Chp 9

Muscles

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

3
Characteristics of a Skeletal Muscle Fiber

• A skeletal muscle cell (“fiber”) has several defining

characteristics:
1. It is multinucleated (myoblasts)
2. It contains many mitochondria.
3. It has special structures called Transverse tubules (T tubules).
4. cannot be replaced by the division of other existing muscle fibers
but new fibers can be formed from undifferentiated cells known
as satellite cells
5. It has myofibrils and sarcomeres.
6. It has specific terms for some of the intracellular structures:
Sarcolemma = Plasma membrane
Sarcoplasm = Cytoplasm
Sarcoplasmic reticulum = Smooth ER

4
 Muscle
• = a number of muscle fibers bound together by
connective tissue
• Skeletal muscles are usually attached to bones by
bundles of collagen fibers known as tendons.
• Some tendons are very long, with the site where the
tendon attaches to the bone far removed from the end
of the muscle (example: some muscles that move the fingers are in the
forearm)

• The transmission of force from muscle to bone is like

a number of people pulling on a rope, each person
corresponding to a single muscle fiber and the rope
corresponding to the connective tissue and tendons.
5
 Myofibrils

• Myofibrils are the structures that give skeletal and

cardiac muscle their characteristic striated
appearance.

• They are orderly arrangements of repeating pattern

along the length of the myofibril of thick and thin
filaments, known as sarcomere:
– Actin (thin) + troponin + tropomyosin
– Myosin (thick)

6
Structure of Skeletal Muscle

7
Structure of a sarcomere within
myofibrils

8
Structure of Sarcomere
The space between
overlapping thick
and thin filaments
is bridged by
projections known
as cross-bridges

9
 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.
• Following contraction, the mechanisms that generate
force are turned off, and tension declines, allowing
relaxation of the muscle fiber.
10
 Sliding Filament Mechanism

• When 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.
• During this shortening of the sarcomeres, there is no change in
the lengths of either the thick or thin filaments. This is known
as the sliding-filament mechanism of muscle contraction.
• The ability of a muscle fiber to generate force and movement
depends on the interaction of the contractile proteins actin and
myosin.

11
Sliding Filament Mechanism

12
 Cross-bridge formation

One stroke of a cross-bridge produces only a very small movement of a thin

filament relative to a thick filament. As long as a muscle fiber remains activated,
however, each cross-bridge repeats its swivelling motion many times, resulting
in large displacements of the filaments.

13
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.

14
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.
15
Thick and Thin Filaments

16
The Cross-bridge Cycle

17
Functions of ATP in Skeletal Muscle
Contraction

18
Roles of Troponin, Tropomyosin, and Ca2+ in
Contraction

19
Action Potentials and Contraction

20
 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 Ca 2+ 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.
21
Excitation-contraction Coupling

22
 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.
• The number of fibers innervated depends on the
muscle, fine motor movements (like typing) rely
on motor units with relatively few fibers in
contrast to those in the leg muscles, for example.

23
Motor Units

24
 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.
25
 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.
26
The Neuromuscular Junction

27
 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 ACh-
mediated 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.

28
Sequence of Events in Muscle Contraction

29
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.
30
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.

31
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.
32
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.
33
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.

34
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.
35
Twitch Contractions

36
 Isometric and Isotonic Twitches:
• Isometric twitches 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.

37
Load-shortening Relationship

38
Load-velocity Relationship

39
 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 (Figure
9.19, 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).
40
Frequency-tension Relationship

41
 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.

42
Length-tension Relationship

43
 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
44
Skeletal Muscle Energy Metabolism

45
 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.
46
 Muscle Fatigue Causes
• Many factors can contribute to the fatigue of skeletal muscle.
Acute fatigue from high-intensity, short-duration exercise is
thought to involve:
– decrease in ATP concentration.
– increase in concentrations of ADP, Pi, Mg2+ , H+ and oxygen free radicals.
• These have been shown to:
– decrease the rate of Ca2+ release, reuptake and storage by the endoplasmic
reticulum.
– decrease the sensitivity of the thin filament proteins to activation by Ca 2+
release.
– directly inhibit the binding and power-stroke motion of the myosin cross-
bridges.
• Each of these has been shown to be important under experimental
conditions but muscle fatigue is still not well understood.

47
 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.

48
Muscle Fatigue

49
 Types of Skeletal Muscle Fibers
• All 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.
50
 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.
These fibers appear darker and muscles containing many of these are
used for long term contractions (like standing) and are sometimes
referred to a “dark meat” (see Figure 9.24).

• In contrast, glycolytic fibers have few mitochondria but possess a high

concentration of glycolytic enzymes and a large store of glycogen. This
allows for quick bursts of activity. Muscles with many of these are
known as “white meat”
51
 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 myosin-ATPase
activity with high glycolytic capacity.

• Note that the fourth theoretical possibility—slow-

glycolytic fibers—is not found.
52
Types of Skeletal Muscle Fibers

53
Comparison of Skeletal Fiber Types

54
Whole-muscle Contraction

55
 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.

56
Control of Muscle Tension

57
 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.

58
 Muscle Adaptation to Exercise
• An increase in the amount of contractile 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)

59
Muscle Movements

60
Muscle Movements

61
Lever Action of Muscles and Bones

62
 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.
63
 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.
64
 Hypocalcemic Tetany
• Hypocalcemic tetany is the involuntary tetanic contraction of
skeletal muscles that occurs when the extracellular Ca 2+
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.
65
 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.
66
 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.

67
 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 actin-

containing filaments, and tropomyosin but NO troponin.

• The thin filaments are anchored either to the plasma

membrane or to cytoplasmic structures known as dense
bodies. 68
 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 sliding-

filament 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.

69
Structure of Smooth Muscle

70
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).

71
 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 plasma-
membrane Ca2+ channels

• To relax, the Ca2+ has to be removed either to the SR

or back to the extracellular fluid.

72
 Membrane Activation
• Smooth muscle responses can be graded.

• Input to smooth muscle can be either

excitatory or inhibitory.

73
Smooth Muscle Contraction and its
Control

74
Cross-bridge Activation

75
 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.

76
 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.

77
 Local Factors
• Local factors, including paracrine signals, acidity, O 2 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 acts 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.
78
 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.
79
 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.

80
Membrane Activation

81
Factors Affecting Smooth Muscle
Contraction

82
 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.

83
 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.

• The nodal 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 interfere with the heart’s ability to pump.

84
Cellular Structure of Cardiac Muscle

85
Excitation-Contraction Coupling in Cardiac Muscle

86
Skeletal vs Cardiac Muscle

87
Characteristics of Muscle Cells

88