MLS 102 Lecture 10: Muscle Tissue

Overview of Muscle Tissues 1. Epimysium

• Types of Muscle Tissue: → Sheath of dense, irregular connective tissue
1. Skeletal muscle wrapping each muscle
2. Cardiac muscle → Allows a muscle to contract and move
3. Smooth Muscle powerfully while maintaining its structural
• Excitability integrity.
→ Plasma membranes can change their electrical 2. Perimysium
states (from polarized to depolarized) → Middle layer of connective tissue enveloping a
→ Send an electrical wave called an ACTION muscle fascicle (individual muscle fiber
POTENTIAL. bundles).
• Nervous system: influence the excitability of 3. Endomysium
cardiac and smooth muscle → Encloses each muscle fiber inside each
• Skeletal muscle completely depends on signaling fascicle
from the nervous system.
• Cardiac muscle and smooth muscle can respond Skeletal Muscle Fibers
to other stimuli (hormones and local stimuli) • Greek sarco, which means “flesh.”
• Muscle contraction (shortening) when actin is pulled • SARCOLEMMA: plasma membrane of muscle
myosin. fibers
• In striated muscle: exposure of actin binding sites • SARCOPLASM: cytoplasm
due to the interaction between calcium ions (Ca++) • SARCOPLASMIC RETICULUM: specialized
and (troponin and tropomyosin) that “shield” the smooth endoplasmic reticulum, which stores,
actin binding sites releases, and retrieves calcium ions (Ca++)
• Ca++: required for the contraction of smooth muscle
• Ca++: activate myosin heads
• Muscles require ATP for contraction, and relax when
Ca++ is removed and the actin-binding sites are
re-shielded.
• ELASTICITY: Muscle can return to its original length
when relaxed
• EXTENSIBILITY: it can stretch or extend
• CONTRACTILITY allows muscle tissue to pull on its
attachment points and shorten with force
• The actin and myosin are arranged regularly in the
cytoplasm of skeletal and cardiac muscle fibers,
which creates a pattern, or stripes, called
STRIATIONS
• Skeletal ms fibers: multinucleated
• Cardiac ms fibers: have one to two nuclei and are
physically and electrically connected to each other
so that the entire heart contracts as one unit (called
a SYNCYTIUM)
• Smooth ms: single nucleus, has a uniform, Sarcomere
nonstriated. • Functional unit of a skeletal muscle fiber
• Contractile myofilaments actin (thin filament) and
Skeletal Muscle myosin (thick filament), along with other support
• Functions: proteins
1. hold a body upright or balanced in any position • The striated appearance of skeletal muscle fibers
2. Keep joints stable is due to the arrangement of the myofilaments of
3. Protect internal organs actin and myosin in sequential order from one end of
4. Maintenance of homeostasis in the body by the muscle fiber to the other
generating heat • Microfilaments and their regulatory proteins,
troponin and tropomyosin
Three layers of Connective Tissue • Z-discs / Z-lines- actin myofilaments are anchored;
border of the sarcomere
• Periodic invaginations in the sarcolemma, called T-
tubules.
• Because the actin and its troponin-tropomyosin
complex (projecting from the Z-discs toward the
center of the sarcomere) form strands that are
thinner than the myosin, it is called the thin filament
of the sarcomere.
• Likewise, because the myosin strands and their
multiple heads (projecting from the center of the
sarcomere, toward but not all to way to, the Z-discs)
have more mass and are thicker, they are called the
thick filament of the sarcomere

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 Motor End-Plate and Innervation. At the NMJ, the axon terminal releases
ACh. The motor end-plate is the location of the ACh-receptors in the muscle
fiber sarcolemma. When ACh molecules are released, they diffuse across a
minute space called the synaptic cleft and bind to the receptors

Neuromuscular Junction
• The site where a motor neuron’s terminal meets the
muscle fiber
• Where the muscle fiber first responds to signaling by
the motor neuron.

Excitation-Contraction Coupling
• Cell’s membrane RESTING POTENTIAL
• Inside of the membrane is usually around -60 to -90
mV
• This is achieved by opening and closing specialized
proteins in the membrane called ion channels.

• Periodic invaginations in the sarcolemma, called T-

tubules
• T-tubules carry the action potential into the interior
of the cell
• TRIAD: arrangement of a T-tubule with the
membranes of SR on either side
→ Surrounds the cylindrical structure called a
myofibril, which contains actin and myosin.

The T-tubule. Narrow T-tubules permit the conduction of electrical

impulses. The SR functions to regulate intracellular levels of calcium. Two
terminal cisternae (where enlarged SR connects to the T-tubule) and one T-
tubule comprise a triad—a “threesome” of membranes, with those of SR on
two sides and the T-tubule sandwiched between them.

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Muscle Contraction and Relaxation

Relaxation of a Muscle Fiber. Ca++ ions are pumped back into the SR,
which causes the tropomyosin to re-shield the binding sites on the actin
strands. A muscle may also stop contracting when it runs out of ATP and
becomes fatigued.

THE SLIDING FILAMENT MODEL OF CONTRACTION

• When signaled by a motor neuron, a skeletal muscle
fiber contracts as the thin filaments are pulled and
then slide past the thick filaments within the fiber’s
sarcomeres.
• The sliding can only occur when myosin-binding
sites on the actin filaments are exposed by a series
of steps that begins with Ca++ entry into the
sarcoplasm.

Contraction of a Muscle Fiber. A cross-bridge forms between actin and

the myosin heads triggering contraction. As long as Ca++ ions remain in the
sarcoplasm to bind to troponin, and as long as ATP is available, the muscle
fiber will continue to shorten
• This zone where thin and thick filaments overlap is
very important to muscle contraction, as it is the site
where filament movement starts.
• Thin filaments, anchored at their ends by the Z-
discs, do not extend completely into the central
region that only contains thick filaments, anchored at
their bases at a spot called the M-line. • Tropomyosin is a protein that winds around the
• A myofibril is composed of many sarcomeres chains of the actin filament and covers the myosin-
running along its length; thus, myofibrils and muscle binding sites to prevent actin from binding to
cells contract as the sarcomeres contract myosin.
• Muscle Contraction Stops: • Tropomyosin binds to troponin to form a troponin-
tropomyosin complex.
→ Prevents the myosin “heads” from binding to
the active sites on the actin microfilaments.
→ Troponin also has a binding site for Ca++ ions.
• To initiate muscle contraction, tropomyosin has to
expose the myosin-binding site on an actin filament
to allow cross-bridge formation between the actin
and myosin microfilaments.
• The first step in the process of contraction is for
Ca++ to bind to troponin so that tropomyosin can
slide away from the binding sites on the actin
strands.

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• This allows the myosin heads to bind to these the power stroke, as movement of the thin filament
exposed binding sites and form cross-bridges. occurs at this step
• The thin filaments are then pulled by the myosin • In the absence of ATP, the myosin head will not
heads to slide past the thick filaments toward the detach from actin.
center of the sarcomere. • One part of the myosin head attaches to the binding
• But each head can only pull a very short distance site on the actin, but the head has another binding
before it has reached its limit and must be “re- site for ATP.
cocked” before it can pull again, a step that requires • ATP binding causes the myosin head to detach from
ATP. the actin
• After this occurs, ATP is converted to ADP and Pi by
ATP and Muscle Contraction the intrinsic ATPase activity of myosin.
• For thin filaments to continue to slide past thick • The energy released during ATP hydrolysis changes
filaments during muscle contraction, myosin heads the angle of the myosin head into a cocked position
must pull the actin at the binding sites, detach, re- • The myosin head is now in position for further
cock, attach to more binding sites, pull, detach, re- movement.
cock, etc. • When the myosin head is cocked, myosin is in a
• This repeated movement is known as the cross- high-energy configuration.
bridge cycle. • This energy is expended as the myosin head moves
through the power stroke, and at the end of the
power stroke, the myosin head is in a low energy
position.
• After the power stroke, ADP is released; however,
the formed cross-bridge is still in place, and actin
and myosin are bound together.
• As long as ATP is available, it readily attaches to
myosin, the cross-bridge cycle can recur, and
muscle contraction can continue.

Sources of ATP
• ATP supplies the energy for muscle contraction to
take place. ATP
• In addition to its direct role in the cross-bridge cycle,
ATP also provides the energy for the active-
transport Ca++ pumps in the SR.
• Muscle contraction does not occur without sufficient
amounts of ATP.
• The amount of ATP stored in muscle is very low, only
sufficient to power a few seconds worth of
contractions.
• As it is broken down, ATP must therefore be
regenerated and replaced ATP quickly to allow for
sustained contraction.
• There are three mechanisms by which ATP can
be regenerated:
1. Creatine phosphate metabolism,
2. Anaerobic glycolysis, and fermentation
3. Aerobic respiration.

Creatinine Phosphate
• Is a molecule that can store energy in its phosphate
bonds.
• In a resting muscle, excess ATP transfers its energy
Skeletal Muscle Contraction. (a) The active site on actin is exposed as to creatine, producing ADP and creatine
calcium binds to troponin. (b) The myosin head is attracted to actin, and phosphate.
myosin binds actin at its actin-binding site, forming the cross-bridge. (c) • This acts as an energy reserve that can be used to
During the power stroke, the phosphate generated in the previous
contraction cycle is released. This results in the myosin head pivoting quickly create more ATP.
toward the center of the sarcomere, after which the attached ADP and • When the muscle starts to contract and needs
phosphate group are released. (d) A new molecule of ATP attaches to the energy, creatine phosphate transfers its phosphate
myosin head, causing the crossbridge to detach. (e) The myosin head
hydrolyzes ATP to ADP and phosphate, which returns the myosin to the back to ADP to form ATP and creatine
cocked position. • This reaction is catalyzed by the enzyme creatine
• Cross-bridge formation occurs when the myosin kinase and occurs very quickly; thus, creatine
head attaches to the actin while adenosine phosphate-derived ATP powers the first few seconds
diphosphate (ADP) and inorganic phosphate (Pi) of muscle contraction.
are still bound to myosin • However, creatine phosphate can only provide
• Pi is then released, causing myosin to form a approximately 15 seconds worth of energy, at which
stronger attachment to the actin, after which the point another energy source has to be used
myosin head moves toward the M-line, pulling the • As the ATP produced by creatine phosphate is
actin along with it. depleted, muscles turn to glycolysis as an ATP
• As actin is pulled, the filaments move approximately source.
10 nm toward the M-line. This movement is called

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 • To compensate, muscles store small amount of
excess oxygen in proteins call myoglobin, allowing
for more efficient muscle contractions and less
fatigue.
• Aerobic training also increases the efficiency of the
circulatory system so that O2 can be supplied to the
muscles for longer periods of time.
• Muscle fatigue occurs when a muscle can no longer
contract in response to signals from the nervous
system.
• The exact causes of muscle fatigue are not fully
known, although certain factors have been
correlated with the decreased muscle contraction
that occurs during fatigue.
• ATP is needed for normal muscle contraction, and
as ATP reserves are reduced, muscle function may
decline
• This may be more of a factor in brief, intense muscle
output rather than sustained, lower intensity efforts.
• Lactic acid buildup may lower intracellular pH,
affecting enzyme and protein activity.
Glycolysis • Imbalances in Na+ and K+ levels as a result of
• Is an anaerobic (non-oxygen-dependent) process membrane depolarization may disrupt Ca++ flow out
that breaks down glucose (sugar) to produce ATP; of the SR.
however, glycolysis cannot generate ATP as quickly • Long periods of sustained exercise may damage the
as creatine phosphate. SR and the sarcolemma, resulting in impaired Ca++
• Thus, the switch to glycolysis results in a slower regulation.
rate of ATP availability to the muscle. • Intense muscle activity results in an oxygen debt,
• The sugar used in glycolysis can be provided by or which is the amount of oxygen needed to
by metabolizing glycogen that is stored in the compensate for ATP produced without oxygen
muscle. during muscle contraction.
• The breakdown of one glucose molecule produces • Oxygen is required to restore ATP and creatine
two ATP and two molecules of pyruvic acid, which phosphate levels, convert lactic acid to pyruvic acid,
can be used in aerobic respiration or when oxygen and, in the liver, to convert lactic acid into glucose or
levels are low, converted to lactic acid. glycogen.
• If oxygen is available, pyruvic acid is used in • Other systems used during exercise also require
aerobic respiration. oxygen, and all of these combined processes result
• However, if oxygen is not available, pyruvic acid is in the increased breathing rate that occurs after
converted to lactic acid, which may contribute to exercise.
muscle fatigue. • Until the oxygen debt has been met, oxygen intake
• This conversion allows the recycling of the enzyme is elevated, even after exercise has stopped.
NAD+ from NADH, which is needed for glycolysis to
continue RELAXATION OF A SKELETAL MUSCLE
• This occurs during strenuous exercise when high • Relaxing skeletal muscle fibers, and ultimately, the
amounts of energy are needed but oxygen cannot skeletal muscle, begins with the motor neuron, which
be sufficiently delivered to muscle. stops releasing its chemical signal, Acetylcholine
• Glycolysis itself cannot be sustained for very long (Ach), into the synapse at the NMJ.
(approximately 1 minute of muscle activity), but it is • The muscle fiber will repolarize, which closes the
useful in facilitating short bursts of high-intensity gates in the SR where Ca++ was being released.
output. • ATP-driven pumps will move Ca++ out of the
• This is because glycolysis does not utilize glucose sarcoplasm back into the SR.
very efficiently, producing a net gain of two ATPs per • This results in the “reshielding” of the actin-binding
molecule of glucose, and the end product of lactic sites on the thin filaments.
acid, which may contribute to muscle fatigue as it • Without the ability to form cross-bridges between the
accumulates. thin and thick filaments, the muscle fiber loses its
tension and relaxes.
Aerobic Respiration
• Is the breakdown of glucose or other nutrients in the MUSCLE STREGNTH
presence of oxygen (O2) to produce carbon • Muscle strength is directly related to the amount of
dioxide, water, and ATP. myofibrils and sarcomeres within each fiber.
• Approximately 95% of the ATP required for resting • Factors, such as hormones and stress (and artificial
or moderately active muscles is provided by aerobic anabolic steroids), acting on the muscle can
respiration, which takes place in mitochondria. increase the production of sarcomeres and
• The inputs for aerobic respiration include glucose myofibrils within the muscle fibers, a change called
circulating in the bloodstream, pyruvic acid, and hypertrophy, which results in the increased mass
fatty acids. and bulk in a skeletal muscle
• Is much more efficient than anaerobic glycolysis, • decreased use of a skeletal muscle results in
producing approximately 36 ATPs per molecule of atrophy, where the number of sarcomeres and
glucose versus four from glycolysis. myofibrils disappear (but not the number of muscle
• Cannot be sustained without a steady supply of O2 fibers).
to the skeletal muscle and is much slower
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• It is common for a limb in a cast to show atrophied
muscles when the cast is removed, and certain
diseases, such as polio, show atrophied muscles

NERVOUS SYSTEM CONTROL OF MUSCLE

TENSION
• To move an object (load), the sarcomeres in the
muscle fibers of the skeletal muscle must shorten.
• The force generated by the contraction of the muscle
(or shortening of the sarcomeres) is called muscle
tension.
• However, muscle tension also is generated when the
muscle is contracting against a load that does not
move, resulting in two main types of skeletal muscle
contractions:
1. Isotonic contractions
2. Isometric contractions

ISOTONIC CONTRACTION
• Tension in the muscle stays constant
• A load is moved as the length of the muscle changes Motor Units
(shortens) • The actual group of muscle fibers in a muscle
• Two types of isotonic contractions: innervated by a single motor neuron
1. Concentric contraction
2. Eccentric contraction • A single motor neuron
supplies a small number of
• Muscle shortening to muscle fibers in a muscle.
Small Motor
move a load. • Permit very fine motor control
unit
• EX: biceps brachii of the muscle
contracting when a hand • Ex: extraocular eye muscles
weight is brought upward that move the eyeballs
Concentric with increasing muscle • Is an arrangement where a
contraction tension. single motor neuron supplies
• As the biceps brachii a large number of muscle
contract, the angle of the fibers in a muscle.
elbow joint decreases as • Large motor units are
the forearm is brought Large Motor
concerned with simple, or
toward the body unit
“gross,” movements, such as
• muscle tension diminishes powerfully extending the
and the muscle knee joint.
lengthens. • Ex: thigh muscles or back
• Ex: hand weight is lowered muscles
in a slow and controlled • This increasing activation of
manner as the amount of motor units produces an
cross bridges being increase in muscle
Eccentric activated by nervous contraction
contraction system stimulation Recruitment
• As more motor units are
decreases. recruited, the muscle
• In this case, as tension is contraction grows
released from the biceps progressively stronger.
brachii, the angle of the
elbow joint increases. THE LENGTH-TENSION RANGE OF A SARCOMERE
•used for movement and • When a skeletal muscle fiber contracts, myosin
balance of the body heads attach to actin to form cross-bridges followed
by the thin filaments sliding over the thick filaments
ISOMETRIC CONTRACTION as the heads pull the actin, and this results in
• Muscle produces tension without changing the angle sarcomere shortening, creating the tension of the
of a skeletal joint. muscle contraction.
• Involve sarcomere shortening and increasing • The cross-bridges can only form where thin and thick
muscle tension, but do not move a load, as the force filaments already overlap, so that the length of the
produced cannot overcome the resistance provided sarcomere has a direct influence on the force
by the load. generated when the sarcomere shortens.
• Ex: one attempts to lift a hand weight that is too • The ideal length of a sarcomere to produce maximal
heavy, there will be sarcomere activation and tension occurs at 80 percent to 120 percent of its
shortening to a point, and ever-increasing muscle resting length, with 100 percent being the state
tension, but no change in the angle of the elbow where the medial edges of the thin filaments are just
joint. at the most-medial myosin heads of the thick
filaments.
• This length maximizes the overlap of actin-binding
sites and myosin heads.

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• If a sarcomere is stretched past this ideal length
(beyond 120 percent), thick and thin filaments do not
overlap sufficiently, which results in less tension
produced.
• If a sarcomere is shortened beyond 80 percent, the
zone of overlap is reduced with the thin filaments
jutting beyond the last of the myosin heads and
shrinks the H zone, which is normally composed of
myosin tails. Eventually, there is nowhere else for
the thin filaments to go and the amount of tension is
diminished.
• If the muscle is stretched to the point where thick and
thin filaments do not overlap at all, no cross-bridges
can be formed, and no tension is produced in that
sarcomere.
• This amount of stretching does not usually occur, as GRADED MUSCLE RESPONSE
accessory proteins and connective tissue oppose • Normal muscle contraction is more sustained, and it
extreme stretching. can be modified by input from the nervous system to
produce varying amounts of force.
• The rate at which a motor neuron fires action
potentials affects the tension produced in the
skeletal muscle.
• At the molecular level, summation occurs because
the second stimulus triggers the release of
• More Ca++ ions, which become available to activate
additional sarcomeres while the muscle is still
contracting from the
• First stimulus. Summation results in greater
contraction of the motor unit.

WAVE SUMMATION
• If the fibers are stimulated
THE FREQUENCY OF MOTOR NEURON while a previous twitch is
STIMULATION still occurring, the second
Twitch twitch will be stronger.
• A single action potential from a motor neuron will • Because the excitation-
produce a single contraction in the muscle fibers of contraction coupling
its motor unit. effects of successive
• Myogram: an instrument that measures the amount motor neuron signaling is
of tension produced over time. summed, or added together
THREE PHASES OF MUSCLE TWITCH INCOMPLETE TETANUS
• AP is propagated along the • If the frequency of motor neuron signaling increases,
sarcolemma and Ca++ are summation and subsequent muscle tension in the
released from the SR motor unit continues to rise until it reaches a peak
Latent period
• Excitation and contraction are point
being coupled • The tension at this point is about three to four times
• Contraction has yet to occur greater than the tension of a single twitch
• Ca++ in the sarcoplasm have • Muscle goes through quick cycles of contraction with
bound to troponin a short relaxation phase for each.
• Tropomyosin has shifted away
Contraction from actin binding sites TETANUS
Phase • Cross-bridges formed, and • If the stimulus
sarcomeres are actively frequency is so high
shortening to the point of peak that the relaxation
tension. phase disappears
• Tension decreases as completely,
contraction stops contractions become
• Ca++ are pumped out of the continuous
Relaxation
sarcoplasm into the SR • The concentration of
Phase
• Cross-bridge cycling stops Ca++ ions in the
• Returning the muscle fibers to sarcoplasm allows
their resting state. virtually all of the sarcomeres to form cross bridges
and shorten, so that a contraction can continue
uninterrupted (until the muscle fatigues and can no
longer produce tension).

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• When a skeletal → Do not possess substantial numbers of
muscle has been mitochondria or significant amounts of
dormant for an myoglobin
extended period → White color
and then activated • Fatigue more quickly than the others permitting them
to contract, with all to only be used for short period
other things being
equal, the initial MOST SKELETAL MUSCLES IN A HUMAN
contractions CONTAIN(S) ALL THREE TYPES, ALTHOUGH IN
generate about one VARYING PROPORTIONS.
-half the force of later contractions. • The speed of contraction is dependent on how
• Muscle tension increases in a graded manner that to quickly myosin’s ATPase hydrolyzes ATP to produce
some looks like a set of stairs. cross-bridge action.
• Muscle contractions become more efficient • Fast fibers hydrolyze ATP approximately twice as
• Results from a higher concentration of Ca++ in the quickly as slow fibers, resulting in much quicker
sarcoplasm resulting from the steady stream of cross-bridge cycling (which pulls the thin filaments
signals from the motor neuron. It can only be toward the center of the sarcomeres at a faster rate).
maintained with adequate ATP. • The primary metabolic pathway used by a muscle
fiber determines whether the fiber is classified as
MUSCLE TONE oxidative or glycolytic.
• Skeletal muscles are rarely completely relaxed, or • If a fiber primarily produces ATP through aerobic
flaccid. pathways, it is oxidative.
• Even if a muscle is not producing movement, it is → More ATP can be produced during each
contracted a small amount to maintain its contractile metabolic cycle, making the fiber more
proteins. resistant to fatigue.
• The tension produced by muscle tone allows • Glycolytic fibers primarily create ATP through
muscles to continually stabilize joints and maintain anaerobic glycolysis, which produces less ATP per
posture. cycle.
→ As a result, glycolytic fibers fatigue at a quicker
• Absence of the low-level rate.
contractions that lead to Oxidative Fibers
muscle tone • Contain more mitochondria than the glycolytic fibers
• Cause: damage to CNS, → Aerobic metabolism, uses O2, occurs in the
HYPOTONIA such as the cerebellum, or mitochondria
from poliomyelitis. • SO fibers = capable of contracting for longer periods
• Flaccid appearance → large amount of ATP produced
• Functional impairments, like → small diameter &don’t produce large amount of
weak reflexes tension
• Excessive muscle tone → SO fibers = supplied with blood capillaries to
• Accompanied by supply O2 from the red blood cells in the
hyperreflexia bloodstream.
• Damage to upper motor → SO fibers = myoglobin, an O2-carrying
neurons in the CNS molecule similar to O2-carrying hemoglobin in
HYPERTONIA • Muscle rigidity (as seen in the red blood cells
Parkinson’s disease) or
spasticity, a phasic change in Slow Oxidative (SO) Fibers
muscle tone, where a limb will • Can function for long periods without fatiguing
“snap” back from passive • Maintaining posture
stretching (as seen in some • Producing isometric contractions
strokes). • Stabilizing bones and joints
• Making small movements that happen often but do
• Contract relatively slowly not require large amounts of energy
SLOW
• Use aerobic respiration • Do not produce high tension
OXIDATIVE
(oxygen and glucose) to • Not used for powerful, fast movements that require
(SO) FIBERS
produce ATP high amounts of energy and rapid cross-bridge
• Fast contractions cycling
• Primarily use aerobic
FAST respiration Fast Oxidative (FO) Fibers
OXIDATIVE • May switch to anaerobic • Intermediate fibers
(FO) FIBERS respiration (glycolysis), can • Characteristics intermediate between fast fibers and
fatigue more quickly than SO slow fibers
fibers • Produce ATP relatively quickly
• Produce high amounts of tension.
TYPES OF MUSCLE FIBERS • Produce ATP aerobically
Fast Glycolytic (FG) Fibers • Possess high amounts of mitochondria
• Have fast contractions; Produce rapid, forceful • Do not fatigue quickly
contractions to make quick, powerful movements.
• Primarily use anaerobic glycolysis
• Do not primarily use aerobic metabolism

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 • Structural proteins are ERYTHROPOIETIN (EPO)
HYPERTROPHY added to muscle fibers. • Boost the availability of oxygen to muscles to
• Increasing cell diameter increase aerobic respiration
• Structural proteins are lost • Produced in the kidneys
ATROPHY • Triggers the production of red blood cells
• Muscle mass decreases
SARCOPENIA • Age-related muscle atrophy • The extra oxygen carried by these blood cells can
then be used by muscles for aerobic respiration.
Endurance Exercise
• Slow fibers are predominantly used HUMAN GROWTH HORMONE (hGH)
• Require little force but involve numerous repetitions • It can facilitate building muscle mass
• Aerobic metabolism used by slow-twitch fibers • Main role is to promote the healing of muscle and
allows them to maintain contractions over long other tissues after strenuous exercise.
periods. • Allow for faster recovery after muscle damage
• Endurance exercise can also increase the amount of • Reducing the rest required after exercise
myoglobin in a cell, as increased aerobic respiration • Allowing for more sustained high-level performance.
increases the need for oxygen.
• Myoglobin is found in the sarcoplasm and acts as an CREATININE PHOSPHATE
oxygen storage supply for the mitochondria. • Provides quick bursts of ATP to muscles in the initial
• The training can trigger the formation of more stages of contraction.
extensive capillary networks around the fiber, a • Produce more
process called ANGIOGENESIS, to supply oxygen • Increase explosive power output
and remove metabolic waste. • Its effectiveness as a supplement has been
• To allow these capillary networks to supply the deep questioned
portions of the muscle, muscle mass does not
greatly increase in order to maintain a smaller area CARDIAC MUSCLE TISSUE
for the diffusion of nutrients and gases • pump blood into the vessels of the circulatory
• All of these cellular changes result in the ability to system.
sustain low levels of muscle contractions for greater • Striated and organized into sarcomeres.
periods without fatiguing. • Shorter than skeletal muscle fibers
• The proportion of SO muscle fibers in muscle • Usually contain only one centrally located nucleus
determines the suitability of that muscle for • Possess many mitochondria and myoglobin
endurance, and may benefit those participating in • ATP is produced primarily through aerobic
endurance activities. metabolism
• Postural muscles have a large number of SO fibers
and relatively few FO and FG fibers, to keep the INTERCALATED DISC
back straight • Allows the cardiac muscle cells to contract in a
wavelike pattern so that the heart can work as a
Resistance Exercise pump
• Require large amounts of FG fibers to produce short, • Connects one cardiac muscle fiber to another
powerful movements that are not repeated over long • Are part of the sarcolemma
periods. • Contain two structures important in cardiac
• The high rates of ATP hydrolysis and cross-bridge muscle contraction:
formation in FG fibers result in powerful muscle 1. Gap junctions
contractions. 2. Desmosomes
• Muscles used for power have a higher ratio of
FG:SO/FO fibers, and trained athletes possess
even higher levels of FG fibers in their muscles.
• Resistance exercise affects muscles by increasing
the formation of myofibrils, thereby increasing
the thickness of muscle fibers.
• This added structure causes hypertrophy, or the
enlargement of muscles, exemplified by the large
skeletal muscles seen in body builders and other
athletes
• Because this muscular enlargement is achieved by GAP JUNCTION
the addition of structural proteins, athletes trying • Forms channels between adjacent cardiac muscle
to build muscle mass often ingest large amounts of fibers
protein.
• Allow the depolarizing current to flow from one
cardiac muscle cell to the next
PERFORMANCE-ENHANCING SUBSTANCES
• This joining is called electric coupling
ANABOLIC STEROIDS
• Allows the quick transmission of action potentials
• Boost muscle mass and increase power output
and the coordinated contraction of the entire heart
• TESTOSTERONE
• This network of electrically connected cardiac
→ Male sex hormone
muscle cells creates a functional unit of contraction
→ Stimulates muscle formation called a SYNCYTIUM.
→ Increased muscle mass

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 DESMOSOMES • T-tubules are not required to reach the interior of the
• anchors the ends of cardiac muscle fibers together cell and therefore not necessary to transmit an
• Cells do not pull apart during the stress of individual action potential deep into the fiber.
fibers contracting • Smooth muscle fibers have a limited calcium-storing
SR (sarcoplasmic reticulum) but have calcium
channels in the sarcolemma (similar to cardiac
muscle fibers) that open during the action potential
along the sarcolemma.
• The influx of extracellular Ca++ ions, which diffuse
into the sarcoplasm to reach the calmodulin,
accounts for most of the Ca++ that triggers
contraction of a smooth muscle cell.
• Muscle contraction continues until ATP-dependent
calcium pumps actively transport Ca++ ions back
into the SR and out of the cell.
PACEMAKER CELLS • However, a low concentration of calcium remains in
• Specialized cardiac muscle cells the sarcoplasm to maintain muscle tone.
• Directly control heart rate. • This remaining calcium keeps the muscle slightly
• Respond to signals from the autonomic nervous contracted, which is important in certain tracts and
system (ANS) to speed up or slow down the heart around blood vessels.
rate. • Because most smooth muscles must function for
• Can also respond to various hormones that long periods without rest, their power output is
modulate heart rate to control blood pressure. relatively low, but contractions can continue without
using large amounts of energy.
AUTORHYTHMICITY PLATEAU • Some smooth muscle can also maintain
• Self-excitable • Relatively long contractions even as Ca++ is removed and myosin
kinase is inactivated/dephosphorylated.
• Able to depolarize to action potentials in
threshold and fire its fibers sustained • This can happen as a subset of cross-bridges
action potentials on depolarization between myosin heads and actin, called latch-
their own bridges
→ Keep the thick and thin filaments linked
PLATEAU together for a prolonged period, and without the
• Is produced by Ca++ entry though voltage-gated need for ATP.
calcium channels in the sarcolemma of cardiac → Maintaining of muscle “tone” in smooth muscle
muscle fibers. that lines arterioles and other visceral organs
with very little energy expenditure.
• Provides for a longer contraction than is produced by
an action potential in skeletal muscle. • Smooth muscle is not under voluntary control; thus,
it is called involuntary muscle.
• Unlike skeletal muscle, a large percentage of the
Ca++ that initiates contraction in cardiac muscles • Smooth muscle is organized in two ways:
comes from outside the cell rather than from the SR. 1. Single-unit smooth muscle (more common)
2. Multiunit smooth muscle
SMOOTH MUSCLE
SINGLE-UNIT MUSCLE
• The two types have different locations in the body
and have different characteristics. Single-unit
muscle has its muscle fibers joined by gap junctions
so that the muscle contracts as a single unit. This
type of smooth muscle is found in the walls of all
visceral organs except the heart (which has cardiac
muscle in its walls), and so it is commonly called
visceral muscle.
• Has a stress-relaxation response
→ Muscle of a hollow organ is stretched, the
mechanical stress of the stretching will trigger
contraction, but this is immediately followed by
relaxation so that the organ does not empty its
Smooth Muscle Tissue Smooth muscle tissue is found around organs in the contents prematurely
digestive, respiratory, reproductive tracts and the iris of the eye
• Produces slow, steady contractions that allow
• Cells do not have striations substances, such as food in the digestive tract, to
• Walls of hollow organs: urinary bladder, uterus, move through the body.
stomach, intestines
• Walls of passageways: arteries and veins MULTIUNIT SMOOTH MUSCLE
• Tracts of the respiratory, urinary, and reproductive • Rarely possess gap junctions
systems • Are not electrically coupled.
• Eyes: functions to change the size of the iris and • Contraction does not spread from one cell to the next
alter the shape of the lens • Confined to the cell that was originally stimulated.
• Skin: hair to stand erect in response to cold
• Stimuli for multiunit smooth muscles come from
temperature or fear
autonomic nerves or hormones but not from
• Smooth muscle contraction relies on the presence of stretching.
Ca2+ ions, smooth muscle fibers have a much • This type of tissue is found around large blood
smaller diameter than skeletal muscle cells. vessels, in the respiratory airways, and in the eyes.
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 SMOOTH MUSCLE FIBERS DEVELOPMENT AND REGENERATION OF MUSCLE
• Spindle-shaped TISSUE
• Single nucleus • Origin: embryonic mesoderm
• Size: 30 to 200 μm • Skeletal ms, excluding those of the head and limbs:
• Produce their own connective tissue, endomysium mesodermal somites
• Do not have striations and sarcomeres • Skeletal ms in the head and limbs develop from
general mesoderm.
DENSE BODY/BODIES
• Is analogous to the Z-discs of skeletal and cardiac • Blocks of cells from Paraxial
muscle fibers mesodermal cells adjacent to
• Is fastened to the sarcolemma SOMITES the neural tube
• Ca++ are supplied by the SR in the fibers and by • Somites give rise to myoblasts
sequestration from the extracellular fluid through
membrane indentations called CALVEOLI. • Is a muscle-forming stem cell
• Where thin filaments are anchored that migrates to different
• The structures invested in the inner membrane of the regions in the body and then
MYOBLAST
sarcolemma (at adherens junctions) that also have fuse(s) to form a syncytium, or
cord-like intermediate filaments attached to them. myotube.
• When the thin filaments slide past the thick
filaments, they pull on the dense bodies, structures • is formed from many different
tethered to the sarcolemma, which then pull on the myoblast cells
intermediate filaments’ networks throughout the • it contains many nuclei, but has
sarcoplasm. a continuous cytoplasm
• This arrangement causes the entire muscle fiber to • skeletal ms cells: multinucleate
contract in a manner whereby the ends are pulled MYOTUBE • the nucleus of myoblast
toward the center, causing the midsection to bulge in remains intact
a corkscrew motion. • cardiac and smooth muscle
cells are not multinucleate
because the myoblasts that
form their cells do not fuse

• similar to a myoblast
• because it is a type of stem cell
CALMODULIN • are incorporated into muscle
• Regulatory protein cells
• Smooth muscle cells do not contain troponin • facilitate the protein synthesis
• Cross-bridge formation is not regulated by the SATELLITE required for repair and growth
troponin-tropomyosin complex CELLS • located outside the sarcolemma
• External Ca++ ions passing through opened calcium • stimulated to grow and fuse with
channels in the sarcolemma, and additional Ca++ muscle cells by growth factors
released from SR, bind to calmodulin. that are released by muscle
• The Ca2+-Calmodulin complex then activates an fibers under certain forms of
enzyme called MYOSIN (light chain) KINASE, which stress
in turn, activates the myosin heads by • found in some small blood
phosphorylating them (Converting ATP to ADP and vessels
PI, with PI attaching to the head)
• allow smooth muscle cells to
→ The heads can then attach to actin-binding regenerate
sites and pull on the thin filaments.
• cardiac muscle does not
regenerate to a great extent
HYPERPLASIA IN SMOOTH MUSCLE PERICYTE • Dead cardiac muscle tissue is
• Smooth muscle can undergo hypertrophy to
replaced by scar tissue, which
increase in size
cannot contract
• Smooth muscle can also divide to produce more
• As scar tissue accumulates, the
cells (HYPERPLASIA)
heart loses its ability to pump
• UTERUS AT PUBERTY = responds to increased because of the loss of
estrogen levels by producing more uterine smooth contractile power.
muscle fibers, and greatly increases the size of the
myometrium

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