MUSCULAR SYSTEM

Mai Elgafarawy
Some of the smallest skeletal muscles control the focus of our eyes;
some of the largest are responsible for the shivering that helps keep us
warm when it is cold. Nearly 40% of body weight in males and about
32% in females is skeletal muscle. Another very important function of
many muscles is to resist movement.
The physical interaction of protein filaments is required for
muscle function:
Muscle cells are excitable, meaning that they contract in response to
chemical and/or electrical signals. All muscles have only one basic
mechanism of action: they contract (shorten), and then they relax,
returning to their original length. Muscle cell contraction relies on the
interaction between protein structures called thin and thick filaments.
The major component of thin filaments is the globular protein actin. In
thin filaments, two strands of polymerized actin are coiled around one
another; similar actin structures called microfilaments function in cell
motility. The thick filaments are staggered arrays of myosin molecules.
Muscle groups that work together to create the same movement are
called synergistic muscles. Muscles that oppose each other are called
antagonistic muscles.
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. The origin is
generally closer to the midline of the body and the insertion is farther
away.
Vertebrate Skeletal Muscle:
A cross section of muscle reveals that it is arranged in bundles called
fascicles, each enclosed in a sheath of a type of fibrous connective
tissue called fascia. Within a typical skeletal muscle is a bundle of long
fibers running along the length of the muscle. Each individual fiber is a
single cell. Within are multiple nuclei, each derived from one of the
embryonic cells that fused to form the fiber. The nuclei are located just
under the cell membrane. Surrounding these nuclei are longitudinal
myofibrils, which consist of bundles of thin and thick filaments.
The myofibrils in muscle fibers
are made up of repeating
sections called sarcomeres, which
are the basic contractile units of
skeletal muscle.
Thin filaments attach at the Z
lines at the sarcomere ends,
while thick filaments are
anchored in the middle of the
sarcomere (M line).
In a resting (relaxed) myofibril,
thick and thin filaments partially
overlap. Near the edge of the
sarcomere there are only thin
filaments, whereas the zone in
the center contains only thick
filaments.
Individual muscle cells
contract and relax:
The Sliding-Filament Model of
Muscle Contraction:
The filaments slide past each
other. According to the well-
accepted sliding-filament model,
the thin and thick filaments
ratchet past each other, powered
by myosin molecules.
Muscle contraction requires
repeated cycles of binding and
release. During each cycle of
each myosin head, the head is
freed from a cross-bridge,
cleaves the newly bound ATP,
and binds again to actin. Each
end of a thick filament
contains approximately 300
heads, each of which forms and re-forms about five cross-bridges per
second, driving the thick and thin filaments past each other.
The Role of Calcium and Regulatory Proteins:
Proteins bound to actin play
crucial roles in controlling muscle
contraction. In a muscle fiber at
rest, tropomyosin, a regulatory
protein, and the troponin
complex, are bound to the actin
strands of thin filaments
(troponin and tropomyosin that
together form the troponin-
tropomyosin protein complex).
Tropomyosin covers the myosin-
binding sites along the thin
filament, preventing actin and myosin from interacting. Motor neurons
enable actin and myosin to interact by triggering a release of calcium
ions (Ca2+) into the cytosol. Once in the cytosol, Ca2+ binds to the
troponin complex, causing the myosin-binding sites on actin to
be exposed.
Within the muscle fiber, the
action potential spreads deep
into the interior, following
infoldings of the plasma
membrane called transverse
(T) tubules. These make close
contact with the sarcoplasmic
reticulum (SR), a specialized
smooth endoplasmic
reticulum.
Several diseases cause paralysis by interfering with the excitation of
skeletal muscle fibers by motor neurons. In amyotrophic lateral
sclerosis (ALS), motor neurons in the spinal cord and brainstem
degenerate, and muscle fibers atrophy. ALS is progressive and usually
fatal within five years after symptoms appear. In myasthenia gravis, a
person produces antibodies to the acetylcholine receptors of skeletal
muscle. Myasthenia gravis can be controlled with drugs that inhibit
acetylcholinesterase. Most commonly impaired are the eye muscles.
Rigor mortis, in which a body becomes stiff during the time period from
about four hours to several days after death, is due to the absence of
ATP. In the absence of ATP, the myosin heads cannot detach from actin,
and so the muscles remain “locked” in the contracted state.
Creatine phosphate can transfer a phosphate group and energy to ADP
and therefore create a new ATP molecule quickly. This reaction is
reversible. Unfortunately, muscles cannot store much more creatine
phosphate than they usually have, even without creatine phosphate
loading. Creatine phosphate also seems to improve muscle
performance in certain neuromuscular diseases, such as amyotrophic
lateral sclerosis (ALS), also known as Lou Gehrig’s Disease.

The activity of muscles can vary:

Isotonic versus isometric contractions:
Isotonic (“same” + “strength” or “tone”) contractions occur whenever a
muscle shortens while maintaining a constant force. In isometric
(“same” + “length”) contractions, force is generated, muscle tension
increases, and the muscle may shorten a little, but bones and objects
do not move.
Nervous Control of Muscle Tension:
Although individual motor units either are contracting or are relaxed,
whole muscles generally
maintain an intermediate level
of force known as muscle tone.
In vertebrates, each branched
motor neuron may form
synapses with many muscle
fibers, although each fiber is
controlled by only one motor
neuron. A motor unit consists
of a single motor neuron and
all the muscle fibers it controls.
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.
Increasing tone (or force) by activating more motor units is called
recruitment.
Some muscles, especially those that hold up the body and maintain
posture, are almost always partially contracted.
In such muscles, the nervous system may alternate activation among
the motor units, reducing the length of time any one set of fibers is
contracted.
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. Muscle cells always respond with a complete cycle of
contraction and relaxation (called a twitch). Muscle cell contraction
lasts longer than neuron activation.
A single action potential produces a twitch lasting about 100
milliseconds or less. If a second action potential arrives before the
muscle fiber has completely relaxed, the two twitches add together,
resulting in greater tension. When the rate is so high that the muscle
fiber cannot relax at all between stimuli, the twitches fuse into one
smooth, sustained contraction called tetanus.
A laboratory recording
of muscle activity,
called a myogram,
reveals that the
stimulus-twitch
relationship has three
stages:
1. Latent period (the time between stimulation and the start of
contraction).
2. Contraction (the time during which the muscle actually shortens).
3. Relaxation (muscle returns to its original length).
Types of Skeletal Muscle Fibers:
Fibers are classified by the source of ATP and the speed of contraction.
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 fibers to extract
oxygen from the blood efficiently. In contrast, glycolytic fibers have a
larger diameter and less myoglobin. Also, glycolytic fibers use glycolysis
as their primary source of ATP and fatigue more readily than oxidative
fibers. These two fiber types are readily apparent in the muscle of
poultry and fish: The dark meat (red muscle) is made up of oxidative
fibers rich in myoglobin, and the light meat (white muscle) is composed
of glycolytic fibers.
Fast-Twitch and Slow-Twitch Fibers:
Fast-twitch fibers develop tension two to three times faster than slow-
twitch fibers. Compared with a fast fiber, a slow fiber has less
sarcoplasmic reticulum and pumps Ca2+ more slowly. Because Ca2+
remains in the cytosol longer, a muscle twitch in a slow fiber lasts about
five times as long as one in a fast fiber.
Most human skeletal muscles contain both fast-twitch and slow-twitch
fibers, the relative proportions of each are genetically determined,
although the muscles of the eye and hand are exclusively fast-twitch.
However, if such a muscle is used repeatedly for activities requiring
high endurance, some fast glycolytic fibers can develop into fast
oxidative fibers. This is because fast oxidative fibers fatigue more slowly
than fast glycolytic fibers.
Slow-twitch fibers contain
are well supplied with blood
vessels, so they draw more
blood and oxygen than fast-
twitch fibers. Myoglobin and
the presence of numerous
blood vessels make slow-
twitch fibers reddish in color,
so they are sometimes called
“red” muscle.
Fast-twitch fibers have fewer mitochondria, fewer blood vessels, and
little or no myoglobin compared to slow-twitch fibers, so they’re called
“white” muscle. They store large amounts of glycogen and tend to rely
heavily on creatine phosphate and anaerobic metabolism for quick
bursts of high energy. They depend on aerobic mechanisms for any
activity that is sustained.
Some vertebrates have skeletal muscle fibers that twitch at rates far
faster than any human muscle. For example, superfast muscles produce
a rattlesnake’s rattle and a dove’s coo. Even faster are the muscles
surrounding the gas-filled swim bladder of the male oyster toadfish. In
producing its “boat whistle” mating call, the toadfish can contract and
relax these muscles more than 200 times per second!
Exercise training improves muscle mass, strength, and endurance:
The two primary types of exercise training are strength (resistance)
training and aerobic (endurance) training. Strength training involves
doing exercises that strengthen specific muscles. Strength training is
generally short. 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.
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 increase. Aerobic exercise also improves the
performance of the cardiovascular and respiratory systems.
Cardiac and smooth muscles have special features:
Vertebrates have cardiac muscle and smooth muscle in addition to
skeletal muscle.
Vertebrate cardiac muscle is found only in the heart. Some cardiac
muscle cells can initiate rhythmic depolarization and contraction
without nervous system input. Normally, cells in one part of the heart
act as a pacemaker to initiate contraction.
Signals from the pacemaker
spread throughout the heart
because specialized regions
called intercalated disks
electrically couple each cardiac
muscle cell to the adjacent cells.
Although these action potentials
last up to 20 times longer than those of skeletal muscle fibers, a long
refractory period prevents summation and tetanus.
Smooth muscle in vertebrates is found in the walls of hollow organs.
Smooth muscle is also found in the eye, where its action controls
focusing and pupil diameter. Smooth muscle cells lack striations
because their actin and myosin filaments are not regularly arrayed
along the length of the cell.
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
are electrically coupled to one
another and can generate action potentials without input from
neurons. Smooth muscles contract and relax more slowly than striated
muscles. Smooth muscle generally is partially contracted all the time.
Although Ca2+ regulates smooth muscle contraction, smooth muscle
cells have no troponin complex or T tubules, and their sarcoplasmic
reticulum is not well developed. During an action potential, Ca2+ 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; in fact, arthropod skeletal muscles are nearly
identical to those of vertebrates. However, the wings of some insects
can actually beat up and down faster than action potentials can arrive
from the central nervous system.
Modification of certain proteins in the muscles that hold a clam’s shell
closed allows them to remain contracted for as long as a month with
only a low rate of energy consumption.

Diseases and disorders of the muscular system:

Muscular dystrophy:
The term actually applies to several different hereditary diseases of
muscle. 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. Eventually much of the
muscle mass is replaced with fibrous connective tissue. At the moment
there is no cure.
Tetanus:
Tetanus is caused by a bacterial infection. 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 (its common name
“lockjaw”). Untreated, tetanus may lead to death due to exhaustion or
respiratory failure.
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.
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.
Fasciitis:
Fasciitis involves inflammation of the 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. Injections of corticosteroid drugs
can relieve severe pain.