1. Chapter Opener 9
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2. Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Bone
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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3. Bone Epimysium Tendon Blood vessel Fascicle Perimysium
Figure 9.1a Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Bone
Epimysium
Tendon
Blood vessel
Perimysium
wrapping a fascicle
Endomysium
(between individual
muscle fibers)
Muscle
fiber
Fascicle
Perimysium
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4. Epimysium Perimysium Endomysium
Figure 9.1b Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Epimysium
Perimysium
Endomysium
Muscle fiber
in middle of
a fascicle
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5. Figure 9.2 Microscopic anatomy of a skeletal muscle fiber.
Photomicrograph of portions
of two isolated muscle
fibers (700x). Notice the
obvious striations (alternating
dark and light bands).
Nuclei
Dark A band
Light I band
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
Light I band
Nucleus
Thin (actin)
filament
Z disc
H zone
Z disc
Small part of one
myofibril enlarged to
show the myofilaments
responsible for the
banding pattern. Each
sarcomere extends from
one Z disc to the next.
Thick (myosin)
filament
I band
A band
I band
M line
Sarcomere
Z disc
M line
Z disc
Enlargement of one
sarcomere (sectioned
lengthwise). Notice the
myosin heads on the
thick filaments.
Thin (actin)
filament
Elastic (titin)
filaments
Thick
(myosin)
filament
Cross-sectional view of a
sarcomere cut through in
different locations.
Myosin
filament
Actin
filament
I band
thin filaments
only
H zone
thick filaments
only
M line
thick filaments linked
by accessory proteins
Outer edge of A band
thick and thin
filaments overlap
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7. B C E A D F

8. Figure 9.2a Microscopic anatomy of a skeletal muscle fiber.
Photomicrograph of portions of two
isolated muscle
fibers (700x). Notice
the obvious striations (alternating dark and
light bands).
Nuclei
Dark A band
Light I band
Fiber
© 2013 Pearson Education, Inc.

9. 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
Light
I band
Nucleus
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10. Figure 9.2c Microscopic anatomy of a skeletal muscle fiber.
Thin (actin)
filament
Z disc
H zone
Z disc
Small part of one
myofibril
enlarged to show
the myofilaments
responsible for the
banding pattern.
Each sarcomere
extends from one Z
disc to the next.
Thick
(myosin)
filament
I band
A band
I band
M line
Sarcomere
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11. Figure 9.2d Microscopic anatomy of a skeletal muscle fiber.
Sarcomere
Thin
(actin)
filament
Z disc
M line
Z disc
Enlargement of
one sarcomere (sectioned length-
wise). Notice the
myosin heads on
the thick filaments.
Elastic
(titin)
filaments
Thick
(myosin)
filament
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12. Figure 9.2e Microscopic anatomy of a skeletal muscle fiber.
Cross-sectional
view of a sarcomere
cut through in different
locations.
Myosin
filament
Actin
filament
I band
thin filaments
only
H zone
thick filaments
only
M line
thick filaments
linked by access-
ory proteins
Outer edge
of A band
thick and thin
filaments overlap
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13. 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 oppositeends of the filament.
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 thick filament
Portion of a thin filament
Myosin head
Tropomyosin
Troponin
Actin
Actin-binding sites
Heads
Tail
ATP-
binding
site
Active sites
for myosin
attachment
Actin subunits
Flexible hinge region
Myosin molecule
Actin subunits
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14. Figure 9.3 Composition of thick and thin filaments. (1 of 3)
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.
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15. Figure 9.3 Composition of thick and thin filaments. (2 of 3)
Thick 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
Actin-binding sites
Heads
Tail
ATP-
binding
site
Flexible hinge region
Myosin molecule
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16. Figure 9.3 Composition of thick and thin filaments. (3 of 3)
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
Active sites
for myosin
attachment
Actin subunits
Actin subunits
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17. Table 9.1 Structure and Organizational Levels of Skeletal Muscle (1 of 3)
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18. Table 9.1 Structure and Organizational Levels of Skeletal Muscle (2 of 3)
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19. Table 9.1 Structure and Organizational Levels of Skeletal Muscle (3 of 3)
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20. Thick filament (myosin)
Figure 9.4 Myosin heads forming cross bridges that generate muscular contractile force.
Thin filament (actin)
Myosin heads
Thick filament (myosin)
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21. Part of a skeletal muscle fiber (cell) I band A band I band Z disc
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
A band
I band
Z disc
H zone
Z disc M
line
Sarcolemma
Myofibril
Triad:
• T tubule
• Terminal
cisterns of
the SR (2)
Sarcolemma
Tubules of
the SR
Myofibrils
Mitochondria
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22. Figure 9.6 Sliding filament model of contraction.1
Fully relaxed sarcomere of a muscle fiber Z H Z I A I 2
Fully contracted sarcomere of a muscle fiber Z Z I A I
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23. Figure 9.6 Sliding filament model of contraction. (1 of 2)
Fully relaxed sarcomere of a muscle fiber Z H Z I A I
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24. Figure 9.6 Sliding filament model of contraction. (2 of 2)
Fully contracted sarcomere of a muscle fiber Z Z I A I
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25. 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).
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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26. Figure 9.7 The phases leading to muscle fiber contraction. (1 of 2)
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
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27. Figure 9.7 The phases leading to muscle fiber contraction. (2 of 2)
AP travels across the entire sarcolemma
AP travels along T tubules
Phase 2:
Excitation-contraction
coupling occurs (see
Figures 9.9 and 9.11).
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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28. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released.
Myelinated axon
of motor neuron
Action
potential (AP)
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
Action potential arrives at axon
terminal of motor neuron. 1
Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient.
Synaptic vesicle
containing ACh 2
Axon terminal
of motor neuron
Synaptic
cleft
Fusing synaptic
vesicles
Ca2+ entry causes ACh (a
neurotransmitter) to be released
by exocytosis. 3
ACh
Junctional
folds of
sarcolemma
ACh diffuses across the synaptic cleft and binds to its receptors on
the sarcolemma. 4
Sarcoplasm of
muscle fiber
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. 5
Postsynaptic
membrane
ion channel opens;
ions pass.
Degraded ACh
ACh
Ion channel closes;
ions cannot pass.
ACh effects are terminated by
its breakdown in the synaptic
cleft by acetylcholinesterase and
diffusion away from the junction. 6
Acetylcho-
linesterase…
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29. Myelinated axon of motor neuron
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. (1 of 3)
Myelinated axon
of motor neuron
Action
potential (AP)
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
Action potential arrives at axon
terminal of motor neuron. 1
Synaptic vesicle
containing ACh
Voltage-gated Ca2+ channels open. Ca2+ enters the axon terminal moving down its electochemical gradient. 2
Axon terminal
of motor neuron
Synaptic
cleft
Fusing synaptic
vesicles
Ca2+ entry causes ACh (a
neurotransmitter) to be released
by exocytosis. 3
ACh
Junctional
folds of
sarcolemma
ACh diffuses across the synaptic cleft and binds to its receptors on
the sarcolemma. 4
Sarcoplasm of
muscle fiber
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30. Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. (1 of 3)
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31. channels in the receptors that allow simultaneous passage of
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. (2 of 3)
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. 5
Postsynaptic membrane
ion channel opens;
ions pass.
© 2013 Pearson Education, Inc.

32. Acetylcholinesterase
Figure 9.8 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released. (3 of 3)
ACh effects are terminated by
its breakdown in the synaptic
cleft by acetylcholinesterase and
diffusion away from the junction. 6
ACh
Degraded ACh
Acetylcholinesterase
Ion channel closes;
ions cannot pass.
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33. Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber.
Open Na+
channel
Closed K+
channel
Na+
− − − − − − − −
− − − − −
− − − − − −
ACh-containing
synaptic vesicle
− − − − K+
Axon terminal of
neuromuscular
junction
Action potential
Ca2+
Ca2+
Synaptic
cleft
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. 2
Wave of
depolarization
Closed Na+
channel
Open K+
channel
An end plate potential is generated at the
neuromuscular junction (see Figure 9.8). 1
Na+  
− − − − − − − −
− − − −
− − − −− − − − − − K+
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. 3
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34. ACh-containing synaptic vesicle 1
Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber. (1 of 3)
ACh-containing
synaptic vesicle
Axon terminal of
neuromuscular
junction
Ca2+
Ca2+
Synaptic
cleft
Wave of
depolarization
An end plate potential is generated at the
neuromuscular junction (see Figure 9.8). 1
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35. − − − − − − − − − − − − − − − − − − − + + + + + + + + + + + +
Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber. (2 of 3)
Open Na+
channel
Closed K+
channel
Na+
− − − − − − − −
− − − − −
− − − − − − 
− − − − K+
Action potential
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. 2
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36. + + + + + + + + + + + + + + + + + + + + + + − − − − − − − − − − − −
Figure 9.9 Summary of events in the generation and propagation of an action potential in a skeletal muscle fiber. (3 of 3)
Closed Na+
channel
Open K+
channel
Na+
+ +
− − − − − − − −
− − − −
− − − − − − − − − − K+ 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.
© 2013 Pearson Education, Inc.

37. Membrane potential (mV)
Figure 9.10 Action potential tracing indicates changes in Na+ and K+ ion channels.
+30
Na+ channels
close, K+ channels
open
Depolarization
due to Na+ entry
Membrane potential (mV)
Repolarization
due to K+ exit
Na+
channels
open
K+ channels
closed
–95 5 10 15 20
Time (ms)
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38. 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:
Sarcolemma
Voltage-sensitive
tubule protein
T tubule
The action potential (AP) propagates along the sarcolemma and down the
T tubules. 1
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.
Ca2+
release
channel
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. 2
Terminal
cistern
of SR
Synaptic
cleft
Axon terminal of
motor neuron at NMJ
Action potential
is generated
ACh
Sarcolemma
Actin
T tubule
Troponin
Tropomyosin
blocking active sites
Terminal
cistern
of SR
Myosin
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. 3
Muscle fiber
Triad
Active sites exposed and
ready for myosin binding
One sarcomere
Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. 4
Myosin
cross
bridge
One myofibril
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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39. The events at the neuromuscular junction (NMJ)
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. (1 of 4)
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
Axon terminal of
motor neuron at NMJ
Action
potential is
generated
ACh
Sarcolemma
T tubule
Terminal
cistern
of SR
Muscle fiber
Triad
One sarcomere
One myofibril
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40. 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. (2 of 4)
Steps in E-C Coupling:
Sarcolemma
The action potential (AP) propagates along the sarcolemma and down the
T tubules. 1
Voltage-sensitive
tubule protein
T tubule
Ca2+
release
channel
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. 2
Terminal
cistern
of SR
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
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. 3
Active sites exposed and
ready for myosin binding
Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. 4
Myosin
cross
bridge
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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41. The action potential (AP) propagates along the sarcolemma and down the
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. (3 of 4)
Steps in E-C Coupling:
Sarcolemma
The action potential (AP) propagates along the sarcolemma and down the
T tubules. 1
Voltage-sensitive
tubule protein
T tubule
Ca2+
release
channel 2
Calcium ions are released.
Terminal
cistern
of SR
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42. The aftermath Actin Troponin Tropomyosin blocking active sites Myosin
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. (4 of 4)
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
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. 3
Active sites exposed and
ready for myosin binding
Contraction begins: Myosin binding to actin forms cross bridges and contraction (cross bridge cycling) begins. At this point, E-C coupling is over. 4
Myosin
cross
bridge
The aftermath
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43. 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
Thick
filament
Myosin
Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming
a cross bridge. 1
ATP
hydrolysis
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.* 4
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. 2
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 detachment. After ATP attaches to myosin, the link between myosin and actin weakens, and the myosin head detaches (the cross bridge “breaks”). 3
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44. Actin Thin filament Myosin
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. (1 of 4)
Actin
Thin filament
Myosin
cross bridge
Thick
filament
Myosin
Cross bridge formation. Energized myosin head attaches to an actin myofilament, forming a cross bridge. 1
© 2013 Pearson Education, Inc.

45. 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. (2 of 4)
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. 2
© 2013 Pearson Education, Inc.

46. 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. (3 of 4)
Cross bridge detachment. After ATP attaches to myosin, the link between myosin and actin weakens, and the myosin head detaches (the cross bridge “breaks”). 3
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47. 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. (4 of 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.* 4
*This cycle will continue as long
as ATP is available and Ca2+ is
bound to troponin.
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48. Figure 9.13 A motor unit consists of one motor neuron and all the muscle fibers it innervates.
Spinal cord
Axon terminals at
neuromuscular junctions
Branching axon
to motor unit
Motor
unit 1
Motor
unit 2
Nerve
Motor neuron
cell body
Motor neuron
axon
Muscle
Muscle
fibers
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.
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49. neuromuscular junctions
Figure 9.13a A motor unit consists of one motor neuron and all the muscle fibers it innervates.
Spinal cord
Axon terminals at
neuromuscular junctions
Motor
unit 1
Motor
unit 2
Nerve
Motor neuron
cell body
Motor
neuron
axon
Muscle
Muscle
fibers
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.
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50. neuromuscular junctions
Figure 9.13b A motor unit consists of one motor neuron and all the muscle fibers it innervates.
Branching axon
to motor unit
Axon terminals at
neuromuscular junctions
Muscle
fibers
Branching axon terminals form
neuromuscular junctions, one
per muscle fiber (photomicro-
graph 330x).
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51. Figure 9.14 The muscle twitch.
Latent
period
Period of
contraction
Period of
relaxation
maximum tension
Percentage of 20 40 60 80
100
120
140
Time (ms)
Single
stimulus
Myogram showing the three phases of an isometric twitch
Latent period
Extraocular muscle (lateral rectus)
Gastrocnemius
Soleus
maximum tension
Percentage of 40 80
120
160
200
Time (ms)
Single
stimulus
Comparison of the relative duration of twitch responses of
three muscles
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52. Figure 9.14a The muscle twitch.
Latent
period
Period of
contraction
Period of
relaxation
maximum tension
Percentage of 20 40 60 80
100
120
140
Time (ms)
Single
stimulus
Myogram showing the three phases of an isometric twitch
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53. Figure 9.14b The muscle twitch.
Latent period
Extraocular muscle (lateral rectus)
Gastrocnemius
Soleus
maximum tension
Percentage of 40 80
120
160
200
Time (ms)
Single
stimulus
Comparison of the relative duration of twitch responses of
three muscles
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54. Figure 9.15 A muscle’s response to changes in stimulation frequency.
Single stimulus single twitch
Tension
Contraction
Maximal tension of a single twitch
Relaxation
Stimulus
100
200
300
Time (ms)
A single stimulus is delivered. The muscle contracts and relaxes.
Low stimulation
frequency
unfused (incomplete)
tetanus
Tension
Partial relaxation
Stimuli
100
200
300
Time (ms)
If another stimulus is applied before the muscle relaxes
completely, then more tension results. This is wave (or
temporal) summation and results in unfused (or
incomplete) tetanus.
High stimulation
frequency
fused (complete)
tetanus
Tension
Stimuli
100
200
300
Time (ms)
At higher stimulus frequencies, there is no relaxation at all
between stimuli. This is fused (complete) tetanus.
© 2013 Pearson Education, Inc.

55. Figure 9.15a A muscle’s response to changes in stimulation frequency.
Single stimulus single twitch
Tension
Contraction
Maximal tension of a single twitch
Relaxation
Stimulus
100
200
300
Time (ms)
A single stimulus is delivered. The muscle contracts and relaxes.
© 2013 Pearson Education, Inc.

56. Figure 9.15b A muscle’s response to changes in stimulation frequency.
Low stimulation
frequency
unfused (incomplete)
tetanus
Partial relaxation
Tension
Stimuli
100
200
300
Time (ms)
If another stimulus is applied before the muscle relaxes
completely, then more tension results. This is wave (or
temporal) summation and results in unfused (or incomplete) tetanus.
© 2013 Pearson Education, Inc.

57. Figure 9.15c A muscle’s response to changes in stimulation frequency.
High stimulation
frequency
fused (complete)
tetanus
Tension
Stimuli
100
200
300
Time (ms)
At higher stimulus frequencies, there is no relaxation at all
between stimuli. This is fused (complete) tetanus.
© 2013 Pearson Education, Inc.

58. Threshold stimulus 1 2 3 4 5 6 7 8 9 10 Maximal contraction
Figure Relationship between stimulus intensity (graph at top) and muscle tension (tracing below).
Stimulus strength
Maximal
stimulus
Stimulus voltage
Threshold stimulus 1 2 3 4 5 6 7 8 9 10
Stimuli to nerve
Proportion of motor units excited
Strength of muscle contraction
Maximal contraction
Tension
Time (ms)
© 2013 Pearson Education, Inc.

59. Figure 9.17 The size principle of recruitment.
Skeletal
muscle
fibers
Tension
Time
Motor
unit 1
recruited
(small
fibers)
Motor
unit 2
recruited
(medium
fibers)
Motor
unit 3
recruited
(large
fibers)
© 2013 Pearson Education, Inc.

60. Figure 9.18 Isotonic (concentric) and isometric contractions.
Isotonic contraction (concentric)
Isometric contraction
On stimulation, muscle develops enough tension (force)
to lift the load (weight). Once the resistance is overcome,
the muscle shortens, and the tension remains constant for
the rest of the contraction.
Muscle is attached to a weight that exceeds the muscle’s
peak tension-developing capabilities. When stimulated, the
tension increases to the muscle’s peak tension-developing
capability, but the muscle does not shorten.
Tendon
Muscle
contracts
(isotonic
contraction)
Muscle
contracts
(isometric
contraction)
3 kg
Tendon
6 kg
6 kg
3 kg 8
Amount of
resistance 8
Muscle
relaxes
Amount of resistance 6
Tension developed
(kg)
Tension developed
(kg) 6
Muscle
relaxes 4
Peak tension
developed 4 2 2
Peak tension
developed
Muscle
stimulus
Muscle
stimulus
100
Resting length
Resting length
100 90
Muscle length (percent
of resting length)
Muscle length (percent
of resting length) 90 80 80 70 70
Time (ms)
Time (ms)
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61. Isotonic contraction (concentric)
Figure 9.18a Isotonic (concentric) and isometric contractions. (1 of 2)
Isotonic contraction (concentric)
On stimulation, muscle develops enough tension (force)
to lift the load (weight). Once the resistance is overcome,
the muscle shortens, and the tension remains constant for
the rest of the contraction.
Tendon
Muscle
contracts
(isotonic
contraction)
3 kg
Tendon
3 kg
© 2013 Pearson Education, Inc.

62. Isotonic contraction (concentric)
Figure 9.18a Isotonic (concentric) and isometric contractions. (2 of 2)
Isotonic contraction (concentric) 8
Amount of
resistance
Muscle
relaxes 6
Tension developed
(kg) 4
Peak tension
developed 2
Muscle
stimulus
Resting length
100 90
Muscle length (percent
of resting length) 80 70
Time (ms)
© 2013 Pearson Education, Inc.

63. Isometric contraction
Figure 9.18b Isotonic (concentric) and isometric contractions. (1 of 2)
Isometric contraction
Muscle is attached to a weight that exceeds the muscle’s
peak tension-developing capabilities. When stimulated, the
tension increases to the muscle’s peak tension-developing
capability, but the muscle does not shorten.
Muscle
contracts
(isometric
contraction)
6 kg
6 kg
© 2013 Pearson Education, Inc.

64. Isometric contraction
Figure 9.18b Isotonic (concentric) and isometric contractions. (2 of 2)
Isometric contraction 8
Amount of resistance 6
Tension developed
(kg)
Muscle
relaxes 4
Peak tension
developed 2
Muscle
stimulus
Resting length
100 90
Muscle length (percent
of resting length) 80 70
Time (ms)
© 2013 Pearson Education, Inc.

65. Figure 9.19 Pathways for regenerating ATP during muscle activity.
Direct phosphorylation
Anaerobic pathway
Aerobic pathway
Coupled reaction of creatine
Phosphate (CP) and ADP
Glycolysis and lactic acid formation
Aerobic cellular respiration
Energy source: CP
Energy source: glucose
Energy source: glucose; pyruvic acid; free
fatty acids from adipose tissue; amino
acids from protein catabolism
Glucose (from
glycogen breakdown or
delivered from blood)
Glucose (from
glycogen breakdown or
delivered from blood)
Creatine
kinase
Glycolysis
in cytosol
Pyruvic acid
Creatine
Fatty
acids 2
Aerobic respiration
in mitochondria
Aerobic respiration
in mitochondria
Amino
acids
Pyruvic acid
net gain 32
Released
to blood
Lactic acid
net gain per
glucose
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration of energy provided:
15 seconds
Oxygen use: None
Products: 2 ATP per glucose, lactic acid
Duration of energy provided: 30-40
seconds, or slightly more
Oxygen use: Required
Products: 32 ATP per glucose, CO2, H2O
Duration of energy provided: Hours
© 2013 Pearson Education, Inc.

66. Figure 9.19a Pathways for regenerating ATP during muscle activity.
Direct phosphorylation
Coupled reaction of creatine
Phosphate (CP) and ADP
Energy source: CP
Creatine
kinase
Creatine
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration of energy provided:
15 seconds
© 2013 Pearson Education, Inc.

67. Figure 9.19b Pathways for regenerating ATP during muscle activity.
Anaerobic pathway
Glycolysis and lactic acid formation
Energy source: glucose
Glucose (from
glycogen breakdown or
delivered from blood)
Glycolysis
in cytosol 2
Pyruvic acid
net gain
Released
to blood
Lactic acid
Oxygen use: None
Products: 2 ATP per glucose, lactic acid
Duration of energy provided: 30-40
seconds, or slightly more
© 2013 Pearson Education, Inc.

68. Figure 9.19c Pathways for regenerating ATP during muscle activity.
Aerobic pathway
Aerobic cellular respiration
Energy source: glucose; pyruvic acid; free
fatty acids from adipose tissue; amino
acids from protein catabolism
Glucose (from
glycogen breakdown or
delivered from blood)
Pyruvic acid
Fatty
acids
Aerobic respiration
in mitochondria
Aerobic respiration
in mitochondria
Amino
acids 32
net gain per
glucose
Oxygen use: Required
Products: 32 ATP per glucose, CO2, H2O
Duration of energy provided: Hours
© 2013 Pearson Education, Inc.

69. Figure Comparison of energy sources used during short-duration exercise and prolonged-duration exercise.
Short-duration exercise
Prolonged-duration exercise
6 seconds
10 seconds
30–40 seconds
End of exercise
Hours
ATP stored in
muscles is
used first.
ATP is formed from
creatine phosphate
and ADP (direct
phosphorylation).
Glycogen stored in muscles is broken down to glucose,
which is oxidized to generate ATP (anaerobic pathway).
ATP is generated by breakdown
of several nutrient energy fuels by
aerobic pathway.
© 2013 Pearson Education, Inc.

70. Short-duration exercise
Figure Comparison of energy sources used during short-duration exercise and prolonged-duration exercise. (1 of 2)
Short-duration exercise
6 seconds
10 seconds
30–40 seconds
End of exercise
ATP stored in
muscles is
used first.
ATP is formed
from creatine phosphate and
ADP (direct
phosphorylation).
Glycogen stored in muscles is broken
down to glucose, which is oxidized to
generate ATP (anaerobic pathway).
© 2013 Pearson Education, Inc.

71. Prolonged-duration exercise
Figure Comparison of energy sources used during short-duration exercise and prolonged-duration exercise. (2 of 2)
Prolonged-duration exercise
Hours
ATP is generated by breakdown
of several nutrient energy fuels by
aerobic pathway.
© 2013 Pearson Education, Inc.

72. Contractile force (more cross bridges attached)
Figure Factors that increase the force of skeletal muscle contraction.
High
frequency of
stimulation
(wave
summation
and tetanus)
Large
number of
muscle
fibers
recruited
Muscle and
sarcomere
stretched to
slightly over 100%
of resting length
Large
muscle
fibers
Contractile force (more cross bridges attached)
© 2013 Pearson Education, Inc.

73. Sarcomeres excessively stretched
Figure Length-tension relationships of sarcomeres in skeletal muscles.
Sarcomeres
greatly
shortened
Sarcomeres at
resting length
Sarcomeres excessively
stretched
75%
100%
170%
100
Tension (percent of maximum)
Optimal sarcomere
operating length
(80%–120% of
resting length) 50 60 80
100
120
140
160
180
Percent of resting sarcomere length
© 2013 Pearson Education, Inc.

74. Predominance of fast glycolytic (fatigable) fibers Small load
Figure Factors influencing velocity and duration of skeletal muscle contraction.
Predominance
of fast glycolytic
(fatigable) fibers
Small load
Predominance
of slow oxidative
(fatigue-resistant)
fibers
Contractile
velocity
Contractile
duration
© 2013 Pearson Education, Inc.

75. Table 9.2 Structural and Functional Characteristics of the Three Types of Skeletal Muscle Fibers
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76. Velocity of shortening
Figure Influence of load on duration and velocity of muscle contraction.
Light load
Distance shortened
Velocity of shortening
Intermediate load
Heavy load 20 40 60 80
100
120
Time (ms)
Increasing load
Stimulus
The greater the load, the less the muscle shortens
and the shorter the duration of contraction
The greater the load, the
slower the contraction
© 2013 Pearson Education, Inc.

77. Light load Intermediate load Heavy load 20 40 60 80 100 120 Stimulus
Figure 9.24a Influence of load on duration and velocity of muscle contraction.
Light load
Distance shortened
Intermediate load
Heavy load 20 40 60 80
100
120
Time (ms)
Stimulus
The greater the load, the less the muscle shortens
and the shorter the duration of contraction
© 2013 Pearson Education, Inc.

78. Velocity of shortening
Figure 9.24b Influence of load on duration and velocity of muscle contraction.
Velocity of shortening
Increasing load
The greater the load, the
slower the contraction
© 2013 Pearson Education, Inc.

79. Figure 9.25 Arrangement of smooth muscle in the walls of hollow organs.
Longitudinal layer of smooth
muscle (shows smooth muscle
fibers in cross section)
Small intestine
Mucosa
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 smooth
muscle fibers)
© 2013 Pearson Education, Inc.

80. Figure 9.25a Arrangement of smooth muscle in the walls of hollow organs.
Small intestine
© 2013 Pearson Education, Inc.

81. Small intestine Mucosa
Figure 9.25b Arrangement of smooth muscle in the walls of hollow organs.
Longitudinal layer of smooth
muscle (shows smooth muscle
fibers in cross section)
Small intestine
Mucosa
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 smooth
muscle fibers)
© 2013 Pearson Education, Inc.

82. Figure 9.26 Innervation of smooth muscle.
Varicosities
Autonomic
nerve fibers
innervate
most smooth
muscle fibers.
Smooth
muscle
cell
Synaptic
vesicles
Mitochondrion
Varicosities release
their neurotransmitters
into a wide synaptic
cleft (a diffuse junction).
© 2013 Pearson Education, Inc.

83. Contracted smooth muscle fiber
Figure Intermediate filaments and dense bodies of smooth muscle fibers harness the pull generated by myosin cross bridges.
Intermediate
filament
Caveolae
Gap junctions
Nucleus
Dense bodies
Relaxed smooth muscle fiber (note that gap junctions connect
adjacent fibers)
Nucleus
Dense bodies
Contracted smooth muscle fiber
© 2013 Pearson Education, Inc.

84. Caveolae Gap junctions Nucleus Dense bodies
Figure 9.27a Intermediate filaments and dense bodies of smooth muscle fibers harness the pull generated by myosin cross bridges.
Intermediate
filament
Caveolae
Gap junctions
Nucleus
Dense bodies
Relaxed smooth muscle fiber (note that gap junctions connect
adjacent fibers)
© 2013 Pearson Education, Inc.

85. Contracted smooth muscle fiber
Figure 9.27b Intermediate filaments and dense bodies of smooth muscle fibers harness the pull generated by myosin cross bridges.
Nucleus
Dense bodies
Contracted smooth muscle fiber
© 2013 Pearson Education, Inc.

86. Extracellular fluid (ECF)
Figure Sequence of events in excitation-contraction coupling of smooth muscle.
Extracellular fluid (ECF)
Ca2+
Plasma membrane
Cytoplasm
Calcium ions (Ca2+)
enter the cytosol from
the ECF via voltage-
dependent or voltage-
independent Ca2+
channels, or from
the scant SR. 1
Ca2+
Ca2+ binds to and
activates calmodulin.
Sarcoplasmic
reticulum 2
Ca2+
Inactive calmodulin
Activated calmodulin
Activated calmodulin
activates the myosin
light chain kinase
enzymes. 3
Inactive kinase
Activated kinase
The activated kinase
enzymes catalyze transfer
of phosphate to myosin,
activating the myosin
ATPases. 4
Inactive myosin
molecule
Activated (phosphory-
lated) myosin molecule
Activated myosin forms
cross bridges with actin of the
thin filaments. Shortening
begins. 5
Thin
filament
Thick
filament
© 2013 Pearson Education, Inc.

87. Extracellular fluid (ECF)
Figure Sequence of events in excitation-contraction coupling of smooth muscle. (1 of 5)
Extracellular fluid (ECF)
Plasma membrane
Cytoplasm
Calcium ions (Ca2+)
enter the cytosol from
the ECF via voltage-
dependent or voltage-
independent Ca2+
channels, or from
the scant SR. 1
Sarcoplasmic
reticulum
© 2013 Pearson Education, Inc.

88. Ca2+ Inactive calmodulin Activated calmodulin
Figure Sequence of events in excitation-contraction coupling of smooth muscle. (2 of 5)
Ca2+ binds to and
activates calmodulin. 2
Ca2+
Inactive calmodulin
Activated calmodulin
© 2013 Pearson Education, Inc.

89. Inactive kinase Activated kinase
Figure Sequence of events in excitation-contraction coupling of smooth muscle. (3 of 5)
Activated calmodulin
activates the myosin
light chain kinase
enzymes. 3
Inactive kinase
Activated kinase
© 2013 Pearson Education, Inc.

90. The activated kinase enzymes catalyze transfer of phosphate
Figure Sequence of events in excitation-contraction coupling of smooth muscle. (4 of 5)
The activated kinase enzymes
catalyze transfer of phosphate
to myosin, activating the myosin
ATPases. 4
Inactive
myosin molecule
Activated (phosphorylated)
myosin molecule
© 2013 Pearson Education, Inc.

91. Activated myosin forms cross bridges with actin of the thin
Figure Sequence of events in excitation-contraction coupling of smooth muscle. (5 of 5)
Activated myosin forms cross
bridges with actin of the thin
filaments. Shortening begins. 5
Thin
filament
Thick
filament
© 2013 Pearson Education, Inc.

92. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (1 of 4)
© 2013 Pearson Education, Inc.

93. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (2 of 4)
© 2013 Pearson Education, Inc.

94. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (3 of 4)
© 2013 Pearson Education, Inc.

95. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (4 of 4)
© 2013 Pearson Education, Inc.

96. Myotube (immature multinucleate muscle fiber) Embryonic mesoderm cells
Figure Myoblasts fuse to form a multinucleate skeletal muscle fiber.
Myotube
(immature
multinucleate
muscle fiber)
Embryonic
mesoderm cells
Myoblasts
Satellite
cell
Mature
skeletal
muscle
fiber
Embryonic
mesoderm cells
called myoblasts
undergo cell div-
ision (to increase
number) and
enlarge. 1
Several
myoblasts fuse
together to form
a myotube. 2
Myotube
matures into
skeletal muscle
fiber. 3
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97. Closer Look 9.1
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98. System Connections 9.1
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