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Muscle Physiology
Chapter 8
There are three kinds of muscle
tissue: skeletal, cardiac, and
smooth.
• These three kinds of muscle tissue compose
about 50 percent of a human’s body weight.
• Skeletal muscle tissue is striated and subject
to voluntary control.
• The skeletal muscles make up the muscular
system.
• The skeletal muscles are innervated by the
somatic nervous system.
A muscle fiber is a skeletal muscle cell. It
is large, elongated, and cylinder-shaped.
The fibers extend the entire length of a
skeletal muscle.
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A muscle fiber contains contractile elements
called myofibrils. A myofibril contains thick
filaments called myosin and thin filaments
(e.g., actin).
Actin and myosin are arranged in units
called sarcomeres. A sarcomere is found
between two Z lines. The sarcomere is the
functional unit of the muscle. Its regions
are:
– A band - myosin (thick) filaments stacked
along with parts of the actin (thin) filaments
– H zone - middle of the A band where actin
does not reach
– M line - extends vertically down the center of
the A band
– I band - has part of actin that do not project
into A band
The thick filaments of myosin have cross
bridges. The cross bridges can attach to
actin binding sites. The cross bridges
also have myosin ATPase activity.
• Actin is the main, thin
structural protein in the
sarcomere. Each actin
molecule has a binding
site that can attach with
a myosin cross bridge.
• Actin and mysoin are
contractile proteins.
Tropomyosin and troponin are
thin proteins. They are
regulatory proteins.
• Tropomyosin covers the actin binding sites,
preventing their union with myosin cross
bridges.
• Troponin has three binding sites: one binds to
tropomyosin, one to actin, and one to Ca
ions.
– When calcium combines with troponin,
tropomyosin slips away from its blocking position
between actin and myosin.
– With this change actin and myosin can interact
Skeletal muscle contraction is a
molecular phenomenon.
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The myosin cross bridges can bind to the actin, pulling these thin
filaments toward the center of the sarcomere. This is the sliding
filament mechanism.
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The width of the A band remains unchanged.
The H zone is shortened horizontally.
The I band decreases in width as the actin overlaps more with the myosin.
Neither the thick nor thin filaments change in length. They change their
position with one another.
– The actin slides closer together between the thick filaments.
By the power stroke the myosin
cross bridges pull the thin actin
filaments inward. The cross bridges
bind to the actin and bend inward.
• A single power stroke pulls the actin inward only a
small percentage of the total shortening distance.
Complete shortening occurs by repeated cycles of
the power stroke.
• This interaction can occur when troponin and
tropomyosin are pulled out of the way by the release
of calcium.
• The link between myosin and actin is broken at the
end of one cross bridge cycle. A cross bridge returns
to its original position and can return to the next actin
molecule position, pulling the actin filament further.
By excitation-coupling a series of events link
muscle excitation to muscle contraction.
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Calcium is the link for this process.
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A somatic efferent sends action potentials to muscle fibers.
This neuron releases acetylcholine at the neuromuscular junction.
This produces an action potential over the entire muscle cell membrane.
This action potential passes along the membrane of the T tubule in the
central part of the muscle fiber.
– This action potential meets the membranes of the adjacent sarcoplasmic
reticulum (SR) deep inside the muscle cell.
– A permeability change is produced in the membranes of the SR, releasing
calcium from the SR.
The release of calcium ions
from the SR into the cytosol
allows it to bind with troponin.
• By this event, tropomyosin is pulled off the binding
sites of actin, allowing the myosin cross bridges to
bind to actin and slide this protein.
– Myosin cross bridges had been previously energized by
splitting ATP into ADP plus P. The cross bridges have
binding sites for this change. This energy places the
myosin cross bridges into a cocked position.
– The contact between myosin and actin “pulls the trigger”,
allowing myosin to pull the actin toward the center of the
sarcomere (power stroke). This shortens the sarcomere.
– P is released from the cross bridges during the power stroke.
ADP is released with power stroke completion.
The addition of a new ATP to myosin
cross bridges detaches them from
actin. The bridges return to their
original conformation.
• The cross bridges return to their original
shape for a repeat of the power stroke cycle.
• By the continued, repetition of the cycle, the
“rowing” of the myosin cross bridges slide the
actin toward the center of the sarcomere for
muscle contraction.
• However, for this repetition, calcium ions must
be available.
Relaxation of a skeletal muscle
depends on the reuptake of
calcium ions, from the cytosol
into the SR.
• With the absence of calcium, troponin and
tropomyosin can resume their blocking role.
• However, calcium can be released again from
the SR into the cytosol if a somatic efferent
neuron signals the muscle cell with another
action potential.
A whole muscle is a group of
muscle fibers.
• A muscle is covered by a sheath of connective tissue.
It divides the muscle internally into bundles. Each
individual muscle fiber is enveloped by a layer of
connective tissue.
• A tendon attaches a muscle to a bone.
• A single action potential is a muscle fiber produces a
twitch.
• Gradations of whole muscle tension depend on the
number of muscle fibers contracting and the tension
developed by each contracting fiber.
A motor unit is one motor neuron
and the muscle fibers it
innervates.
• Whole muscle tension depends on the size of the
muscle, the extend of motor unit recruitment, and
the size of each motor unit.
• The number of muscle fibers varies among different
motor units.
– Muscles performing refined, delicate movements have few
muscle fibers per motor unit.
– Muscles performing coarse, controlled movements have a
large number of fibers per motor unit.
– The asynchronous recruitment of motor units delays or
prevents muscle fatigue.
The tension developed by a muscle
depends on the frequency of
stimulation.
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Repetitive stimulation of a muscle
increases its tension by twitch
summation.
Contractile responses (twitches)
can add together by two actions
potentials signaling a muscle fiber
closely together in time.
If a muscle fiber is stimulated
very rapidly, it cannot relax
between stimuli. The twitches
merge into a smooth, sustained,
maximal contraction called
tetanus.
Twitch summation results from
sustained elevation of calcium in
the cytosol.
The tension of a tetanic contraction
also depends on the length of the
fiber at the onset of contraction.
– The optimal length is the resting muscle
length. It offers the maximal opportunity for
cross-bridge interaction.
– At lengths other than the optimal length, not
all cross bridges are able to interact for
muscle shortening.
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Whole muscle tension also depends on he
extent of fatigue and the thickness of the
fiber.
Muscle tension is transmitted to bone as the
contractile component tightens the serieselastic component.
– The origin is the fixed end of attachment of a
muscle to a bone. The insertion is the
movable end of attachment. If
– If muscle tension overcomes a load, it pulls
the insertion toward the origin.
The two primary types of contraction
are isotonic and isometric.
• By isometric contraction the
muscle tension developed is
less than its opposing load.
The muscle cannot shorten
and lift the object with that
load.
• By isotonic contraction the
muscle tension developed is
greater than its opposing load.
The muscle usually shortens
and lifts an object. The muscle
maintains a constant tension
throughout the period of
shortening.
• The velocity of muscle
shortening is inversely
proportional to the magnitude
of the load.
Skeletal muscles can perform
work.
• Work is calculated by multiplying the
magnitude of the load times the
distance the load is moved (Force times
distance).
– Much of the energy applied is converted
into heat.
– About 25 percent is realized work.
– About 75 percent is converted to heat.
Bones, muscles, and joints interact to
form lever systems.
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A lever is a rigid structure capable of moving around a pivot.
The pivot is the fulcrum.
The power arm is the part of the lever between the fulcrum and the point
where an upward force is applied.
The load arm is the part of the lever between the fulcrum and the
downward force from the load.
Often the velocity and distance of muscle shortening is increased to
increase the speed and range of motion of the body part moved by muscle
contraction. The muscle must exert more force than the opposing load for
this increased speed and range.
ATP is generated three ways for the
muscle contraction.
• Creatine phosphate plus ADP is converted enzymatically to
creatine plus ATP. This is the first source of ATP for the first
minute or less of exercise.
• Oxidative phosphorylation generates large amounts of ATP in
the mitochondria if oxygen is available for the muscle cell. This
supports aerobic exercise. Some types of muscle fibers have
myoglobin which can transfer oxygen into muscle cells.
• Glycolysis makes a small amount of ATP in the absence of
oxygen. A net of 2ATPs is formed per glucose molecule. This
process uses large quantities of stored glycogen and produces
lactic acid. The accumulation of this acid produces muscle
soreness.
• Glycolysis supports anaerobic exercise. One glucose molecule
is converted into two molecules of pyruvic acid.
• It the absence of oxygen for the muscle cell, pyruvic acid does
not enter oxidative phosphorylation. It is converted to pyruvic
acid.
These are two types of
fatigue.
• Muscle fatigue occurs when an exercising muscle
can no longer respond to the same degree of
stimulation with the same degree of contractile
activity.
– Factors for this include an increase in inorganic phosphate,
accumulation of lactic acid, and the depletion of energy
reserves. Increased oxygen consumption is needed to
recover from exercise (paying off an oxygen debt).
• Central fatigue occurs when the CNS can no longer
activate motor neurons supplying working muscles.
– It is often psychological and is related to biochemical
changes at the synapses in the brain.
The three types of skeletal
muscle fibers are:
– slow oxidative (type I) fibers
– fast-oxidative (type IIa) fibers
– fast-glycolytic (type IIb) fibers
• Most humans have a mixture of all three types of
fibers.
• They are classified by the pathway used for ATP
synthesis (oxidative vs. glycolytic) and the rapidity by
which they split ATP and contract (fast vs. slow).
• Oxidative fibers are red with a high concentration of
myoglobin.
Muscle fibers can adapt to the
different demands placed on
them.
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Regular endurance exercise (e.g., long-distance jogging) promotes
improved oxidative capacity in oxidative fibers.
The fibers use oxygen more efficiently.
High-intensity resistance training promotes hypertrophy of fast
glycolytic fibers. The fibers increase diameter. Testosterone promotes
protein synthesis for this increase.
The extent of training determines the interconversion of the two types
of fast-twitch fibers. Whether a fiber is fast- twitch or slow-twitch
depends on its nerve supply.
Fast-twitch and slow-twitch fibers are interconvertible. For example
weight training can convert fast -oxidative fibers to fast-glycolytic fibers.
Skeletal muscles atrophy when not used. There is disuse atrophy and
denervation atrophy.
Skeletal muscles have a capacity for limited repair.
Multiple neural inputs influence
motor unit output. There are
three inputs of control for motor
neuron output.
• (1) spinal reflex pathways that arise from afferent
neurons
• (2) corticospinal (pyramidal) motor system that arise
from the primary motor cortex; It is involved mainly
with the intricate movements of the hands.
• (3) pathways of the multineuronal (extrapyramidal)
motor system that originate from the brain stem; It is
involved mainly with postural adjustments and
involuntary movements of the trunk and limbs.
Muscle receptors provide afferent
information needed to control
skeletal muscle activity.
– This input can communicate changes in muscle length
(monitored by muscle spindles) and muscle tension
(monitored by Golgi tendon organs). Golgi tendon organs
are located in the tendons of muscles.
• A stretch reflex is triggered when a whole muscle is
passively stretched.
– Muscle spindles are stretched. This triggers the reflex
contraction of that muscle. This response resists passive
changes in muscle length.
– The classic example of the stretch reflex is the patellartendon or knee jerk reflex.
Smooth muscle composes the internal,
contractile organs except the heart. The
heart is composed of cardiac muscle.
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Smooth muscle cells are small and unstriated.
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These cells have actin and myosin. Their
arrangement is not organized compared to skeletal
muscle cells. Therefore, smooth muscle cells are not
striated.
Smooth muscle cells contract when calcium ions
enter the cells from the ECF. Calcium is also
released from intracellular stores.
This release activates a series of biochemical
reactions leading to myosin cross bridge movement.
Myosin cross bridges are phosphorylated and bind to
actin.
Multiunit smooth muscle is
neurogenic.
• It has properties partway between skeletal muscle and singleunit smooth muscle.
• Smooth muscle is supplied by the involuntary autonomic
nervous system.
• Multi-unit smooth muscle is found in the walls of large vessels,
the large airways of the lungs. the ciliary muscle, the iris of the
eye, and the base of hair follicles.
• Single-unit smooth muscle cells form functional syncytia.
• A syncyticium is a group of interconnected cells. When an
action potential develops in one cell, it quickly spreads to other
cells.
• Therefore, the cells in a syncyticium contract as a single,
coordinated unit.
Single-unit smooth muscle is
myogenic.
• It is self-excitable. It does not require
nervous stimulation for contraction. It can
develop pacemaker potentials or slow-wave
potentials.
• Automatic shifts in ion concentrations in the
ECF and ICF cause spontaneous
depolarizations to threshold potential.
• By myogenic activity the smooth muscle
develops nerve-independent contractile
activity. It is initiated by the muscle itself.
Single-unit smooth muscle
can produce gradations of
contraction.
• It differs from the mechanism for producing the gradations of
skeletal muscle contraction.
• It depends on the level of calcium ions in the cytosol.
• Many single-unit smooth muscle cells have enough calcium in
the cytosol to maintain tone (low level of tension). This occurs in
the absence of action potentials.
• Signaling by the ANS and hormones alter the strength of selfinduced, smooth muscle contractions.
• Other factors, such as local metabolites and certain drugs, alter
the contraction of smooth muscle.
• All of these influences alter the level of calcium ions in the cells’
cytosol.
Smooth muscle can develop
tension when it is stretched
significantly. It inherently
relaxes when stretched.
• Its contraction is slow and energyefficient.
– Single-unit smooth muscle can exist at a
many lengths without a change in tension.
It is well-suited for forming the walls of
distensible, hollow organs.
Cardiac muscle has properties
of skeletal and smooth
muscle.
• It is found in the walls of the heart.
• It is highly organized and striated.
These are similarities to skeletal muscle
tissue.
• It can generate action potentials which
spread throughout the walls of the
heart. This is similar to single-unit
smooth muscle.