© 2013 Pearson Education, Inc. Muscle Tissue Nearly half of body's mass Transforms chemical energy...

© 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



• Cardiac muscle– Only in heart; bulk of heart walls – Striated– Can contract without nervous system

stimulation – Involuntary



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


Special Characteristics of Muscle Tissue

• Excitability (responsiveness or irritability): 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

Myofibril

NucleusLight I band

Dark A band


Striations

• H zone: lighter region in midsection of dark A band where filaments do not overlap

• M line: line of protein myomesin bisects H zone• Z disc (line): coin-shaped sheet of proteins on

midline of light I band that anchors thin filaments and connects myofibrils to one another

• Thick filaments: run entire length of an A band• Thin filaments: run length of I band and

partway into A band• Sarcomere: region between two successive Z

discs


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


Myofibril Banding Pattern

• Orderly arrangement of actin and myosin myofilaments within sarcomere– Actin myofilaments = thin filaments

• Extend across I band and partway in A band• Anchored to Z discs

– Myosin myofilaments = thick filaments• Extend length of A band• Connected at M line


Ultrastructure of Thick Filament

• Composed of protein myosin

• Each composed of 2 heavy and four light polypeptide chains– Myosin tails contain 2 interwoven, heavy

polypeptide chains– Myosin heads contain 2 smaller, light

polypeptide chains that act as cross bridges during contraction

• Binding sites for actin of thin filaments• Binding sites for ATP• ATPase enzymes


Ultrastructure of Thin Filament

• Twisted double strand of fibrous protein F actin

• F actin consists of G (globular) actin subunits

• G actin bears active sites for myosin head attachment during contraction

• Tropomyosin and troponin - regulatory proteins bound to actin


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 of

regulatory 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.


Structure of Myofibril

• Elastic filament– Holds thick filaments in place; helps recoil

after stretch; resists excessive stretching

• Dystrophin– Links thin filaments to proteins of sarcolemma

• Nebulin, myomesin, C proteins bind filaments or sarcomeres together; maintain alignment


Sarcoplasmic Reticulum (SR)

• Network of smooth endoplasmic reticulum surrounding each myofibril– Most run longitudinally

• Pairs of terminal cisternae form perpendicular cross channels

• Functions in regulation of intracellular Ca2+ levels– Stores and releases Ca2+


T Tubules

• Continuations of sarcolemma

• Lumen continuous with extracellular space

• Increase muscle fiber's surface area

• Penetrate cell's interior at each A band–I band junction

• Associate with paired terminal cisterns to form triads that encircle each sarcomere


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


Triad Relationships

• T tubules conduct impulses deep into muscle fiber; every sarcomere

• Integral proteins protrude into intermembrane space from T tubule and SR cistern membranes–act as voltage sensors

• SR foot proteins: gated channels that regulate Ca2+ release from SR cisterns


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 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


Physiology of Skeletal Muscle Fibers

• For skeletal muscle to contract– Activation (at neuromuscular

junction)• Must be nervous system stimulation• Must generate action potential in

sarcolemma

– Excitation-contraction coupling• Action potential propagated along

sarcolemma• Intracellular Ca2+ levels must rise briefly


Phase 1Motor neuronstimulatesmuscle fiber(see Figure 9.8).

Phase 2:Excitation-contraction coupling occurs (see Figures 9.9 and 9.11).

Action potential (AP) arrives at axonterminal at neuromuscular junction

ACh released; binds to receptorson sarcolemma

Ion permeability of sarcolemma changes

Local change in membrane voltage(depolarization) occurs

Local depolarization (end platepotential) ignites AP in sarcolemma

AP travels across the entire sarcolemma

AP travels along T tubules

SR releases Ca2+; Ca2+ binds totroponin; myosin-binding sites(active sites) on actin exposed

Myosin heads bind to actin;contraction begins

Figure 9.7 The phases leading to muscle fiber contraction.


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 2

Synaptic vesiclecontaining ACh

Synaptic cleft

Axon terminalof motor neuron

Fusing synaptic vesiclesa

ACh Junctionalfolds of sarcolemma

Sarcoplasm ofmuscle fiber

Action potential arrives at axon terminal of motor neuron.1




Synaptic cleft





Action potential arrives at axon terminal of motor neuron.

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

1

2




Synaptic cleft







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

1

2

3




Synaptic cleft







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

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

1

2

3

4



Postsynaptic membraneion channel opens;ions pass.

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



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

6

Degraded AChACh

Acetylcholinesterase

Ion channel closes;ions cannot pass.


Neuromuscular Junction (NMJ)

• Situated midway along length of muscle fiber• Axon terminal and muscle fiber separated by

gel-filled space called synaptic cleft• Synaptic vesicles of axon terminal contain

neurotransmitter acetylcholine (ACh)• Junctional folds of sarcolemma contain ACh

receptors • NMJ includes axon terminals, synaptic cleft,

junctional folds


A&P Flix™: Events at the Neuromuscular Junction

Events at the Neuromuscular Junction

• Nerve impulse arrives at axon terminal ACh released into synaptic cleft

• ACh diffuses across cleft and binds with receptors on sarcolemma

• Electrical events generation of action potential

PLAYPLAY


Destruction of Acetylcholine

• ACh effects quickly terminated by enzyme acetylcholinesterase in synaptic cleft – Breaks down ACh to acetic acid and choline– Prevents continued muscle fiber contraction in

absence of additional stimulation


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 6

Myosin

Tropomyosinblocking active sites

Actin

Troponin

The aftermath



Slide 7

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.

Active sites exposed and ready for myosin binding

Myosin


Actin

Troponin

The aftermath

3



Slide 8


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

Myosincross bridge


Myosin


Actin

Troponin

The aftermath

3

4



A&P Flix™: Excitation-contraction coupling.

PLAYPLAY

Slide 9

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:

Terminal cisternof SR

Ca2+

releasechannel

Voltage-sensitivetubule protein

T tubule

Sarcolemma


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


Myosin


Actin

Troponin

2

1

3

4


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 6

A&P Flix™: The Cross Bridge Cycle

PLAYPLAY

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


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

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