Muscular Histology and Physiology. Human Anatomy and Physiology, 7e by Elaine Marieb & Katja Hoehn...

Muscular Histology and Physiology

Human Anatomy and Physiology, 7eby Elaine Marieb & Katja Hoehn

Copyright © 2007 Pearson Education, Inc.,publishing as Benjamin Cummings.

Photomicrograph of the capillary network surrounding skeletal muscle fibers



Microscopic anatomy of a skeletal muscle fiber

Nuclei Fiber

NucleusLightI band

DarkA band

Sarcolemma

Mitochondrion

H zone(b)

Myofibril

(a)

(c)

Thin (actin) filament

Thick (myosin) filament

Z disc Z disc



Composition of thick and thin filaments

(b)

(c)

(d)

(e)

(a)

Heads

Flexible hinge region

Tail

Myosin head

Troponin complex Tropomyosin Actin

Thin filamentThick filament

Thin filament (actin) Thick filament (myosin)Myosin heads

Myosin molecule

Portion of a thick filament

Portion of a thin filament

Longitudinal section of filaments within one sarcomere of a myofibril

Transmission electron micrograph of part of a sarcomere



Microscopic anatomy of a skeletal muscle fiber

I band

Z disc Z disc

I bandA band

H zone

(c)

(d)

(e)




Elastic (titin) filaments

Z disc Z disc

M line

M line

Sarcomere


I bandthin filaments

only

H zonethick filaments

only

M linethick filaments linkedby accessory proteins

Outer edge of A band

thick and thinfilaments overlap



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

MyofibrilMyofibrils

Triad

Tubules of sarcoplasmic reticulum

Sarcolemma

Sarcolemma

Mitochondrion

I band I bandA band

H zone Z discZ disc

Part of a skeletal muscle fiber (cell)

T tubule

Terminal cisternaof the sarcoplasmic reticulum

Mline



Sliding filament model of contraction

A

Z Z

II A

Z Z

A

Z Z

H

1

2

3



Connective tissue sheaths of skeletal muscle

(b)

(a)

Bone

PerimysiumEndomysiumBlood

vessel

Muscle fiber(cell)

Fascicle(wrapped byperimysium)

Endomysium(betweenfibers)

Epimysium

Tendon

Epimysium

Muscle fiberin middle of a fascicle

Perimysium

Blood vessel

Endomysium

Figure 4.30



The neuromuscular junction

(a)

(b) (c)

Axon terminal ofa motor neuron

Junctionalfolds of thesarcolemmaat motor endplate

Part of amyofibril

Mitochondrion

Synaptic cleft

T tubule

Binding of Achto receptor opensNa+/K+ channel

Acetylcholinesterase

Synapticcleft

ACh molecules

Fusing synapticvesicle

Synapticvesicle Acetic acid

Choline

Axon terminal

Actionpotential Axon terminal at

neuromuscular junction

Sarcolemmaof themuscle fiber

Nucleus

Na+K+

Myelinated axonof motor neuron

Ca2+



(a)

Actionpotential

Axon terminal atneuromuscular junction

Sarcolemmaof themuscle fiber

Nucleus

Myelinated axonof motor neuron

Figure 9.7a: The neuromuscular junction, p. 290.




(b)

Axon terminal ofa motor neuron

Junctionalfolds of thesarcolemmaat motor endplate

Part of amyofibril

Mitochondrion

Synaptic cleft

T tubule

Synapticvesicle

Ca2+

Muscle Contraction Physiology



(c)

Binding of Achto receptor opensNa+/K+ channel

Acetylcholinesterase

Synapticcleft

ACh molecules

Fusing synapticvesicle

Acetic acid

Choline

Axon terminal

Na+K+




An action potential in a skeletal muscle fiber

(b)

(c)

(d)

(a)

(b) Step 1: Depolarization and generation of the action potential.Production of an end plate potential at the motor end plate causes adjacent areas of the sarcolemma to become permeable to sodium (voltage-gated sodium channels open). As sodium ions diffuse rapidly into the cell, the resting potential is decreased (i.e., depolarization occurs). If the stimulus is strong enough, an action potential is initiated.

(c) Step 2: Propagation of the action potential.The positive charge inside the initial patch of sarcolemma changes the permeability of an adjacent patch, opening voltage-gated Na+ channels there. Consequently the membrane potential in that region decreases and depolarization occurs there as well. Thus, the action potential travels rapidly over the entire sarcolemma.

(d) Step 3: Repolarization.Immediately after the depolarization wave passes, the sarcolemma's permeability changes once again: Na+ channels close and K+ channels open, allowing K+ to diffuse from the cell. This restores the electrical conditions of the resting (polarized) state. Repolarization occurs in the same direction as depolarization, and must occur before the muscle fiber can be stimulated again. The ionic concentrations of the resting state are restored later by the sodium-potassium pump

(a) Electrical conditions of a resting (polarized) sarcolemma.The outside face is positive, while the inside face is negative. The predominant extracellular ion is sodium (Na+); the predominant intracellular ion is potassium (K+). The sarcolemma is relatively impermeable to both ions.

Na+

Stimulus

[Na+] [K+]

K+

[K+] [Na+]



0 1 2 3 4

–70

–55

0

+30

Time (ms)

Na+ channelsclose

Action potential

K+ channelsopen

Na+

channelsopen Threshold

Action potential scan showing changing sarcolemma permeability to Na+ and K+ ions

Mem

bra

ne

po

ten

tial

(m

V)

Rel

ativ

e m

emb

ran

e p

erm

eab

ilit

y



Excitation-contraction coupling

ADP

Pi

Net entry of Na+ initiatesan action potential which is propagated along thesarcolemma and downthe T tubules.

T tubuleSarcolemma

SR tubules (cut)

SynapticcleftSynaptic

vesicle

Axon terminal

ACh ACh ACh

Neurotransmitter released diffuses across the synaptic cleft and attaches to ACh

Action potentialin T tubule activatesvoltage-sensitive receptors, which in turn trigger Ca2+

release from terminalcisternae of SRinto cytosol.

Calcium ions bind to troponin;troponin changes shape, removingthe blocking action of tropomyosin;actin active sites exposed.

Contraction; myosin heads alternately attach toactin and detach, pulling the actin filaments towardthe center of the sarcomere; release of energy byATP hydrolysis powers the cycling process.

Removal of Ca2+ by active transportinto the SR after the actionpotential ends.

SR

Tropomyosin blockagerestored, blocking myosinbinding sites onactin; contraction ends and muscle fiber relaxes.

Ca2+

Ca2+

Ca2+

Ca2+

Ca2+Ca2+

Ca2+

Ca2+

Ca2+

Ca2+

1

2

6

5

4

3



Role of ionic calcium in the contraction mechanism

(a) (b) (c) (d)

Actin

Actin

Tnl

TnT

Tropomyosin

Myosinbindingsites

Troponincomplex

TnC

Myosinhead

Myosinbindingsite

Additionalcalciumionsbind

Additionalcalciumionsbindto TnC

Myosinhead

Actin

Overview

Troponin

TropomyosinMyosinhead

Plane of (a) Plane of (d)

+ Ca2+



The cross bridge cycle

ATP

ADP

ADPATPhydrolysis

ADP

ATP

Pi

Pi

Myosin head(high-energyconfiguration)

Myosin head attaches to the actinmyofilament, forming a cross bridge.

Thin filament

As ATP is split into ADP and Pi, the myosinhead is energized (cocked into the high-energyconformation).

Inorganic phosphate (Pi) generated in theprevious contraction cycle is released, initiatingthe power (working) stroke. The myosin headpivots and bends as it pulls on the actin filament,sliding it toward the M line. Then ADP is released.

Myosin head(low-energyconfiguration)

Thick filament

As new ATP attaches to the myosin head, the link betweenMyosin and actin weakens, and the cross bridge detaches.

1

2

3

4



, p. 296.

(b)(a)

Spinal cord

Motor neuroncell body

Muscle

Branching axonto motor unit

Muscle fibers

Nerve

Motorunit 1

Motorunit 2

Musclefibers

Motor neuronaxon

Axon terminals atneuromuscular junctions



The muscle twitch

Latentperiod

Period ofcontraction

Period ofrelaxation

Per

cen

tag

e o

fm

axim

um

ten

sio

n

Time (ms)

0 200

(a)

40 60 80 100 120 140Singlestimulus

Latent period

Extraocular muscle (lateral rectus)

GastrocnemiusSoleus

Per

cen

tag

e o

fm

axim

um

ten

sio

n

Time (ms)

0 400 80 120 160 200Singlestimulus(b)



Methods of regenerating ATP during muscle activity

Creatine

Energy source: CP

Oxygen use: NoneProducts: 1 ATP per CP, creatineDuration of energy provision: 15s

(a) Direct phosphorylation [coupled reaction of creatine phosphate (CP) and ADP]

(b) Anaerobic mechanism (glycolysis and lactic acid formation)

(c) Aerobic mechanism (aerobic cellular respiration)

Energy source: glucose

Oxygen use: NoneProducts: 2 ATP per glucose, lactic acidDuration of energy provision: 30–60 s.

Energy source: glucose; pyruvic acid; free fatty acids from adipose tissue; amino acids from protein catabolism

Oxygen use: RequiredProducts: 38 ATP per glucose, CO2, H2ODuration of energy provision: Hours

O2

O2

ATP ATP

net gain

Glucose (fromglycogen breakdown ordelivered from blood)

Pyruvic acid

Glycolysisin cytosol

Glucose (fromglycogen breakdown ordelivered from blood)

Pyruvic acid

2

ATP

net gain per glucose

38Lactic acidReleased

to blood

O2

H2O

O2

Fattyacids

Aminoacids

CP ADP

Aerobic respirationin mitochondria

CO2



Factors influencing force, velocity, and duration of skeletal muscle contraction

(a) (b) (c)Increasedcontractileforce

Large numberof musclefibers activated

Largemusclefibers

Asynchronoustetaniccontractions

Muscle andsarcomerelength slightlyover 100% ofresting length

Predominanceof fast glycolytic(fatigable) fibers

Predominanceof slow oxidative(fatigue-resistant)fibers

Small load

Increasedcontractilevelocity

Increasedcontractileduration



Influence of load on contraction velocity and duration

(a)

Time (ms)

60

Dis

tan

ce s

ho

rten

ed

0 20 40 80 100 120

Single actionpotential initiated (b)

Increasing load

0

Vel

oci

ty o

f sh

ort

enin

g

Intermediate load

Light load

Heavy load



Innervation of smooth muscle

Smooth muscle cell

Mucosa

Varicosities

Autonomic nervefiber

Varicosity

Synaptic vesicles

Mitochondrion

Submucosa

Serosa

Muscularisexterna



Sequence of events in excitation-contraction coupling of smooth muscle

ATP

Pi

Pi

Pi

Pi

ADP

Calcium ions (Ca2+) enterthe cytosol from the ECFor from the scant SR.

Ca2+ binds to andactivates calmodulin.

Ca2+

Ca2+

Ca2+Sarcoplasmic reticulum

Plasma membrane

Activated calmodulin activatesthe myosin light chain kinaseenzymes.

Inactivecalmodulin

Activatedcalmodulin

Inactivekinase

Activatedkinase

Extracellular fluid

Cytoplasm

The activated kinase enzyme catalyzes transfer of phosphate to myosin heads, activating themyosin head ATPases.

Phosphorylated myosin heads form cross bridges with actin of the thin filaments and shorteningoccurs.

Inactive myosinmolecule

Activated(phosphorylated)myosin molecule

Thin myofilament

Thick filament

Cross bridge activity ends when phosphate is removed from the myosin heads by phosphorylase enzymes and intracellular Ca2+ levels fall.

1

2

3

4

5

6

Muscular Histology and Physiology. Human Anatomy and Physiology, 7e by Elaine Marieb & Katja Hoehn...

Documents

Transcript of Muscular Histology and Physiology. Human Anatomy and Physiology, 7e by Elaine Marieb & Katja Hoehn...