1. 9
Muscles and Muscle Tissue: Part A

2. Nearly half of body's mass
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
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3. Types of Muscle Tissue Skeletal muscles
Elongated cells called muscle fibers
Striated (striped)
Voluntary (i.e., conscious control)
Contract rapidly; tire easily; powerful
Require nervous system stimulation
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4. Types of Muscle Tissue Cardiac muscle Only in heart Striated
Can contract without nervous system stimulation
Involuntary
More details in Chapter 18
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5. Types of Muscle Tissue Smooth muscle
In walls of hollow organs, e.g., stomach, urinary bladder, and airways
Not striated
Can contract without nervous system stimulation
Involuntary
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6. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (1 of 4)
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7. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (2 of 4)
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8. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (3 of 4)
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9. Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle (4 of 4)
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10. Special Characteristics of Muscle Tissue
Excitability (responsiveness): 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
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11. Four important functions
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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12. 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
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13. Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
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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14. 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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15. Microscopic Anatomy of a Skeletal Muscle Fiber
Long, cylindrical cell
Multiple peripheral nuclei
Sarcolemma = plasma membrane
Sarcoplasm = cytoplasm
Glycosomes for glycogen storage, myoglobin for O2 storage
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16. Sarcolemma Mitochondrion Dark A band Light I band Nucleus
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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17. Smallest contractile unit (functional unit) of muscle fiber
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
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18. Z disc H zone Z disc I band A band I band M line Sarcomere
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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19. 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
Myosin myofilaments = thick filaments
Extend length of A band
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20. Ultrastructure of Thin Filament
Tropomyosin and troponin - regulatory proteins bound to actin
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21. Portion of a thick filament Portion of a thin filament
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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22. Sarcoplasmic Reticulum (SR)
Network of smooth endoplasmic reticulum surrounding each myofibril
Functions in regulation of intracellular Ca2+ levels
Stores and releases Ca2+
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23. 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
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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24. 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)
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25. 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
PLAY
A&P Flix™: Events at the Neuromuscular Junction
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26. 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
© 2013 Pearson Education, Inc.

27. Figure 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 1
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.
© 2013 Pearson Education, Inc.

28. The events at the neuromuscular junction (NMJ)
Figure 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.
Synaptic
cleft
Axon terminal of
motor neuron at NMJ
Action poten-
tial is
generated
ACh
Sarcolemma
T tubule
Terminal
cistern
of SR
Muscle
fiber
Triad
One sarcomere
One myofibril
© 2013 Pearson Education, Inc.

29. Figure 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 3
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.
© 2013 Pearson Education, Inc.

30. The action potential (AP) propagates along the sarcolemma and down the
Figure 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 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
Terminal
cistern
of SR
© 2013 Pearson Education, Inc.

31. The action potential (AP) propagates along the sarcolemma and down the
Figure 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
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
© 2013 Pearson Education, Inc. 31

32. The aftermath Actin Troponin Tropomyosin blocking active sites Myosin
Figure 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 6
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
The aftermath
© 2013 Pearson Education, Inc.

33. The aftermath Actin Troponin Tropomyosin blocking active sites Myosin
Figure 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 7
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
The aftermath
© 2013 Pearson Education, Inc.

34. The aftermath Actin Troponin Tropomyosin blocking active sites Myosin
Figure 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 8
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
© 2013 Pearson Education, Inc.

35. A&P Flix™: Excitation-contraction coupling.
Figure 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:
Sarcolemma
The action potential (AP) propagates along the sarcolemma and down the
T tubules. 1
Voltage-sensitive
tubule protein
T tubule
PLAY
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
A&P Flix™: Excitation-contraction coupling.
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.
© 2013 Pearson Education, Inc.

36. Figure 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 10
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.
© 2013 Pearson Education, Inc. 36

37. 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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