Muscular system

Muscle cell function relies on neurofibrils microfilaments, which are divided to the thin
actin filaments and thick myosin filaments of the cytoskeleton. That microfilaments, like
microtubules, function in cell motility. Muscle contraction is the product of
microfilament movement powered by chemical energy; muscle extension occurs only
passively.
Muscle: any flesh in the body, tissue have the ability to contract and relax.
The number of muscles in the human body is about 620 (skeletal) muscles (not assured
by scientists). The muscles are divided into three types which are cardiac (heart
muscle), smooth (walls of hollow organs) and skeletal (attached to bone) muscles. The
skeletal muscle for example is attached to the bones with connective tissues called
tendons. Without these tendons, the muscle cannot transmit the motion (contraction and
relaxation) to the body. Muscle groups that work together to create the same movement
are called synergistic muscles. Muscles that oppose each other are called
antagonistic muscles.
Function of muscles:
1- Movement, Stability and Posture: the contraction and relaxation of the muscle
which lead to the motion that divided into transport and positional movement (head,
hand, fingers and organs). Also maintaining the balance by the hypothalamus.
2- Calcium storage in its smooth ER: the smooth ER of the muscular tissue is called
sarcoplasmic reticulum which stores Ca++ in its tissues. This calcium is used up in
transmitting the nerve impulses along the body, muscle contraction and the bone
formation. In the nerve impulses, if the nervous tissues defect in the calcium
concentration, they take calcium from the sarcoplasmic reticulum.
3- Circulation: using the three types of muscles in the circulation of the blood in the
whole body in which:
- Heart that pump blood to the whole body (cardiac muscle).
- Artery that transfer blood from heart to body by contraction and relaxation.
(smooth muscle).
- Veins that return the blood from body to heart by contraction and relaxation of
muscles (skeletal muscle)
4- Breathing: controlling the breath rate by intercoastal muscles (skeletal muscle)
which help in the inhalation and exhalation. Breathing muscles can be affected by
some diseases and gases such as sarin gas and botulism disease.
5- Digestion: movement of elementary canal muscles such as esophagus, duodenum,
ileum, large intestine which all help in peristalsis of the food inside the digestive
system helping in the mechanical digestion by contraction and relaxation mixing it
with digestive enzymes leading to the digestion.
6- Urination: With the using of the urinary bladder and sphincters smooth muscles,
the sympathetic and parasympathetic systems make orders with relaxation and
contraction of muscles leading to the urination of the urine.

-101-
7- Childbirth: oxytocin hormone stimulates the uterus wall (smooth muscle) leading to
relaxation and contraction to facilitate the delivery of the baby.
8- Vision: focusing by the ciliary muscles, moving the eyeball and the motion of the iris
by relaxation and contraction (smooth muscles)
9- Organ protection: such as eye lids and abdominal muscles protect the abdominal
organs such as small intestine and large intestine.
10- Temperature generation and regulation: when the body temperature decreases, the
body shivers by the smooth muscles and shrink the skin by erector muscles.

Vertebrate skeletal muscle:

1- Skeletal muscle, with its associated connective tissue, constitutes
approximately 40% of body weight.
2- Attaches with bones and that is the reason for their name.
3- Multinucleated muscle fiber that is discussed by that more than one cell fused.
4- Voluntary which is controlled by the PNS efferent motor neurons.
5- Striated (appear in parallel lines) because transverse bands, or striations, can be seen
in the muscle under the microscope.
6- Can have fatigue.
7- One end of a skeletal muscle, called its origin, joins to a bone that remains
relatively stationary. The other end of the muscle, called its insertion, attaches to
another bone across a joint. When the muscle contracts, the insertion is pulled
toward the origin. The origin is generally closer to the midline of the body and the
insertion is farther away.
Structure of skeletal muscle:
Each muscle is surrounded by a membrane called epimysium
wrapping the entire muscle. Every muscle consists of many
fascicles or fasciculi, each fascicle is surrounded by a
membrane called perimysium. Each fascicle is consisted of
many muscle fibers, each muscle fiber is surrounded by a
membrane called endomysium. All of these membranes are
gathered and coiled to form the tendon that attach the muscle to
the bone or a sheet-like aponeurosis, which indirectly attaches
the muscle to bone, cartilage, or another connective tissue
covering. If the tendon is only formed from the epimysium,
with any contraction to the muscle, the inner fibers will detach
from the outer membrane, so it is formed from all the
membranes. The muscle fibers are parallel to the fascicles
parallel to the axis of the muscle.
Examining the structure of a muscle fiber helps us understand
the mechanism of muscle contraction. A muscle fiber is a

-102-
 single cylindrical fiber, with several nuclei located at its periphery as more than one cell
are fused. The largest human muscle fibers are up to 30 cm long and 0.15 mm in
diameter. Such giant cells may contain several thousand nuclei.
The muscle fiber is surrounded by a membrane called sarcolemma. It has a cytosol
called sarcoplasm that includes organelles that has more than one nuclei and that why it
called multinucleated. Along the surface of the sarcolemma are m any tube-like
invaginations, called transverse tubules, or T tubules, which occur at regular intervals
along the muscle fiber and extend inward into it. The T tubules are associated with a
highly organized smooth ER which called sarcoplasmic reticulum and myofibril which
is divides into thin filaments of actin and thick filaments of myosin. The sarcoplasmic
reticulum has a relatively high concentration of Ca2+, which plays a major role in
muscle contraction.
Striation of muscle fibers:
The actin and myosin myofilaments are arranged
into highly ordered certain manner represented in
repeating units called sarcomeres, which are
joined end-to-end to form the myofibrils.
The sarcomere is the basic structural unit of
skeletal muscle because it is the smallest portion
of skeletal muscle capable of contracting. While,
the functional unit of the muscles is a group of muscle fibers supplied by a motor nerve.
 The separate components of the sarcomere can slide past each other, causing the
sarcomeres to shorten. When the sarcomeres shorten, the myofibrils shorten, which
is the ultimate cause of contraction of the muscle fiber during a contraction.
 Each sarcomere extends from one Z disk to an adjacent Z disk. So that, the number
of Z lines = number of sarcomeres + 1
Each Z disk is a network of protein fibers forming an
attachment site for actin myofilaments and it is made
of actin.
 The arrangement of the actin and myosin
myofilaments in sarcomeres:
 A light I band, which consists only of actin
myofilaments, spans each Z disk and ends at the
myosin myofilaments.
 A darker, central region in each sarcomere,
called an A band, extends the length of the myosin myofilaments. The actin and
myosin myofilaments overlap for some distance at both ends of the A band.
 In the center of each sarcomere is a second semi-light zone, called the H zone,
which consists only of myosin myofilaments.
 The myosin myofilaments are anchored in the center of the sarcomere at a dark-
staining band, called the M line.

-103-
 The alternating I bands and A bands of the sarcomeres are responsible for the striations
in skeletal muscle fibers observed through the microscope. It is the close association of
the sarcomeres, the T tubules, and the sarcoplasmic reticulum that enables a nerve
stimulus to initiate contraction of the muscle fiber.
Muscle contraction:
Contraction of skeletal muscle tissue occurs as actin and myosin myofilaments slide
past one another, causing the sarcomeres to shorten.
 Many sarcomeres are joined end-to-end
to form myofibrils. Shortening of the
sarcomeres causes myofibrils to shorten,
thereby causing the entire muscle to
shorten.
 The sliding of actin myofilaments past
myosin myofilaments during contraction
is called the sliding filament model of muscle contraction which was made by
Huxley.
 During contraction, neither the actin nor the myosin fibers shorten but the Z lines get
closer to each other leading to shorten of I bands only. This is done in the non-
completed contraction. While in the full-contracted muscles, the length of the actin
filaments shortens as the actin filaments overlap each other so the I band disappear.
The H zones disappear in both completed and non-completed contractions, but the
A bands do not change in length.
 During muscle relaxation, sarcomeres lengthen. This lengthening requires an
opposing force, such as that produced by other muscles or by gravity
Actin and Myosin Myofilaments:
Actin myofilaments, or thin filaments, are made up of three components:
actin, troponin, and tropomyosin.
 The actin strands, which resemble two-minute strands of pearls twisted together, have
attachment binding sites for the myosin myofilaments.
 Troponin complex molecules are attached at specific intervals along the actin
myofilaments. These molecules have binding sites for Ca2+.
 Tropomyosin filaments are located along the groove between the twisted strands of
actin myofilament subunits. The tropomyosin filaments block the myosin
myofilament binding sites on the actin myofilaments in an unstimulated muscle. In
other words, if no Ca2+ is present, the tropomyosin filaments cover the attachment
sites on the actin myofilament. However, when Ca2+ is present, it binds to troponin,
which causes the tropomyosin filaments to expose the attachment sites on the
actin -myofilaments.
 Myosin myofilaments, or thick myofilaments, consists of two heads and tails. The
parts of the myosin molecule that resemble golf club heads are referred to as myosin

-104-
 heads made of globular protein. The tails of the myosin filaments are connected to
each other in the M line.
In order to make the contraction of the muscle, the heads of myosin should bind to the
heads of actin, but there are two main problems which are that the actin heads are short
and the binding cites are covered. The myosin heads have three important properties:
 The heads can bind to attachment sites on the actin myofilaments
 They can bend and straighten during contraction
 They can break down ATP, releasing energy.
Mechanism of relaxation and contraction using Ca and ATP:
Calcium ions (Ca+2) and proteins bound to
actin play crucial roles in both muscle cell
contraction and relaxation. Tropomyosin, a
regulatory protein, and the troponin complex, a
set of additional regulatory proteins, are bound
to the actin strands of thin filaments. In a
muscle fiber at rest, tropomyosin covers the
myosin-binding sites along the thin filament,
preventing actin and myosin from interacting.
When Ca+2 accumulates in the cytosol, it
binds to the troponin complex, causing
tropomyosin bound along the actin strands to
shift position and expose the myosin binding sites on the thin filament.
 Thus, when the Ca+2 concentration rises in the cytosol, the thin and thick filaments
slide past each other, and the muscle fiber contracts.
 When the Ca+2 concentration falls, the binding sites are
covered, and contraction stops.
 Motor neurons cause muscle contraction by triggering
the release of Ca+2 into the cytosol of muscle cells with
which they form synapses.
The head, which extends to the side, can bind ATP and
hydrolyze it to ADP and inorganic phosphate.
 Hydrolysis of ATP converts myosin to a high-energy
form. This form of myosin binds to actin, forms a cross-
bridge changing the angle of myosin, and pulls the thin actin filament toward the
center of the sarcomere. The cross-bridge is broken when a new molecule of ATP
binds to the myosin head.

-105-
Storage energy compounds:
For making any activity, the muscle cells need a source of energy, so they depend on
direct energy and stored energy resources. Direct energy represented in ATP which
the muscle cells store only enough for about 10 seconds’ (3 to 9 contractions) worth of
maximal activity. Once this is used up the cells must produce more ATP from other
stored energy sources, including creatine phosphate, glycogen,
glucose, and fatty acids.
 Creatine phosphate (creatine-P) which is a high-energy molecule
with an attached phosphate group. Creatine phosphate can transfer a
phosphate group and energy to ADP and therefore create a new
ATP molecule quickly.
This reaction is reversible: if ATP is not needed to power muscle
contractions, the excess ATP can be used to build a fresh supply of
creatine phosphate, which is stored until needed. Creatine phosphate
also seems to improve muscle performance in certain neuromuscular
diseases.
 The combination of previously available ATP plus stored creatine
phosphate produces only enough energy from 15 up to 30–40
seconds of heavy activity.
Beyond that for more difficult activities, muscles must rely on stored
glycogen, acomplex sugar (polysaccharide) composed of many
smaller molecules of glucose.
 For the first three to five minutes of sustained activity, a muscle
cell draws on its internal supply of stored glycogen. Glucose
molecules are removed from the glycogen, and their energy is
used to synthesize ATP. And this can be done by two ways:
 Part of the process of the breakdown of glucose (proper source)
can happen without oxygen (called anaerobic metabolism) fairly
quickly, but anaerobic metabolism yields only two ATP
molecules per glucose molecule. It also has the unfortunate side
effect of producing lactic acid, which causes the burning
sensation one feels right at the end of a heavy weightlifting
session, just as exhaustion sets in. It can last about one minute
with these 2 ATPs.
 The most efficient long-term source of energy is the aerobic
metabolism of glucose in the blood, fatty acids derived from
stored fat in fat cells, and other high-energy molecules such as
lactic acid. Aerobic metabolism takes place in mitochondria and
requires oxygen. The next time you engage in strenuous exercise,
notice that it may take a minute or two for your respiratory rate to
increase dramatically. Your heart rate also increases because

-106-
 there is an increase in blood flow to the exercising muscle. The increased respiration
and heart rate are signs that aerobic metabolism is now taking place. Until aerobic
metabolism kicks in, however, your cells are relying on stored ATP, creatine
phosphate, and anaerobic metabolism of glycogen. The aerobic metabolism
generates from 28 to 32 ATPs from the oxidation of lipids. It can last from 40
minutes to hours with these 32 ATPs.
Weight lifters can rely almost exclusively on stored energy because their muscles
perform for relatively short periods of time. Long-distance runners start out by
depending on stored energy, but within several minutes they are relying almost
exclusively on aerobic metabolism. If they could not, they would collapse in exhaustion.
After you finish exercising, note that you continue to breathe heavily for a period of
time. These rapid, deep breaths help reverse your body’s oxygen debt, incurred because
your muscles used more ATP early on than was provided by aerobic metabolism. The
additional ATP was produced by anaerobic metabolism, with the subsequent buildup of
lactic acid.
 After exercise, you still need oxygen to metabolize the lactic acid by aerobic
pathways and to restore the muscle’s stores of ATP and creatine phosphate to their
resting levels. The ability of muscle tissue to accumulate an oxygen debt and then
repay it later allows muscles to perform at a near-maximal rate even before aerobic
metabolism has increased.

ATP role in the muscle contraction:

1) Starting with the myosin head bonding to ATP without hydrolyzing in its low energy
configuration.
2) Hydrolyzation of the ATP to ADP and phosphate and leaving the myosin head in
high energy configuration.
3) The myosin head binds to actin binding site forming a cross bridge (called also
transverse links) because of the change of its angle.
4) Releasing the ADP and phosphate from the myosin returning it to low energy
configuration. In a response, the myosin tends to return the ADP bond so it moves
towards the center of the muscle and it is still attached to the actin.
5) Bonding a new ATP molecule to the myosin leading it to release the myosin head
from the actin. The process loops leading to contraction.

-107-
 Notes:
1) If there is absence in no. of
ATP after contraction, the muscle
cannot return to its relaxation state
again. And that what happens actually
in death, if there were contracted
muscles, they will remain contracted
calling it rigor mortis (stiffness +
death).
2) Number of ATP in one cross
bridge is one ATP as if there was more
than one ATP, it will make more than
one cross bridge. The ATP bonds at
first with myosin and then hydrolyze
making the cross bridge until another
ATP makes the same mechanism
again.

Nerve Supply and Muscle fiber Stimulation:

Skeletal muscle fibers do not contract unless they are stimulated by motor neurons.
Motor neurons generate action potentials that travel to skeletal muscle fibers. Axons of
these neurons enter muscles and send out branches to several muscle fibers. Each
branch forms a junction with a muscle fiber, called a neuromuscular junction.
Neuromuscular junctions are located near the center of a muscle fiber. A single motor
neuron and all the skeletal muscle fibers it innervates constitute a motor unit. A motor
unit in a small, precisely controlled muscle, such as in the hand, may have only one or a
few muscle fibers per unit whereas the motor units of large thigh muscles may have as
many as 1000 muscle fibers per motor unit.
Therefore, the fewer fibers there are in the motor units of a muscle, the greater
control you have over that muscle. Many motor units constitute a single muscle.
A neuromuscular junction is formed by a cluster of enlarged axon terminals
resting in indentations of the muscle fiber’s cell membrane. An enlarged axon
terminal is the presynaptic terminal; the space between the presynaptic terminal
and the muscle fiber membrane is the synaptic cleft; and the muscle fiber
membrane is the postsynaptic membrane which is called motor endplate. It has two
types of channel receptors which are sodium ligand and voltage gated ion channels.
1) When an action potential reaches the presynaptic terminal, it causes Ca2+
channels to open.
2) Calcium ions enter the presynaptic terminal and cause several
synaptic vesicles to release acetylcholine into the synaptic cleft by exocytosis.
3) The acetylcholine diffuses across the synaptic cleft and binds to acetylcholine
receptor sites on the Na+ channels in the muscle fiber cell membrane.
4) The combination of acetylcholine with its receptor opens Na+ channels and
therefore makes the membrane more permeable to Na+.

-108-
 5) The resultant movement of Na+ into the muscle fiber will initiate an action potential
once threshold is reached. The action potential travels along the length in the two
directions of the membrane of the muscle fiber and causes it to contract. The action
potential goes in the two directions because both of the sides of sarcolemma are in
polarization state leading to depolarizing the adjacent sides in the two directions (as the
artificial stimulation to the axon in neurons).
6) The acetylcholine released into the synaptic cleft between the neuron and the
muscle fiber is rapidly broken down by an enzyme, acetylcholinesterase. This
enzymatic breakdown ensures that one action potential in the neuron yields only
one action potential in the skeletal muscle fibers of that motor unit and only one
contraction of each muscle fiber.
7) Within the muscle fiber, the action potential spreads deep into the interior, following
infoldings of the plasma membrane called transverse (T) tubules.
8) The T tubules make close contact with the sarcoplasmic reticulum (SR), a
specialized endoplasmic reticulum. As the action potential spreads along the T tubules,
it triggers changes in the SR, opening Ca+2 channels.
9) Calcium ions stored in the interior of the SR flow through these open channels into the
cytosol and bind to the troponin complex, initiating contraction of the muscle fiber.
10) The bond of calcium with troponin complex shift the tropomyosin position and
expose the myosin binding sites on the thin filament.
11) Making each sarcomere to contract with this mechanism leads to the contraction of
muscle.
12) To relax the muscle again, the membrane of the muscle makes repolarization by
opening the potassium sodium pumps using ATP to let out the sodium ions that
entered the membrane, leading to the repolarization of the T-tubules and the
sarcoplasmic reticulum. So, the sarcoplasmic reticulum closes the calcium ion
channels
13) When the calcium concentration becomes very high in the cytosol as it came out from
the sarcoplasmic reticulum, it enters again the sarcoplasmic reticulum by a calcium
pump using ATP.
14) With decreasing the calcium concentration of calcium in the cytosol, the calcium
bonded with troponin complex leave leading to blocking again the myosin site
receptors in the actin with the tropomyosin.

-109-
 Note: For a single contraction for the muscles, the ATP used in three places which are:
 The sodium potassium ion pump in repolarization of the muscle fiber membrane.
 Making the myosin heads with high energy to bond with the actin filaments.
 Calcium ion pump to return the calcium into the sarcoplasmic reticulum.
Several diseases cause paralysis by interfering with the excitation of skeletal muscle
fibers by motor neurons:
1) Amyotrophic lateral sclerosis (ALS):
Amyotrophic lateral sclerosis, or ALS, is a progressive nervous system disease that
affects nerve cells in the brainstem and spinal cord, causing loss of muscle control.
ALS affects the nerve cells that control voluntary muscle movements such as
walking and talking (motor neurons). ALS causes the motor neurons to gradually
deteriorate, and then die. Motor neurons extend from the brain to the spinal cord to
muscles throughout the body. When motor neurons are damaged, they stop sending
messages to the muscles, so the muscles can't function.
ALS is inherited in 5% to 10% of people. For the rest, the cause isn't known.
Researchers continue to study possible causes of ALS. Most theories center on a
complex interaction between genetic and environmental factors.
2) Myasthenia gravis:
It is an autoimmune disease in which a person produces antibodies to the
acetylcholine receptors on skeletal muscle fibers. As the number of these receptors
decreases, synaptic transmission between motor neurons and muscle fibers declines
preventing muscle contraction. Fortunately, effective treatments are available for
myasthenia gravis.
3) Muscular dystrophy:
Serious diseases of muscle are relatively uncommon, but foremost among them is
muscular dystrophy. The term actually applies to several different hereditary diseases of
muscle (dystrophy means “abnormal growth”).

-110-
 In Duchenne muscular dystrophy, a single defective gene results in the lack of a
particular muscle cell protein. The normal gene, when present, directs the cell to produce
a protein called dystrophin that is part of the muscle cell membrane. The function of
dystrophin is to limit the inflow of calcium into muscle cells through calcium “leak”
channels. People with muscular dystrophy lack dystrophin, and as a result too much
calcium leaks into the muscle cell through the leak channels.
 The high intracellular calcium concentration activates enzymes that damage muscle
proteins and ultimately may kill the cell. The result is a loss of muscle fibers and
muscle wasting. Eventually much of the muscle mass is replaced with fibrous
connective tissue. Many people with muscular dystrophy die before age 30, usually
because of failure of the heart muscle or the skeletal muscles used for breathing. At
the moment there is no cure; however, it is an area of intense research interest, and
progress is being made on several fronts.
4) Tetanus:
 Tetanus is caused by a bacterial infection. The disorder is called tetanus because this
is the technical term for a maximal (tetanic) muscle contraction or spasm.
 Generally, the infection is acquired by a puncture wound to a muscle. The bacteria
produce a toxin that overstimulates the nerves controlling muscle activity, resulting in
tetanic contractions.
 The toxin affects a variety of skeletal muscles, but especially those of the jaws and
neck. Jaw muscles may contract so forcefully that they seem locked shut (the origin of
its common name, “lockjaw”). Untreated, tetanus may lead to death due to exhaustion
or respiratory failure.
5) Muscle cramps:
Muscle cramps are painful, uncontrollable, reflex-mediated muscle contractions.
They are thought to be caused by the dehydration and ion imbalances that sometimes
occur with heavy exercise.
 The most likely culprit is a shift in potassium ions between the intracellular and
extracellular fluid. Muscle cramps generally can be soothed by increasing the
circulation to the affected muscle through gentle stretching and massage.
6) Pulled muscles:
Pulled muscles, sometimes called torn muscles, result from stretching a muscle
too far, causing some of the fibers to tear apart. Internal bleeding, swelling,
and pain often accompany a pulled muscle.
7) Fasciitis:
Fasciitis involves inflammation of the connective tissue sheath, or fascia, that
surrounds a muscle. It is usually caused by straining or tearing the fascia.
Most often it affects the sole of the foot (plantar fasciitis), where it is a common
cause of heel pain. Like tendons and ligaments, fascia mend slowly. Treatment
includes resting the area and protecting it from pressure. Injections of
corticosteroid drugs can relieve severe pain.

-111-
 Muscle fatigue:
It is defined as a decline in muscle performance during exercise. The most common
cause of fatigue is insufficient energy to meet metabolic demands, due to depletion
of ATP, creatine phosphate, and glycogen stores within the muscle. However,
fatigue can also be caused by psychological factors, including discomfort or the
boredom of repetitive tasks. The fatigue is occurred from the accumulation of lactic
acid in the anaerobic cellular respiration despite being useful. It is useful in using as
a fuel by conversion to pyruvate that make energy in mitochondria.
Muscle strength: Our strength and ability to move effectively depend on how forcefully
our muscles contract. The mechanical force that muscles generate when they contract is
called muscle tension.
How much tension is generated by a muscle depends on three factors:
 The number of muscle cells in each motor unit (motor unit size)
 The number of motor units active at any one time
 The frequency of stimulation of individual motor units. If the frequency increased a
lot, it causes spasm such as tetanus.
Motor unit:
A single muscle may consist of thousands of individual muscle cells. The individual
cells in any muscle are organized into groups of cells that all work together. Each group
of cells is controlled by a single nerve cell called a motor neuron (because it affects
movement). The motor neuron and all of the muscle cells it controls are called a
motor unit. Also, it is called Motor nerve fiber.
 A motor unit is the smallest functional unit of muscle contraction, because
when the motor neuron is activated, all the muscle cells in that motor unit are
activated together.
While when we ask on the motor endplates, we mean also the neuromuscular junctions
and synaptic terminals.
Controlling the motor unit:
1) Motor unit size:
It can vary widely from one muscle to the next. The number of muscle cells per motor
unit is a tradeoff between brute strength and fine control.
 Larger motor units generate more force but offer less control. In the thigh
muscle, where strength is more important than fine control, a single motor unit may
consist of as many as a thousand muscle cells.
 In muscles of the eye, where fine control is essential, a motor unit may consist of
only 10 muscle cells. According to the all-or-none principle, muscle cells are
completely under the control of their motor neuron.
 Muscle cells always respond with a complete cycle of contraction and relaxation
(called a twitch) every time they are stimulated by an electrical impulse, called an
action potential, from their motor neuron.

-112-
  Although individual motor units either are contracting or are relaxed, whole muscles
generally maintain an intermediate level of force known as muscle tone. Muscle tone
exists because, at any one time, some of the muscle’s motor units are contracting
while others are relaxed.
 The number of motor units active at any one time
 Increasing tone (or force) by activating more motor units is called recruitment. The
maintenance of muscle tone depends on the nervous system. In recruitment, the
number of muscle fibers contracting is increased by increasing the number of motor
units stimulated, and the muscle contracts with more force.
 When only a few motor units are stimulated, a small force of contraction is
produced because only a small number of muscle fibers are contracting.
 As the number of motor units stimulated increases, more muscle fibers are
stimulated to contract, and the force of contraction increases.
Maximum force of contraction is produced in a given muscle when all the motor units of
that muscle are stimulated (recruited).
There are two important conclusions which are:
 when the nerve impulse goes in the motor unit, all the muscle fibers from this motor
unit contract at the same time.
 The motor unit isn’t attached with the contraction of other motor units at the same
time.
2) The frequency of stimulation of individual motor units:
 A laboratory recording of muscle activity, called a
myogram, reveals that the stimulus-twitch
relationship has three stages:
1. Latent period (or lag period) (the time between
stimulation and the start of contraction). This is
the time it takes for the nerve impulse to travel to
the sarcoplasmic reticulum, for calcium to be
released, and for the myosin heads to bind to the
actin filaments.
2. Contraction (the time during which the muscle actually shortens). Actin
filaments are pulled toward the center of the sarcomere and myofibrils shorten.
3. Relaxation (muscle returns to its original length). Calcium is transported back
into the sarcoplasmic reticulum, the troponin-tropomyosin protein complex shifts
back into its original position, and the sarcomere stretches passively to its original
length.
 A key point is that the contraction/relaxation cycle of the muscle twitch lasts longer
than the stimulus that caused the contraction in the first place. If additional stimuli
arrive at the muscle before the muscle has had a chance to transport calcium back into
the sarcoplasmic reticulum and relax completely, the total force produced becomes
greater than the force produced by one twitch alone. In effect, the force becomes

-113-
 greater because more calcium is present. Increasing muscle force by increasing the
rate of stimulation of motor units is called summation.
 There is a limit to summation, however. If stimulation becomes so frequent that the
muscle cannot relax at all, it will remain in a state of maximum contraction called
tetanus or a tetanic contraction. On a myogram, tetanus appears as a straight
horizontal line representing the fusion of the peaks and valleys of individual twitches.
A tetanic contraction may lead eventually to muscle fatigue.
Called also Isotonic

Types of muscle contraction:

Types of Skeletal Muscle Fibers:
1) According to the source of ATP used to power muscle activity:
They are divided into Oxidative and Glycolytic Fibers:
Fibers that rely mostly on aerobic respiration are called oxidative fibers. Such fibers
are specialized in ways that enable them to make use of a steady energy supply:
They have many mitochondria, a rich blood supply, and a large amount of an oxygen-
storing protein called myoglobin. A brownish red pigment, myoglobin binds oxygen
more tightly than does hemoglobin, enabling oxidative fiber to extract oxygen from
the blood efficiently. So, it has no muscle fatigue.

-114-
In contrast to oxidative fibers, glycolytic fibers use glycolysis as their primary source of
ATP. They have a larger diameter and less myoglobin than oxidative fibers and thus
fatigue much more readily.
These different fiber types are readily apparent in the muscle of poultry and fish: The
dark meat is made up of oxidative fibers rich in myoglobin, and the light meat is
composed of glycolytic fibers.
2) The speed of muscle contraction:
Fast twitch fibers Slow twitch fibers
Fast-twitch fibers develop tension two Slow fibers, often found in muscles that
to three times faster than slow-twitch maintain posture, can
fibers. sustain long contractions.
Fast fibers enable brief, rapid, A slow fiber has less sarcoplasmic
powerful contractions. reticulum and pumps Ca+2 more slowly
than a fast fiber.
can contract more quickly than slow- Because Ca+2 remains in the cytosol
twitch fibers because they break down longer, a muscle twitch in a slow fiber
ATP more quickly. lasts about five times as long as one in a
fast fiber.
have fewer mitochondria, fewer blood break down ATP slowly, and so they
vessels, and little or no myoglobin contract slowly. They tend to make ATP
compared to slow-twitch fibers as they need it by aerobic metabolism.
This is done to keep their posture.
store large amounts of glycogen and contain many mitochondria and are
tend to rely heavily on creatine well supplied with blood vessels, so
phosphate and anaerobic they draw more blood and oxygen than
metabolism for quick bursts of high fast-twitch fibers.
energy.
Their contractions are rapid and store very little glycogen because they
powerful but cannot be sustained for can obtain glucose and fatty acids
long. quickly from the blood
Fast-twitch fibers depend on aerobic
mechanisms for any activity
Have fatigue as they accumulate lactic Don’t have fatigue as they are rich in
acid. oxygen
Examples: Eyeball and Eyelashes Examples: Trunk muscles
Which type of fiber is better?
 It depends on the activity. Because slow-twitch fibers offer more endurance, they are
most useful for steady activities such as jogging, swimming, and biking. Slow-twitch
fibers are also important for maintaining body posture.

-115-
Many of the muscles of the leg and back, for example, contain a high percentage of
slow-twitch fibers because they must contract for long periods to support us when we
stand.
 Fast-twitch fibers are more often used to power brief, high intensity activities such as
sprinting for short distances, lifting weights, or swinging a tennis racquet. Muscles in
our hands, for example, contain a high proportion of fast twitch fibers, allowing the
muscles to contract quickly and strongly when necessary.
 The percentage of slow- and fast-twitch fibers varies not only from muscle to muscle
but from person to person. The percentages are determined in part by inheritance, and
they can influence athletic ability. For example, most world-class marathoners have a
higher-than-average percentage of slow-twitch fibers in their legs.
Exercise training improves muscle mass, strength, and endurance:
 Although part of your athletic potential might be influenced by inheritance, a
consistent, planned program of physical exercise (sometimes called exercise
training) can improve your strength, endurance, and skill at any athletic
endeavor.
 The extent of muscle development depends on many factors, including the amount
of resistance used, the duration and frequency of exercise, and your own
genetic predisposition. However, even low to moderate weights can lead to
noticeable improvements in muscle strength.
 Whether primarily strength or endurance is improved by exercise training
depends on the type and intensity of training. The two primary types of exercise
training are strength (resistance) training and aerobic (endurance) training.
 Strength training involves doing exercises that strengthen specific muscles,
usually by providing some type of resistance that makes them work harder.
 Strength training is generally short, intense exercise such as weightlifting using free
weights or weight machines. It builds more myofibrils, particularly in fast-twitch
fibers, and causes the fast-twitch fibers to store more glycogen and creatine
phosphate as quick energy sources. This increases the size of individual muscle cells
and builds muscle mass and muscle strength, but it does not increase the number of
muscle cells.
 Aerobic training involves activities in which the body increases its oxygen intake
to meet the increased demands for oxygen by muscles. Whereas resistance
training strengthens muscles, aerobic training builds endurance.
 With aerobic training, the number of blood capillaries supplying muscle increases.
In addition, the number of mitochondria in muscle cells and the amount of
myoglobin available to store oxygen both increases. The muscle fibers themselves
do not increase much in mass, nor do they increase in number. Aerobic exercise also
improves the performance of the cardiovascular and respiratory systems.
 Less intense than strength training but carried out for prolonged periods, aerobic
exercises include jogging, walking, biking, and swimming.

-116-
 It’s a good idea to combine any athletic activity with stretching exercises. Gentle
stretching before exercise increases your heart rate gradually, pumping additional
blood to your muscles and preparing you for more strenuous exertion. This lowers
your risk of sprains and pulled muscles. After exercising, let your heart rate and
breathing return gradually to normal as you walk slowly and do more stretching.
 Regular stretching improves joint mobility and range of motion. Whenever
you stretch, do it gradually and hold each position for 30 seconds. You should
feel a gentle pull in your muscles, but not pain. Try not to bounce, because
abrupt stretches could cause your muscles to contract quickly in response, increasing
the risk of injury.
Summary: A motor unit consists of a motor neuron and all of the muscle cells it
controls. Greater muscle force is produced by activation of more motor units and/or
increased frequency of stimulation of motor units. Most muscles contain a combination
of slow-twitch and fast-twitch fibers. Slow-twitch fibers rely on aerobic metabolism and
are most useful for endurance. Fast-twitch fibers are most useful where strength is
required. Exercise increases aerobic capacity, muscle mass, and muscle strength but
does not increase the number of muscle cells.
Most of the overall muscle mass of the body is skeletal muscle. Nevertheless,
both cardiac and smooth muscle have unique features that suit them ideally for
their roles in the body.
Cardiac muscles (heart muscles only):
Although all cardiac muscle cells are capable of beating
spontaneously and establishing their own cycle of contraction
and relaxation (involuntary), those with the fastest rhythm are
called pacemaker cells because the rest of the cells follow
their faster pace.
 Cardiac muscles are striated also but without light and
dark bands.
 Cardiac muscles are Uni-nucleated (one nucleus) branched
in each fiber.
 Cardiac muscle cells have an intrinsic ability to generate and
conduct electrical impulses that stimulate these same cells to
contract rhythmically. These properties are intrinsic to the
heart muscle itself and do not depend on extrinsic nerve
impulses. Even if all nerve connections to the heart are
severed, the heart continues to beat rhythmically.
The impulse that signals each heartbeat begins at the sinoatrial
(SA) node, a crescent-shaped mass of specialized cardiac
muscle cells that lies in the wall of the right atrium, just inferior
to the entrance of the superior vena cava. The SA node sets the

-117-
basic heart rate by generating 70–80 electrical impulses per minute making its own
action potential.
 Cardiac muscle cells are joined at their blunt ends by structures called intercalated
discs. The intercalated discs contain gap junctions that permit one cell to
electrically stimulate the next one. This is made because the two heart atriums or
ventricles for example need to contract and relax in the same time, so it connects the
two sides with each other transferring the contraction. In effect, the pacemaker cells
dictate the rate of contraction of the whole heart, because their faster pace activates
the slower cells before the slower cells would be activated by their own inherent
rhythm.
Action potentials of cardiac muscle cells last up to 20 times longer than those of the
skeletal muscle fibers. Cardiac muscle cells go through rhythmic cycles of contraction
and relaxation. The relaxation periods are necessary periods of rest so that the muscle
doesn’t fatigue. A long refractory period prevents summation and tetanus.
Smooth muscles:
Smooth muscles are the lining wall of all hollow organs (except heart) such as arteries,
veins, uterus, alimentary canals, urinary bladder, iris and ciliary muscles.
 They are uni-nucleated in each cell, involuntary and take the spindle shape.
 Smooth muscle lacks the striated appearance of skeletal and cardiac muscle because
their actin and myosin filaments are not regularly arrayed along the length of the cell . It is
called “smooth” for this reason.
 Smooth muscle cells are also joined by gap junctions
that permit the cells to activate each other, so that
the whole tissue contracts together in a coordinated
fashion. (In contrast to smooth and cardiac muscle,
skeletal muscle cells are activated only by motor
neurons. This is why the skeletal muscles of a person
with a severed spinal cord are completely paralyzed
below the point of injury.)
 Even though cardiac and smooth muscle cells can
contract without signals from the nerves, they do
respond to nerve activity as well. In both types of
muscle, the nerves belong to the autonomic nervous
system.
 The effect of nerve activity may be either inhibitory or
stimulatory. Changes in both inhibitory and stimulatory
nerve activity to the heart are responsible for the increase in
your heart rate when you exercise, for example. Nerve
stimulation can also change the contractile force of smooth
muscle.

-118-
 Smooth muscle generally is partially contracted all the time. This makes it ideally
suited for situations in which contractions need to be sustained. Nevertheless, it almost
never fatigues because it contracts so slowly that its ATP usage is always less than its
production capability. Smooth muscle is a key player in the homeostatic regulation of
blood pressure because it can maintain the diameter of blood vessels indefinitely,
adjusting them slightly as necessary.
Instead, the thick filaments are scattered throughout the cytoplasm, and the thin
filaments are attached to structures called dense bodies, some of which are tethered to
the plasma membrane.
 There is less myosin than in striated muscle fibers, and the myosin is not associated
with specific actin strands.
Some smooth muscle cells contract only when stimulated by neurons of the autonomic
nervous system. Others can generate action potentials without input from neurons they
are electrically coupled to one another.
Smooth muscle cells have no troponin complex or T tubules, and their sarcoplasmic
reticulum is not well developed. During an action potential, Ca+2 enters the cytosol
mainly through the plasma membrane. Calcium ions cause contraction by binding to the
protein calmodulin, which activates an enzyme that phosphorylates the myosin head,
enabling cross-bridge activity. Invertebrates have muscle cells similar to vertebrate
skeletal and smooth muscle cells, and arthropod skeletal muscles are nearly identical to
those of vertebrates.
However, because the flight muscles of insects are capable of independent, rhythmic
contraction, the wings of some insects can actually beat faster than action potentials can
arrive from the central nervous system. Another interesting evolutionary adaptation has
been discovered in the muscles that hold a clam’s shell closed. The thick filaments in
these muscles contain a protein called paramyosin that enables the muscles to remain
contracted for as long as a month with only a low rate of energy consumption.

-119-