Three Types of Muscle Tissue
1. Skeletal muscle tissue:
•
Attached to bones and skin
•
Striated
•
Voluntary (i.e., conscious control)
•
Powerful
•
Primary topic of this chapter
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Three Types of Muscle Tissue
2. Cardiac muscle tissue:
•
Only in the heart
•
Striated
•
Involuntary
•
More details in Chapter 18
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Three Types of Muscle Tissue
3. Smooth muscle tissue:
•
In the walls of hollow organs, e.g., stomach,
urinary bladder, and airways
•
Not striated
•
Involuntary
•
More details later in this chapter
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Copyright © 2010 Pearson Education, Inc.
Table 9.3
Special Characteristics of Muscle Tissue
• Excitability (responsiveness or irritability):
ability to receive and respond to stimuli
• Contractility: ability to shorten when
stimulated
• Extensibility: ability to be stretched
• Elasticity: ability to recoil to resting length
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Muscle Functions
1. Movement of bones or fluids (e.g., blood)
2. Maintaining posture and body position
3. Stabilizing joints
4. Heat generation (especially skeletal muscle)
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Skeletal Muscle
• Each muscle is served by one artery, one
nerve, and one or more veins
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Skeletal Muscle
• Connective tissue sheaths of skeletal muscle:
• Epimysium: dense regular connective tissue
surrounding entire muscle
• Perimysium: fibrous connective tissue surrounding
fascicles (groups of muscle fibers)
• Endomysium: fine areolar connective tissue
surrounding each muscle fiber
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Epimysium
Bone Epimysium
Perimysium
Endomysium
Tendon
(b)
Perimysium Fascicle
(a)
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Muscle fiber
in middle of
a fascicle
Blood vessel
Fascicle
(wrapped by perimysium)
Endomysium
(between individual
muscle fibers)
Muscle fiber
Figure 9.1
Skeletal Muscle: Attachments
• Muscles attach:
• Directly—epimysium of muscle is fused to the
periosteum of bone or perichondrium of
cartilage
• Indirectly—connective tissue wrappings extend
beyond the muscle as a ropelike tendon or
sheetlike aponeurosis
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Table 9.1
Microscopic Anatomy of a Skeletal Muscle
Fiber
• Cylindrical cell 10 to 100 m in diameter, up to
30 cm long
• Multiple peripheral nuclei
• Many mitochondria
• Glycosomes for glycogen storage, myoglobin
for O2 storage
• Also contain myofibrils, sarcoplasmic
reticulum, and T tubules
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Myofibrils
• Densely packed, rodlike elements
• ~80% of cell volume
• Exhibit striations: perfectly aligned repeating
series of dark A bands and light I bands
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Sarcolemma
Mitochondrion
Myofibril
Dark A band Light I band Nucleus
(b) Diagram of part of a muscle fiber showing the myofibrils. One
myofibril is extended afrom the cut end of the fiber.
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Sarcomere
• Smallest contractile unit (functional unit) of a
muscle fiber
• The region of a myofibril between two
successive Z discs
• Composed of thick and thin myofilaments
made of contractile proteins
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Features of a Sarcomere
• Thick filaments: run the entire length of an A band
• Thin filaments: run the length of the I band and
partway into the A band
• Z disc: coin-shaped sheet of proteins that anchors
the thin filaments and connects myofibrils to one
another
• H zone: lighter midregion where filaments do not
overlap
• M line: line of protein myomesin that holds adjacent
thick filaments together
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Thin (actin)
filament
Thick (myosin)
filament
Z disc
H zone
Z disc
I band
A band
Sarcomere
I band
M line
(c) 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.
Sarcomere
Z disc
M line
Z disc
Thin (actin)
filament
Elastic (titin)
filaments
Thick
(myosin)
filament
(d) Enlargement of one sarcomere (sectioned lengthwise). Notice the
myosin heads on the thick filaments.
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Figure 9.2c, d
Ultrastructure of Thick Filament
• Composed of the protein myosin
• Myosin tails contain:
• 2 interwoven, heavy polypeptide chains
• Myosin heads contain:
• 2 smaller, light polypeptide chains that act as cross
bridges during contraction
• Binding sites for actin of thin filaments
• Binding sites for ATP
• ATPase enzymes
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Ultrastructure of Thin Filament
• Twisted double strand of fibrous protein F
actin
• F actin consists of G (globular) actin subunits
• G actin bears active sites for myosin head
attachment during contraction
• Tropomyosin and troponin: regulatory proteins
bound to actin
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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
A thin filament consists of two strands
myosin molecules whose heads protrude of actin subunits twisted into a helix
at opposite ends of the filament.
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
ATPbinding
site
Heads
Tail
Flexible hinge region
Myosin molecule
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Active sites
for myosin
attachment
Actin
subunits
Actin subunits
Figure 9.3
Sarcoplasmic Reticulum (SR)
• Network of smooth endoplasmic reticulum
surrounding each myofibril
• Pairs of terminal cisternae form perpendicular
cross channels
• Functions in the regulation of intracellular
Ca2+ levels
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T Tubules
• Continuous with the sarcolemma
• Penetrate the cell’s interior at each A band–I
band junction
• Associate with the paired terminal cisternae to
form triads that encircle each sarcomere
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Part of a skeletal
muscle fiber (cell)
Myofibril
I band
A band
I band
Z disc
H zone
Z disc
M line
Sarcolemma
Sarcolemma
Triad:
• T tubule
• Terminal
cisternae
of the SR (2)
Tubules of
the SR
Myofibrils
Mitochondria
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Figure 9.5
Triad Relationships
• T tubules conduct impulses deep into muscle
fiber
• Integral proteins protrude into the
intermembrane space from T tubule and SR
cisternae membranes
• T tubule proteins: voltage sensors
• SR foot proteins: gated channels that regulate
Ca2+ release from the SR cisternae
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Contraction
• The generation of force
• Does not necessarily cause shortening of the
fiber
• Shortening occurs when tension generated by
cross bridges on the thin filaments exceeds
forces opposing shortening
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Sliding Filament Model of Contraction
• In the relaxed state, thin and thick filaments
overlap only slightly
• During contraction, myosin heads bind to
actin, detach, and bind again, to propel the
thin filaments toward the M line
• As H zones shorten and disappear,
sarcomeres shorten, muscle cells shorten,
and the whole muscle shortens
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Z
Z
H
A
I
I
1 Fully relaxed sarcomere of a muscle fiber
Z
I
Z
A
I
2 Fully contracted sarcomere of a muscle fiber
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Figure 9.6
Requirements for Skeletal Muscle
Contraction
1. Activation: neural stimulation at a
neuromuscular junction
2. Excitation-contraction coupling:
•
Generation and propagation of an action
potential along the sarcolemma
•
Final trigger: a brief rise in intracellular Ca2+
levels
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Events at the Neuromuscular Junction
• Skeletal muscles are stimulated by somatic
motor neurons
• Axons of motor neurons travel from the
central nervous system via nerves to skeletal
muscles
• Each axon forms several branches as it
enters a muscle
• Each axon ending forms a neuromuscular
junction with a single muscle fiber
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Action
potential (AP)
Myelinated axon
of motor neuron
Axon terminal of
neuromuscular
junction
Nucleus
Sarcolemma of
the muscle fiber
1 Action potential arrives at
axon terminal of motor neuron.
2 Voltage-gated Ca2+ channels
open and Ca2+ enters the axon
terminal.
Ca2+
Ca2+
Axon terminal
of motor neuron
Synaptic vesicle
containing ACh
Mitochondrion
Synaptic
cleft
Fusing synaptic
vesicles
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Figure 9.8
Neuromuscular Junction
• Situated midway along the length of a muscle
fiber
• Axon terminal and muscle fiber are separated
by a gel-filled space called the synaptic cleft
• Synaptic vesicles of axon terminal contain the
neurotransmitter acetylcholine (ACh)
• Junctional folds of the sarcolemma contain
ACh receptors
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Events at the Neuromuscular Junction
• Nerve impulse arrives at axon terminal
• ACh is released and binds with receptors on
the sarcolemma
• Electrical events lead to the generation of an
action potential
PLAY
A&P Flix™: Events at the Neuromuscular Junction
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Myelinated axon
of motor neuron
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
Action
potential (AP)
Nucleus
1 Action potential arrives at
axon terminal of motor neuron.
2
Voltage-gated Ca2+ channels
Ca2+
Ca2+
open and Ca2+ enters the axon
terminal.
Axon terminal
of motor neuron
3 Ca2+ entry causes some
Fusing synaptic
vesicles
synaptic vesicles to release
their contents (acetylcholine)
by exocytosis.
ACh
4 Acetylcholine, a
neurotransmitter, diffuses across
the synaptic cleft and binds to
receptors in the sarcolemma.
Na+
K+
channels that allow simultaneous
passage of Na+ into the muscle
fiber and K+ out of the muscle
fiber.
by its enzymatic breakdown in
the synaptic cleft by
acetylcholinesterase.
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Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
5 ACh binding opens ion
6 ACh effects are terminated
Synaptic vesicle
containing ACh
Mitochondrion
Synaptic
cleft
Ach–
Degraded ACh
Na+
Acetylcholinesterase
Postsynaptic membrane
ion channel opens;
ions pass.
Postsynaptic membrane
ion channel closed;
ions cannot pass.
K+
Figure 9.8
Destruction of Acetylcholine
• ACh effects are quickly terminated by the
enzyme acetylcholinesterase
• Prevents continued muscle fiber contraction in
the absence of additional stimulation
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Events in Generation of an Action Potential
1. Local depolarization (end plate potential):
•
ACh binding opens chemically (ligand)
gated ion channels
•
Simultaneous diffusion of Na+ (inward) and
K+ (outward)
•
More Na+ diffuses, so the interior of the
sarcolemma becomes less negative
•
Local depolarization – end plate potential
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Events in Generation of an Action Potential
2. Generation and propagation of an action
potential:
•
End plate potential spreads to adjacent
membrane areas
•
Voltage-gated Na+ channels open
•
Na+ influx decreases the membrane voltage
toward a critical threshold
•
If threshold is reached, an action potential is
generated
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Events in Generation of an Action Potential
• Local depolarization wave continues to
spread, changing the permeability of the
sarcolemma
• Voltage-regulated Na+ channels open in the
adjacent patch, causing it to depolarize to
threshold
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Events in Generation of an Action Potential
3. Repolarization:
•
Na+ channels close and voltage-gated K+
channels open
•
K+ efflux rapidly restores the resting polarity
•
Fiber cannot be stimulated and is in a
refractory period until repolarization is
complete
•
Ionic conditions of the resting state are
restored by the Na+-K+ pump
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Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh
ACh
Na+ K+
Na+ K+
++
++ +
+
K+
Action potential
+
+ +++
+
2 Generation and propagation of
the action potential (AP)
1 Local depolarization:
generation of the end
plate potential on the
sarcolemma
Sarcoplasm of muscle fiber
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Closed Na+ Open K+
Channel
Channel
Na+
K+
3 Repolarization
Figure 9.9
Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh
ACh
Na+ K+
Na+
K+
K+
++
++ +
+
Action potential
+
+ +++
+
1 Local depolarization: generation of the
end plate potential on the sarcolemma
Sarcoplasm of muscle fiber
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Figure 9.9, step 1
Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh
ACh
Na+ K+
Na+
K+
K+
++
++ +
+
Action potential
+
+ +++
+
2 Generation and propagation of the
action potential (AP)
1 Local depolarization: generation of the
end plate potential on the sarcolemma
Sarcoplasm of muscle fiber
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Figure 9.9, step 2
Closed Na+
Channel
Open K+
Channel
Na+
K+
3 Repolarization
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Figure 9.9, step 3
Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh
ACh
Na+ K+
Na+ K+
++
++ +
+
K+
Action potential
+
+ +++
+
2 Generation and propagation of
the action potential (AP)
1 Local depolarization:
generation of the end
plate potential on the
sarcolemma
Sarcoplasm of muscle fiber
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Closed Na+ Open K+
Channel
Channel
Na+
K+
3 Repolarization
Figure 9.9
Depolarization
due to Na+ entry
Na+ channels
close, K+ channels
open
Repolarization
due to K+ exit
Na+
channels
open
Threshold
K+ channels
close
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Figure 9.10
Excitation-Contraction (E-C) Coupling
• Sequence of events by which transmission of
an AP along the sarcolemma leads to sliding
of the myofilaments
• Latent period:
• Time when E-C coupling events occur
• Time between AP initiation and the beginning
of contraction
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Events of Excitation-Contraction (E-C)
Coupling
• AP is propagated along sarcomere to T
tubules
• Voltage-sensitive proteins stimulate Ca2+
release from SR
• Ca2+ is necessary for contraction
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Setting the stage
Axon terminal
of motor neuron
Action potential
Synaptic cleft
is generated
ACh
Sarcolemma
Terminal cisterna of SR
Muscle fiber Ca2+
Triad
One sarcomere
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Figure 9.11, step 1
Steps in E-C Coupling:
Sarcolemma
Voltage-sensitive
tubule protein
T tubule
1 Action potential is propagated along
the sarcolemma and down the T tubules.
Ca2+
release
channel
2 Calcium ions are released.
Terminal
cisterna
of SR
Ca2+
Actin
Troponin
Ca2+
Tropomyosin
blocking active sites
Myosin
3 Calcium binds to troponin and
removes the blocking action of
tropomyosin.
Active sites exposed and
ready for myosin binding
4 Contraction begins
Myosin
cross
bridge
The aftermath
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Figure 9.11, step 2
1 Action potential is
Steps in
E-C Coupling:
propagated along the
sarcolemma and down
the T tubules.
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cisterna
of SR
Ca2+
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Figure 9.11, step 3
1 Action potential is
Steps in
E-C Coupling:
propagated along the
sarcolemma and down
the T tubules.
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cisterna
of SR
2 Calcium
ions are
released.
Ca2+
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Figure 9.11, step 4
Actin
Ca2+
Troponin
Tropomyosin
blocking active sites
Myosin
The aftermath
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Figure 9.11, step 5
Actin
Ca2+
Troponin
Tropomyosin
blocking active sites
Myosin
3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin.
Active sites exposed and
ready for myosin binding
The aftermath
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Figure 9.11, step 6
Actin
Ca2+
Troponin
Tropomyosin
blocking active sites
Myosin
3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin.
Active sites exposed and
ready for myosin binding
4 Contraction begins
Myosin
cross
bridge
The aftermath
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Figure 9.11, step 7
Steps in E-C Coupling:
Sarcolemma
Voltage-sensitive
tubule protein
T tubule
1 Action potential is propagated along
the sarcolemma and down the T tubules.
Ca2+
release
channel
2 Calcium ions are released.
Terminal
cisterna
of SR
Ca2+
Actin
Troponin
Ca2+
Tropomyosin
blocking active sites
Myosin
3 Calcium binds to troponin and
removes the blocking action of
tropomyosin.
Active sites exposed and
ready for myosin binding
4 Contraction begins
Myosin
cross
bridge
The aftermath
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Figure 9.11, step 8
Role of Calcium (Ca2+) in Contraction
• At low intracellular Ca2+ concentration:
• Tropomyosin blocks the active sites on actin
• Myosin heads cannot attach to actin
• Muscle fiber relaxes
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Role of Calcium (Ca2+) in Contraction
• At higher intracellular Ca2+ concentrations:
• Ca2+ binds to troponin
• Troponin changes shape and moves
tropomyosin away from active sites
• Events of the cross bridge cycle occur
• When nervous stimulation ceases, Ca2+ is
pumped back into the SR and contraction ends
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Cross Bridge Cycle
• Continues as long as the Ca2+ signal and
adequate ATP are 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 the cross bridge detaches
• “Cocking” of the myosin head—energy from
hydrolysis of ATP cocks the myosin head into
the high-energy state
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Thin filament
Actin
Ca2+
Myosin
cross bridge
ADP
Pi
Thick
filament
Myosin
Cross
bridge
formation.
1
ADP
ADP
Pi
ATP
Pi
hydrolysis
2 The power (working)
stroke.
4 Cocking of myosin head.
ATP
ATP
3 Cross bridge
detachment.
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Figure 9.12
Actin
Ca2+
Myosin
cross bridge
Thin filament
ADP
Pi
Thick filament
Myosin
1 Cross bridge formation.
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Figure 9.12, step 1
ADP
Pi
2 The power (working) stroke.
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Figure 9.12, step 3
ATP
3 Cross bridge detachment.
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Figure 9.12, step 4
ADP
ATP
Pi
hydrolysis
4 Cocking of myosin head.
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Figure 9.12, step 5
Thin filament
Actin
Ca2+
Myosin
cross bridge
ADP
Pi
Thick
filament
Myosin
Cross
bridge
formation.
1
ADP
ADP
Pi
ATP
Pi
hydrolysis
2 The power (working)
stroke.
4 Cocking of myosin head.
ATP
ATP
3 Cross bridge
detachment.
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Figure 9.12
Review Principles of Muscle Mechanics
1. Same principles apply to contraction of a
single fiber and a whole muscle
2. Contraction produces tension, the force
exerted on the load or object to be moved
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Review Principles of Muscle Mechanics
3. Contraction does not always shorten a
muscle:
•
Isometric contraction: no shortening; muscle
tension increases but does not exceed the
load
•
Isotonic contraction: muscle shortens
because muscle tension exceeds the load
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Review Principles of Muscle Mechanics
4. Force and duration of contraction vary in
response to stimuli of different frequencies
and intensities
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Motor Unit: The Nerve-Muscle Functional
Unit
• Motor unit = a motor neuron and all (four to
several hundred) muscle fibers it supplies
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Spinal cord
Motor Motor
unit 1 unit 2
Axon terminals at
neuromuscular junctions
Nerve
Motor neuron
cell body
Motor
Muscle
neuron
axon
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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Figure 9.13a
Motor Unit
• Small motor units in muscles that control fine
movements (fingers, eyes)
• Large motor units in large weight-bearing
muscles (thighs, hips)
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Motor Unit
• Muscle fibers from a motor unit are spread
throughout the muscle so that a single motor
unit causes weak contraction of entire muscle
• Motor units in a muscle usually contract
asynchronously; helps prevent fatigue
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Muscle Twitch
• Response of a muscle to a single, brief
threshold stimulus
• Simplest contraction observable in the lab
(recorded as a myogram)
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Muscle Twitch
• Three phases of a twitch:
• Latent period: events of excitation-contraction
coupling
• Period of contraction: cross bridge formation;
tension increases
• Period of relaxation: Ca2+ reentry into the SR;
tension declines to zero
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Latent Period of
period contraction
Period of
relaxation
Single
stimulus
(a) Myogram showing the three phases of an isometric twitch
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Figure 9.14a
Muscle Twitch Comparisons
Different strength and duration of twitches are
due to variations in metabolic properties and
enzymes between muscles
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Latent period
Extraocular muscle (lateral rectus)
Gastrocnemius
Soleus
Single
stimulus
(b) Comparison of the relative duration of twitch responses of
three muscles
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Figure 9.14b
Graded Muscle Responses
• Variations in the degree of muscle contraction
• Required for proper control of skeletal
movement
Responses are graded by:
1. Changing the frequency of stimulation
2. Changing the strength of the stimulus
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Response to Change in Stimulus Frequency
• A single stimulus results in a single contractile
response—a muscle twitch
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Single stimulus
single twitch
Contraction
Relaxation
Stimulus
A single stimulus is delivered. The muscle
contracts and relaxes
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Figure 9.15a
Response to Change in Stimulus Frequency
• Increase frequency of stimulus (muscle does
not have time to completely relax between
stimuli)
• Ca2+ release stimulates further contraction 
temporal (wave) summation
• Further increase in stimulus frequency 
unfused (incomplete) tetanus
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Low stimulation frequency
unfused (incomplete) tetanus
Partial relaxation
Stimuli
(b) If another stimulus is applied before the muscle
relaxes completely, then more tension results.
This is temporal (or wave) summation and results
in unfused (or incomplete) tetanus.
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Figure 9.15b
Response to Change in Stimulus Frequency
• If stimuli are given quickly enough, fused
(complete) tetany results
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High stimulation frequency
fused (complete) tetanus
Stimuli
(c) At higher stimulus frequencies, there is no relaxation
at all between stimuli. This is fused (complete) tetanus.
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Figure 9.15c
Response to Change in Stimulus Strength
• Threshold stimulus: stimulus strength at which
the first observable muscle contraction occurs
• Muscle contracts more vigorously as stimulus
strength is increased above threshold
• Contraction force is precisely controlled by
recruitment (multiple motor unit summation),
which brings more and more muscle fibers
into action
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Stimulus strength
Maximal
stimulus
Threshold
stimulus
Proportion of motor units excited
Strength of muscle contraction
Maximal contraction
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Figure 9.16
Response to Change in Stimulus Strength
• Size principle: motor units with larger and
larger fibers are recruited as stimulus intensity
increases
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Motor
unit 1
Recruited
(small
fibers)
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Motor
unit 2
recruited
(medium
fibers)
Motor
unit 3
recruited
(large
fibers)
Figure 9.17
Muscle Tone
• Constant, slightly contracted state of all
muscles
• Due to spinal reflexes that activate groups of
motor units alternately in response to input
from stretch receptors in muscles
• Keeps muscles firm, healthy, and ready to
respond
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Isotonic Contractions
• Muscle changes in length and moves the load
• Isotonic contractions are either concentric or
eccentric:
• Concentric contractions—the muscle shortens
and does work
• Eccentric contractions—the muscle contracts
as it lengthens
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Figure 9.18a
Isometric Contractions
• The load is greater than the tension the
muscle is able to develop
• Tension increases to the muscle’s capacity,
but the muscle neither shortens nor lengthens
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Figure 9.18b
Muscle Metabolism: Energy for Contraction
• ATP is the only source used directly for
contractile activities
• Available stores of ATP are depleted in 4–6
seconds
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Muscle Metabolism: Energy for Contraction
• ATP is regenerated by:
• Direct phosphorylation of ADP by creatine
phosphate (CP)
• Anaerobic pathway (glycolysis)
• Aerobic respiration
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(a) Direct phosphorylation
Coupled reaction of creatine
phosphate (CP) and ADP
Energy source: CP
CP
ADP
Creatine
kinase
Creatine
ATP
Oxygen use: None
Products: 1 ATP per CP, creatine
Duration of energy provision:
15 seconds
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Figure 9.19a
Anaerobic Pathway
• At 70% of maximum contractile activity:
• Bulging muscles compress blood vessels
• Oxygen delivery is impaired
• Pyruvic acid is converted into lactic acid
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Anaerobic Pathway
• Lactic acid:
• Diffuses into the bloodstream
• Used as fuel by the liver, kidneys, and heart
• Converted back into pyruvic acid by the liver
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(b) Anaerobic pathway
Glycolysis and lactic acid formation
Energy source: glucose
Glucose (from
glycogen breakdown or
delivered from blood)
Glycolysis
in cytosol
2
O2
ATP
Pyruvic acid
net gain
O2
Released
to blood
Lactic acid
Oxygen use: None
Products: 2 ATP per glucose, lactic acid
Duration of energy provision:
60 seconds, or slightly more
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Figure 9.19b
Aerobic Pathway
• Produces 95% of ATP during rest and light to
moderate exercise
• Fuels: stored glycogen, then bloodborne
glucose, pyruvic acid from glycolysis, and free
fatty acids
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(c) 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)
O2
Pyruvic acid
Fatty
acids
O2
Aerobic
respiration
Aerobic respiration
in mitochondria
mitochondria
Amino
acids
32
CO2
H2O
ATP
net gain per
glucose
Oxygen use: Required
Products: 32 ATP per glucose, CO2, H2O
Duration of energy provision: Hours
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Figure 9.19c
Short-duration exercise
ATP stored in
muscles is
used first.
ATP is formed
from creatine
Phosphate
and ADP.
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Glycogen stored in muscles is broken
down to glucose, which is oxidized to
generate ATP.
Prolonged-duration
exercise
ATP is generated by
breakdown of several
nutrient energy fuels by
aerobic pathway. This
pathway uses oxygen
released from myoglobin
or delivered in the blood
by hemoglobin. When it
ends, the oxygen deficit is
paid back.
Figure 9.20
Muscle Fatigue
• Physiological inability to contract
• Occurs when:
• Ionic imbalances (K+, Ca2+, Pi) interfere with EC coupling
• Prolonged exercise damages the SR and
interferes with Ca2+ regulation and release
• Total lack of ATP occurs rarely, during states
of continuous contraction, and causes
contractures (continuous contractions)
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Oxygen Deficit
Extra O2 needed after exercise for:
• Replenishment of
• Oxygen reserves
• Glycogen stores
• ATP and CP reserves
• Conversion of lactic acid to pyruvic acid,
glucose, and glycogen
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Heat Production During Muscle Activity
• ~ 40% of the energy released in muscle
activity is useful as work
• Remaining energy (60%) given off as heat
• Dangerous heat levels are prevented by
radiation of heat from the skin and sweating
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Force of Muscle Contraction
• The force of contraction is affected by:
• Number of muscle fibers stimulated
(recruitment)
• Relative size of the fibers—hypertrophy of
cells increases strength
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Force of Muscle Contraction
• The force of contraction is affected by:
• Frequency of stimulation— frequency allows
time for more effective transfer of tension to
noncontractile components
• Length-tension relationship—muscles contract
most strongly when muscle fibers are 80–
120% of their normal resting length
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Large
number of
muscle
fibers
activated
Large
muscle
fibers
High
frequency of
stimulation
Muscle and
sarcomere
stretched to
slightly over 100%
of resting length
Contractile force
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Figure 9.21
Sarcomeres
greatly
shortened
Sarcomeres at
resting length
Sarcomeres excessively
stretched
75%
100%
170%
Optimal sarcomere
operating length
(80%–120% of
resting length)
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Figure 9.22
Velocity and Duration of Contraction
Influenced by:
1. Muscle fiber type
2. Load
3. Recruitment
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Muscle Fiber Type
Classified according to two characteristics:
1. Speed of contraction: slow or fast,
according to:
•
Speed at which myosin ATPases split ATP
•
Pattern of electrical activity of the motor
neurons
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Muscle Fiber Type
2. Metabolic pathways for ATP synthesis:
•
Oxidative fibers—use aerobic pathways
•
Glycolytic fibers—use anaerobic glycolysis
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Muscle Fiber Type
Three types:
• Slow oxidative fibers
• Fast oxidative fibers
• Fast glycolytic fibers
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Copyright © 2010 Pearson Education, Inc.
Table 9.2
Predominance
of fast glycolytic
(fatigable) fibers
Contractile
velocity
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Small load
Predominance
of slow oxidative
(fatigue-resistant)
fibers
Contractile
duration
Figure 9.23
FO
SO
FG
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Figure 9.24
Influence of Load
 load   latent period,  contraction, and 
duration of contraction
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Light load
Intermediate load
Heavy load
Stimulus
(a) The greater the load, the less the muscle
shortens and the shorter the duration of
contraction
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(b) The greater the load, the
slower the contraction
Figure 9.25
Influence of Recruitment
Recruitment  faster contraction and 
duration of contraction
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Effects of Exercise
Aerobic (endurance) exercise:
• Leads to increased:
• Muscle capillaries
• Number of mitochondria
• Myoglobin synthesis
• Results in greater endurance, strength, and
resistance to fatigue
• May convert fast glycolytic fibers into fast oxidative
fibers
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Effects of Resistance Exercise
• Resistance exercise (typically anaerobic)
results in:
• Muscle hypertrophy (due to increase in fiber
size)
• Increased mitochondria, myofilaments,
glycogen stores, and connective tissue
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The Overload Principle
• Forcing a muscle to work hard promotes
increased muscle strength and endurance
• Muscles adapt to increased demands
• Muscles must be overloaded to produce
further gains
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Smooth Muscle
• Found in walls of most hollow organs
(except heart)
• Usually in two layers (longitudinal and
circular)
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Longitudinal layer
of smooth muscle
(shows smooth
muscle fibers in
cross section)
Small
intestine
(a)
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Mucosa
(b) 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)
Figure 9.26
Peristalsis
• Alternating contractions and relaxations of
smooth muscle layers that mix and squeeze
substances through the lumen of hollow
organs
• Longitudinal layer contracts; organ dilates and
shortens
• Circular layer contracts; organ constricts and
elongates
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Microscopic Structure
• Spindle-shaped fibers: thin and short
compared with skeletal muscle fibers
• Connective tissue: endomysium only
• SR: less developed than in skeletal muscle
• Pouchlike infoldings (caveolae) of
sarcolemma sequester Ca2+
• No sarcomeres, myofibrils, or T tubules
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Copyright © 2010 Pearson Education, Inc.
Table 9.3
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Table 9.3
Innervation of Smooth Muscle
• Autonomic nerve fibers innervate smooth
muscle at diffuse junctions
• Varicosities (bulbous swellings) of nerve fibers
store and release neurotransmitters
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Varicosities
Autonomic
nerve fibers
innervate
most smooth
muscle fibers.
Smooth
muscle
cell
Synaptic
vesicles
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Mitochondrion
Varicosities release
their neurotransmitters
into a wide synaptic
cleft (a diffuse junction).
Figure 9.27
Myofilaments in Smooth Muscle
• Ratio of thick to thin filaments (1:13) is much
lower than in skeletal muscle (1:2)
• Thick filaments have heads along their entire
length
• No troponin complex; protein calmodulin binds
Ca2+
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Myofilaments in Smooth Muscle
• Myofilaments are spirally arranged, causing
smooth muscle to contract in a corkscrew
manner
• Dense bodies: proteins that anchor
noncontractile intermediate filaments to
sarcolemma at regular intervals
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Figure 9.28a
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Figure 9.28b
Contraction of Smooth Muscle
• Slow, synchronized contractions
• Cells are electrically coupled by gap junctions
• Some cells are self-excitatory (depolarize
without external stimuli); act as pacemakers
for sheets of muscle
• Rate and intensity of contraction may be
modified by neural and chemical stimuli
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Contraction of Smooth Muscle
• Sliding filament mechanism
• Final trigger is  intracellular Ca2+
• Ca2+ is obtained from the SR and extracellular
space
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Role of Calcium Ions
• Ca2+ binds to and activates calmodulin
• Activated calmodulin activates myosin (light
chain) kinase
• Activated kinase phosphorylates and activates
myosin
• Cross bridges interact with actin
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Copyright © 2010 Pearson Education, Inc.
Table 9.3
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Table 9.3
Extracellular fluid (ECF)
Ca2+
Plasma membrane
Cytoplasm
1 Calcium ions (Ca2+)
enter the cytosol from
the ECF via voltagedependent or voltageindependent Ca2+
channels, or from
the scant SR.
2 Ca2+ binds to and
activates calmodulin.
Ca2+
Sarcoplasmic
reticulum
Ca2+
Inactive calmodulin
3 Activated calmodulin
activates the myosin
light chain kinase
enzymes.
Inactive kinase
4 The activated kinase enzymes
catalyze transfer of phosphate
to myosin, activating the myosin
ATPases.
Activated calmodulin
Activated kinase
ATP
ADP
Pi
Pi
Inactive
myosin molecule
Activated (phosphorylated)
myosin molecule
5 Activated myosin forms cross
bridges with actin of the thin
filaments and shortening begins.
Thin
filament
Thick
filament
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Figure 9.29
Extracellular fluid (ECF)
Ca2+
Plasma membrane
Cytoplasm
1 Calcium ions (Ca2+)
enter the cytosol from
the ECF via voltagedependent or voltageindependent Ca2+
channels, or from
the scant SR.
Ca2+
Sarcoplasmic
reticulum
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Figure 9.29, step 1
2 Ca2+ binds to and
activates calmodulin.
Ca2+
Inactive calmodulin
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Activated calmodulin
Figure 9.29, step 2
3 Activated calmodulin
activates the myosin
light chain kinase
enzymes.
Inactive kinase
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Activated kinase
Figure 9.29, step 3
4 The activated kinase enzymes
catalyze transfer of phosphate
to myosin, activating the myosin
ATPases.
ATP
ADP
Pi
Pi
Inactive
myosin molecule
Copyright © 2010 Pearson Education, Inc.
Activated (phosphorylated)
myosin molecule
Figure 9.29, step 4
5 Activated myosin forms cross
bridges with actin of the thin
filaments and shortening begins.
Thin
filament
Thick
filament
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Figure 9.29, step 5
Extracellular fluid (ECF)
Ca2+
Plasma membrane
Cytoplasm
1 Calcium ions (Ca2+)
enter the cytosol from
the ECF via voltagedependent or voltageindependent Ca2+
channels, or from
the scant SR.
2 Ca2+ binds to and
activates calmodulin.
Ca2+
Sarcoplasmic
reticulum
Ca2+
Inactive calmodulin
3 Activated calmodulin
activates the myosin
light chain kinase
enzymes.
Inactive kinase
4 The activated kinase enzymes
catalyze transfer of phosphate
to myosin, activating the myosin
ATPases.
Activated calmodulin
Activated kinase
ATP
ADP
Pi
Pi
Inactive
myosin molecule
Activated (phosphorylated)
myosin molecule
5 Activated myosin forms cross
bridges with actin of the thin
filaments and shortening begins.
Thin
filament
Thick
filament
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Figure 9.29
Contraction of Smooth Muscle
• Very energy efficient (slow ATPases)
• Myofilaments may maintain a latch state for
prolonged contractions
Relaxation requires:
• Ca2+ detachment from calmodulin
• Active transport of Ca2+ into SR and ECF
• Dephosphorylation of myosin to reduce
myosin ATPase activity
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Regulation of Contraction
Neural regulation:
• Neurotransmitter binding   [Ca2+] in
sarcoplasm; either graded (local) potential or
action potential
• Response depends on neurotransmitter
released and type of receptor molecules
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Regulation of Contraction
Hormones and local chemicals:
• May bind to G protein–linked receptors
• May either enhance or inhibit Ca2+ entry
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Special Features of Smooth Muscle
Contraction
Stress-relaxation response:
• Responds to stretch only briefly, then adapts to
new length
• Retains ability to contract on demand
• Enables organs such as the stomach and
bladder to temporarily store contents
Length and tension changes:
• Can contract when between half and twice its
resting length
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Special Features of Smooth Muscle
Contraction
Hyperplasia:
• Smooth muscle cells can divide and increase
their numbers
• Example:
• estrogen effects on uterus at puberty and
during pregnancy
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Table 9.3
Types of Smooth Muscle
Single-unit (visceral) smooth muscle:
• Sheets contract rhythmically as a unit (gap
junctions)
• Often exhibit spontaneous action potentials
• Arranged in opposing sheets and exhibit
stress-relaxation response
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Types of Smooth Muscle: Multiunit
Multiunit smooth muscle:
• Located in large airways, large arteries,
arrector pili muscles, and iris of eye
• Gap junctions are rare
• Arranged in motor units
• Graded contractions occur in response to
neural stimuli
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Developmental Aspects
• All muscle tissues develop from embryonic
myoblasts
• Multinucleated skeletal muscle cells form by
fusion
• Growth factor agrin stimulates clustering of
ACh receptors at neuromuscular junctions
• Cardiac and smooth muscle myoblasts
develop gap junctions
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Developmental Aspects
• Cardiac and skeletal muscle become amitotic,
but can lengthen and thicken
• Myoblast-like skeletal muscle satellite cells
have limited regenerative ability
• Injured heart muscle is mostly replaced by
connective tissue
• Smooth muscle regenerates throughout life
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Developmental Aspects
• Muscular development reflects neuromuscular
coordination
• Development occurs head to toe, and
proximal to distal
• Peak natural neural control occurs by
midadolescence
• Athletics and training can improve
neuromuscular control
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Developmental Aspects
• Female skeletal muscle makes up 36% of
body mass
• Male skeletal muscle makes up 42% of body
mass, primarily due to testosterone
• Body strength per unit muscle mass is the
same in both sexes
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Developmental Aspects
• 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 and severe
pain in leg muscles
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Muscular Dystrophy
• Group of inherited muscle-destroying
diseases
• Muscles enlarge due to fat and connective
tissue deposits
• Muscle fibers atrophy
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Muscular Dystrophy
Duchenne muscular dystrophy (DMD):
• Most common and severe type
• Inherited, sex-linked, carried by females and
expressed in males (1/3500) as lack of dystrophin
• Victims become clumsy and fall frequently; usually die
of respiratory failure in their 20s
• No cure, but viral gene therapy or infusion of stem
cells with correct dystrophin genes show promise
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