Download Chap 9 Muscle Physiology

CHAPTER
9
Muscles and
Muscle
Physiology
Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (1 of 4)
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Special Characteristics of Muscle Tissue
• Excitability:
• Contractility:
• Extensibility:
• Elasticity:
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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"
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Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Bone
Epimysium
Epimysium
Perimysium
Tendon
Endomysium
Muscle fiber
in middle of
a fascicle
Blood vessel
Perimysium
wrapping a fascicle
Endomysium
(between individual
muscle fibers)
Muscle
fiber
Fascicle
Perimysium
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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
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Table 9.1 Structure and Organizational Levels of Skeletal Muscle (1 of 3)
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Table 9.1 Structure and Organizational Levels of Skeletal Muscle (2 of 3)
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Figure 9.2b Microscopic anatomy of a skeletal muscle fiber.
Diagram of part
of a muscle
fiber showing
the myofibrils.
One myofibril
extends from the
cut end of the
fiber.
Sarcolemma
Mitochondrion
Myofibril
Dark
A band
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Light Nucleus
I band
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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
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Figure 9.2c Microscopic anatomy of a skeletal muscle fiber.
Thin (actin)
filament
Small part of one
myofibril
enlarged to show
the myofilaments
responsible for the
banding pattern.
Thick
Each sarcomere
extends from one Z (myosin)
filament
disc to the next.
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Z disc
I band
H zone
Z disc
I band
A band
Sarcomere
M line
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Striations
• H zone:
• M line:
• Z disc (line):
• Thick filaments:
• Thin filaments:
• Sarcomere:
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Figure 9.2c Microscopic anatomy of a skeletal muscle fiber.
Thin (actin)
filament
Small part of one
myofibril
enlarged to show
the myofilaments
responsible for the
banding pattern.
Thick
Each sarcomere
extends from one Z (myosin)
filament
disc to the next.
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Z disc
I band
H zone
Z disc
I band
A band
Sarcomere
M line
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Figure 9.2d Microscopic anatomy of a skeletal muscle fiber.
Z disc
Enlargement of
one sarcomere
(sectioned lengthwise). Notice the
myosin heads on
the thick filaments.
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Sarcomere
M line
Z disc
Thin
(actin)
filament
Elastic
(titin)
filaments
Thick
(myosin)
filament
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Figure 9.3 Composition of thick and thin filaments.
Longitudinal section of filaments within one
sarcomere of a myofibril
Thick filament
Thin filament
In the center of the sarcomere, the thick filaments
lack myosin heads. Myosin heads are present only
in areas of myosin-actin overlap.
Thick filament.
Thin filament
Each thick filament consists of many myosin
molecules whose heads protrude at opposite ends
of the filament.
Portion of a thick filament
Myosin head
A thin filament consists of two strands of actin
subunits twisted into a helix plus two types of
regulatory proteins (troponin and tropomyosin).
Portion of a thin filament
Tropomyosin
Troponin Actin
Actin-binding sites
Heads
ATPbinding
site Flexible hinge region
Myosin molecule
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Tail
Active sites
for myosin
attachment
Actin subunits
Actin subunits
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Figure 9.5 Relationship of the sarcoplasmic reticulum and T tubules to myofibrils of skeletal muscle.
Part of a skeletal
muscle fiber (cell)
I band
Z disc
Myofibril
A band
H zone
M
line
I band
Z disc
Sarcolemma
Triad:
• T tubule
• Terminal
cisterns of
the SR (2)
Sarcolemma
Tubules of
the SR
Myofibrils
Mitochondria
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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
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Sliding Filament Model of Contraction
• 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
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Figure 9.6 Sliding filament model of contraction.
Slide 1
1 Fully relaxed sarcomere of a muscle fiber
H
A
Z
I
Z
I
2 Fully contracted sarcomere of a muscle fiber
Z
Z
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I
A
I
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Sliding Filament Model of Contraction
• 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)
• Review Sliding Filament Theory on IP
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Figure 9.6 Sliding filament model of contraction.
Slide 4
1 Fully relaxed sarcomere of a muscle fiber
H
A
Z
I
Z
I
2 Fully contracted sarcomere of a muscle fiber
Z
Z
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I
A
I
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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
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Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released.
Slide 1
Myelinated axon
of motor neuron
Action
potential (AP)
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
1 Action potential arrives at axon
terminal of motor neuron.
2 Voltage-gated Ca2+ channels
open. Ca2+ enters the axon terminal
moving down its electochemical
gradient.
Synaptic vesicle
containing ACh
Axon terminal
of motor neuron
Fusing synaptic
vesicles
3 Ca2+ entry causes ACh (a
neurotransmitter) to be released
by exocytosis.
ACh
4 ACh diffuses across the synaptic
cleft and binds to its receptors on
the sarcolemma.
5 ACh binding opens ion
channels in the receptors that
allow simultaneous passage of
Na+ into the muscle fiber and K+
out of the muscle fiber. More Na+
ions enter than K+ ions exit,
which produces a local change
in the membrane potential called
the end plate potential.
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6 ACh effects are terminated by
its breakdown in the synaptic
cleft by acetylcholinesterase and
diffusionMDufilho
away from the junction.
Synaptic
cleft
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
Postsynaptic
membrane
ion channel opens;
ions pass.
ACh
Acetylcholinesterase
Degraded ACh
Ion channel closes;
ions cannot pass.
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Figure 9.7 The phases leading to muscle fiber contraction.
Action potential (AP) arrives at axon
terminal at neuromuscular junction
ACh released; binds to receptors
on sarcolemma
Phase 1
Motor neuron
stimulates
muscle fiber
(see Figure 9.8).
Ion permeability of sarcolemma changes
Local change in membrane voltage
(depolarization) occurs
Local depolarization (end plate
potential) ignites AP in sarcolemma
AP travels across the entire sarcolemma
AP travels along T tubules
Phase 2:
Excitation-contraction
coupling occurs (see
Figures 9.9 and 9.11).
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SR releases Ca2+; Ca2+ binds to
troponin; myosin-binding sites
(active sites) on actin exposed
Myosin heads bind to actin;
contraction begins
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Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal
muscle fiber.
Open Na+
Closed K+
channel
Slide 1
channel
Na+
ACh-containing
synaptic vesicle
Ca2+
Ca2+


++++++++
++++
++++ 
K+
Axon terminal of
neuromuscular
junction
Synaptic
cleft
 ++++
Action potential
2 Depolarization: Generating and propagating an action
potential (AP). The local depolarization current spreads to adjacent
areas of the sarcolemma. This opens voltage-gated sodium channels
there, so Na+ enters following its electrochemical gradient and initiates
the AP. The AP is propagated as its local depolarization wave spreads to
adjacent areas of the sarcolemma, opening voltage-gated channels there.
Again Na+ diffuses into the cell following its electrochemical gradient.
Wave of
depolarization
Closed Na+
channel
1 An end plate potential is generated at the
neuromuscular junction (see Figure 9.8).
Open K+
channel
Na+
++++ ++++
++++


++++ ++++++
 
K+
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3 Repolarization: Restoring the sarcolemma to its initial
polarized state (negative inside, positive outside). Repolarization
occurs as Na+ channels close (inactivate) and voltage-gated K+ channels
open. Because K+ concentration is substantially higher inside the cell
than in the extracellular fluid, K+ diffuses rapidly out of the muscle fiber.25
Membrane potential (mV)
Figure 9.10 Action potential tracing indicates changes in Na+ and K+ ion channels.
+30
0
Na+ channels
close, K+ channels
open
Depolarization
due to Na+ entry
Repolarization
due to K+ exit
Na+
channels
open
K+ channels
closed
–95
0
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10
Time (ms)
15
20
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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
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Figure 9.11 Excitation-contraction (E-C) coupling is the sequence of events by which transmission of an
action potential along the sarcolemma leads to the sliding of myofilaments.
Slide 2
Setting the stage
The 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.
Axon terminal of
motor neuron at NMJ
Action potential is
generated
Synaptic
cleft
ACh
Muscle
fiber
Sarcolemma
T tubule
Terminal
cistern
of SR
Triad
One sarcomere
One myofibril
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Figure 9.11 Excitation-contraction (E-C) coupling is the sequence of events by which transmission of an
action potential along the sarcolemma leads to the sliding of myofilaments.
Slide 9
Steps in E-C Coupling:
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
2 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.
Ca2+
release
channel
PLAY
Terminal
cistern
of SR
A&P Flix™:
Excitationcontraction
coupling.
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
Active sites exposed and
ready for myosin binding
Myosin
cross
bridge
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1 The action potential (AP)
propagates along the
sarcolemma and down the
T tubules.
3 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.
4 Contraction begins:
Myosin binding to actin
forms cross bridges and
contraction (cross bridge
cycling) begins. At this
point, E-C coupling is over.
The aftermath
When 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
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E-C coupling is repeated.
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Figure 9.11 Excitation-contraction (E-C) coupling is the sequence of events by which transmission of an action
potential along the sarcolemma leads to the sliding of myofilaments.
Steps in E-C Coupling:
Voltage-sensitive
tubule protein
Setting the stage
The 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.
Synaptic
cleft
Sarcolemma
T tubule
1 The action potential (AP)
propagates along the
sarcolemma and down the
T tubules.
Ca2+
release
channel
2
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.
Terminal
cistern
of SR
Axon terminal of
motor neuron at NMJ
Action potential
is generated
ACh
Actin
Sarcolemma
Troponin
T tubule
Terminal
cistern
of SR
Muscle fiber
Tropomyosin
blocking active sites
Myosin
Triad
Active sites exposed and
ready for myosin binding
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.
4
One sarcomere
One myofibril
3
Myosin
cross
bridge
Contraction begins:
Myosin binding to actin forms
cross bridges and contraction
(cross bridge cycling) begins. At
this point, E-C coupling is over.
The aftermath
When 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.
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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
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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
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Figure 9.12 The cross bridge cycle is the series of events during which myosin heads pull thin filaments
toward the center of the sarcomere.
Actin
Ca2+ Thin filament
Myosin
cross bridge
PLAY
A&P Flix™: The
Cross Bridge
Cycle
Slide 6
Thick
filament
Myosin
1 Cross bridge formation.
Energized myosin head attaches
to an actin myofilament, forming
a cross bridge.
ATP
hydrolysis
4 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. *
*This cycle will continue as long
as ATP is available and Ca2+ is
bound to troponin.
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2 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.
In the absence
of ATP, myosin
heads will not
detach, causing
rigor mortis.
3 Cross bridge detachment. After ATP
attaches to myosin, the link between myosin
and actin weakens, and the myosin head
detaches (the cross bridge “breaks”).
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Role of Calcium (Ca2+) in Contraction
• At low intracellular Ca2+ concentration?
-
• At high intracellular Ca2+ concentration?
-
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ATP is needed ……
• To re-establish RMP at sarcolemma and
synaptic knob
• For detachment and “re-cocking” of
myosin heads
• For sarcoplasmic reticulum to reabsorb
Ca++ ( by ATP dependant calcium pump)
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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
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What if??????
• Ach were not removed from synaptic cleft.
• Little or no ATP could be produced
• The CNS sends volleys of high frequency
impulses to various muscles
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