MUSCULAR SYSTEM

INTRODUCTION
Muscles make up the bulk of the body and
account for about one-third of its weight.
Their ability to contract not only enables the
body to move, but also provides the force
that pushes substances, such as blood and
food, through the body. Without the
muscular system, none of the other organ
systems would be able to function.
Muscles move cows, snakes, worms and
humans. Muscles move you! Without
muscles you couldn't open your mouth,
speak, shake hands, walk, talk, or move
your food through your digestive system.
There would be no smiling, blinking,
breathing. You couldn't move anything
inside or outside you. The fact is, without
muscles, you wouldn't be alive for very long!
Muscle tissue is found everywhere within
the body, not only beneath the skin but deep
within the body, surrounding many internal
organs and blood vessels.
The size and location of muscle tissue helps
determine the shape of our bodies and the
way we move.

2. Regulates organ volume. It sustains

contractions of smooth muscles that may
prevent outflow of the contents of a hollow
organ. For example, temporary storage of
food in the stomach or urine in the urinary
bladder.
3. Stabilizes body position. Besides
producing movements, skeletal muscle
contractions maintain the body in a stable
position, such as standing or sitting.
4. Generates Body Heat. Heat is the byproduct of contraction of muscles. In fact, it
is believed to contribute to 85% of all body
heat.

CHARACTERISTICS OF MUSCLES:
1. Excitability. Ability to respond to certain
stimuli by producing electrical signals called
action potentials impulses).
2. Elasticity. Ability of the muscle to return
to its original shape after contracting or
extending.
3. Contractility. Ability of the muscle tissue
to shorten and thicken (contract), thus
DO YOU KNOW THAT?
generating force to do work.
On the average, probably 40% of your body 4. Extensibility. Ability of the muscle to be
weight is in muscles. You have over 630 extended (stretched) without damaging the
muscles that move you. Muscles can't push. tissue.
They pull. You may ask yourself, if muscles
can't push how can you wiggle your fingers TYPES OF MUSCLES:
in both directions, back and forth, back and 1. CARDIAC MUSCLE. Found solely in the
forth? The answer? Muscles often work in heart; striated, but are NOT under voluntary
pairs so that they can pull in different or control. The cardiac muscle cell contains
opposite directions.
ONE nucleus located near the center,
adjacent cells form branching fibers that
FUNCTIONS OF MUSCLES:
allow nerve impulses to pass from cell to
1. Provides movement. Movements rely on cell.
the integrated functioning of bones, joints,
and skeletal muscles. These includes 2. SKELETAL MUSCLE. Responsible for
unseen movements like the beating of the moving parts of the body, such as the limbs,
heart, the churning of food in the stomach, trunk, and face;
generally attached to
and contraction of urinary bladder to expel bones;
responsible
for
VOLUNTARY
urine.
MOVEMENT; made of elongated cells called
MUSCLE FIBERS. Varying movements
require contraction of variable numbers of
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muscles fibers in a muscle. Skeletal muscle

fibers are grouped into dense bundles
called FASCICLES.
Viewed under a
microscope,
they
appear
to
have
STRIATIONS. Thus the name STRIATED
MUSCLES. MOST SKELETAL MUSCLES ARE
CONSCIOUSLY CONTROLLED BY THE
CENTRAL NERVOUS SYSTEM. Skeletal
muscle cells are LARGE and have MORE
THAN 1 NUCLEUS. Because they are so
long and slender, they are often called
MUSCLE FIBERS rather than muscle cells.
Muscle Fiber together with the connective
tissue, blood vessels, and nerves form a
skeletal muscle.

the bone that moves when the muscle

contracts.

Muscles that cause the same action at a

joint are SYNERGISTS. For example, all the
muscles that extend the knee joint. Muscles
that produce opposing actions are
ANTAGONISTS. For example, muscles that
flex a joint are antagonists to muscles that
extend that joint. All the muscles that make
up the triceps are synergists because they
cause the same action. All the muscles that
make up the biceps are synergists because
they cause the same action. Biceps, on the
other hand, are antagonists to triceps
because they have opposite actions. Biceps
3. SMOOTH MUSCLES. Usually not under cause flexion, while triceps cause extension.
voluntary control; spindle-shaped and have
a single nucleus, are not striated and When you lift a weight by contracting
interlace to form sheets of smooth muscle muscles in your biceps, the force produced
tissue; found in many internal organs like by the muscle is greater than the force of
stomach, intestines, and walls of blood gravity on the object you are lifting. In this
vessels.
Smooth muscle fibers are case, the muscle and all of its fibers shorten
surrounded by connective tissue, but the in length. This type of contraction is called
connective tissue does not unite to form ISOTONIC CONTRACTION because the
TENDONS as it does in skeletal muscles. force of contraction remains relatively
Most smooth muscle cells can contract constant
throughout
the
shortening
WITHOUT
nervous
stimulation.
Its process.
Before isotonic contraction
movements cannot be
consciously however, the muscle begins to contract but
controlled, thus they are referred to as the tension is absorbed by the tendons and
INVOLUNTARY muscles. The contractions in other elastic tissue associated with the
smooth muscles move food through our muscle. The muscle therefore does not
digestive tract, control the way blood flows change in length. This is called ISOMETRIC
through the circulatory system, and CONTRACTION.
increases the size of the pupils of our eyes
in bright light.
THE MICROSTRUCTURE OF SKELETAL
MUSCLES
Skeletal muscles produce movement of a 1. FASCIA a sheet of connective tissue
skeleton when they contract. Usually, the beneath the skin or around muscles and
two ends of a skeletal muscle are attached other organs of the body.
to different bones (although in some cases,
A. SUPERFICIAL FASCIA. Immediately
one or both ends may be connected to some found deep in the skin; composed of adipose
other kind of structure, such as the skin. The tissue and areolar connective tissue. Its
attachments to bone are made by means of functions include:
tendons.
a. storing water and fat.
One attachment of the muscle is the
b. forming a layer of insulation that
ORIGIN. This remains relatively stationary protects the body from heat loss.
during a contraction. The other end of the
c. providing mechanical protection
muscle is the INSERTION. It is attached to against traumatic blows.
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d. providing a pathway for nerves and

A. THICK FILAMENT. Made up of about
blood vessels to enter and exit muscles.
200 molecules of myosin molecules.
B. DEEP FASCIA. Dense, irregular
MYOSIN MOLECULE
connective tissue that lines the body wall
shaped like two golf clubs twisted
and extremities and holds muscles together.
together.
Allows free movement of muscles, carries
Projecting myosin heads are called
nerves & lymph & lymphatic vessels, & fills
cross bridges.
spaces between muscles. It includes the
The tail part points towards the
following.
center of the sarcomere. Tails lying
a.
The
ENDOMYSIUM,
which
parallel to each other forms the
penetrates the interior of each fascicle and
shaft of the thick filament
separates muscle fibers from one another. It
B. ELASTIC FILAMENT. It is composed of
is continuous with the connective tissue that the protein TITIN (connectin).
envelopes muscle bundles, the perimysium.
TITIN
b. The PERIMYSIUM, which surrounds
the 3rd most plentiful protein in the
muscle bundles or fascicles of 10-100 or
skeletal muscle.
more individual muscle fiber. It is
Titin is a large elastic, protein
continuous with the connective tissue that
molecule that has 25,000 amino
envelops the muscle, the epimysium.
acids. Together with nubulin, it
c. The EPIMYSIUM, which is the
ensures a proper alignment of
outermost layer, encircling the whole
filaments.
muscle. It is continuous with the tendon or
Two primary functions:
Stabilizes
aponeurosis.
the position of the contractile
filaments by anchoring thick
All three may extend beyond the muscle
filaments to the Z discs, AND it
fibers as TENDON a cord of dense
returns stretched muscles to their
connective tissue that attaches a muscle to
resting length.
the periosteum or bone.
It spans from 1 Z disk to the next M
line
2. MUSCLE FIBERS. The cells of muscles. It
is long, cylindrical, and it lies parallel to one C. THIN FILMENT. They extend from the
another. It arose from the fusion of many anchoring points in the Z disc. Its main
smaller cells, thus has many nuclei to direct component are the actin molecules.
protein synthesis. Nuclei are at its periphery Individual actin molecules appear to be
next to the sarcolemma. It has mitochondria shaped like kidney beans. They join to form
that lie in rows strategically close to the an actin filament that is twisted into a helix.
muscle proteins that use ATP to carry on the Each actin molecule contains a myosincontraction
process. binding site, a site where a cross bridge can
attach. Also present are smaller amounts of
two
regulatory
proteins
The
TROPOMYOSIN, which covers the myosinbinding sites on actin and thus blocks
attachment of myosin cross-bridges to
actin.and the TROPONIN.
3. SARCOLEMMA (sarco = flesh; lemma =
D. SARCOPLASMIC RETICULUM. The
sheath). Muscle fibers plasma membrane
smooth endoplasmic reticulum found in
4. SARCOPLASM. Mscle fibers cytoplasm
striated muscle fibers which stores calcium
5. MYOFIBRILS. Contractile elements of the
phosphate salts in a gelatinous state until
skeletal muscle. About 1 to 2 m in diameter
the muscle is stimulated at which point the
with 3 types of myofilaments:
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Ca2+ release channels open, permitting

Ca2+ ions to diffuse into the general
sarcoplasm where they serve as the second
messenger, triggering the sliding filament
mechanism of contraction.
E. Ca2+ RELEASE CHANNELS. Integral
membrane proteins which have the ability,
when regulated to be open, to permit
calcium ions to diffuse from one side of the
membrane to the other; e.g., the calcium
release channels in the sarcoplasmic
reticulum membranes of skeletal muscle
cells which release calcium ions into the
sarcoplasm when muscle contraction is to
be initiated.
F. TRANSVERSE or T TUBULES. The
irregular network of tiny tunnel-like
extensions of the sarcolemma which
penetrate into the interior of striated muscle
cells and make intimate contact with the
membranes of the terminal cisterns of the
sarcoplasmic reticulum; when the striated
muscle
cell
is
stimulated
by
neurotransmitter and depolarization occurs,
the wave of depolarization is propagated
along the transverse tubules and the
depolarization is transferred to the
membrane of the sarcoplasmic reticulum
causing its depolarization and the opening
of the Ca2+ release channels.
G. SARCOMERE. The smallest contractile
unit of the skeletal muscle cell. The entire
structure self-assembles through multiple

molecular associations to form an ordered

array of thick (myosin-containing) and thin
(actin-containing) filaments. Myofilaments
do not run the length of the muscle fiber.
They are contained in these compartments,
the sarcomeres. The A band is the dark
band. It takes up the length of the thick
filament and it also overlaps with the thin
filaments at the end. The H zone includes
the thick filaments only. The M line is the
attachment site for the thick filaments. The Z

disk is the attachment site for the thin

filaments and it also marks the boundary of
the sarcomere. The I band includes the thin
filaments only. This is the light band. A
sarcomere therefore, runs from one Z disk
to another Z disk.

MUSCLE CONTRACTION

1. Nerve impulse arrives at the axon terminal of

channels that passes small cations,
motor neuron, also called the synaptic endespecially sodium.
bulb. These axon terminals contain many 4. Because sodium is positively charged, its
membrane-enclosed sacs called synaptic
entrance into the membrane will cause a
vesicles which contain thousands of
change in the resting membrane potential of
neurotransmitters. The one present in motor
the cell and will trigger a muscle action
neuron synaptic vesicles and released at
potential that will travel along the muscle
neuromuscular junction (NMJ) a synapse
cell membrane (sarcolemma) and initiates
formed between a motor neuron and a
the events leading to muscle contraction.
skeletal muscle fiber is the acetylcholine or 5. In a relaxed muscle fiber, the concentration
ACh.
of Ca++ in the sarcoplasm is low. This is
2. When nerve impulse (action potential)
because the SR membrane contains Ca++
reaches the axon terminal, it triggers
active transport pumps that remove Ca++
exocytosis of synaptic vesicles. In so doing,
from the sarcoplasm and keeps it inside the
it fuses with the plasma membrane and
SR. The SR has a powerful Ca++ pump that
liberates ACh, which diffuses into the
keeps the
synaptic cleft between the motor neuron and 6. concentration of Ca++ inside the SR at a
the motor end plate.
level about 2000 times higher than in the
3. On the muscle side of the synaptic cleft, the
sarcoplasm (cytoplasm). The sarcoplasm
acetylcholine receptors (integral membrane
also has electrosensitive Ca++ gates and
proteins that recognize and bind specifically
presumably work much the same as Na+ and
to ACh) binds ACh to it, thus opening
K+ gates work.
5

7. However, as muscle action potential travels 14. This continues until the action potentials
along the sarcolemma and into the
stop.
transverse tubule system, Ca++ release
channels open in the SR membrane. This HOW ARE MUSCLES RELAXED?
results in the flooding of Ca++ in the 1. Action potentials stop coming from the
sarcoplasm around the thick and thin brain down the motor neuron, thus
filaments.
acetylcholine is no longer released.
8. The calcium gets into the sarcomeres and 2. The always present acetylcholinesterase in
binds to receptor sites on the troponin the neuromuscular junction chews up the last
molecules (which are resting on the of the acetylcholine. (The acetic acid wanders
tropomyosin and actin filaments). The off and gets used by cells in the Kreb's cycle.
binding of the calcium causes a shape The choline gets reabsorbed so it can combine
change in the troponin protein such that it with a newly made acetic acid molecule in the
leads to a shape change in the tropomyosin motor neuron.)
molecule. The tropomyosin is changed in 3. Without any acetylcholine, the action
shape such that it uncovers the actin and potentials in the muscle stop.
exposes the myosin binding site that resides 4. Without any action potentials in the muscle
on the actin. The myosin can now bind to the (and the T-system), then the Ca++ gates of the
actin. (Normally tropomyosin blocks the sarcoplasmic reticulum can close.
binding of myosin with actin).
5. The Ca++ active transport pumps (which
9. The myosin, with an already bound ATP were working constantly all along) are no
molecule, binds to the actin.
longer overwhelmed by the leak and thus they
10. As the ATP reacts to form ADP, the released successfully
pump
calcium
from
the
energy is used to bend the myosin head such sarcoplasm back into the sarcoplasmic
that the actin filament slides along relative to reticulum.
the myosin filament. During contraction the 6. Without bound Ca++ the troponinfilaments of actin and myosin not change tropomyosin regain their resting shape. The
length but the distance between Z bands very next time the myosin releases from the
does. Thus, developed the sliding filament actin, the troponin-tropomyosin will sneak
theory versus contracting proteins.
back in between and prevent any further
11. As the ATP reacts to form ADP, the released interaction between the actin and myosin.
energy is used to bend the myosin head such 7. Without the actin myosin bonding, the
that the actin filament slides along relative to sarcomeres and muscle can no longer
the myosin filament. During contraction the contract, thus the muscle elastically moves
filaments of actin and myosin not change back to its resting position (or more commonly
length but the distance between Z bands , is passively pulled to a new position by a
does. Thus, developed the sliding filament more dominant antagonistic muscle).
theory versus contracting proteins.
12. The ADP is dropped by the myosin, myosin MUSCLE ENERGY
binds another ATP and only then does it A. All possible energy sources for muscle
release from the actin. The process is contraction must be converted to an ATP
repeated. Several repetitions cause a energy. This is the ONLY energy source
significant movement. At full contraction the myosin can use.
myosin is still trying to pull on the actin and
ATP + H2O
ADP + H3PO4 + energy
ATP is still being used.
B. ATP is needed for several aspects of muscle
13. Rigor mortis is where ATP is not available contraction and relaxation:
and the myosin can not release from the
1. Myosin ATPase.
actin. Certain types of cramps are caused by
the same phenomenon.
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2. Na+-K+ ATPase for developing a

membrane potential (sarcolemma and nerve
cell)
3. ATPase for sarcoplasmic reticulum Ca++
pump.
C. Since the normal concentration of ATP
stored in a muscle cell is very small, then any
significant contraction must involve indirect
energy sources that lead to ATP formation:
1.
After
the
reser
ves
of
ATP are used (~5 sec), the first indirect source
of energy generally used is Creatine
phosphate (CP)(phosphocreatine) (~15 sec):
creatine phosphate + ADP ----> creatine +
ATP
2. Next, glucose is used as an energy
source:
a. ANAEROBIC glucose breakdown to
make ATP. (~40 sec)
1a.

2b. Fast but inefficient.

3c. The excess lactate must eventually
be dealt with. A small amount of it is oxidized
itself, the rest is converted back to glycogen.
After the exercise, the amount that has to be
oxidized is the amount necessary to bring the
ATP, CP, lactate and the rest of the muscle
back to homeostasis. This exactly corresponds
to the amount of exercise that was done and
the amount of oxygen necessary to reachieve
this homeostasis is called the oxygen debt.
b. AEROBIC glucose breakdown to make ATP.
1a. C6H12O6 + 6O2 + 38 ADP ------> 6CO2 +
6H2O + 38 ATP
2b. Slow, but very efficient usage of glucose.
c. Glucose source. Often the amount of
glucose stored as such is not sufficient for
repeated muscle contractions. More glucose
can be derived from stores of glycogen in the
muscle itself and in the blood. The liver also

plays a very important role in converting

glycogen to glucose. The conversion of
glycogen to glucose is relatively rapid
compared to other methods of glucose
formation (e.g. the development of glucose
from fats would be very slow).
3. As a last ditch energy source, the ADP can
be used in an unusual fashion to make ATP
using the enzyme myokinase:
2 ADP ---->
ATP + AMP
D. After contraction the reserves of ATP and
creatine phosphate must be reestablished and
the excess of lactic acid and AMP must be
removed. Such processes must ultimately
require aerobic respiration. The amount of
oxygen required to reestablish such a
homeostasis after a muscle contraction is
referred to as an OXYGEN DEBT.
MUSCLE DISORDERS
Muscle disorders, or myopathies, can result
from an inherited genetic defect, or can be
caused by external factors such as alcohol or
steroid hormones. People who suffer from the
disease experience moderate to severe
weakness of the muscles and may become
wheelchair-bound. The disorder develops at
the mean age of 28 years. It is often
accompanied by cardiomyopathy, a heart
disorder that can cause heart failure and
sudden death.
FIBROMYALGIA
DEFINITION:
Fibromyalgia
is
a
common
condition
characterized by widespread pain in joints,
muscles, tendons, and other soft tissues.
Some other problems commonly linked with
fibromyalgia include fatigue, morning stiffness,
sleep problems, headaches, numbness in
hands and feet, depression, and anxiety.
Fibromyalgia can develop on its own, or
secondary
to
other
musculoskeletal
conditions, such as rheumatoid arthritis, or
systemic lupus.
ALTERNATIVE NAMES:
Fibromyositis; Fibrositis; Myofascial pain
syndrome
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MUSCULAR DYSTROPHY
DEFINITION
The muscular dystrophies (MD) are a group of
genetic diseases characterized by progressive
weakness and degeneration of the skeletal
muscles which control movement. There are
many forms of muscular dystrophy, some
noticeable at birth (congenital muscular
dystrophy), others in adolescence (Becker
MD), but the 3 most common types are
Duchenne,
facioscapulohumeral,
and
myotonic. These three types differ in terms of
pattern of inheritance, age of onset, rate of
progression, and distribution of weakness.
Duchenne MD primarily affects boys and is the
result of mutations in the gene that regulates
dystrophin - a protein involved in maintaining
the integrity of muscle fiber. Onset is between

3-5 years and progresses rapidly. Most boys

become unable to walk at 12, and by 20 have
to
use
a
respirator
to
breathe.
Facioscapulohumeral
MD
appears
in
adolescence
and
causes
progressive
weakness in facial muscles and certain
muscles in the arms and legs. It progresses
slowly and can vary in symptoms from mild to
disabling.
Myotonic MD varies in the age of onset and is
characterized by myotonia (prolonged muscle
spasm) in the fingers and facial muscles; a
floppy-footed, high-stepping gait; cataracts;
cardiac
abnormalities;
and
endocrine
disturbances. Individuals with myotonic MD
have long faces and drooping eyelids; men
have frontal baldness.