Chapter 11
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11-1
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Muscle Tissue
• Types and Characteristics of Muscle Tissue
• Microscopic Anatomy of Skeletal Muscle
• Behavior of Skeletal Muscle Fibers
• Behavior of Whole Muscles
• Muscle Metabolism
• Cardiac and Smooth Muscle
11-2
Introduction to Muscle
• Create movement
• muscle cells convert chemical energy of ATP
into mechanical energy
• types of muscle
– skeletal, cardiac, and smooth
• physiology of skeletal muscle
– basis of warm-up, quickness, strength,
endurance, and fatigue
11-3
Characteristics of Muscle
• responsiveness (excitability)
– chemical signals, stretch and electrical changes
• 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
Nucleus
• striations - alternating light
and dark transverse bands
– results from an overlapping of
internal contractile proteins
Muscle fiber
Endomysium
Striations
• voluntary – usually subject
to conscious control
Figure 11.1
• muscle cell, muscle fiber,
(myofiber) as long as 30 cm
11-5
Connective Tissue Elements
• 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 and thus with bones
• collagen
– stretches slightly under tension and recoils when released
• protects muscle from injury
• contribute to power output and muscle efficiency
11-6
The Muscle Fiber
• sarcolemma – plasma membrane of a muscle fiber
• sarcoplasm – cytoplasm of a muscle fiber
• myofibrils – long protein bundles in main portion of sarcoplasm
– glycogen – provides energy
– myoglobin – red pigment – stores oxygen
– mitochondria – packed in spaces between myofibrils
• sarcoplasmic reticulum (SR) - smooth ER that forms a
network around each myofibril – calcium reservoir
• terminal cisternae – end-sacs of SR which cross muscle fiber
• T tubules – tubular infoldings of the sarcolemma which
penetrate through the cell and emerge on the other side
11-7
Structure of a Skeletal Muscle
Fiber
Muscle
fiber
Nucleus
A band
I band
Z disc
Openings into
transverse tubules
Mitochondria
Sarcoplasmic
reticulum
Triad:
Terminal cisternae
Transverse tubule
Sarcolemma
Sarcoplasm
Myofibrils
Myofilaments
Figure 11.2
11-8
Myofibrils:Thick Myofilaments
Tail
Head
(a) Myosin molecule
Myosin head
(b) Thick filament
• made of several hundred myosin molecules
– shaped like a golf club
– 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
11-9
Thin Myofilaments
• actin - two intertwined strands
– string of globular subunits each with an active site that
can bind to head of myosin molecule
• tropomyosin molecules
– each blocking 6 or 7 active sites on actin subunits
• troponin molecule - small, calcium-binding protein
on each tropomyosin molecule
Tropomyosin
(c) Thin filament
Troponin complex
G actin
Figure 11.3c
11-10
Regulatory and Contractile Proteins
• contractile proteins - myosin and actin
– do the work
• regulatory proteins - tropomyosin and troponin
– like a switch that determines if the fiber can contract
– contraction activated by calcium binding to troponin,
– troponin changes shape and moves tropomyosin off the
active sites on actin
11-11
Overlap of Thick and Thin Filaments
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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
11-12
Striations
• myosin and actin occur in all cells
• organized in a precise way in skeletal and cardiac muscle
– A band – dark
– I band – alternating lighter band
– z disc – provides anchorage for thin filaments and elastic
filaments - bisects I band
– sarcomere – the segment of the myofibril from one z disc to
the next
I band
(b)
Z disc
Sarcomere
A band
H band
Thick filament
Thin filament
M line
Elastic filament
I band
Titin
Z disc
11-13
Striations and Sarcomeres
Nucleus
M line
Z disc
H band
A band
I band
1
I band
2
3
4
Individual myofibrils
5
Sarcomere
(a)
Visuals Unlimited
sarcomere - segment from Z disc to Z disc
- functional contractile unit of muscle fiber
11-14
Sarcomeres
• muscle cells shorten b/c 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, linking proteins also pull on
extracellular proteins
– transfers pull to extracellular tissue
11-15
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
• somatic motor neurons – nerve cells that serve
skeletal muscles
– each muscle fiber is supplied by only one motor neuron
(but one motor neuron may lead to many muscle fibers)
11-16
Motor Neurons
axon
axon terminal
muscle fiber
11-17
• motor unit – one nerve fiber and
all the muscle fibers innervated
by it
Motor Units
Spinal cord
• muscle fibers of one motor unit
– dispersed throughout the
muscle
– contract in unison
– weak contraction over wide
area
Neuromuscular
junction
– can sustain long-term
contraction as motor units take Skeletal
muscle
turns contracting (postural
fibers
control)
– effective contraction usually
requires the contraction of
several motor units at once
Motor
neuron 1
Motor
neuron 2
11-18
• average motor unit – 200 muscle
fibers for each motor unit
Motor Units
Spinal cord
• small motor units - fine degree
of control
– 3-6 muscle fibers per neuron
– eye and hand muscles
• large motor units – more
strength than control
– many muscle fibers per motor
unit
– powerful contractions –
gastrocnemius – 1000 muscle
fibers per neuron
Motor
neuron 1
Motor
neuron 2
Neuromuscular
junction
Skeletal
muscle
fibers
11-19
The Neuromuscular Junction
• synapse – point where a nerve fiber meets its
target cell
• neuromuscular junction (NMJ) - when target
cell is a muscle fiber
• one nerve fiber stimulates the muscle fiber at
several points within the NMJ
• action potential - the electrical signal that is
produced by the nerve cell and transferred to
the muscle fiber
11-20
Neuromuscular Junction - LM
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Motor nerve
fibers
Neuromuscular
junction
Muscle fibers
Figure 11.7a
(a)
100 µm
Victor B. Eichler
11-21
Neuromuscular Toxins
• toxins that interfere with synaptic function can paralyze muscles
• spastic paralysis - continual contraction of the muscles
– some pesticides prevent signal from “turning off”
– possible suffocation
– tetanus (lockjaw) is a form of spastic paralysis caused by
toxin of 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
• flaccid paralysis – muscles are limp and cannot contract
– curare – blocks nerve signals - plant poison used by S.
American natives on blowgun darts
– botulism – type of food poisoning caused by a toxin
secreted by the bacterium Clostridium botulinum
11-22
Muscle Contraction & Relaxation
• four major phases of contraction and relaxation
1.) excitation
• the process in which nerve action potentials lead to
muscle action potentials
2.) excitation-contraction coupling
• linking action potentials on the sarcolemma to activation of
the myofilaments, thereby preparing them to contract
3.) contraction
• muscle fiber develops tension and may shorten
4.) relaxation
• when its work is done, muscle fiber relaxes and returns to
11-23
its resting length
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11-24
Excitation-Contraction Coupling
(steps 6 and 7)
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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
• action potential spreads down into T tubules
• opens Ca+2 channels in SR
• Ca+2 enters the cytosol
7 Calcium released from
terminal cisternae
11-25
Excitation-Contraction Coupling
(steps 8 and 9)
Ca2+
Troponin
Tropomyosin
Ca2+
8 Binding of calcium
to troponin
Actin
Thin filament
Active sites
Myosin
9 Shifting of tropomyosin;
exposure of active sites
on actin
• calcium binds to troponin in thin filaments
• troponin-tropomyosin complex changes shape and exposes
active sites on actin
11-26
Contraction (steps 10 and 11)
• myosin ATPase
enzyme in myosin
head hydrolyzes
an ATP molecule
TroponinTropomyosin
ADP
Pi
Myosin
10Hydrolysis of ATP to ADP + Pi;
activation and cocking of myosin head
• activates the head
“cocking” it in an
extended position
– ADP + Pi remain
attached
• head binds to actin
active site forming
11Formation of myosin–actin cross-bridge
a myosin - actin
cross-bridge
Cross-bridge:
Actin
Myosin
Figure 11.10 (10-11)
11-27
Contraction (steps 12 and 13)
• 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 5
power strokes per second
– each stroke utilizes one
molecule of ATP
ATP
13Binding of new ATP;
breaking of cross-bridge
ADP
ADP
P
Pii
12Power stroke; sliding of thin
filament over thick filament
Figure 11.10 (12-13)
11-28
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11-29
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11-30
Relaxation (step 16)
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• Nerve signal stops
• Ca+2 pumped back into SR by
active transport. Ca+2 binds to
calsequestrin while in storage
Terminal cisterna
of SR
Ca2+
Ca2+
• ATP is needed for muscle
relaxation as well as muscle
contraction.
16 Reabsorption of calcium ions by
sarcoplasmic reticulum
11-31
Relaxation (steps 17 and 18)
• Ca+2 removed from troponin
is pumped back into SR
Ca2+
• tropomyosin reblocks the
active sites
ADP
Pi
Ca2+
17Loss of calcium ions
from troponin
• muscle fiber ceases to
produce or maintain tension
Tropomyosin
• muscle fiber returns to its
resting length
– recoil of elastic components
& contraction of antagonistic
muscles
ATP
18Return of tropomyosin to position
blocking active sites of actin
Figure 11.11 (17-18)
11-32
Rigor Mortis
• rigor mortis - stiffening of muscles 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
11-33
Length-Tension Relationship
• Length – Tension Relationship - the force of contraction
depends on how stretched or contracted the muscle was before it
was stimulated
• if overly contracted at rest, - weak contraction
– thick filaments too close to Z discs and can’t slide
• if too stretched before stimulated, - weak contraction
– not enough overlap of thin and thick filaments
• optimum resting length produces greatest force when muscle
contracts
– muscle tone – central nervous system maintains a state of
partial contraction called muscle tone
– maintains optimum length and makes the muscles ideally
ready for action
11-34
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
11-35
Behavior of Whole Muscles
• myogram – a chart of the timing
and strength of a muscle’s
contraction
• threshold - the 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
Relaxation
phase
Contraction
phase
Muscle tension
• weak, subthreshold electrical
stimulus causes no contraction
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Latent
period
Time of
stimulation
Time
Figure 11.13
11-36
Phases of a Twitch Contraction
• latent period - 2 msec delay between the onset of stimulus
and onset of twitch response
– time required to get things going
– internal tension – force generated during latent period and no
shortening of the muscle occurs
• contraction phase – filaments slide and muscle shortens
– once elastic components are taut, muscle begins to produce
external tension – in muscle that moves a load
• relaxation phase - SR reabsorbs Ca+2, myosin releases thin
filaments and tension declines
– muscle returns to resting length
– entire twitch lasts from 7 to 100 msec
11-37
Behavior of Whole Muscles
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Relaxation
phase
Muscle tension
Contraction
phase
Latent
period
Figure 11.13
Time of
stimulation
Time
11-38
Contraction Strength of Twitches
• at threshold intensity and above - a twitch is produced
– higher voltage does not mean stronger twitch
• not entirely all-or-none– twitches vary in strength depending upon:
• stimulus frequency - stimuli arriving closer together
mean stronger twitches
• concentration of Ca+2 in sarcoplasm
• how stretched muscle was before stimulation
• temperature of the muscles – warm muscle contracts
more strongly – enzymes work more quickly
• lower than normal pH weakens the contraction - fatigue
• state of hydration of muscle affects overlap of thick &
thin filaments
11-39
Isometric and Isotonic Contractions
Muscle develops
tension but does
not shorten
Muscle shortens,
tension remains
constant
Movement
No movement
(a) Isometric contraction
(b) Isotonic concentric contraction
Muscle lengthens
while maintaining
tension
Movement
(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 posture and joint stabilization
11-40
Isometric and Isotonic Contractions
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Muscle develops
tension but does
not shorten
Muscle shortens,
tension remains
constant
Muscle lengthens
while maintaining
tension
Movement
No movement
(a) Isometric contraction
Movement
(b) Isotonic concentric contraction (c) Isotonic eccentric contraction
• isotonic muscle contraction
– muscle changes in length with no change in tension
– concentric contraction – muscle shortens while
maintains tension
– eccentric contraction – muscle lengthens as it maintains
tension
11-41
Muscle Metabolism
• all muscle contraction depends on ATP
• ATP supply depends on availability of:
– oxygen
– organic energy sources such as glucose and fatty acids
• 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
11-42
Modes of ATP Synthesis
During Exercise
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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)
Figure 11.18
Aerobic
respiration
supported by
cardiopulmonary
function
11-43
Immediate Energy Needs
• short, intense exercise (100 m dash)
– oxygen first 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
• creatine kinase – obtains Pi from a phosphate-storage
molecule creatine phosphate (CP)
• phosphagen system – ATP and CP collectively
– provides nearly all energy for short bursts of intense activity
• important in activities requiring brief but maximum effort
– football, baseball, and weight lifting
11-44
Immediate Energy Needs
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ADP
ADP
Pi
Myokinase
ATP
AMP
ADP
Creatine
phosphate
Pi
Figure 11.19
Creatine
Creatine
kinase
ATP
11-45
Short-Term Energy Needs
• 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
– converts glucose (from glycogen) to lactic acid
• produces enough ATP for 30 – 40 seconds of maximum
activity
11-46
Long-Term Energy Needs
• 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
• aerobic respiration produces 36 ATP per glucose
– oxygen consumption rises for 3-4 minutes & then levels off
– little lactic acid accumulates
– 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
11-47
Fatigue
• muscle fatigue - progressive weakness and loss of contractility from
prolonged use of the muscles
• causes of muscle fatigue
– ATP synthesis declines as glycogen is consumed
– ATP shortage slows down the Na+ - K+ pumps
• lowers excitability of the muscle fibers
– lactic acid lowers pH of sarcoplasm
• inhibits enzymes involved in contraction, ATP synthesis, etc.
– release of K+ with each action potential causes the accumulation
of extracellular K+
• makes the muscle fiber less excitable
– motor nerve fibers use up their signalling chemicals
• less capable of stimulating muscle fibers
– central nervous system, where all motor commands originate,
fatigues by unknown processes
11-48
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 person
11-49
Oxygen Debt
• heavy breathing continues after strenuous exercise
– excess post-exercise oxygen consumption
(EPOC) – the difference between the resting rate of
oxygen consumption and the elevated rate following
exercise.
– typically about 11 liters extra is needed after
strenuous exercise
– repaying the oxygen debt
11-50
Oxygen Debt
• needed for the following purposes:
– replace oxygen reserves depleted in the 1st min. of exercise
– replenishing the phosphagen system
• synthesized ATP to donate phosphate groups back to
creatine until resting levels of ATP and CP are restored
– oxidizing lactic acid
• reconverted to pyruvic acid in the kidneys, cardiac muscle,
and especially the liver
• liver converts most pyruvic acid back to glucose to replace
the muscle glycogen stores
– serving the elevated metabolic rate
• body temperature is elevated & consumes more oxygen
11-51
Beating Muscle Fatigue
• taking oral creatine increases level of creatine phosphate in
muscle tissue and increases speed of ATP regeneration
– useful in burst type exercises – weight-lifting
– risks are not well known
• muscle cramping, electrolyte imbalances, dehydration,
water retention, stroke
• kidney disease from overloading kidney with metabolite
creatinine
• carbohydrate loading – dietary regimen
– packs extra glycogen into muscle cells
– extra glycogen is hydrophilic and adds 2.7 g water/ g
glycogen
• sense of heaviness may outweigh benefits
11-52
Physiological Classes of Muscle Fibers
• slow oxidative (SO), slow-twitch, red, or type I fibers
– abundant mitochondria, myoglobin and capillaries - deep
red color
• adapted for aerobic respiration and fatigue
resistance
– relative long twitch lasting about 100 msec
– soleus of calf and postural muscles of the back
•
11-53
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
– phosphagen and glycogen-lactic acid systems generate lactic
acid, causing fatigue
– poor in mitochondria, myoglobin, and blood capillaries which
gives pale appearance
• SR releases & reabsorbs Ca+2 quickly so contractions are
quicker
– extrinsic eye muscles, gastrocnemius and biceps
brachii
• ratio of different fiber types have genetic predisposition – “born
sprinter,” etc.
11-54
FG and SO Muscle Fibers
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FG
SO
Figure 11.20
11-55
Strength and Conditioning
• muscular strength depends on:
– primarily muscle size
• cross-sectional area
– fascicle arrangement
• pennate stronger than parallel, parallel stronger than circular
– size of motor units
• larger the motor unit the stronger the contraction
– multiple motor unit summation – recruitment
• if stronger contraction required, nervous system activates
more motor units
– temporal summation
• more frequent stimulation means stronger contraction
– length – tension relationship
• a muscle at optimal length contracts more forcefully
– fatigue
• fatigued muscles contract more weakly than rested muscles
11-56
Strength and Conditioning
• resistance training (weight lifting)
– contraction of a muscles 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
11-57
Strength and Conditioning
• endurance training (aerobic exercise)
– improves fatigue resistance
– 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
11-58
Cardiac Muscle
• limited to the heart where it functions to pump blood
• required 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
11-59
Cardiac Muscle
• characteristics of cardiac muscle cells
– striated like skeletal muscle, but cells shorter and thicker
– each cell joined to several others at the uneven, notched
linkages – intercalated discs
• electrical gap junctions allow each cell to directly stimulate
its neighbors
• mechanical junctions keep the myocytes from pulling apart
– 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 11-60
Cardiac Muscle
branched cell
cardiac nuclei
intercalated discs
11-61
Cardiac Muscle
– can contract without need for nervous stimulation
• built-in pacemaker - rhythmically sets off wave of
electrical excitation
• wave travels through the muscle and triggers
contraction of chambers
• autorhythmic – ability to contract rhythmically and
independently
11-62
Cardiac Muscle
– very slow twitches
• gives the heart time to expel blood
– uses aerobic respiration almost exclusively
– very adaptable with respect to fuel used
– very vulnerable to interruptions of oxygen supply
– highly fatigue resistant
11-63
Smooth Muscle
smooth muscle cell
nuclei
11-64
Smooth Muscle
• composed of myocytes that have a fusiform shape
• there is only one nucleus
• no visible striations
• z discs are absent and replaced by dense bodies (protein
masses in cytoplasm)
– protein plaques on the inner face of the plasma membrane
• cytoplasm contains extensive cytoskeleton of intermediate
filament
– attach to the membrane plaques and dense bodies
• capable of mitosis
• injured smooth muscle regenerates well
11-65
Layers of Visceral Muscle
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Mucosa:
Epithelium
Lamina propria
Muscularis
mucosae
Muscularis externa:
Circular layer
Longitudinal
layer
Figure 11.22
11-66
Stimulation 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
11-67
Contraction and Relaxation
• contraction begins in response to Ca+2 that enters the
cell from ECF
– voltage, ligand, and mechanically-gated (stretching)
Ca+2 channels open to allow Ca+2 to enter cell
• although there are no sarcomeres, there are still thick
and thin filaments
– 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
11-68
Contraction and Relaxation
• contraction and relaxation very slow in comparison to
skeletal muscle
• 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
11-69
Plaque
Intermediate filaments
of cytoskeleton
Contraction
of Smooth
Muscle
Actin filaments
Dense body
Myosin
(a) Relaxed smooth muscle cells
(b) Contracted smooth
muscle cells
Figure 11.24
11-70
Contraction and Stretching
• 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
• 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 it is empty
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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 sex-linked
recessive trait (1 of 3500 live-born boys)
– most common form
– mutation in gene for muscle protein dystrophin
• actin not linked to sarcolemma and cell membranes
damaged during contraction, necrosis and scar tissue
results
– severe effects on respiratory and cardiac muscle
• facioscapulohumeral MD - autosomal dominant trait affecting
both sexes equally
– facial and shoulder muscles
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Myasthenia Gravis
• autoimmune disease in which antibodies attack
neuromuscular junctions
– disease of women between 20 and 40
– fiber becomes less and less sensitive to stimulus
– 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
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Myasthenia Gravis
• treatments
– cholinesterase inhibitors retard breakdown of stimulus
chemicals
– immunosuppressive agents suppress the production
of anti-self antibodies
– thymus removal (thymectomy) – helps to dampen the
overactive immune response
– plasmapheresis –technique to remove harmful
antibodies from blood plasma
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