1. © 2016 Pearson Education, Inc.

2. Table 9.3-1 Comparison of Skeletal, Cardiac, and Smooth Muscle
© 2016 Pearson Education, Inc.

3. Perimysium wrapping a fascicle
Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Epimysium
Epimysium
Bone
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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4. Epimysium Bone Tendon Blood vessel Perimysium wrapping a fascicle
Figure 9.1a Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Epimysium
Bone
Tendon
Blood vessel
Perimysium wrapping
a fascicle
Endomysium
(between individual
muscle fibers)
Muscle
fiber
Fascicle
Perimysium
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5. Table 9.1-1 Structure and Organizational Levels of Skeletal Muscle
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6. 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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7. Figure 9.2a Microscopic anatomy of a skeletal muscle fiber.
Photomicrograph of portions
of two isolated muscle
fibers (700×). Notice the
obvious striations (alternating
dark and light bands).
Nuclei
Dark A band
Light I band
Fiber
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8. 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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9. Figure 9.2de Microscopic anatomy of a skeletal muscle fiber.
Sarcomere
M line
Z disc
Z disc
Thin (actin)
filament
Enlargement of
one sarcomere
(sectioned
lengthwise). Notice
the myosin heads
on the thick
filaments.
Elastic
filaments
Thick
(myosin)
filament
Myosin
filament
Cross-sectional
view of a
sarcomere cut
through in different
locations.
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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10. Figure 9.3-2 Composition of thick and thin filaments.
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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11. Figure 9.3-3 Composition of thick and thin filaments.
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
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12. 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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13. Figure 9.6-1 Sliding filament model of contraction.
Fully relaxed sarcomere of a muscle fiber Z H Z l A l
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14. Figure 9.6-2 Sliding filament model of contraction.
Fully contracted sarcomere of a muscle fiber Z Z l A l
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15. 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 Focus
Figure 9.1).
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
Figure 9.8 and Focus
Figure 9.2).
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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16. Postsynaptic membrane ion channel opens; ions pass.
Focus Figure 9.1 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released.
Slide 6
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
Ca2+
Voltage-gated Ca2+
channels open. Ca2+ enters the axon terminal, moving down its electrochemical gradient. 2
Ca2+
Synaptic vesicle
containing ACh
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
Na+ K+
Postsynaptic membrane
ion channel opens;
ions pass.
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17. Postsynaptic membrane ion channel opens; ions pass.
Focus Figure 9.1 When a nerve impulse reaches a neuromuscular junction, acetylcholine (ACh) is released.
Slide 7
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
Ca2+
Voltage-gated Ca2+
channels open. Ca2+ enters the axon terminal, moving down its electrochemical gradient. 2
Ca2+
Synaptic vesicle
containing ACh
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
Na+ K+
Postsynaptic membrane
ion channel opens;
ions pass.
ACh effects are terminated by its breakdown in the synaptic cleft by acetylcholinesterase and diffusion away from the junction. 6
ACh
Degraded ACh
Ion channel closes;
ions cannot pass.
Na+
Acetylcholin-
esterase K+
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18. © 2016 Pearson Education, Inc.
Focus Figure 9.2 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 5
Steps in E-C Coupling:
Sarcolemma 1
Voltage-sensitive
tubule protein
T tubule
The action potential (AP) propagates along the sarcolemma and down the T tubules.
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 Ca release channels in the terminal cisterns of the sarcoplasmic reticulum (SR), allowing Ca to flow into the cytosol. 2+ 2
Terminal
cistern
of SR
Ca2+
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
Calcium binds to troponin and removes the blocking action of tropomyosin. When Ca binds, troponin changes shape, exposing binding sites for myosin (active sites) on the thin filaments. 2+ 3
Ca2+
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
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19. © 2016 Pearson Education, Inc.
Focus Figure 9.3 The cross bridge cycle is the series of events during which myosin heads pull thin filaments toward the center of the sarcomere.
Slide 5
Actin
Ca2+
Thin filament
Myosin
cross bridge
ADP Pi
Thick filament
Myosin
Cross bridge formation. Energized
myosin head attaches to an actin myofilament, forming a cross bridge. 1
ADP
ADP
ATP
hydrolysis Pi Pi
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.
ATP
ATP
*This cycle will continue as long as ATP is
available and Ca2+ is bound to troponin. If ATP is not available, the cycle stops between steps 2 and 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”). 3
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20. Clinical – Homeostatic Imbalance 9.2
Rigor mortis
3–4 hours after death, muscles begin to stiffen
Peak rigidity occurs about 12 hours postmortem
Intracellular calcium levels increase because ATP is no longer being synthesized, so calcium cannot be pumped back into SR
Results in cross bridge formation
ATP is also needed for cross bridge detachment
Results in myosin head staying bound to actin, causing constant state of contraction
Muscles stay contracted until muscle proteins break down, causing myosin to release
© 2016 Pearson Education, Inc.

21. Figure 9.22 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 running at
right angles to each other.
Circular layer of smooth muscle
(shows longitudinal views of smooth
muscle fibers)
© 2016 Pearson Education, Inc.

22. Figure 9.23 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).
© 2016 Pearson Education, Inc.

23. Figure 9.24a Intermediate filaments and dense bodies of smooth muscle fibers harness the pull generated by myosin cross bridges.
Intermediate
filaments
Gap junctions
Nucleus
Dense bodies
Relaxed smooth muscle fiber (note that gap junctions connect
adjacent fibers)
© 2016 Pearson Education, Inc.

24. Figure 9.24b Intermediate filaments and dense bodies of smooth muscle fibers harness the pull generated by myosin cross bridges.
Nucleus
Dense bodies
Contracted smooth muscle fiber
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25. Table 9.3-1 Comparison of Skeletal, Cardiac, and Smooth Muscle
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26. Table 9.3-2 Comparison of Skeletal, Cardiac, and Smooth Muscle (continued)
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27. Table 9.3-3 Comparison of Skeletal, Cardiac, and Smooth Muscle (continued)
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28. Table 9.3-4 Comparison of Skeletal, Cardiac, and Smooth Muscle (continued)
© 2016 Pearson Education, Inc.

29. Developmental Aspects of Muscle
All muscle tissues develop from embryonic myoblasts
Multinucleated skeletal muscle cells form by fusion of many myoblasts
Growth factor stimulates clustering of ACh receptors at neuromuscular junctions
Cardiac and smooth muscle myoblasts do not fuse, but develop gap junctions
Cardiac muscle cells start pumping when embryo is 3 weeks old
© 2016 Pearson Education, Inc.

30. Figure 9.26 Myoblasts fuse to form a multinucleate skeletal muscle fiber.
Embryonic
mesoderm cells
Myoblasts
Myotube
(immature
multinucleate
muscle fiber)
Satellite cell
Mature skeletal
muscle fiber
Embryonic mesoderm cells called myoblasts undergo cell division (to increase number) and enlarge. 1
Several myoblasts fuse together to form a myotube. 2
Myotube matures into skeletal muscle fiber. 3
© 2016 Pearson Education, Inc.

31. Developmental Aspects of Muscle
Regeneration of muscle:
Myoblast-like skeletal muscle satellite cells have limited regenerative ability
Cardiomyocytes can divide at modest rate, but injured heart muscle is mostly replaced by connective tissue
Smooth muscle regenerates throughout life
Cardiac and skeletal muscle can lengthen and thicken in growing child
In adults, leads to hypertrophy
© 2016 Pearson Education, Inc.

32. Developmental Aspects of Muscle
Muscular development in infants reflects neuromuscular coordination
Development occurs head to toe, and proximal to distal
A baby can lift its head before it is able to walk
Peak natural neural control occurs by midadolescence
Athletics and training can continue to improve neuromuscular control
© 2016 Pearson Education, Inc.

33. Developmental Aspects of Muscle
Difference in muscle mass between sexes:
Female skeletal muscle makes up 36% of body mass
Male skeletal muscle makes up 42% of body mass, primarily as a result of testosterone
Males have greater ability to enlarge muscle fibers, also because of testosterone
Body strength per unit muscle mass is the same in both sexes
© 2016 Pearson Education, Inc.

34. Developmental Aspects of Muscle
Aging muscles:
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 (limping) and severe pain in leg muscles
© 2016 Pearson Education, Inc.

35. Clinical – Homeostatic Imbalance 9.4
Muscular dystrophy: group of inherited muscle-destroying diseases
Generally appear in childhood
Muscles enlarge as a result of fat and connective tissue deposits, but then atrophy and degenerate
Duchenne muscular dystrophy (DMD) is the most common and severe type
Caused by defective gene for dystrophin
Inherited, sex-linked trait, carried by females and expressed in males (1/3600)
© 2016 Pearson Education, Inc.

36. Clinical – Homeostatic Imbalance 9.4
Dystrophin is a cytoplasmic protein that links the cytoskeleton to the extracellular matrix, stabilizing the sarcolemma
Fragile sarcolemma tears during contractions, causing entry of excess Ca2+
Leads to damaged contractile fibers
Inflammatory cells accumulate
Muscle mass declines
Victims become clumsy and fall frequently
Usually appears between ages 2 and 7
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37. Clinical – Homeostatic Imbalance 9.4
Currently no cure is known
Prednisone can improve muscle strength and function
Myoblast transfer therapy has been disappointing
Coaxing dystrophic muscles to produce more utrophin (protein similar to dystrophin) has been successful in mice
Viral gene therapy and infusion of stem cells with correct dystrophin genes show promise
Patients usually die of respiratory failure in their early 20s
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