Chapter 11
Lecture PowerPoint
Muscular Tissue
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Introduction
• Movement is a fundamental characteristic of all
living organisms
• Three types of muscular tissue—skeletal,
cardiac, and smooth
• Important to understand muscle at the
molecular, cellular, and tissue levels of
organization
11-2
Types and Characteristics of
Muscular Tissue
• Expected Learning Outcomes
– Describe the physiological properties that all muscle
types have in common.
– List the defining characteristics of skeletal muscle.
– Discuss the possible elastic functions of the
connective tissue components of a muscle.
11-3
Universal Characteristics of Muscle
• Responsiveness (excitability)
– To chemical signals, stretch, and electrical changes across the
plasma membrane
• Conductivity
– Local electrical change triggers a wave of excitation that travels
along the muscle fiber
• Contractility
– Shortens when stimulated
• Extensibility
– Capable of being stretched between contractions
• Elasticity
– Returns to its original resting length after being stretched
11-4
Skeletal Muscle
• Skeletal muscle—
voluntary, striated muscle
attached to one or more
bones
• Striations—alternating
light and dark transverse
bands
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Nucleus
Muscle fiber
– Results from an
overlapping of internal
contractile proteins
• Voluntary—usually
subject to conscious
control
• Muscle cell, muscle fiber
(myofiber)—as long as 30
cm
Endomysium
Striations
© Ed Reschke
Figure 11.1
11-5
Skeletal Muscle
• Tendons are attachments between muscle and bone matrix
–
–
–
–
–
Endomysium: connective tissue around muscle cells
Perimysium: connective tissue around muscle fascicles
Epimysium: connective tissue surrounding entire muscle
Continuous with collagen fibers of tendons
In turn, with connective tissue of bone matrix
• Collagen is somewhat extensible and elastic
– Stretches slightly under tension and recoils when released
• Resists excessive stretching and protects muscle from injury
• Returns muscle to its resting length
• Contributes to power output and muscle efficiency
11-6
Microscopic Anatomy of
Skeletal Muscle
• Expected Learning Outcomes
– Describe the structural components of a muscle fiber.
– Relate the striations of a muscle fiber to the
overlapping arrangement of its protein filaments.
– Name the major proteins of a muscle fiber and state
the function of each.
11-7
The Muscle Fiber
• Sarcolemma—plasma membrane of a muscle
fiber
• Sarcoplasm—cytoplasm of a muscle fiber
• Myofibrils—long protein bundles that occupy
the main portion of the sarcoplasm
– Glycogen: stored in abundance to provide energy
with heightened exercise
– Myoglobin: red pigment; stores oxygen needed for
muscle activity
11-8
The Muscle Fiber
• Multiple nuclei—flattened nuclei pressed
against the inside of the sarcolemma
– Myoblasts: stem cells that fuse to form each muscle
fiber
– Satellite cells: unspecialized myoblasts remaining
between the muscle fiber and endomysium
• May multiply and produce new muscle fibers to some
degree
• Mitochondria—packed into spaces between
myofibrils
11-9
The Muscle Fiber
• Sarcoplasmic reticulum (SR)—smooth ER
that forms a network around each myofibril:
calcium reservoir
– Calcium activates the muscle contraction process
• Terminal cisternae—dilated end-sacs of SR
which cross the muscle fiber from one side to
the other
• T tubules—tubular infoldings of the
sarcolemma which penetrate through the cell
and emerge on the other side
• Triad—a T tubule and two terminal cisterns
11-10
The Muscle Fiber
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Muscle
fiber
Nucleus
A band
I band
Z disc
Openings into
transverse tubules
Mitochondria
Sarcoplasmic
reticulum
Triad:
Terminal cisternae
Transverse tubule
Sarcolemma
Myofibrils
Sarcoplasm
Myofilaments
Figure 11.2
11-11
Myofilaments
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Head
Tail
(a) Myosin molecule
Myosin head
(b) Thick filament
Figure 11.3a,b
• Thick filaments—made of several hundred myosin
molecules
– Shaped like a golf club
• Two chains intertwined to form a shaftlike tail
• Double globular head
– Heads directed outward in a helical array around the bundle
• Heads on one half of the thick filament angle to the left
• Heads on the other half angle to the right
• Bare zone with no heads in the middle
11-12
Myofilaments
• Thin filaments
– Fibrous (F) actin: two intertwined strands
• String of globular (G) actin subunits each with an active site
that can bind to head of myosin molecule
– Tropomyosin molecules
• Each blocking six or seven active sites on G actin subunits
– Troponin molecule: small, calcium-binding protein on
each tropomyosin molecule
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Tropomyosin
Troponin complex
G actin
(c) Thin filament
Figure 11.3c
11-13
Myofilaments
• Elastic filaments
–
–
–
–
–
Titin (connectin): huge, springy protein
Flank each thick filament and anchor it to the Z disc
Help stabilize the thick filament
Center it between the thin filaments
Prevent overstretching
11-14
Myofilaments
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Myosin head
(b) Thick filament
Tropomyosin
(c) Thin filament
Troponin complex
G actin
Figure 11.3b,c
• Contractile proteins—myosin and actin do the work
• Regulatory proteins—tropomyosin and troponin
– Like a switch that determines when the fiber can contract and when it
cannot
– Contraction activated by release of calcium into sarcoplasm and its
binding to troponin
– Troponin changes shape and moves tropomyosin off the active sites on
actin
11-15
Myofilaments
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Thick filament
Thin filament
Bare zone
(d) Portion of a sarcomere showing the overlap
of thick and thin filaments
Figure 11.3d
11-16
Myofilaments
• At least seven other
accessory proteins in or
associated with thick or thin
filaments
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Endomysium
Linking proteins
Basal lamina
– Anchor the myofilaments,
regulate length of
myofilaments, keep alignment
for optimal contractile
effectiveness
Sarcolemma
Dystrophin
Thin filament
Thick filament
Figure 11.4
11-17
Myofilaments
• Dystrophin—most clinically
important
– Links actin in outermost
myofilaments to transmembrane
proteins and eventually to
fibrous endomysium
surrounding the entire muscle
cell
– Transfers forces of muscle
contraction to connective tissue
around muscle cell
– Genetic defects in dystrophin
produce disabling disease
muscular dystrophy
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Endomysium
Linking proteins
Basal lamina
Sarcolemma
Dystrophin
Thin filament
Thick filament
Figure 11.4
11-18
Striations
• Myosin and actin are proteins that occur in all cells
– Function in cellular motility, mitosis, transport of intracellular
material
• Organized in a precise way in skeletal and cardiac
muscle
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Sarcomere
A band
I band
I band
H band
(b)
Z disc
Thick filament
Thin filament
Elastic filament
M line
Figure 11.5b
Titin
Z disc
11-19
Striations
– A band: dark; A stands for anisotropic
• Part of A band where thick and thin filaments overlap is
especially dark
– H band: middle of A band; thick filaments only
– M line: middle of H band
– I band: alternating lighter band; I stands for isotropic
• The way the bands reflect polarized light
– Z disc: provides anchorage for thin filaments and
elastic filaments
• Bisects I band
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Sarcomere
A band
I band
I band
H band
(b)
Z disc
Thick filament
Thin filament
Elastic filament
M line
Figure 11.5b
Titin
Z disc
11-20
Striations
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Nucleus
M line
Z disc
H band
A band
I band
1
I band
2
3
4
Individual myofibrils
5
Sarcomere
(a)
Visuals Unlimited
Figure 11.5a
11-21
Striations
• Sarcomere—segment from Z disc to Z disc
– Functional contractile unit of muscle fiber
• Muscle cells shorten because their individual
sarcomeres shorten
– Z disc (Z lines) are pulled closer together as thick and thin
filaments slide past each other
• Neither thick nor thin filaments change length during
shortening
– Only the amount of overlap changes
• During shortening dystrophin and linking proteins also
pull on extracellular proteins
– Transfers pull to extracellular tissue
11-22
The Nerve—Muscle Relationship
• Expected Learning Outcomes
– Explain what a motor unit is and how it relates to
muscle contraction.
– Describe the structure of the junction where a nerve
fiber meets a muscle fiber.
– Explain why a cell has an electrical charge difference
across its plasma membrane and, in general terms,
how this relates to muscle contraction.
11-23
The Nerve—Muscle Relationship
• Skeletal muscle never contracts unless
stimulated by a nerve
• If nerve connections are severed or poisoned, a
muscle is paralyzed
– Denervation atrophy: shrinkage of
paralyzed muscle when connection not
restored
11-24
Motor Neurons and Motor Units
• Somatic motor neurons—nerve cells whose
cell bodies are in the brainstem and spinal cord
that serve skeletal muscles
• Somatic motor fibers—their axons that lead to
the skeletal muscle
– Each nerve fiber branches out to a number of muscle
fibers
– Each muscle fiber is supplied by only one motor
neuron
11-25
Motor Neurons and Motor Units
• Motor unit—one nerve fiber
and all the muscle fibers
innervated by it
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Spinal cord
• Muscle fibers of one motor
unit
– Dispersed throughout the
muscle
– Contract in unison
– Produce weak contraction
over wide area
– Provides ability to sustain
long-term contraction as
motor units take turns
contracting (postural control)
– Effective contraction usually
requires the contraction of
several motor units at once
Motor
neuron 1
Motor
neuron 2
Neuromuscular
junction
Skeletal
muscle
fibers
Figure 11.6
11-26
Motor Neurons and Motor Units
• Average motor unit—200 muscle fibers for
each motor unit
• Small motor units—fine degree of control
– Three to six muscle fibers per neuron
– Eye and hand muscles
• Large motor units—more strength than control
– Powerful contractions supplied by large motor units
(e.g., gastrocnemius has 1,000 muscle fibers per
neuron)
– Many muscle fibers per motor unit
11-27
The Neuromuscular Junction
• Synapse—point where a nerve fiber meets its
target cell
• Neuromuscular junction (NMJ)—when target cell
is a muscle fiber
• Each terminal branch of the nerve fiber within the
NMJ forms separate synapse with the muscle fiber
• One nerve fiber stimulates the muscle fiber at
several points within the NMJ
11-28
The Neuromuscular Junction
• Synaptic knob—swollen end of nerve fiber
– Contains synaptic vesicles filled with acetylcholine
(ACh)
• Synaptic cleft—tiny gap between synaptic knob
and muscle sarcolemma
• Schwann cell envelops and isolates all of the NMJ
from surrounding tissue fluid
• Synaptic vesicles undergo exocytosis releasing
ACh into synaptic cleft
11-29
The Neuromuscular Junction
• Synaptic vesicles undergo exocytosis releasing
ACh into synaptic cleft
• 50 million ACh receptors—proteins incorporated
into muscle cell plasma membrane
– Junctional folds of sarcolemma beneath synaptic knob
• Increase surface area holding ACh receptors
– Lack of receptors leads to paralysis in disease myasthenia
gravis
11-30
The Neuromuscular Junction
• Basal lamina—thin layer of collagen and
glycoprotein separates Schwann cell and entire
muscle cell from surrounding tissues
– Contains acetylcholinesterase (AChE) that breaks
down ACh after contraction causing relaxation
11-31
The Neuromuscular Junction
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Motor nerve fiber
Myelin
Synaptic knob
Schwann cell
Basal lamina
Synaptic vesicles
(containing ACh)
Sarcolemma
Synaptic cleft
Nucleus
ACh receptor
Junctional folds
Mitochondria
Nucleus
Sarcoplasm
(b)
Myofilaments
Figure 11.7b
11-32
The Neuromuscular Junction
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Motor nerve
fibers
Neuromuscular
junction
Muscle fibers
Figure 11.7a
(a)
100 µm
Victor B. Eichler
11-33
Electrically Excitable Cells
• Muscle fibers and neurons are electrically
excitable cells
– Their plasma membrane exhibits voltage changes in
response to stimulation
• Electrophysiology—the study of the electrical
activity of cells
• Voltage (electrical potential)—a difference in
electrical charge from one point to another
• Resting membrane potential—about −90 mV
– Maintained by sodium–potassium pump
11-34
Electrically Excitable Cells
• In an unstimulated (resting) cell
– There are more anions (negative ions) on the inside of the
plasma membrane than on the outside
– The plasma membrane is electrically polarized (charged)
– There are excess sodium ions (Na+) in the extracellular
fluid (ECF)
– There are excess potassium ions (K+) in the intracellular
fluid (ICF)
– Also in the ICF, there are anions such as proteins, nucleic
acids, and phosphates that cannot penetrate the plasma
membrane
– These anions make the inside of the plasma membrane
negatively charged by comparison to its outer surface
11-35
Electrically Excitable Cells
• Stimulated (active) muscle fiber or nerve cell
– Ion gates open in the plasma membrane
– Na+ instantly diffuses down its concentration gradient into the
cell
– These cations override the negative charges in the ICF
– Depolarization: inside of the plasma membrane becomes
briefly positive
– Immediately, Na+ gates close and K+ gates open
– K+ rushes out of cell
– Repelled by the positive sodium charge and partly because
of its concentration gradient
– Loss of positive potassium ions turns the membrane
negative again (repolarization)
11-36
Electrically Excitable Cells
• Stimulated (active) muscle fiber or nerve cell (cont.)
– Action potential: quick up-and-down voltage shift from the
negative RMP to a positive value, and back to the negative
value again
– RMP is a stable voltage seen in a waiting muscle or nerve
cell
– Action potential is a quickly fluctuating voltage seen in an
active stimulated cell
– An action potential at one point on a plasma membrane
causes another one to happen immediately in front of it, which
triggers another one a little farther along and so forth
11-37
Neuromuscular Toxins and Paralysis
• Toxins that interfere with synaptic function can paralyze the
muscles
• Some pesticides contain cholinesterase inhibitors
– Bind to acetylcholinesterase and prevent it from degrading
Ach
– Spastic paralysis: a state of continual contraction of the
muscles; possible suffocation
• Tetanus (lockjaw) is a form of spastic paralysis caused by
toxin Clostridium tetani
– Glycine in the spinal cord normally stops motor neurons from
producing unwanted muscle contractions
– Tetanus toxin blocks glycine release in the spinal cord and
causes overstimulation and spastic paralysis of the muscles
11-38
Neuromuscular Toxins and Paralysis
• Flaccid paralysis—a state in which the muscles are limp
and cannot contract
– Curare: compete with ACh for receptor sites, but do not
stimulate the muscles
– Plant poison used by South American natives to poison
blowgun darts
• Botulism—type of food poisoning caused by a
neuromuscular toxin secreted by the bacterium Clostridium
botulinum
– Blocks release of ACh causing flaccid paralysis
– Botox cosmetic injections for wrinkle removal
11-39
Behavior of Skeletal Muscle Fibers
• Expected Learning Outcomes
– Explain how a nerve fiber stimulates a skeletal
muscle fiber.
– Explain how stimulation of a muscle fiber activates its
contractile mechanism.
– Explain the mechanism of muscle contraction.
– Explain how a muscle fiber relaxes.
– Explain why the force of a muscle contraction
depends on sarcomere length prior to stimulation.
11-40
Behavior of Skeletal Muscle Fibers
• Four major phases of contraction and relaxation
– Excitation
• The process in which nerve action potentials lead to muscle
action potentials
– Excitation–contraction coupling
• Events that link the action potentials on the sarcolemma to
activation of the myofilaments, thereby preparing them to contract
– Contraction
• Step in which the muscle fiber develops tension and may shorten
– Relaxation
• When its work is done, a muscle fiber relaxes and returns to its
resting length
11-41
Excitation
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Nerve signal
Motor
nerve
fiber
Ca2+ enters
synaptic knob
Synaptic
knob
Sarcolemma
Synaptic
vesicles
ACh
Synaptic
cleft
ACh
receptors
1 Arrival of nerve signal
2 Acetylcholine (ACh) release
Figure 11.8 (1, 2)
• Nerve signal opens voltage-gated calcium channels in synaptic
knob
• Calcium stimulates exocytosis of ACh from synaptic vesicles
• ACh released into synaptic cleft
11-42
Excitation
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ACh
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ACh
K+
ACh receptor
Sarcolemma
Na+
4 Opening of ligand-regulated ion gate;
creation of end-plate potential
3 Binding of ACh to receptor
Figure 11.8 (3, 4)
• Two ACh molecules bind to each receptor protein, opening Na+ and K+
channels
• Na+ enters; shifting RMP goes from −90 mV to +75 mV, then K+ exits and
RMP returns to −90 mV; quick voltage shift is called an end-plate
potential (EPP)
11-43
Excitation
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K+
Plasma
membrane
of synaptic
knob
Na+
Voltage-regulated
ion gates
Sarcolemma
Figure 11.8 (5)
5 Opening of voltage-regulated ion gates;
creation of action potentials
• Voltage change (EPP) in end-plate region opens nearby voltagegated channels producing an action potential that spreads over
muscle surface
11-44
Excitation–Contraction Coupling
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Figure 11.9 (6, 7)
Terminal
cisterna
of SR
T tubule
T tubule
Sarcoplasmic
reticulum
Ca2+
Ca2+
6 Action potentials propagated
down T tubules
7 Calcium released from
terminal cisternae
• Action potential spreads down into T tubules
• Opens voltage-gated ion channels in T tubules and Ca+2 channels in SR
11-45
• Ca+2 enters the cytosol
Excitation–Contraction Coupling
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Ca2+
Troponin
Tropomyosin
Active sites
Actin
Thin filament
Myosin
Ca2+
8 Binding of calcium
9 Shifting of tropomyosin;
to troponin
exposure of active sites
on actin
Figure 11.9 (8, 9)
• Calcium binds to troponin in thin filaments
• Troponin–tropomyosin complex changes shape and exposes active sites
11-46
on actin
Contraction
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Troponin
• Myosin ATPase
enzyme in myosin
head hydrolyzes an
ATP molecule
Tropomyosin
• Activates the head
“cocking” it in an
extended position
ADP
Pi
Myosin
10 Hydrolysis of ATP to ADP + Pi;
activation and cocking of myosin head
– ADP + Pi remain
attached
Cross-bridge:
Actin
Myosin
11 Formation of myosin–actin cross-bridge
Figure 11.10 (10, 11)
• Head binds to actin
active site forming a
myosin–actin crossbridge
11-47
Contraction
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• Myosin head releases
ADP and Pi, flexes pulling
thin filament past thick—
power stroke
• Upon binding more ATP,
myosin releases actin
and process is repeated
– Each head performs five
power strokes per second
– Each stroke utilizes one
molecule of ATP
ATP
13
Binding of new ATP;
breaking of cross-bridge
ADP
ADP
PPii
12
Power stroke; sliding of thin
filament over thick filament
Figure 11.10 (12, 13)
11-48
Relaxation
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Figure 11.11 (14, 15)
AChE
ACh
14 Cessation of nervous stimulation
and ACh release
15 ACh breakdown by
acetylcholinesterase (AChE)
• Nerve stimulation and ACh release stop
• AChE breaks down ACh and fragments reabsorbed into synaptic knob
• Stimulation by ACh stops
11-49
Relaxation
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Terminal cisterna
of SR
Ca2+
Ca2+
16 Reabsorption of calcium ions by
sarcoplasmic reticulum
Figure 11.11 (16)
• Ca+2 pumped back into SR by active transport
• Ca+2 binds to calsequestrin while in storage in SR
• ATP is needed for muscle relaxation as well as muscle contraction
11-50
Relaxation
•
Ca+2
removed from troponin
is pumped back into SR
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Ca2+
• Tropomyosin reblocks the
active sites
ADP
Pi
17
Ca2+
Loss of calcium ions from troponin
• Muscle fiber ceases to
produce or maintain tension
Tropomyosin
• Muscle fiber returns to its
resting length
– Due to recoil of elastic
components and
contraction of antagonistic
muscles
ATP
18
Return of tropomyosin to position
blocking active sites of actin
Figure 11.11 (17, 18)
11-51
The Length–Tension Relationship
and Muscle Tone
• Length–tension relationship—the amount of tension
generated by a muscle and the force of contraction
depends on how stretched or contracted it was before it
was stimulated
• If overly contracted at rest, a weak contraction results
– Thick filaments too close to Z discs and cannot slide
• If too stretched before stimulated, a weak contraction
results
– Little overlap of thin and thick does not allow for very
many cross-bridges to form
11-52
The Length–Tension Relationship
and Muscle Tone
• Optimum resting length produces greatest
force when muscle contracts
– Muscle tone: central nervous system continually
monitors and adjusts the length of the resting
muscle, and maintains a state of partial contraction
called muscle tone
– Maintains optimum length and makes the muscles
ideally ready for action
11-53
Length–Tension Relationship
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Optimum resting length
(2.0–2.25µm)
z
z
Overly contracted
z
z
Overly stretched
z
z
Tension (g) generated
upon stimulation
1.0
0.5
0.0
1.0
2.0
3.0
Sarcomere length (µm) before stimulation
Figure 11.12
4.0
11-54
Rigor Mortis
• Rigor mortis—hardening of muscles and stiffening of
body beginning 3 to 4 hours after death
–
–
–
–
Deteriorating sarcoplasmic reticulum releases Ca+2
Deteriorating sarcolemma allows Ca+2 to enter cytosol
Ca+2 activates myosin-actin cross-bridging
Muscle contracts, but cannot relax
• Muscle relaxation requires ATP, and ATP production is no
longer produced after death
– Fibers remain contracted until myofilaments begin to decay
• Rigor mortis peaks about 12 hours after death, then
diminishes over the next 48 to 60 hours
11-55
Behavior of Whole Muscles
• Expected Learning Outcomes
– Describe the stages of a muscle twitch.
– Explain why muscle does not contract in an all-ornone manner.
– Explain how successive muscle twitches can add up
to produce stronger muscle contractions.
– Distinguish between isometric and isotonic
contraction.
– Distinguish between concentric and eccentric
contraction.
11-56
Threshold, Latent Period, and Twitch
• Myogram—a chart of the
timing and strength of a
muscle’s contraction
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Relaxation
phase
Contraction
phase
Muscle tension
• The response of a muscle
to weak electrical stimulus
seen in frog
gastrocnemius—sciatic
nerve preparation
Latent
period
Time of
stimulation
Time
Figure 11.13
11-57
Threshold, Latent Period, and Twitch
• Weak, subthreshold
electrical stimulus causes no
contraction
Relaxation
phase
Contraction
phase
Muscle tension
• Threshold—minimum
voltage necessary to
generate an action potential
in the muscle fiber and
produce a contraction
– Twitch—a quick cycle of
contraction when stimulus
is at threshold or higher
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Latent
period
Time of
stimulation
Time
Figure 11.13
11-58
Threshold, Latent Period, and Twitch
• Latent period—2 ms delay between the onset of
stimulus and the onset of twitch response
– Time required for excitation, excitation–contraction coupling,
and tensing of elastic components of the muscle
– Internal tension: force generated during latent period and
no shortening of the muscle occurs
• Contraction phase—phase in which filaments slide
and the muscle shortens
– Once elastic components are taut, muscle begins to
produce external tension in muscle that moves a load
– Short-lived phase
11-59
Threshold, Latent Period, and Twitch
• Relaxation phase—SR quickly reabsorbs Ca2+,
myosin releases the thin filaments, and tension
declines
– Muscle returns to resting length
– Entire twitch lasts from 7 to 100 ms
11-60
Contraction Strength of Twitches
• At subthreshold stimulus—no contraction
at all
• At threshold intensity and above—a twitch
is produced
– Twitches caused by increased voltage are no
stronger than those at threshold
11-61
Contraction Strength of Twitches
• Not exactly true that muscle fiber obeys an all-ornone law—contracting to its maximum or not at all
– Electrical excitation of a muscle follows all-or-none law
– Not true that muscle fibers follow the all-or-none law
– Twitches vary in strength depending upon:
• Stimulus frequency—stimuli arriving closer together
produce stronger twitches
• Concentration of Ca+2 in sarcoplasm can vary the
frequency
11-62
Contraction Strength of Twitches
Cont.
• How stretched muscle was before it was stimulated
• Temperature of the muscles—warmed-up muscle contracts
more strongly; enzymes work more quickly
• Lower than normal pH of sarcoplasm weakens contraction—
fatigue
• State of hydration of muscle affects overlap of thick and
thin filaments
• Muscles need to be able to contract with variable
strengths for different tasks
11-63
Contraction Strength of Twitches
Stimulus voltage
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Threshold
1
2
3
Stimuli to nerve
4
5
6
7
8
9
Proportion of nerve fibers excited
Tension
Maximum contraction
1
2
3
4
5
6
7
8
9
Figure 11.14
Responses of muscle
• Stimulating the nerve with higher and higher voltages produces
stronger contractions
– Higher voltages excite more and more nerve fibers in the motor nerve
which stimulates more and more motor units to contract
• Recruitment or multiple motor unit (MMU) summation—the
process of bringing more motor units into play
11-64
Contraction Strength of Twitches
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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Treppe
Twitch
Muscle twitches
(a)
Stimuli
Figure 11.15a,b
(b)
• When stimulus intensity (voltage) remains constant
twitch strength can vary with the stimulus frequency
• Up to 10 stimuli per second
– Each stimulus produces identical twitches and full
recovery between twitches
11-65
Contraction Strength of Twitches
• 10–20 stimuli per second produces treppe (staircase)
phenomenon
– Muscle still recovers fully between twitches, but each
twitch develops more tension than the one before
– Stimuli arrive so rapidly that the SR does not have time
between stimuli to completely reabsorb all of the Ca2+ it
released
– Ca2+ concentration in the cytosol rises higher and higher
with each stimulus causing subsequent twitches to be
stronger
– Heat released by each twitch causes muscle enzymes
such as myosin ATPase to work more efficiently and
produce stronger twitches as muscle warms up
11-66
Contraction Strength of Twitches
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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Complete tetanus
Incomplete tetanus
Fatigue
(c)
(d)
Figure 11.15c,d
• 20–40 stimuli per second produces incomplete tetanus
– Each new stimulus arrives before the previous twitch is over
– New twitch “rides piggy-back” on the previous one
generating higher tension
– Temporal summation: results from two stimuli arriving close
together
11-67
Contraction Strength of Twitches
Cont.
– Wave summation: results from one wave of
contraction added to another
– Each twitch reaches a higher level of tension than the
one before
– Muscle relaxes only partially between stimuli
– Produces a state of sustained fluttering contraction
called incomplete tetanus
11-68
Contraction Strength of Twitches
• 40–50 stimuli per second produces complete
tetanus
– Muscle has no time to relax between stimuli
– Twitches fuse to a smooth, prolonged contraction
called complete tetanus
– A muscle in complete tetanus produces about four
times the tension as a single twitch
– Rarely occurs in the body, which rarely exceeds 25
stimuli per second
– Smoothness of muscle contractions is because motor
units function asynchronously
• When one motor unit relaxes, another contracts and takes
over so the muscle does not lose tension
11-69
Isometric and Isotonic Contraction
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Figure 11.16
Muscle develops
tension but does
not shorten
Muscle shortens,
tension remains
constant
Muscle lengthens
while maintaining
tension
Movement
Movement
No movement
(a) Isometric contraction
(b) Isotonic concentric contraction
(c) Isotonic eccentric contraction
• Isometric muscle contraction
– Muscle is producing internal tension while an external
resistance causes it to stay the same length or become
longer
– Can be a prelude to movement when tension is absorbed by
elastic component of muscle
– Important in postural muscle function and antagonistic muscle
joint stabilization
11-70
Isometric and Isotonic Contraction
• Isotonic muscle contraction
– Muscle changes in length with no change in tension
– Concentric contraction: muscle shortens as it
maintains tension
– Eccentric contraction: muscle lengthens as it
maintains tension
11-71
Isometric and Isotonic Contraction
Length or Tension
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Muscle
tension
Muscle
length
Isometric
phase
Isotonic
phase
Figure 11.17
Time
• At the beginning of contraction—isometric phase
– Muscle tension rises but muscle does not shorten
• When tension overcomes resistance of the load
– Tension levels off
• Muscle begins to shorten and move the load—isotonic phase
11-72
Muscle Metabolism
• Expected Learning Outcomes
– Explain how skeletal muscle meets its energy
demands during rest and exercise.
– Explain the basis of muscle fatigue and soreness.
– Define oxygen debt and explain why extra oxygen is
needed even after an exercise has ended.
– Distinguish between two physiological types of
muscle fibers, and explain their functional roles.
– Discuss the factors that affect muscular strength.
– Discuss the effects of resistance and endurance
exercises on muscles.
11-73
ATP Sources
• All muscle contraction depends on ATP
• ATP supply depends on availability of:
– Oxygen
– Organic energy sources such as glucose and fatty
acids
11-74
ATP Sources
• Two main pathways of ATP synthesis
– Anaerobic fermentation
• Enables cells to produce ATP in the absence of oxygen
• Yields little ATP and toxic lactic acid, a major factor in muscle
fatigue
– Aerobic respiration
• Produces far more ATP
• Less toxic end products (CO2 and water)
• Requires a continual supply of oxygen
11-75
ATP Sources
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0
10 seconds
40 seconds
Duration of exercise
Repayment of
oxygen debt
Mode of ATP synthesis
Aerobic respiration
using oxygen from
myoglobin
Phosphagen
system
Glycogen–
lactic acid
system
(anaerobic
fermentation)
Aerobic
respiration
supported by
cardiopulmonary
function
Figure 11.18
11-76
Immediate Energy
• Short, intense exercise (100 m dash)
– Oxygen need is briefly supplied by myoglobin for a limited
amount of aerobic respiration at onset—rapidly depleted
– Muscles meet most of ATP demand by borrowing phosphate
groups (Pi) from other molecules and transferring them to
ADP
• Two enzyme systems control these phosphate
transfers
– Myokinase: transfers Pi from one ADP to another,
converting the latter to ATP
– Creatine kinase: obtains Pi from a phosphate-storage
molecule creatine phosphate (CP)
• Fast-acting system that helps maintain the ATP level while
other ATP-generating mechanisms are being activated
11-77
Immediate Energy
• Phosphagen system—ATP and CP collectively
– Provides nearly all energy used for short bursts of
intense activity
• 1 minute of brisk walking
• 6 seconds of sprinting or fast swimming
• Important in activities requiring brief but maximum
effort
– Football, baseball, and weightlifting
11-78
Immediate Energy
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
ADP
ADP
Pi
Myokinase
ATP
AMP
ADP
Creatine
phosphate
Pi
Figure 11.19
Creatine
Creatine
kinase
ATP
11-79
Short-Term Energy
• As the phosphagen system is exhausted muscles shift
to anaerobic fermentation
– Muscles obtain glucose from blood and their own stored
glycogen
– In the absence of oxygen, glycolysis can generate a net
gain of 2 ATP for every glucose molecule consumed
– Converts glucose to lactic acid
• Glycogen–lactic acid system—the pathway from
glycogen to lactic acid
• Produces enough ATP for 30 to 40 seconds of
maximum activity
11-80
Long-Term Energy
• After 40 seconds or so, the respiratory and
cardiovascular systems “catch up” and deliver
oxygen to the muscles fast enough for aerobic
respiration to meet most of the ATP demands
11-81
Long-Term Energy
• Aerobic respiration produces 36 ATP per glucose
– Efficient means of meeting the ATP demands of
prolonged exercise
– One’s rate of oxygen consumption rises for 3 to 4
minutes and levels off to a steady state in which aerobic
ATP production keeps pace with demand
11-82
Long-Term Energy
Cont.
– Little lactic acid accumulates under steady-state
conditions
– Depletion of glycogen and blood glucose, together with
the loss of fluid and electrolytes through sweating, set
limits on endurance and performance even when lactic
acid does not
11-83
Fatigue and Endurance
• Muscle fatigue—progressive weakness and loss of
contractility from prolonged use of the muscles
– Repeated squeezing of rubber ball
– Holding textbook out level to the floor
• Fatigue is thought to result from:
– ATP synthesis declines as glycogen is consumed
– ATP shortage slows down the Na+–K+ pumps
• Compromises their ability to maintain the resting
membrane potential and excitability of the muscle fibers
– Lactic acid lowers pH of sarcoplasm
• Inhibits enzymes involved in contraction, ATP synthesis,
and other aspects of muscle function
11-84
Fatigue and Endurance
• Fatigue is thought to result from (cont.):
– Release of K+ with each action potential causes the
accumulation of extracellular K+
• Hyperpolarizes the cell and makes the muscle fiber less
excitable
– Motor nerve fibers use up their ACh
• Less capable of stimulating muscle fibers—junctional
fatigue
– Central nervous system, where all motor commands
originate, fatigues by unknown processes, so there is less
signal output to the skeletal muscles
11-85
Fatigue and Endurance
• Endurance—the ability to maintain high-intensity
exercise for more than 4 to 5 minutes
– Determined in large part by one’s maximum oxygen
uptake (VO2max)
– Maximum oxygen uptake: the point at which the rate
of oxygen consumption reaches a plateau and does not
increase further with an added workload
•
•
•
•
Proportional to body size
Peaks at around age 20
Usually greater in males than females
Can be twice as great in trained endurance athletes as in
untrained persons
– Results in twice the ATP production
11-86
Oxygen Debt
• Heavy breathing continues after strenuous exercise
– Excess postexercise oxygen consumption (EPOC):
the difference between the resting rate of oxygen
consumption and the elevated rate following exercise
– Typically about 11 L extra is needed after strenuous
exercise
• Needed for the following purposes:
– Replace oxygen reserves depleted in the first minute
of exercise
• Oxygen bound to myoglobin and blood hemoglobin,
oxygen dissolved in blood plasma and other
extracellular fluid, and oxygen in the air in the lungs
11-87
Oxygen Debt
• Needed for the following purposes (cont.):
– Replenishing the phosphagen system
• Synthesizing ATP and using some of it to donate the
phosphate groups back to creatine until resting levels
of ATP and CP are restored
– Oxidizing lactic acid
• 80% of lactic acid produced by muscles enter
bloodstream
11-88
Oxygen Debt
Cont.
• Reconverted to pyruvic acid in the kidneys, cardiac
muscle, and especially the liver
• Liver converts most of the pyruvic acid back to glucose
to replenish the glycogen stores of the muscle
– Serving the elevated metabolic rate
• Occurs while the body temperature remains elevated
by exercise and consumes more oxygen
11-89
Physiological Classes of
Muscle Fibers
• Slow oxidative (SO), slow-twitch, red, or type I fibers
– Abundant mitochondria, myoglobin, capillaries: deep red
color
• Adapted for aerobic respiration and fatigue resistance
– Relative long twitch lasting about 100 ms
– Soleus of calf and postural muscles of the back
11-90
Physiological Classes of
Muscle Fibers
• Fast glycolytic (FG), fast-twitch, white, or type II fibers
– Fibers are well adapted for quick responses, but not for fatigue
resistance
– Rich in enzymes of phosphagen and glycogen–lactic acid
systems generate lactic acid, causing fatigue
– Poor in mitochondria, myoglobin, and blood capillaries which
gives pale appearance
• SR releases and reabsorbs Ca2+ quickly so contractions are
quicker (7.5 ms/twitch)
– Extrinsic eye muscles, gastrocnemius, and biceps
brachii
11-91
Physiological Classes of
Muscle Fibers
• Ratio of different fiber types
have genetic predisposition—
born sprinter
– Muscles differ in fiber
types: gastrocnemius is
predominantly FG for
quick movements
(jumping)
– Soleus is predominantly
SO used for endurance
(jogging)
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FG
SO
Dr. Gladden Willis/Visuals Unlimited, Inc.
Figure 11.20
11-92
Muscular Strength and Conditioning
• Muscles can generate more tension than the bones
and tendons can withstand
• Muscular strength depends on:
– Primarily muscle size
• A muscle can exert a tension of 3 or 4 kg/cm2 of crosssectional area
– Fascicle arrangement
• Pennate are stronger than parallel, and parallel stronger
than circular
– Size of motor units
• The larger the motor unit the stronger the contraction
11-93
Muscular Strength and Conditioning
• Muscular strength depends on (cont.)
– Multiple motor unit summation: recruitment
• When stronger contraction is required, the nervous system
activates more motor units
– Temporal summation
• Nerve impulses usually arrive at a muscle in a series of closely
spaced action potentials
• The greater the frequency of stimulation, the more strongly a
muscle contracts
11-94
Muscular Strength and Conditioning
Cont.
– Length–tension relationship
• A muscle resting at optimal length is prepared to contract more
forcefully than a muscle that is excessively contracted or
stretched
– Fatigue
• Fatigued muscles contract more weakly than rested muscles
11-95
Muscular Strength and Conditioning
• Resistance training (weightlifting)
– Contraction of a muscle against a load that resists
movement
– A few minutes of resistance exercise a few times a
week is enough to stimulate muscle growth
– Growth is from cellular enlargement
– Muscle fibers synthesize more myofilaments and
myofibrils and grow thicker
11-96
Muscular Strength and Conditioning
• Endurance training (aerobic exercise)
– Improves fatigue-resistant muscles
– Slow twitch fibers produce more mitochondria,
glycogen, and acquire a greater density of blood
capillaries
– Improves skeletal strength
– Increases the red blood cell count and oxygen
transport capacity of the blood
– Enhances the function of the cardiovascular,
respiratory, and nervous systems
11-97
Cardiac and Smooth Muscle
• Expected Learning Outcomes
– Describe the structural and physiological differences
between cardiac muscle and skeletal muscle.
– Explain why these differences are important to
cardiac function.
– Describe the structural and physiological differences
between smooth muscle and skeletal muscle.
– Relate the unique properties of smooth muscle to its
locations and functions.
11-98
Cardiac Muscle
• Limited to the heart where it functions to pump
blood
• Properties of cardiac muscle
– Contraction with regular rhythm
– Muscle cells of each chamber must contract in
unison
– Contractions must last long enough to expel blood
– Must work in sleep or wakefulness, without fail, and
without conscious attention
– Must be highly resistant to fatigue
11-99
Cardiac Muscle
• Characteristics of cardiac muscle cells
– Striated like skeletal muscle, but myocytes (cardiocytes)
are shorter and thicker
– Each myocyte is joined to several others at the uneven,
notched linkages—intercalated discs
• Appear as thick, dark lines in stained tissue sections
• Electrical gap junctions allow each myocyte to directly stimulate
its neighbors
• Mechanical junctions that keep the myocytes from pulling apart
11-100
Cardiac Muscle
• Sarcoplasmic reticulum less developed, but T
tubules are larger and admit supplemental Ca2+
from the extracellular fluid
• Damaged cardiac muscle cells repair by
fibrosis
– A little mitosis observed following heart attacks
– Not in significant amounts to regenerate functional
muscle
11-101
Cardiac Muscle
• Can contract without need for nervous
stimulation
– Contains a built-in pacemaker that rhythmically sets
off a wave of electrical excitation
– Wave travels through the muscle and triggers
contraction of heart chambers
– Autorhythmic: able to contract rhythmically and
independently
11-102
Cardiac Muscle
– Autonomic nervous system does send nerve fibers to
the heart
• Can increase or decrease heart rate and contraction
strength
– Very slow twitches; does not exhibit quick twitches like
skeletal muscle
• Maintains tension for about 200 to 250 ms
• Gives the heart time to expel blood
– Uses aerobic respiration almost exclusively
• Rich in myoglobin and glycogen
• Has especially large mitochondria
– 25% of volume of cardiac muscle cell
– 2% of skeletal muscle cell with smaller mitochondria
11-103
Smooth Muscle
• Sarcoplasmic reticulum is scanty and there are no
T tubules
• Ca2+ needed for muscle contraction comes from
the ECF by way of Ca2+ channels in the
sarcolemma
• Some smooth muscles lack nerve supply, while
others receive autonomic fibers, not somatic
motor fibers as in skeletal muscle
• Capable of mitosis and hyperplasia
• Injured smooth muscle regenerates well
11-104
Myocyte Structure
• Myocytes have a fusiform shape
– There is only one nucleus, located near the middle of the
cell
– No visible striations
– Reason for the name “smooth muscle”
– Thick and thin filaments are present, but not aligned with
each other
• Z discs are absent and replaced by dense bodies
– Well-ordered array of protein masses in cytoplasm
– Protein plaques on the inner face of the plasma
membrane
11-105
Myocyte Structure
• Cytoplasm contains extensive cytoskeleton of
intermediate filament
– Attach to the membrane plaques and dense bodies
– Provide mechanical linkages between the thin
myofilaments and the plasma membrane
11-106
Types of Smooth Muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
• Multiunit smooth muscle
Autonomic
nerve fibers
– Occurs in some of the largest
arteries and pulmonary air
passages, in piloerector
muscles of hair follicle, and in
the iris of the eye
Synapses
– Autonomic innervation similar
to skeletal muscle
• Terminal branches of a nerve
fiber synapse with individual
myocytes and form a motor
unit
• Each motor unit contracts
independently of the others
(a) Multiunit
smooth muscle
Figure 11.23a
11-107
Types of Smooth Muscle
• Single-unit smooth muscle
– More widespread
– Occurs in most blood
vessels, in the digestive,
respiratory, urinary, and
reproductive tracts
– Also called visceral muscle
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Autonomic
nerve fibers
Varicosities
• Often in two layers: inner
circular and outer
longitudinal
– Myocytes of this cell type are
electrically coupled to each
other by gap junctions
– They directly stimulate each
other and a large number of
cells contract as a single
unit
Gap junctions
(b) Single-unit
smooth muscle
Figure 11.23b
11-108
Types of Smooth Muscle
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Autonomic
nerve fiber
Varicosities
Mitochondrion
Synaptic
vesicle
Single-unit
smooth muscle
Figure 11.21
11-109
Types of Smooth Muscle
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Figure 11.22
Mucosa:
Epithelium
Lamina propria
Muscularis
mucosae
Muscularis externa:
Circular layer
Longitudinal
layer
11-110
Excitation of Smooth Muscle
• Smooth muscle is involuntary and can contract
without nervous stimulation
– Can contract in response to chemical stimuli
• Hormones, carbon dioxide, low pH, and oxygen deficiency
• In response to stretch
• Single-unit smooth muscle in stomach and intestines has
pacemaker cells that set off waves of contraction throughout
the entire layer of muscle
11-111
Excitation of Smooth Muscle
• Most smooth muscle is innervated by autonomic
nerve fibers
– Can trigger and modify contractions
– Stimulate smooth muscle with either acetylcholine or
norepinephrine
– Can have contrasting effects
• Relax the smooth muscle of arteries
• Contract smooth muscles of the bronchioles
11-112
Excitation of Smooth Muscle
• In single-unit smooth, each autonomic nerve
fiber has up to 20,000 beadlike swellings called
varicosities
– Each contains synaptic vesicles and a few
mitochondria
– Nerve fiber passes amid several myocytes and
stimulates all of them at once when it releases its
neurotransmitter
• No motor end plates, but receptors scattered throughout the
surface—diffuse junctions—no one-to-one relationship
between nerve fiber and myocyte
11-113
Contraction and Relaxation
• Contraction is triggered by Ca2+, energized by
ATP, and achieved by sliding thin past thick
filaments
• Contraction begins in response to Ca2+ that
enters the cell from ECF, a little internally from
sarcoplasmic reticulum
– Voltage, ligand, and mechanically gated (stretching)
– Ca2+ channels open to allow Ca2+ to enter cell
11-114
Contraction and Relaxation
• Calcium binds to calmodulin on thick filaments
– Activates myosin light-chain kinase; adds
phosphate to regulatory protein on myosin head
– Myosin ATPase, hydrolyzing ATP
• Enables myosin similar power and recovery strokes like
skeletal muscle
11-115
Contraction and Relaxation
Cont.
– Thick filaments pull on thin ones, thin ones pull on
dense bodies and membrane plaques
– Force is transferred to plasma membrane and entire
cell shortens
– Puckers and twists like someone wringing out a wet
towel
11-116
Contraction and Relaxation
• Contraction and relaxation very slow in
comparison to skeletal muscle
– Latent period in skeletal 2 ms, smooth muscle 50 to
100 ms
– Tension peaks at about 500 ms (0.5 sec)
– Declines over a period of 1 to 2 seconds
– Slows myosin ATPase enzyme and pumps that
remove Ca2+
– Ca2+ binds to calmodulin instead of troponin
• Activates kinases and ATPases that hydrolyze ATP
11-117
Contraction and Relaxation
• Latch-bridge mechanism is resistant to fatigue
– Heads of myosin molecules do not detach from actin
immediately
– Do not consume any more ATP
– Maintains tetanus tonic contraction (smooth muscle
tone)
• Arteries—vasomotor tone; intestinal tone
– Makes most of its ATP aerobically
11-118
Smooth Muscle Contraction
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Plaque
Intermediate filaments
of cytoskeleton
Actin filaments
Dense body
Myosin
(b) Contracted smooth
muscle cells
Figure 11.24a,b
(a) Relaxed smooth muscle cells
11-119
Response to Stretch
• Stretch can open mechanically gated calcium
channels in the sarcolemma causing contraction
– Peristalsis: waves of contraction brought about by food
distending the esophagus or feces distending the colon
• Propels contents along the organ
• Stress–relaxation response (receptive relaxation)—
helps hollow organs gradually fill (urinary bladder)
– When stretched, tissue briefly contracts then relaxes;
helps prevent emptying while filling
11-120
Response to Stretch
• Skeletal muscle cannot contract forcefully if
overstretched
• Smooth muscle contracts forcefully even when
greatly stretched
– Allows hollow organs such as the stomach and
bladder to fill and then expel their contents
efficiently
11-121
Response to Stretch
• Smooth muscle can be anywhere from half to
twice its resting length and still contract powerfully
• Three reasons
– There are no Z discs, so thick filaments cannot butt
against them and stop contraction
– Since the thick and thin filaments are not arranged in
orderly sarcomeres, stretching does not cause a
situation where there is too little overlap for crossbridges to form
– The thick filaments of smooth muscle have myosin
heads along their entire length, so cross-bridges can
form anywhere
11-122
Response to Stretch
• Plasticity—the ability to adjust its tension to the
degree of stretch
– A hollow organ such as the bladder can be greatly
stretched yet not become flabby when empty
11-123
Muscular Dystrophy
• Muscular dystrophy―group of hereditary diseases in
which skeletal muscles degenerate and weaken, and
are replaced with fat and fibrous scar tissue
• Duchenne muscular dystrophy is caused by a sexlinked recessive trait (1 of 3,500 live-born boys)
– Most common form
– Disease of males; diagnosed between 2 and 10 years of age
– Mutation in gene for muscle protein dystrophin
• Actin not linked to sarcolemma and cell membranes damaged
during contraction; necrosis and scar tissue result
– Rarely live past 20 years of age due to effects on respiratory
and cardiac muscle; incurable
11-124
Myasthenia Gravis
• Autoimmune disease in which antibodies attack
neuromuscular junctions and bind ACh receptors
together in clusters
– Disease of women between 20 and 40
– Muscle fibers then remove the clusters of receptors from
the sarcolemma by endocytosis
– Fiber becomes less and less sensitive to Ach
– Effects usually first appear in facial muscles
• Drooping eyelids and double vision, difficulty swallowing, and
weakness of the limbs
– Strabismus: inability to fixate on the same point with
both eyes
11-125
Myasthenia Gravis
Cont.
• Treatments
– Cholinesterase inhibitors retard breakdown of ACh
allowing it to stimulate the muscle longer
– Immunosuppressive agents suppress the production
of antibodies that destroy ACh receptors
– Thymus removal (thymectomy) helps to dampen the
overactive immune response that causes myasthenia
gravis
– Plasmapheresis: technique to remove harmful
antibodies from blood plasma
11-126
Myasthenia Gravis
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Figure 11.25
• Drooping eyelids and weakness of muscles of eye
movement upon upward gaze
11-127