Download Chapter 9 Muscle - Dr. Eric Schwartz

Chapter 09
Lecture Outline*
Muscle
Eric P. Widmaier
Boston University
Hershel Raff
Medical College of Wisconsin
Kevin T. Strang
University of Wisconsin - Madison
*See PowerPoint Image Slides for all
figures and tables pre-inserted into
PowerPoint without notes.
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1
Muscle Physiology
• Muscle is classified as:
• Skeletal muscle
• Smooth muscle
• Cardiac muscle
• Each type of muscle has specific
characteristics and functions.
2
Types of Muscle
Fig. 9-1
3
Characteristics of a Skeletal Muscle Fiber
• Skeletal Muscle has some defining characteristics:
1. It is multinucleated
2. It contains many mitochondria
3. It has special structures called Transverse
tubules (T tubules)
4. It has myofibrils and sarcomeres
5. It has specific terms for some of the intracellular
structures:
Sarcolemma = Plasma membrane
Sarcoplasm = Cytoplasm
Sarcoplasmic reticulum = Smooth ER
4
Myofibrils
• Myofibrils are the structures that give skeletal and
cardiac muscle their characteristic striated
appearance.
• They are orderly arrangements of thick and thin
filaments:
– Actin (thin)
– Myosin (thick)
5
Structure of Skeletal Muscle
Fig. 9-2
6
Structure of Sarcomere
Fig. 9-3
7
Molecular Mechanisms of Skeletal Muscle
Contraction
• The term contraction does not necessarily mean
“shortening.”
• It simply refers to activation of the force-generating
sites within muscle fibers—the cross-bridges.
• For example, holding a dumbbell at a constant position
requires muscle contraction, but not muscle shortening.
8
Sliding Filament Mechanism
• In this model of contraction force generation
produces shortening of a skeletal muscle fiber, the
overlapping thick and thin filaments in each
sarcomere move past each other, propelled by
movements of the cross-bridges.
• The ability of a muscle fiber to generate force and
movement depends on the interaction of the
contractile proteins actin and myosin.
9
Sliding Filament Mechanism
Fig. 9-5
10
Fig. 9-6
11
Thin Filaments and Associated Proteins
• Actin:
• Contractile protein
• Each G actin has a binding site for myosin.
• Think of pearls strung together on a string and then
the strands of pearls are twisted together.
• Tropomyosin:
• Regulatory protein
• Overlaps binding sites on actin for myosin and
inhibits interaction when in the relaxed state.
12
Thin Filaments and Associated Proteins
• Troponin:
• Regulatory protein
• Forms a complex with the other proteins of the thin
filament (actin and tropomyosin).
• Troponin binds Ca2+ reversibly and once bound
changes conformation to pull tropomyosin away from
the myosin interaction sites.
• Ca2+ binding to troponin regulates skeletal muscle
contraction because it moves the tropomyosin away
and allows myosin to interact with the actin.
13
Fig. 9-7
14
The Cross-bridge Cycle
Fig. 9-8
15
Roles of Troponin, Tropomyosin, and Ca2+ in
Contraction
Fig. 9-9
16
Action Potentials and Contraction
Fig. 9-10 17
Excitation-contraction Coupling
Fig. 9-12 18
Sarcoplasmic Reticulum
• The sarcoplasmic reticulum (SR) in muscle is homologous to
the endoplasmic reticulum found in most cells. Ca2+ is stored and
is released following membrane excitation.
• The T-tubules and SR are connected with junctions. These
junctions involve two integral membrane proteins, one in the
T-tubule membrane, and the other in the membrane of the
sarcoplasmic reticulum.
• The T-tubule protein is a modified voltage-sensitive Ca2+ channel
known as the dihydropyridine (DHP) receptor, which acts as a
voltage sensor. The protein embedded in the SR membrane is
known as the ryanodine receptor, which forms a Ca2+channel.
19
Motor Unit
• A motor unit is defined as the motor neuron
and the skeletal muscle fibers it innervates.
• One motor neuron innervates many
muscle fibers, but one muscle fiber is
innervated by only one motor neuron.
• Within a whole muscle there are many motor
units.
20
Motor Units
Fig. 9-13 21
The Neuromuscular Junction
• Stimulation of the nerve fibers to a skeletal muscle is
the only mechanism by which action potentials are
initiated in skeletal muscle.
• The nerve cells whose axons innervate skeletal
muscle fibers are known as motor neurons (or
somatic efferent neurons), and their cell bodies are
located in either the brainstem or the spinal cord.
• The axons of motor neurons are myelinated and are
the largest-diameter axons in the body. They
propagate action potentials at high velocities,
allowing signals from the central nervous system to
travel to skeletal muscle fibers with minimal delay.
22
The Neuromuscular Junction
• The axon terminals of a motor neuron contain
vesicles similar to the vesicles found at synaptic
junctions between two neurons.
• The vesicles contain the neurotransmitter
acetylcholine (ACh).
• The region of the muscle fiber plasma membrane that
lies directly under the terminal portion of the axon is
known as the motor end plate.
• The junction of an axon terminal with the motor end
plate is known as a neuromuscular junction.
23
The Neuromuscular Junction
Fig. 9-15
24
The Neuromuscular Junction
• All neuromuscular junctions are excitatory.
• In addition to receptors for ACh, the synaptic
junction contains the enzyme acetylcholinesterase,
which breaks down ACh, just as it does at AChmediated synapses in the nervous system.
• Table 9–2 summarizes the sequence of events that
lead from an action potential in a motor neuron to the
contraction and relaxation of a skeletal muscle fiber.
25
26
Disruption of Neuromuscular Signaling
• Curare is a deadly arrowhead poison used by indiginous
peoples of South America. It binds strongly to nicotinic ACh
receptors. It does not open their ion channels, however, and
acetylcholinesterase does not destroy it.
• When a receptor is occupied by curare, ACh cannot bind to the
receptor. Therefore, although the motor nerves still conduct
normal action potentials and release ACh, there is no resulting
EPP in the motor end plate and no contraction.
• Because the skeletal muscles responsible for breathing, like all
skeletal muscles, depend upon neuromuscular transmission to
initiate their contraction, curare poisoning can cause death by
asphyxiation.
27
Disruption of Neuromuscular Signaling
• Neuromuscular transmission can also be blocked by inhibiting
acetylcholinesterase. Some organophosphates, which are the
main ingredients in certain pesticides and “nerve gases” (the
latter developed for chemical warfare), inhibit this enzyme.
This results in skeletal muscle paralysis and death from
asphyxiation.
• Nerve gases also cause ACh to build up at muscarinic
synapses, where parasympathetic neurons inhibit cardiac
pacemaker cells. Thus, the antidote for organophosphate and
nerve gas exposure includes both pralidoxime, which
reactivates acetlycholinesterase, and the muscarinic receptor
antagonist atropine.
28
Disruption of Neuromuscular Signaling
• Drugs that block neuromuscular transmission are sometimes used
in small amounts to prevent muscular contractions during certain
types of surgical procedures.
• One example is succinylcholine, which actually acts as an agonist
to the ACh receptors and produces a depolarizing/desensitizing
block similar to acetylcholinesterase inhibitors.
• Nondepolarizing neuromuscular junction blocking drugs that act
more like curare and last longer are also used, such as rocuronium
and vecuronium.
• The use of such paralytic agents in surgery reduces the required
dose of general anesthetic, allowing patients to recover faster and
with fewer complications. Patients must be artificially ventilated,
however, to maintain respiration until the drug has been removed
from the system.
29
Disruption of Neuromuscular Signaling
• The toxin produced by the bacterium Clostridium botulinum,
blocks the release of acetylcholine from nerve terminals.
• Botulinum toxin is an enzyme that breaks down proteins of the
SNARE complex that are required for the binding and fusion of
ACh vesicles with the plasma membrane of the axon terminal.
• This toxin, which produces the food poisoning called botulism, is
one of the most potent poisons known because of the very small
amount necessary to produce an effect.
• Application of botulinum toxin is increasingly being used for
clinical and cosmetic procedures, including the inhibition of
overactive extraocular muscles, prevention of excessive sweat
gland activity, treatment of migraine headaches, and reduction of
aging-related skin wrinkles.
30
Mechanics of Single-fiber Contractions
• A muscle fiber generates force called tension
in order to oppose a force called the load,
which is exerted on the muscle by an object.
• The mechanical response of a muscle fiber to a
single action potential is known as a twitch.
31
The Phases of a Twitch Contraction
• There are 3 major phases to a twitch contraction:
1. Latent Period
This is the period of time from the action potential to the
onset of contraction. The time delay is due to the
excitation-contraction coupling.
2. Contraction Phase
This is the time that tension is developing due to the
cross-bridge cycling.
3. Relaxation Phase
This is the time that the tension is decreasing (i.e.,
relaxing) and is longer than the contraction phase. This is
due to the amount of time it takes to get all the Ca2+
sequestered.
32
Twitch Contractions
Fig. 9-16
33
Isometric and Isotonic Twitches:
• Isometric twitches do generate tension but do not
shorten the muscle (load is greater than the force
generated by the muscle…i.e., postural muscles).
• Isotonic twitches do shorten the muscle.
34
Load-shortening Relationship
Fig. 9-17 35
Load-velocity Relationship
Fig. 9-18 36
Frequency-tension Relationship
• Because a single action potential in a skeletal muscle fiber
lasts only 1 to 2 ms but the twitch may last for 100 ms, it is
possible for a second action potential to be initiated during the
period of mechanical activity.
• When a stimulus is applied before a fiber has completely
relaxed from a twitch, it induces a contractile response with a
peak tension greater than that produced in a single twitch (S3
and S4).
• The increase in muscle tension from successive action
potentials occurring during the phase of mechanical activity is
known as summation.
• A maintained contraction in response to repetitive stimulation
is known as a tetanus (tetanic contraction).
37
Frequency-tension Relationship
Fig. 9-19
Fig. 9-20
38
Length-tension Relationship
• The spring-like characteristic of the protein titin is responsible for most of the
passive elastic properties of relaxed muscle fibers.
• With increased stretch, the passive tension in a relaxed fiber increases, not
from active cross-bridge movements but from elongation of the titin filaments.
If the stretched fiber is released, it will return to an equilibrium length, much
like what occurs when releasing a stretched rubber band.
• By a different mechanism, the amount of active tension a muscle fiber
develops during contraction can also be altered by changing the length of the
fiber. If you stretch a muscle fiber to various lengths and tetanically stimulate it
at each length, the magnitude of the active tension will vary with length, as
Figure 9–21 shows. The length at which the fiber develops the greatest
isometric active tension is termed the optimal length, L0.
39
Length-tension Relationship
Fig. 9-21 40
Skeletal Muscle Energy Metabolism
• As we have seen, ATP performs three functions directly
related to muscle fiber contraction and relaxation.
• There are three ways a muscle fiber can form ATP:
1. Phosphorylation of ADP by creatine phosphate
2. Oxidative phosphorylation of ADP in the
mitochondria
3. Phosphorylation of ADP by the glycolytic pathway
in the cytosol
41
Skeletal Muscle Energy Metabolism
Fig. 9-22 42
Muscle Fatigue
• When a skeletal muscle fiber is repeatedly stimulated,
the tension the fiber develops eventually decreases even
though the stimulation continues.
• This decline in muscle tension as a result of previous
contractile activity is known as muscle fatigue.
• Additional characteristics of fatigued muscle are a
decreased shortening velocity and a slower rate of
relaxation. The onset of fatigue and its rate of
development depend on the type of skeletal muscle fiber
that is active, the intensity and duration of contractile
activity, and the degree of an individual’s fitness.
43
Muscle Fatigue Causes
• Many factors can contribute to the fatigue of skeletal muscle.
Fatigue from high-intensity, short-duration exercise is thought to
involve at least three different mechanisms:
1. Conduction Failure
– The muscle action potential can fail to be conducted into the fiber
along the T-tubules, which halts the release of Ca2+ from the
sarcoplasmic reticulum.
• This conduction failure results from the buildup of potassium ions
in the small volume of the T-tubule during the repolarization of
repetitive action potentials. Elevated external potassium ion
concentration leads to a persistent depolarization of the membrane
potential, and eventually causes a failure to produce action
potentials in the T-tubular membrane.
44
Muscle Fatigue Causes
2. Lactic Acid Buildup
– Elevated hydrogen ion concentration alters protein
conformation and activity.
– Thus, the acidification of muscle by lactic acid may alter a
number of muscle proteins, including the proteins involved in
Ca2+ release.
– The function of the Ca2+-ATPase pumps of the sarcoplasmic
reticulum is also affected, which may in part explain the
impaired relaxation of fatigued muscle.
45
Muscle Fatigue Causes
3. Inhibition of Cross-Bridge Cycling
– The buildup of ADP and Pi within muscle fibers during intense
activity may directly inhibit cross-bridge.
– Slowing the rate of this step delays cross-bridge detachment
from actin, and thus slows the overall rate of cross-bridge
cycling.
– These changes contribute to the reduced shortening velocity
and impaired relaxation observed in muscle fatigue resulting
from high-intensity exercise.
46
Muscle Fatigue Causes
• Central Command Fatigue
– Another type of fatigue quite different from muscle fatigue
occurs when the appropriate regions of the cerebral cortex fail
to send excitatory signals to the motor neurons.
– This may cause a person to stop exercising even though the
muscles are not fatigued.
– An athlete’s performance depends not only on the physical
state of the appropriate muscles but also upon the “will to
win”—that is, the ability to initiate central commands to
muscles during a period of increasingly distressful sensations.
47
Muscle Fatigue
Fig. 9-23 48
Types of Skeletal Muscle Fibers
• Skeletal muscle fibers do not all have the same
mechanical and metabolic characteristics. Fibers are
classified on the basis of:
1. Their maximal velocities of shortening (fast or slow)
2. The major pathway they use to form ATP—oxidative or glycolytic
• Fast and slow fibers contain forms of myosin that differ
in the maximal rates at which they use ATP.
• This determines the maximal rate of cross-bridge cycling
and thus the maximal shortening velocity.
49
Types of Skeletal Muscle Fibers
• The second means of classifying skeletal muscle fibers is
according to the type of enzymatic machinery available for
synthesizing ATP.
• Some fibers contain numerous mitochondria and thus have a high
capacity for oxidative phosphorylation. These fibers are classified
as oxidative fibers.
•
Most of the ATP such fibers produce is dependent upon blood
flow to deliver oxygen and fuel molecules to the muscle and
contain myoglobin.
• In contrast, glycolytic fibers have few mitochondria but possess a
high concentration of glycolytic enzymes and a large store of
glycogen.
50
Types of Skeletal Muscle Fibers
• On the basis of these two characteristics, three principal
types of skeletal muscle fibers can be distinguished:
1. Slow-oxidative fibers (Type I) combine low myosin-ATPase
activity with high oxidative capacity.
2. Fast-oxidative-glycolytic fibers (Type IIa) combine high
myosin-ATPase activity with high oxidative capacity and
intermediate glycolytic capacity.
3. Fast-glycolytic fibers (Type IIb) combine high myosinATPase activity with high glycolytic capacity.
• Note that the fourth theoretical possibility—slowglycolytic fibers—is not found.
51
Types of
Skeletal
Muscle
Fibers
Fig. 9-25
52
53
Whole-muscle Contraction
Fig. 9-26 54
Control of Muscle Tension
• The total tension a muscle can develop depends
upon two factors:
1. The amount of tension developed by each fiber
2. The number of fibers contracting at any time
• By controlling these two factors, the nervous
system controls whole-muscle tension as well
as shortening velocity.
55
Control of Muscle Tension
56
Control of Shortening Velocity
• Shortening velocity of a whole muscle depends
upon the load on the muscle, the types of
motor units in the muscle, and the number of
motor units recruited to work against the load.
57
Muscle Adaptation to Exercise
• An increase in the amount of contratile activity
increases the size of muscle fibers and increases their
capacity for ATP production.
• “Use it or lose it.” Muscles that are not used will
atrophy. There are 2 types of atrophy:
– Disuse atrophy (like an arm in a cast)
– Denervation atrophy (nerve damage = loss of function)
58
Muscle Movements
Fig. 9-27 59
Muscle Movements
Fig. 9-28
60
Lever Action of Muscles and Bones
Fig. 9-30 61
Skeletal Muscle Disorders
• A number of conditions and diseases can affect the
contraction of skeletal muscle.
• Many of them are caused by defects in the parts of the
nervous system that control contraction of the muscle
fibers rather than by defects in the muscle fibers
themselves.
• For example, poliomyelitis is a viral disease that
destroys motor neurons, leading to the paralysis of
skeletal muscle, and may result in death due to
respiratory failure.
62
Muscle Cramps
• Involuntary tetanic contraction of skeletal muscles produces muscle
cramps.
• During cramping, action potentials fire at abnormally high rates, a
much greater rate than occurs during maximal voluntary contraction.
• The specific cause of this high activity is uncertain, but it is probably
related to electrolyte imbalances in the extracellular fluid surrounding
both the muscle and nerve fibers.
• These imbalances may arise from overexercise or persistent
dehydration, and they can directly induce action potentials in motor
neurons and muscle fibers.
• Another theory is that chemical imbalances within the muscle stimulate
sensory receptors in the muscle, and the motor neurons to the area are
activated by reflex when those signals reach the spinal cord.
63
Hypocalcemic Tetany
• Hypocalcemic tetany is the involuntary tetanic contraction of
skeletal muscles that occurs when the extracellular Ca2+
concentration falls to about 40 percent of its normal value.
• This may seem surprising, because we have seen that Ca2+ is
required for excitation-contraction coupling. However, recall that
this Ca2+ is sarcoplasmic reticulum Ca2+, not extracellular Ca2+.
• The effect of changes in extracellular Ca2+ is exerted not on the
sarcoplasmic reticulum Ca2+, but directly on the plasma
membrane.
• Low extracellular Ca2+ (hypocalcemia) increases the opening of
Na+ channels in excitable membranes, leading to membrane
depolarization and the spontaneous firing of action potentials.
64
Muscular Dystrophy
• This disease is one of the most frequently encountered genetic diseases,
affecting an estimated one in every 3,500 males (but many fewer females).
Muscular dystrophy is associated with the progressive degeneration of
skeletal and cardiac muscle fibers, weakening the muscles and leading
ultimately to death from respiratory or cardiac failure.
• Muscular dystrophies are caused by the absence or defect of one or more
proteins that make up the costameres in striated muscle. Costameres
(costa = "rib") are clusters of structural and regulatory proteins that link
the Z-disks of the outermost myofibrils to the sarcolemma and
extracellular matrix.
• Duchenne muscular dystrophy is a sex-linked recessive disorder caused
by a defect in a gene on the X chromosome that codes for the protein,
dystrophin. Dystrophin was the first costamere protein discovered to be
related to a muscular dystrophy, which is how it earned its name.
65
Myasthenia Gravis
• It affects about one out of every 7,500 Americans, occurring more
often in women than men.
• The most common cause is the destruction of nicotinic ACh receptor
proteins of the motor end plate, mediated by antibodies of a person’s
own immune system.
• A number of approaches are currently used to treat the disease. One
is to administer acetylcholinesterase inhibitors (e.g., neostygmine).
This can partially compensate for the reduction in available ACh
receptors by prolonging the time that acetylcholine is available at
the synapse.
• Other therapies aim at blunting the immune response. Treatment
with glucocorticoids is one way that immune function is suppressed.
• Plasmapheresis is a treatment that involves replacing the liquid
fraction of blood (plasma), which contains the offending antibodies.
66
Structure of Smooth Muscle
• Each smooth muscle cell is spindle-shaped, with a diameter
between 2 and 10 µm, and length ranging from 50 to 400 µm.
• They are much smaller than skeletal muscle fibers, which are
10 to 100 µm wide and can be tens of centimeters long.
• Smooth muscle cells (SMC) have a single nucleus and have
the capacity to divide throughout the life of an individual.
• SMCs have thick myosin-containing filaments and thin actincontaining filaments, and tropomyosin but NO troponin.
• The thin filaments are anchored either to the plasma membrane
or to cytoplasmic structures known as dense bodies.
67
Structure of Smooth Muscle
• The thick and thin filaments are not organized into
myofibrils, and there are NO sarcomeres, which
accounts for the absence of a banding pattern.
• Smooth muscle contraction occurs by a slidingfilament mechanism.
• Smooth muscles surround hollow structures and
organs that undergo changes in volume with
accompanying changes in the lengths of the smooth
muscle fibers in their walls.
68
Structure of Smooth Muscle
Fig. 9-33 69
Smooth Muscle Contraction and its Control
• Cross-Bridge Activation:
– Cross-bridge cycling in smooth muscle is controlled by a
Ca2+regulated enzyme that phosphorylates myosin. Only
the phosphorylated form of smooth muscle myosin can
bind to actin and undergo cross-bridge cycling.
– This is done by myosin light chain kinase (MLCK).
– To relax a contracted smooth muscle, myosin must be
dephosphorylated because dephosphorylated myosin is
unable to bind to actin. This dephosphorylation is mediated
by the enzyme myosin light-chain phosphatase (MLCP)
70
Sources of Cytosolic Ca2+
• Two sources of Ca2+ contribute to the rise in cytosolic
Ca2+ that initiates smooth muscle contraction:
1. The sarcoplasmic reticulum
2. Extracellular Ca2+ entering the cell through plasmamembrane Ca2+ channels.
• To relax, the Ca2+ has to be removed either to the SR
or back to the extra cellular fluid.
71
Membrane Activation
• Smooth muscle responses can be graded.
• Input to smooth muscle can be either
excitatory or inhibitory.
72
Smooth Muscle Contraction and its Control
Fig. 9-34 73
Cross-bridge Activation
Fig. 9-35 74
Nerves and Hormones
• The contractile activity of smooth muscles is influenced by
neurotransmitters released by autonomic neuron endings.
• Unlike skeletal muscle fibers, smooth muscle cells do not have a
specialized motor end-plate region. They have swollen regions known as
varicosities .
• Each varicosity contains many vesicles filled with neurotransmitter,
some of which are released when an action potential passes the
varicosity.
• Varicosities from a single axon may be located along several muscle
cells, and a single muscle cell may be located near varicosities belonging
to postganglionic fibers of both sympathetic and parasympathetic
neurons.
• Therefore, a number of smooth muscle cells are influenced by the
neurotransmitters released by a single neuron, and a single smooth
muscle cell may be influenced by neurotransmitters from more than one
neuron.
75
Nerves and Hormones
• Whereas some neurotransmitters enhance contractile activity, others
decrease contractile activity.
• A given neurotransmitter may produce opposite effects in different
smooth muscle tissues. For example, norepinephrine, the
neurotransmitter released from most postganglionic sympathetic
neurons, enhances contraction of most vascular smooth muscle by
acting on alpha-adrenergic receptors, but produces relaxation of
airway (bronchiolar) smooth muscle by acting on beta-2 adrenergic
receptors.
• Thus, the type of response (excitatory or inhibitory) depends not on
the chemical messenger per se, but on the receptors the chemical
messenger binds to in the membrane and on the intracellular signaling
mechanisms those receptors activate.
76
Local Factors
• Local factors, including paracrine signals, acidity, O2 and CO2
levels, osmolarity, and the ion composition of the extracellular fluid,
can also alter smooth muscle tension.
• Responses to local factors provide a means for altering smooth
muscle contraction in response to changes in the muscle’s
immediate internal environment, independent of long-distance
signals from nerves and hormones.
• Many of these local factors induce smooth muscle relaxation. Nitric
oxide (NO) which produces smooth muscle relaxation. NO in a
paracrine manner.
• Some smooth muscles can also respond by contracting when they
are stretched. Stretching opens mechanosensitive ion channels,
leading to membrane depolarization. The resulting contraction
opposes the forces acting to stretch the muscle.
77
Spontaneous Electrical Activity
• Some types of smooth muscle cells generate action potentials
spontaneously in the absence of any neural or hormonal input.
• The membrane potential change occurring during the spontaneous
depolarization to threshold is known as a pacemaker potential.
• Other smooth muscle pacemaker cells have a slightly different pattern of
activity. The membrane potential drifts up and down due to regular
variation in ion flux across the membrane. These periodic fluctuations
are called slow waves.
• Pacemaker cells are found throughout the gastrointestinal tract, and thus
gut smooth muscle tends to contract rhythmically even in the absence of
neural input.
• Some cardiac muscle fibers and a few neurons in the central nervous
system also have pacemaker potentials and can spontaneously generate
action potentials in the absence of external stimuli.
78
Souces of Cytosolic Calcium
• Calcium that initiates smooth muscle
contraction comes from both the sarcoplasmic
reticulum and from the extracellular fluid
entering through plasma-membrane channels.
79
Membrane Activation
Fig. 9-37 80
81
Types of Smooth Muscle
• Single-unit smooth muscles respond to stimuli
as a single unit because cells are connected by
gap junctions.
• Multi-unit smooth muscles contain cells that
respond to stimuli independently and they
contain few gap junctions.
82
Cardiac Muscle
• Cardiac muscle cells have one to two nuclei that are centrally located.
• They are striated and use the sliding filament mechanism to contract.
• They are branching cells with intercalated discs with desmosomes and
gap junctions. The gap junctions are critical to the heart’s ability to be
electrically coupled.
• They have large mitochondia that produce the energy needed and
prevent the heart from fatiguing.
• The node cells have the ability to stimulate their own action potentials.
This is called automaticity or autorhythmicity.
• The absolute refractory period is about 250 ms. This prevents tetanic
contractions which would interfer with the heart’s ability to pump.
83
Cellular Structure of Cardiac Muscle
Fig. 9-39 84
ExcitationContraction
Coupling in
Cardiac Muscle
Fig. 9-40
85
Skeletal vs Cardiac Muscle
Fig. 9-41
86
87