PHYSIOLOGY OF MUSCLE
Morphology of Skeletal Muscle Fiber
About 40 % of the body is skeletal muscle, and another 10 % is smooth
and cardiac muscle .
Skeletal muscle is a striated, voluntary (neurogenic) muscle, i.e. needs
nerve supply to work. All skeletal muscles are composed of many fibers.
Muscle fiber is a single cell, multinucleated cylindrical shape surrounded
by cell membrane called sarcolemma and each fiber extends the entire
length of the muscle and is usually innervated by only one nerve ending,
located near the middle of the fiber. Each of these muscle fibers is made
up of successively smaller subunits called (myofibrils). Each myofibrils
composed of actin and myosin about 1500 myosin filaments and 3000
actin filaments. (fig 1)
Actin and myosin
The thick filament (myosin): composed of several hundreds of myosin
molecules, each molecule consists of 6 polypeptide chains (4 light and 2
heavy chains). 2 heavy chain wrap spirally form the tail and on the end of
the tail folded bilaterally will form the arm and the head. The head of
myosin molecule form the cross-bridges which bind with actin. The head
of myosin molecule contains actin binding sites and 2 ATPase activity
sites (to produce the energy necessary for contraction). (Fig 2)
(Fig2)
The thin filament (actin): actin filaments composed of three proteins,
actin, tropomyosin and troponin(fig 3)
Actin contain active sits on its surface in which the cross –bridges of
myosin attached
Tropomyosin: lie on the top of the active site of actin strands
Troponin: are 3 loosely bound protein subunits
-Troponin I :has strong affinity to actin .The troponin(I) binds to actin so
inhibit interaction between actin and myosin
-Troponin C :has strong affinity to Ca ion, which is necessary to initiate
contraction
-Troponin T :has affinity for tropomyosin form troponin tropomyosin
complex
(Fig 3)
The myosin and actin filaments partially interdigitate and thus
cause the myofibrils to have alternate light and dark bands, as The light
bands contain only actin filaments and are called I bands . The dark
bands contain myosin filaments, as well as the ends of the actin filaments
where they overlap the myosin, and are called A bands, therefore the
entire muscle fiber has light and dark bands giving the skeletal and
cardiac muscle the striated appearance
The ends of the actin filaments are attached to the Z disc. From this
disc, these filaments extend in both directions .actin held in place by Z
disc
myosin held in place by Z disc but its attachment to Z-disc by protein
titin
Z -disc: is a filamentous protein passes across the myofibril and from
one myofibrils to anther attaching myofibrils to one anther. The ends of
the actin filaments attached to Z-disc
Sarcomere: is the portion of myofibrils that lie between two successive Z
–disc. It is a smallest functional unit of amyofibril necessary to produce
contraction (fig 3)
Sarcolemma :cell membrane of muscle fiber
Sarcoplasm :is the cytoplasm of the muscle fiber contain mitochondria,
myofibrils and sarcoplasmic reticulum
The sarcotubular system: It is composed of:
a)The transverse tubules(T-tubules): originate as invaginations from cell
membrane, penetrating the muscle fiber from one side to the opposite
side, thus communicating with the ECF. T-tubules help for rapid
transmission of action potential from the membrane deep into the muscle.
b) The sarcoplasmic reticulum which composed of:
1-Longitudinal tubules.
2-Terminal cisterns: large chambers adjacent to T-tubules giving the
appearance of triad(1 T-tubule and 2 cisternae). It stores calcium ions
with abundant Ca channels and Ca pumps.(fig 4 ).
Fig 4
Molecular mechanism of muscle contraction
In the relaxed muscle the troponin-I is tightly bound to actin;
tropomyosin covers the active sites of actin thus, troponin-tropomyosin
complex represent the relaxing proteins which inhibit interaction
between actin and myosin
When the Ca ion bind with troponin C this uncover the active sites of the
actin. Then the activated head of myosin cross-bridges attaches to an
active sites of actin, here the head automatically tilts towards the arm
(called power stroke) so dragging the actin filaments along with it
immediately after tilting the head released from the active site then return
to its normal perpendicular direction and then it combined with new
active site of actin, then the head tilts again, and the actin filament moves
another step. Thus, the heads of the cross-bridges step by step walk along
the actin filament, pulling the ends of two successive actin filaments
toward the center of the myosin this is called “walk-along” theory .(fig
5)
Fig 5
neuromuscular junction: As the motor nerve reaches the muscle
fiber, it loses its myelin and divides into a number of terminals. The axon
terminal contains many small vesicles of the neurotransmitter
acetylcholine. The nerve ending invaginates into a thickened, folded
depression in the muscle membrane called the motor end plate (figure
6).Usually there is one junction for each muscle fiber, this invagination is
called synaptic gutter and the space between the axon terminal and the
muscle fiber is called synaptic cleft(contain acetylcholinesterase that
destroy acetylcholine (Ach).
Fig 6
Excitation- contraction coupling
1-when action potential travel along a motor nerve to its ending ,voltage
gated calcium channels(near dense bars ) open and allow calcium ions to
diffuse to the interior of the nerve terminal.
2- The calcium ions exert an attractive influence on the acetylcholine
vesicles, drawing them to the neural membrane adjacent to the dense
bars. The vesicles then fuse with the neural membrane and empty their
acetylcholine into the synaptic space by the process of exocytosis
3-The acetylcholine open the acetylcholine- gated channels, which
allows sodium ion to flow into muscle fiber, this initiate end plate
potential (The sudden entrance of sodium ions into the muscle fiber
causes the electrical potential inside the fiber to increase in the positive
direction as much as 50 to 75 millivolts), which is necessary to initiate an
A.P
4-The action potential travels along the muscle fiber membrane causing
the sarcoplasmic reticulum to release calcium ion into myofibrils
5-The Ca ions uncover the active sites of actin and initiates attractive
force between the actin and myosin cross-bridges causing the actin
filaments to slid inward among the myosin filaments .This is the
contractile process which is occur by sliding filament mechanism. The
energy for this mechanism is supplied by the ATP cleavage by ATPase
enzyme present in the myosin head.
6-After a fraction of a second the Ca ion are pumped back into the
sarcoplasmic reticulum where they remain stored until another muscle
A.P arrives again .this removal of Ca ion from myofibrils causes muscle
contraction to cease.
Note :When active re-pumping of calcium is inhibited, relaxation cannot
occur and muscle stays in contraction.
Why sodium ions flow through the acetylcholine gated channels than
any other ions?
1-high concentration of sodium ions in the extracellular fluid
2-the very negative potential on the inside of the muscle membrane, –80
to –90 millivolts, pulls the positively charged sodium ions .
The acetylcholine then it is removed rapidly by two means:
(1)Most of the acetylcholine
acetylcholinesterase
is
destroyed
by
the
enzyme
(2) A small amount of acetylcholine diffuses out of the synaptic space or
re-uptake by process of pinocytosis. fig (7 ,8)
fig 7
fig 8
Muscle Action Potential
Almost everything regarding initiation and conduction of action
potentials in nerve fibers applies equally to skeletal muscle fibers, except
for quantitative differences.
1-Resting membrane potential: about –80 to –90 millivolts in skeletal
fibers—the same as in large myelinated nerve fibers.
2-Duration of action potential: 1 to 5 milliseconds in skeletal muscle—
about five times as long as in large myelinated nerves
3-Velocity of conduction: 3 to 5 m/sec—about 1/13the velocity of
conduction in the large myelinated nerve fibers .
Simple muscle twitch:
The contraction of a muscle in response to a stimulus , its occur in 3
parts: (fig 9)
latent period :The time between application of stimulus to the motor
nerve and the beginning of contraction
contraction period : the time during which contraction occurs, muscle
shortens & does its work
relaxation period: time during which relaxation occurs ,muscle elongates
& returns to original position
refractory period: the refractory period is short which means that skeletal
muscle can under go summation and tetanization via repeated stimulation
(e.g. Lifting heavy weight)
fig 9
Note :An action potential is an electrochemical
event(less than 2 ms)
But contraction is a mechanical event which requires up
to 1 second to occur.
Degree of actin and myosin filaments overlaps on the
tension developed by the contracting muscle.
At a point A- the two actin filaments begin to overlapped causing muscle tension to decrease , the sarcomere length less than 2 micrometer .
At a point B and C- at a sarcomere length 2 micrometer, full tension is
maintained because all the cross– bridges of myosin overlapped by the
actin at this length it's capable of generating maximum force of
contraction
At a point D- at very long sarcomere length a muscle can not develop
tension because there is no over lap between actin and myosin filaments
(fig10)
Fig 10
Motor unit
All the muscle fibers which is innervated by a single motor nerve are
called motor unit(fig 11)
Muscle that react rapidly for precise function may have only 2-3 muscle
fibers in motor unit e.g laryngeal muscle.
While muscle that don’t need precise function may have 100 muscle fiber
in motor unit.
fig 11
Stimulus strength and muscle contraction
Muscle tension = force exerted by contracting muscle; force is
applied to a load
Load = weight of object being acted upon
An isolated skeletal muscle fiber produces contraction of equal
force in response to each action potential (all-or-none law of skeletal
muscle contraction).
When brief electric stimuli of increasing strength are applied to
muscle fiber ,the following events occur:
1-Subthreshold stimulus does not produce an AP, and no muscle
contraction occurs.
2-A threshold stimulus produces an AP and results in contraction of the
muscle fiber.
3-A stronger than threshold stimulus produces an AP of the same
magnitude as the threshold stimulus and therefore produces an identical
contraction.
Like individual muscle fiber , motor units respond in all-or-none fashion.
Increasing the force of contraction occurs by summation and in two
ways:
1-Multiple motor unit Summation. By increasing the number of motor
units contracting at the same time. When the central nervous system
sends a weak signal to contract a muscle, smaller number of motor units
may be stimulate Then, strength of the signal increases, larger and larger
number of motor units begin to be excited as well.
whole muscle responds to stimuli in a graded fashion, (figure 12). which
means the strength of the contraction can range from weak to strong
depending on the strength of the stimuli.
fig 12
2-Frequency Summation andTetanization by increasing the frequency of
contraction. As the frequency increases, here comes a point where each
new contraction occurs before the preceding one is over. As a result, the
second contraction is added to the first one, so that the total strength of
contraction rises progressively.When the frequency reaches a critical
level, the successive contractions become so rapid that they fuse together,
and the whole muscle contraction appears to be completely smooth and
continuous without relaxation This is called tetanization .So that any
additional increase in frequency beyond that point has no further effect
This occurs because Ca ion is accumulated in sarcoplasm.(fig 13)
fig 13
Types of muscle contraction :
Two types, isometric and isotonic
Isometric: tension of muscle increase but do not change in length e.g
when person push against the wall
Isotonic contraction: there is change in length but the tension not
changed e.g lifts an object
Most contractions are a mixture of the two(e.g: running)
Types of muscle fibers:
Two types according to the twitch duration fast muscle fiber (few)
and slow muscle fiber (hundreds). Most of body muscles are a mixture of
the two types.
Fast muscle fibers
a-Large fibers and innervated by large nerve
b-Extensive sarcoplasmic reticulum for rapid release of calcium ions to
initiate contraction.
c-Large amounts of glycolytic enzymes for rapid release of energy by the
glycolytic process.
d-Less blood supply and few mitochondria because oxidative metabolism
is of secondary importance.
e-easy fatigability
f-Adapted for very rapid and very strong contraction(short distance
running, jumping.)
g-less myoglobin(an iron containing protein similar to hemoglobin in red
blood cells) ,deficit of red myoglobin in fast muscle gives it the name
white muscle
Slow Fibers
a-Smaller fibers. and innervated by smaller nerve fibers.
b- More extensive blood vessel system and capillaries to supply extra
amounts of oxygen.
c-resist fatigue
d-Greatly increased numbers of mitochondria, to support high levels of
oxidative metabolism.
d-Contain large amounts of myoglobin red muscle. The myoglobin gives
the slow muscle a reddish appearance and the name
e-Adapted for prolonged muscular activity(marathon races, postural
muscles which support body against gravity(
Energy expenditure during contraction:
Energy is needed for
1-Sliding of actin on myosin filaments
2-Repumping of calcium ions from sarcoplasm into sarcoplasmic
.reticulum to start muscle relaxation
3-Maintenance of resting membrane potential by Na-K pump-
Source of energy for muscle contractions
1-The immediate source of energy is ATP.The concentration of ATP in
the muscle fiber is sufficient to maintain full contraction for only 1 to 2
seconds
2-glycolysis of glycogen (previously stored in the muscle cells). The
glycolytic reactions can occur even in the absence of oxygen
3-oxidative metabolism. (This means combining oxygen with the glucose
and fatty acids) to liberate ATP.
Muscle Fatigue: Prolonged and strong contraction of a muscle leads
to the state of muscle fatigue. Muscle fatigue is directly proportion to the
rate of depletion of muscle glycogen and ATP.
Skeletal Muscle Tone: Even when muscles are at rest they are in
state of continuous small degree of contraction called muscle tone which
is probably due to reflex impulses from the spinal cord. Muscle tone
decreases during sleep and absent in death
Myasthenia Gravis
Is an autoimmune disease in which the patients have developed
antibodies against their own acetylcholine-gated ion channels. The end
plate potentials that occur in the muscle fibers are too weak to stimulate
the muscle fibers and the patient dies of paralysis.
Drugs That Stimulate the Muscle Fiber by Acetylcholine-LikeAction.
Many compounds, including methacholine, carbachol,and nicotine,
have the same effect on the muscle fiber as does acetylcholine. The
difference between these drugs and acetylcholine is that the drugs are not
destroyed by cholinesterase
Drugs That Stimulate the Neuromuscular Junction by Inactivating
Acetylcholinesterase.
Neostigmine, physostigmine, inactivate the acetylcholinesterase in
the synapses so that it no longer hydrolyzes acetylcholine. Therefore,
acetylcholine accumulates and stimulates the muscle fiber repetitively
Drugs That Block Transmission at the Neuromuscular
Junction.
A drugs can prevent passage of impulses from the nerve ending
into the muscle. as, D-tubocurarine this drug compete with acetylcholine
on its receptor sites.
Poisoning with curare(Ach receptor blocker) cause weak endplate
potential, the same effect occurs with the botulinium toxin(bacterial
toxin)which decreases the release of Ach by nerve terminals
Muscle Hypertrophy
Forceful muscular activity increases total mass of a muscle. All muscle
hypertrophy results from an Increase in the number of actin and myosin
filaments in each muscle fiber, causing enlargement the size of the
muscle .
Muscle atrophy
Occur when a muscle remains unused for many weeks cause a decreases
in muscle mass, the rate of decay of the contractile proteins is more rapid
.than the rate of replacement
Rigor
when muscle fibers are completely depleted of ATP, they develop a state
of extreme rigidity called rigor, when occur after death it is called rigor
mortis, here, all actin filaments bind to myosin filaments permanently in a
fixed way no ATP to detach myosin head and SR can not absorb Ca
Physiology of Smooth Muscle
Morphology: smooth muscle is unstriated, involuntary muscle and differ
from skeletal and cardiac muscle fiber being much smaller; the
sarcoplasmic reticulum is poorly developed. The contractile proteins are
actin, myosin, and tropomyosin but no troponin.
There are two main types of smooth muscle, the visceral(unitary) and the
multiunit (figure 15).
I-Multi-Unit Smooth Muscle.
1-non-syncytial i.e this type of smooth muscle is composed of separate
smooth muscle fibers .Each fiber operates independently of the others
often is innervated by a single nerve ending
2-Neurogenic: controlled by external nerve supply.
3-Contraction not spread widely therefore needed for fine localized
contractions (eg: ciliary muscle and iris of the eye)
4-Very sensitive to acetylcholine and noradrenaline
II-Single-unit Smooth Muscle.
Also called “unitary” or
syncytial or visceral smooth muscle it means a mass of hundreds to
thousands of smooth muscle fibers that contract together as a single unit
(either the whole muscle contracts or the whole muscle relaxes). The
fibers usually are arranged in bundles, and their cell membranes are
adherent to one another at multiple points called gap junction through
which ions and A.P can flow freely from one muscle cell to the next
e.x gut muscle, bile ducts, ureters, uterus, and many blood vessels.
Fig14
Physical Basis for Smooth Muscle Contraction
Comparison of contractile unit within a smooth muscle cell with the
skeletal muscle
1- large numbers of actin filaments radiating from two dense bodies;
the ends of these filaments overlap a myosin filament. In fact, the
dense bodies of smooth muscle serve the same role as the Z discs
in skeletal muscle. This contractile unit is similar to the contractile
unit of skeletal muscle, but randomly arranged .(Fig 15)
2- Most of the myosin filaments have “side polar” cross-bridges
arranged so that the bridges on one side hinge in one direction and
those on the other side hinge in the opposite direction. This allows
the myosin to pull an actin filament in one direction on one side
while simultaneously pulling another actin filament in the opposite
direction on the other side. The value of this organization is that it
allows smooth muscle cells to contract as much as 80 per cent of
their length.
Fig 15
Comparison of Smooth Muscle contraction with
skeletal muscle contraction
Contraction of smooth muscle also occur by sliding filament
mechanism, the difference in contraction are:
I-Although most skeletal muscles contract and relax rapidly, most smooth
muscle contraction is prolonged tonic contraction, sometimes lasting
hours or even days. This is due to
1-Slow Cycling of the Myosin Cross-Bridges. Their attachment to actin,
then release from the actin, and reattachment for the next cycle—is much
slower in smooth muscle than in skeletal muscle
2-low Energy Required to Sustain Smooth Muscle Contraction. only1/10
as energy is required to sustain the same contraction in skeletal muscle.
II-Force of Muscle Contraction is often greater than that of skeletal
muscle, this is results from the prolonged period of attachment of the
myosin cross-bridges to the actin filaments.
III - The role of calcium in excitation-contraction coupling: similar to
skeletal muscle with the following differences:
1-The main source of calcium ions is the ECF rather than sarcoplasmic
reticulum (which is not well developed) ,therefore, Smooth muscle
membrane contains large number of Ca ion channels. .
2-smooth muscle contain tropomyosin but it uncover the active site and
does not contain troponin, in state of it the regulatory protein called
calmodulin which present in cytoplasm of the cell will activate myosin
cross-bridges this occur by:
Calcium ions binds with calmodulin, this binding will cause
activation of myosin light chain kinase, a phosphorylating enzyme
hydrolyzes ATP and takes the inorganic phosphate (Pi) from the ATP and
puts it on the myosin , cause activation of myosin heads this activated
head bind with actin and cause muscle contraction. At the end of
contraction, Calcium ions are pumped back again to the ECF and to the
sarcoplasmic reticulum ,the enzyme myosin phosphatase( located in the
fluids of the smooth muscle cell), which splits the phosphate from the
myosin head then the cycle stop and contraction ceases and causes
relaxation.
Neuromuscular Junctions of Smooth Muscle
I-Neuromuscular junctions of the highly structured type found on skeletal
muscle fibers do not occur in smooth muscle. Instead, the autonomic
nerve fibers that innervate smooth muscle branch diffusely on top of a
sheet of muscle fibers, these fibers do not make direct contact with the
cell membranes but instead they form diffuse junctions that secrete their
transmitter substance into the matrix coating of the smooth muscle ;then
the transmitter substance diffuse to the cell. (fig16)
II-The axons that innervate smooth muscle fibers divides into many
branch, each branch containing series of swollen region called
varicosities contain vesicles that contain neurotransmitter substance.
III-the vesicles of the autonomic nerve fiber endings contain
acetylcholine in some fibers and norepinephrine in others but they are
never secreted by the same nerve fibers. Acetylcholine is excitatory in
some organs and inhibitory in others, the same is true for noradrenaline.
this is depend on the type of receptor(excitatory or inhibitory receptors).
When Ach excite muscle fiber, noradrenaline will inhibit it and vice
versa.
Most blood vessels respond to norepinephrine and epinephrine (from
sympathetic stimulation) by producing vasoconstriction (this response is
mediated through alpha 1-adrenergic receptors). Blood vessels in skeletal
muscle and cardiac muscle respond to these catecholamines producing
vasodilation because the smooth muscle possess beta-adrenergic
receptors
In the multi-unit type of smooth muscle, the varicosities are separated
from the muscle cell membrane by as little as 20 to 30 nanometers—the
same width as the synaptic cleft that occurs in the skeletal muscle
junction. These are called contact junctions (fig 17)
fig 16
Fig 17
Membrane Potentials and Action Potentials in
Smooth Muscle
The normal resting membrane potential is usually about -50 to -60
millivolts, which is about 30 millivolts less negative than in skeletal
muscle.
The action potentials of visceral smooth muscle occur in one of two
forms:
)1(Spike Potentials. rapid depolarization followed by rapid
repolarization. Occurs in most types of visceral smooth muscle. The
smooth muscle cell membrane has more voltage-gated calcium channels
than skeletal muscle but few voltage gated sodium channels .Therefore,
flow of calcium ions to the interior of the fiber is mainly responsible for
the action potential.
)2(Action Potentials with Plateaus. Rapid depolarization followed by
plateau then repolarization .Plateau is responsible for the prolonged
contraction of smooth muscle, is due to the opening of slow calcium
channels , and they remain open much longer. Occurs in the ureter,
uterus, some blood vessels.
Spontaneous electrical activity and slow wave
Some type of smooth muscle cell generate action potential
spontaneously, plasma membrane of these cell do not maintain constant
resting potential instate they gradually depolarized until they reach the
threshold potential and produce A.P fallowing repolarization ,membrane
begin to depolarized again lead to rhythmical state of contractile activity
these cell are pace maker cell
other pace maker cell have different pattern of activity, the
membrane potential go up and down due to regular variation in Na ion
flow across cell membrane this is called slow wave. slow wave rhythm
of the membrane potential not an action potential, but when an excitatory
in put (as food in intestine ) super imposed, slow wave depolarized above
threshold and A.P occur lead to muscle contraction.(fig 18,19(
Fig 18
Fig 19
Excitation of smooth muscles by stretch.
When visceral (unitary) smooth muscle is stretched sufficiently,
spontaneous action potentials usually are generated. They result from a
combination of
)1( the normal slow wave potentials
)2(stretch open mechanosensitive ion channels lead to depolarization
and contraction
This response to stretch allows the gut wall, when excessively stretched,
to contract automatically and rhythmically.
Smooth Muscle Contraction in Response to Local
Tissue Factors.
As occurs in small vessels(arterioles, metarterioles and precapillary
sphincters) which have little or no nerve supply but still can undergoes
powerful vasoconstriction or vasodilation in response to local interstitial
factors and this is called autoregulation of tissue blood flow
1- Lack of oxygen in the local tissues causes smooth muscle relaxation
and vasodilatation.
2-Excess carbon dioxide causes vasodilatation.
3- Increased hydrogen ion concentration causes vasodilatation.
4-nitric oxide from endothelial cell cause local vasodilatation
Effects of Hormones on Smooth Muscle Contraction
A hormone will cause contraction of smooth muscle when act on
excitatory receptors while cause relaxation of smooth muscle when act on
inhibitory receptors. Noradrenaline, vasopressin, and angiotensin
hormones are powerful vasoconstrictors lasting for hours.
Some hormone open sodium or calcium channels and cause
depolarization of the membrane, other hormone closes the sodium and
calcium channels or opening of potassium channels cause
hyperpolarization and inhibition of the muscles .
Sympathetic stimulation(noradrenaline) decreases smooth muscle activity
Parasympathetic stimulation(acetylcholine) has opposite effects (increase
force and frequancy of contraction)
Stretch and cold produce similar effects of acetylcholine on visceral
smooth muscle
Cardiac Muscle
Morphology and physiological characteristics:
The heart actually two separate pumps: a right heart Receive blood
from the peripheral organ and pumps blood to the lungs, and a left heart
receive blood from lung and pumps blood to the peripheral organs. The
heart is composed of three major types of cardiac muscle: atrial muscle,
ventricular muscle, and specialized excitatory and conductive muscle
fibers.
Cardiac muscle is striated, branching, involuntary have single
nucleus, and have typical myofibrils that contain actin and myosin
filaments (troponin and tropomyosin also present) and their organization
give the striated appearance of cardiac muscle fiber ;these filaments lie
side by side and slide along one another during contraction in the same
manner as occurs in skeletal muscle. Cardiac muscle has a smooth
sarcoplasmic reticulum(SR) but less abundant and less organized than in
skeletal muscle. Cardiac muscle are connected by intercalated discs (they
are actually cell membranes that separate individual cardiac muscle cells
from one another). The intercalated disc contains desmosomes(provide
strong mechanical union between cardiac muscle fiber) and gap junction
(protein- tunnels, allow direct transmission of the depolarizing from cell
to cell provide electrical union between cardiac muscle fiber); thus
cardiac muscle act as a single unit(syncytium), in which the cardiac cells
are so interconnected that when one of these cells becomes excited, the
action potential spreads to all of them, Normally, potentials are not
conducted from the atrial syncytium into the ventricular syncytium
directly. Instead, they are conducted only by a specialized conductive
system called the A-V bundle .Cardiac muscle fiber is myogenic (can
work without nerve supply). cardiac muscle cell has rich mitochondria
and blood supply, thus cardiac muscle resist fatigue. (fig 20)

fig 20
Action Potentials in Cardiac Muscle
Resting memberane potential in cardiac muscle is about -85 millivolts,
Rises to a slightly positive value, during each beat. After the initial
spike, the membrane remains depolarized for about 0.2 second ( plateau) ,
followed at the end of the plateau by abrupt repolarization. The presence
of this plateau causes ventricular contraction to last as much as 15 times
as longer than in skeletal muscle.
a. Depolarization: increased Na permeability (fast Na channels).
b. Plateau: increased Ca permeability (slow Ca channels)
c. Repolarization: increased K permeability(K efflux).(figure 21).
Skletal M
Cardiac M
Figure(21) Comparison of action potential in skeletal and cardiac muscle
What Causes the Plateau?
1-slow calcium channels, which are also called calcium-sodium channels.
they are slower to open and, remain open for longer time.
2- decreases the permeability of the cardiac muscle membrane for
potassium ions .
Refractory Period of Cardiac Muscle.is the interval of time, during
which a normal cardiac impulse can not re-excite an already excited area
of cardiac muscle. The normal refractory period of the ventricle is 0.25 to
0.30 second, which is about the duration of the prolonged plateau,
therefore, cardiac muscle cannot be tetanized, a condition which is fatal.
There is an additional relative refractory period about 0.05 second during
which the muscle can be excited by a very strong excitatory signal, this
may develop ventricular fibrillation, a fatal condition unless immediately
treated.
Excitation-Contraction Coupling
As in skeletal muscle, when an action potential passes over the
cardiac muscle membrane, the action potential spreads to the interior of
the cardiac muscle fiber along the membranes of the transverse tubules
and cause sarcoplasmic reticulum to release calcium ions into the muscle
sarcoplasm, these calcium ions diffuse into the myofibrils and catalyze
the chemical reactions that promote sliding of the actin and myosin
filaments along one another; this produces the muscle contraction.
In addition to the calcium ions that are released from the sarcoplasmic
reticulum, a large quantity of extra calcium ions also diffuses into the
sarcoplasm from the T tubules themselves Indeed, without this extra
calcium from the T tubules, the strength of cardiac muscle contraction
would be reduced why??
a-the sarcoplasmic reticulum is less developed than skeletal muscle
b-the T tubules of cardiac muscle have a diameter 5 times as great as that
of the skeletal muscle tubules, which means a volume 25 times as greater.
Frank-Starling Law: Increase the initial length of cardiac muscle
fiber, within physiological limits, will increase the force of contraction
When an extra amount of blood flows into the ventricles, the cardiac
muscle itself is stretched .This in turn causes the muscle to contract with
increased force because the actin and myosin filaments are brought to a
optimal degree of overlap for force generation
Catecholamines (epinephrine and nor epinephrine)increases force of
contraction (positive inotropic effect). This effect is mediated via beta
adrenergic receptors which increase Ca influx from ECF, Ca bind to
troponin-C resulting in forceful contraction.
Spontaneous rhythmicity:
cutting the cardiac nerves does not
stop heart beating, this is due to the presence of a specialized pace maker
tissue that can initiate AP, the pace maker tissue makes up the conductive
system of the heart(SA node, AV node, bundle of His, and Purkinji
fibers) which normally spread impulses throughout the heart.
The pace maker tissue has unstable membrane potential which decline
steadily after each AP until the firing level is reached and another AP is
generated(figure22)
The unstable pacemaker potential is due to:
-Decrease K efflux (membrane potential becomes less negative).
-Na or Ca-Na in the resting condition
fig 22
parameters
Morphology
Skeletal muscles
Striated
cylindrical
Voluntary
Position
Skelton
Nucleus
Multinucleated
Nerve supply
Motor nerve
Autorhythmicity Not present
Tetaniztion
Possible
SR
platue
Well developed
Not present
Pace maker
Source of Ca
No pace maker
sarcoplasm
Neuromuscular
junction
Synaptic cleft
rmp
-90
Smooth muscles
Un striated
spindle
In voluntary
Viscera
Single nucleus
Autonomic
Present
Partially
possible
Not well define
Present in some
fiber
In some fiber
ECF
Cardiac muscles
Striated
Branching
In voluntary
In heart
Sing nucleus
Autonomic
Present
Not possible
Not well define
present
present
ECF
and
sarcoplasm
Contact junction
Diffusion
junction
-50 - -60
-85