

• Due to spinal reflexes – Groups of motor units alternately activated in

response to input from stretch receptors in muscles

• Keeps muscles firm, healthy, and ready to respond


Muscle Metabolism: Energy for Contraction

• ATP only source used directly for contractile activities– Move and detach cross bridges, calcium

pumps in SR, return of Na+ & K+ after excitation-contraction coupling

• Available stores of ATP depleted in 4–6 seconds


Muscle Metabolism: Energy for Contraction

• ATP regenerated by:– Direct phosphorylation of ADP by creatine

phosphate (CP) – Anaerobic pathway (glycolysis lactic acid) – Aerobic respiration


Figure 9.19a Pathways for regenerating ATP during muscle activity.

Direct phosphorylation

Coupled reaction of creatine Phosphate (CP) and ADP

Energy source: CP

Oxygen use: NoneProducts: 1 ATP per CP, creatine

Duration of energy provided:15 seconds

Creatinekinase

Creatine


Anaerobic Pathway

• Glycolysis – does not require oxygen– Glucose degraded to 2 pyruvic acid molecules

• Normally enter mitochondria aerobic respiration

• At 70% of maximum contractile activity– Bulging muscles compress blood vessels;

oxygen delivery impaired– Pyruvic acid converted to lactic acid


Anaerobic Pathway

• Lactic acid– Diffuses into bloodstream

– Used as fuel by liver, kidneys, and heart– Converted back into pyruvic acid or glucose

by liver– Anaerobic respiration yields only 5% as much

ATP as aerobic respiration, but produces ATP 2½ times faster


Figure 9.19b Pathways for regenerating ATP during muscle activity.

Anaerobic pathway

Glycolysis and lactic acid formation

Energy source: glucose

Glucose (fromglycogen breakdown ordelivered from blood)

Glycolysisin cytosol

Pyruvic acidnet gain

Releasedto blood

Lactic acid

Oxygen use: NoneProducts: 2 ATP per glucose, lactic acid

Duration of energy provided: 30-40 seconds, or slightly more

2


Aerobic Pathway

• Produces 95% of ATP during rest and light to moderate exercise; slow

• Series of chemical reactions that require oxygen; occur in mitochondria– Breaks glucose into CO2, H2O, and large

amount ATP

• Fuels - stored glycogen, then bloodborne glucose, pyruvic acid from glycolysis, and free fatty acids


Figure 9.19c Pathways for regenerating ATP during muscle activity.

Aerobic pathway

Aerobic cellular respiration

Energy source: glucose; pyruvic acid; freefatty acids from adipose tissue; amino

acids from protein catabolism

Glucose (fromglycogen breakdown ordelivered from blood)

Pyruvic acidFattyacids

Aminoacids

net gain perglucose

Oxygen use: RequiredProducts: 32 ATP per glucose, CO2, H2O

Duration of energy provided: Hours

Aerobic respirationin mitochondria

Aerobic respirationin mitochondria

32


Energy Systems Used During Sports

• Aerobic endurance– Length of time muscle contracts using aerobic

pathways

• Anaerobic threshold– Point at which muscle metabolism converts to

anaerobic


Figure 9.20 Comparison of energy sources used during short-duration exercise and prolonged-duration exercise.

Short-duration exercise

6 seconds

ATP stored inmuscles isused first.

10 seconds

ATP is formed fromcreatine phosphate

and ADP (directphosphorylation).

30–40 seconds

Glycogen stored in muscles is broken down to glucose,which is oxidized to generate ATP (anaerobic pathway).

End of exercise

Prolonged-duration exercise

Hours

ATP is generated by breakdownof several nutrient energy fuels by

aerobic pathway.


Muscle Fatigue

• Physiological inability to contract despite continued stimulation

• Occurs when– Ionic imbalances (K+, Ca2+, Pi) interfere with

E‑C coupling– Prolonged exercise may damage SR and

interferes with Ca2+ regulation and release

• Total lack of ATP occurs rarely, during states of continuous contraction, and causes contractures (continuous contractions)


Excess Postexercise Oxygen Consumption

• To return muscle to resting state– Oxygen reserves replenished

– Lactic acid converted to pyruvic acid– Glycogen stores replaced– ATP and creatine phosphate reserves

replenished

• All require extra oxygen; occur post exercise


Heat Production During Muscle Activity

• ~40% of energy released in muscle activity useful as work

• Remaining energy (60%) given off as heat

• Dangerous heat levels prevented by radiation of heat from skin and sweating

• Shivering - result of muscle contractions to generate heat when cold


Force of Muscle Contraction

• Force of contraction depends on number of cross bridges attached, which is affected by

• Number of muscle fibers stimulated (recruitment)

• Relative size of fibers—hypertrophy of cells increases strength

• Frequency of stimulation• Degree of muscle stretch


Force of Muscle Contraction

• As more muscle fibers are recruited (as more are stimulated) more force

• Relative size of fibers – bulkier muscles & hypertrophy of cells more force

• Frequency of stimulation - ↑ frequency time for transfer of tension to noncontractile components more force

• Length-tension relationship – muscle fibers at 80–120% normal resting length more force


Figure 9.21 Factors that increase the force of skeletal muscle contraction.

Largenumber of

musclefibers

recruited

Largemusclefibers

Highfrequency ofstimulation

(wavesummation

and tetanus)

Muscle andsarcomerestretched to

slightly over 100%of resting length

Contractile force (more cross bridges attached)


Velocity and Duration of Contraction

• Influenced by:– Muscle fiber type

– Load– Recruitment


Muscle Fiber Type

• Classified according to two characteristics– Speed of contraction: slow or fast fibers

according to• Speed at which myosin ATPases split ATP

• Pattern of electrical activity of motor neurons

– Metabolic pathways for ATP synthesis• Oxidative fibers—use aerobic pathways

• Glycolytic fibers—use anaerobic glycolysis


Muscle Fiber Type

• Three types – Slow oxidative fibers; Fast oxidative

fibers; Fast glycolytic fibers

• Most muscles contain mixture of fiber types range of contractile speed, fatigue resistance– All fibers in one motor unit same type– Genetics dictate individual's percentage of

each


Table 9.2 Structural and Functional Characteristics of the Three Types of Skeletal Muscle Fibers


Adaptations to Exercise

• Aerobic (endurance) exercise– Leads to increased

• Muscle capillaries

• Number of mitochondria

• Myoglobin synthesis

– Results in greater endurance, strength, and resistance to fatigue

– May convert fast glycolytic fibers into fast oxidative fibers


Effects of Resistance Exercise

• Resistance exercise (typically anaerobic) results in– Muscle hypertrophy

• Due primarily to increase in fiber size

– Increased mitochondria, myofilaments, glycogen stores, and connective tissue

Increased muscle strength and size


A Balanced Exercise Program

• Overload principle– Forcing muscle to work hard promotes

increased muscle strength and endurance– Muscles adapt to increased demands– Muscles must be overloaded to produce

further gains– Overuse injuries may result from lack of rest– Best programs alternate aerobic and

anaerobic activities


Homeostatic Imbalance

• Disuse atrophy– Result of immobilization

– Muscle strength declines 5% per day

• Without neural stimulation muscles atrophy to ¼ initial size– Fibrous connective tissue replaces lost

muscle tissue rehabilitation impossible


Smooth Muscle

• Found in walls of most hollow organs(except heart)

• Usually in two layers (longitudinal and circular)


Figure 9.25 Arrangement of smooth muscle in the walls of hollow organs.

Small intestineMucosa

Cross section of the intestine showing the smooth muscle layers (one circular and the other longitudinal) running at right angles to each other.

Circular layer of smooth muscle(shows longitudinal views of smoothmuscle fibers)

Longitudinal layer of smooth muscle (shows smooth musclefibers in cross section)


Microscopic Structure

• Spindle-shaped fibers - thin and short compared with skeletal muscle fibers; only one nucleus; no striations

• Lacks connective tissue sheaths; endomysium only

• SR - less developed than in skeletal muscle • Pouchlike infoldings (caveolae) of sarcolemma

sequester Ca2+ - most calcium influx from outside cell; rapid

• No sarcomeres, myofibrils, or T tubules


Microscopic Structure of Smooth Muscle Fibers

• Longitudinal layer– Fibers parallel to long axis of organ; contraction

dilates and shortened

• Circular layer– Fibers in circumference of organ; contraction

constricts lumen, elongates organ

• Allows peristalsis - Alternating contractions and relaxations of smooth muscle layers that mix and squeeze substances through lumen of hollow organs


Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (1 of 4)




Innervation of Smooth Muscle

• No NMJ as in skeletal muscle

• Autonomic nerve fibers innervate smooth muscle at diffuse junctions

• Varicosities (bulbous swellings) of nerve fibers store and release neurotransmitters into diffuse junctions


Figure 9.26 Innervation of smooth muscle.

Varicosities

Autonomicnerve fibersinnervatemost smoothmuscle fibers.

Smoothmusclecell

Synapticvesicles

Mitochondrion Varicosities releasetheir neurotransmittersinto a wide synaptic cleft (a diffuse junction).


Myofilaments in Smooth Muscle

• Ratio of thick to thin filaments (1:13) is much lower than in skeletal muscle (1:2)

• Thick filaments have heads along entire length

• No troponin complex; protein calmodulin binds Ca2+


Myofilaments in Smooth Muscle

• Myofilaments are spirally arranged, causing smooth muscle to contract in corkscrew manner

• Dense bodies– Proteins that anchor noncontractile

intermediate filaments to sarcolemma at regular intervals

– Correspond to Z discs of skeletal muscle


Intermediatefilament

Caveolae Gap junctions

Nucleus Dense bodies

Relaxed smooth muscle fiber (note that gap junctions connect adjacent fibers)

Figure 9.27a Intermediate filaments and dense bodies of smooth muscle fibers harness the pull generated by myosincross bridges.


NucleusDense bodies

Contracted smooth muscle fiber

Figure 9.27b Intermediate filaments and dense bodies of smooth muscle fibers harness the pull generated by myosincross bridges.


Contraction of Smooth Muscle

• Slow, synchronized contractions

• Cells electrically coupled by gap junctions– Action potentials transmitted from fiber to fiber

• Some cells self-excitatory (depolarize without external stimuli); act as pacemakers for sheets of muscle – Rate and intensity of contraction may be

modified by neural and chemical stimuli



• Actin and myosin interact by sliding filament mechanism

• Final trigger is ↑ intracellular Ca2+

– Ca2+ is obtained from the SR and extracellular space

• ATP energizes sliding process







• Slow to contract and relax but maintains for prolonged periods with little energy cost– Slow ATPases– Myofilaments may latch together to save

energy

• Relaxation requires– Ca2+ detachment from calmodulin; active

transport of Ca2+ into SR and ECF; dephosphorylation of myosin to reduce myosin ATPase activity


Regulation of Contraction

• By nerves, hormones, or local chemical changes

• Neural regulation– Neurotransmitter binding → ↑ [Ca2+] in

sarcoplasm; either graded (local) potential or action potential

– Response depends on neurotransmitter released and type of receptor molecules


Regulation of Contraction

• Hormones and local chemicals– Some smooth muscle cells have no nerve

supply• Depolarize spontaneously or in response to

chemical stimuli that bind to G protein–linked receptors

– Some respond to both neural and chemical stimuli

– Chemical factors include hormones, CO2, pH


Special Features of Smooth Muscle Contraction

• Stress-relaxation response – Responds to stretch only briefly, then adapts

to new length– Retains ability to contract on demand– Enables organs such as stomach and bladder

to temporarily store contents

• Length and tension changes– Can contract when between half and twice its

resting length


Special Features of Smooth Muscle Contraction

• Hyperplasia– Smooth muscle cells can divide and increase

numbers– Example

• Estrogen effects on uterus at puberty and during pregnancy




Types of Smooth Muscle

• Smooth muscle varies in different organs– Fiber arrangement and organization

– Innervation– Responsiveness to various stimuli

• Categorized as unitary and multi unit


Types of Smooth Muscle

• Unitary (visceral) smooth muscle– In all hollow organs except heart

– Arranged in opposing sheets– Innervated by varicosities – Often exhibit spontaneous action potentials– Electrically coupled by gap junctions– Respond to various chemical stimuli


Types of Smooth Muscle: Multiunit

• Multiunit smooth muscle– Located in large airways, large arteries,

arrector pili muscles, and iris of eye– Gap junctions; spontaneous depolarization

rare– Independent muscle fibers; innervated by

autonomic NS; graded contractions occur in response to neural stimuli

– Has motor units; responds to hormones


Developmental Aspects

• All muscle tissues develop from embryonic myoblasts

• Multinucleated skeletal muscle cells form by fusion

• Growth factor agrin stimulates clustering of ACh receptors at neuromuscular junctions

• Cardiac and smooth muscle myoblasts develop gap junctions



• ~ All muscle tissue develops from myoblasts• Cardiac and skeletal muscle become amitotic,

but can lengthen and thicken in growing child

• Myoblast-like skeletal muscle satellite cells have limited regenerative ability

• Cardiomyocytes can divide at modest rate, but injured heart muscle mostly replaced by connective tissue

• Smooth muscle regenerates throughout life



• Muscular development reflects neuromuscular coordination

• Development occurs head to toe, and proximal to distal

• Peak natural neural control occurs by midadolescence

• Athletics and training can improve neuromuscular control



• Female skeletal muscle makes up 36% of body mass

• Male skeletal muscle makes up 42% of body mass, primarily due to testosterone

• Body strength per unit muscle mass same in both sexes



• With age, connective tissue increases and muscle fibers decrease

• By age 30, loss of muscle mass (sarcopenia) begins

• Regular exercise reverses sarcopenia

• Atherosclerosis may block distal arteries, leading to intermittent claudication and severe pain in leg muscles


Muscular Dystrophy

• Group of inherited muscle-destroying diseases; generally appear in childhood

• Muscles enlarge due to fat and connective tissue deposits

• Muscle fibers atrophy and degenerate


Muscular Dystrophy

• Duchenne muscular dystrophy (DMD):– Most common and severe type

– Inherited, sex-linked, carried by females and expressed in males (1/3500) as lack of dystrophin

• Cytoplasmic protein that stabilizes sarcolemma• Fragile sarcolemma tears Ca2+ entry

damaged contractile fibers inflammatory cells muscle mass drops

– Victims become clumsy and fall frequently; usually die of respiratory failure in 20s


Muscular Dystrophy

– No cure– Prednisone improves muscle strength and

function

– Myoblast transfer therapy disappointing– Coaxing dystrophic muscles to produce more

utrophin (protein similar to dystrophin) successful in mice

– Viral gene therapy and infusion of stem cells with correct dystrophin genes show promise

Ch 09 Muslces and Muslce Tissue Gillette College

Science