2. 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.
• Striated (skeletal and cardiac) and unstriated (smooth)
• Voluntary (skeletal) and involuntary (cardiac and smooth)
• The skeletal muscles make up the muscular system.
• The skeletal muscles are innervated by the somatic nervous
system.
• Skeletal muscle fibers lie parallel to one another
4. 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.
• 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
5. 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 myosin are contractile
proteins.
• Each cross bridge has two site
crucial to the contractile process:
1. an actin-binding site
2. Myosin ATPase site
6. Thin filaments consist of three proteins:
actin, tropomyosin, and troponin
• Actin is the primary structural protein (backbone) of the thin filament.
• Actin has special myosin cross bridge binding site.
• Tropomyosin and troponin 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 Ca2+ 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 and muscle contraction can
occur.
7.
8. Skeletal muscle contraction is a
molecular phenomenon.
• 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.
• 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.
9. 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.
10. By excitation-coupling a series of events link muscle
excitation (action potential in muscle fiber) to muscle
contraction (cross bridge activity).
• Skeletal muscle contraction stimulated by release of Ach at neuromuscular junction
• Transverse tubules and sarcoplasmic reticulum in muscle fiber play a in the link.
• Calcium is the link for this process.
• 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.
11. 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.
• ATP binds to myosin at ATPase binding site
• 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.
12. 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.
• The need for ATP in separating myosin and actin is
shown in rigor mortis (stiffness of death)
13. Relaxation of a skeletal muscle
depends on the reuptake of calcium
ions, from the cytosol into the SR.
•Ca2+-ATPase pump on SR transports Ca2+
from cytosol to lateral sacs.
•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.
14. 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 in a
muscle fiber produces a twitch.
• Gradations of whole muscle
tension depend on:
1. the number of muscle fibers
contracting and
2. the tension developed by
each contracting fiber.
15. A motor unit is one motor neuron and
the muscle fibers it innervates.
• One motor neuron innervates a number of muscle
fibers, but each muscle fiber is supplied by only one
motor neuron
• 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. (alternates motor unit activity)
Larger muscles with more muscle fibers generate more tension
than smaller muscles with fewer fibers
16. The tension developed by a muscle
depends on the frequency of stimulation.
• Factors influence extent for
development of tension: frequency
of stimulation, length of the fiber,
extent of fatigue, and thickness of
fiber
• 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.
17. 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.
• Whole muscle tension also depends on the
extent of fatigue and the thickness of the fiber.
• Muscle tension is transmitted to bone as the
contractile component tightens the series-
elastic component.
• The origin is the fixed end of attachment of a
muscle to a bone. The insertion is the movable
end of attachment.
• If muscle tension overcomes a load, it pulls the
insertion toward the origin.
18. The two primary types of contraction
are isotonic and isometric.
• For muscle to shorten during
contraction, the tension developed in
muscle must exceed the forces that
oppose movement of the bone which
muscle insertion is attached, e.g.
elbow flexion
• By isometric contraction the muscle
tension developed is less than its
opposing load. The muscle cannot
shorten and lift the object with that
load. Constant length of the muscle
despite development of tension.
• 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.
• Concentric isotonic contractions: muscle
shortens
• Eccentric isotonic contractions: the
muscle lengthens from being stretched,
e.g lowering a load to the ground
• The velocity of muscle shortening is
inversely proportional to the
magnitude of the load.
• The greater the load, the lower the
velocity for muscles to shorten.
19. Skeletal muscles can perform work.
• Muscle accomplishes work in a physical sense only when an
object is moved.
• 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.
20. Bones, muscles, and joints interact to
form lever systems.
• A lever (bones) is a rigid structure capable of moving around a pivot.
• The pivot is the fulcrum (joints).
• (The skeletal muscles provide the force to move the bones).
• 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.
21. ATP is generated three ways for the
muscle contraction.
• Creatine phosphate (goes through hydrolysis) 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 lactic acid.
22. 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.
23. The three types (based on differences in
ATP hydrolysis and synthesis) 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).
• Fibers with greater ATP formation capacity (oxidative
fibers) are more resistant to fatigue.
• Oxidative fibers are red with a high concentration of
myoglobin (helps support O2 dependency).
• Glycolytic fibers contain glycogen enzymes.
• Fast fibers have higher myosin ATPase activity than
slow fibers.
24. Muscle fibers can adapt to the different
demands placed on them.
• Regular endurance exercise (e.g., long-distance jogging) promotes improved
oxidative capacity in oxidative fibers.
• The fibers use oxygen more efficiently.
• Skeletal muscle has a high degree of plasticity.
• Two types of changes can be induced in muscle fibers: changes in their ATP
synthesizing capacity and changes in their diameter
• 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 fibers are interconvertible. For example weight training can convert fast -
oxidative fibers to fast-glycolytic fibers.
• Slow and fast fibers are not interconvertible
• Skeletal muscles atrophy when not used. There is disuse atrophy and denervation
atrophy.
• Slow-twitch fibers are supplied by motor neurons that exhibit a low-frequency pattern
of electrical activity.
• fast-twitch fibers are innervated by motor neurons that display intermittent rapid bursts
of electrical activity.
• Skeletal muscles have a capacity for limited repair.
25. 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.
26. Muscle receptors provide afferent
information needed to control
skeletal muscle activity.
• This information is necessary for establishing a neuronal pattern of
activity to perform the desired movement
• Two types of muscle receptors: muscle spindles and Golgi tendon
organs
• 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. Muscle
spindles are distributed throughout the fleshy part of a skeletal muscle
• Both these receptor types are activated by muscle stretch
• 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 patellar-tendon or knee
jerk reflex.
• Stretch reflex (HW)
28. Smooth muscle composes the internal,
contractile organs except the heart. The heart
is composed of cardiac muscle.
• Supplied by involuntary autonomic nervous system
• Smooth muscle cells are small and unstriated, and found in
walls of organs and tubes
• These cells have actin and myosin. Their arrangement is
not organized compared to skeletal muscle cells.
Therefore, smooth muscle cells are not striated.
• No troponin and tropomyosin, but myosin light chains
• Light chain is phosphorylated for actin and myosin
interaction
• 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.
29. Smooth muscles can be classified into
phasic or tonic, multiunit or single-unit,
and neurogenic or myogenic
• Classification depends on the timing and means of increasing
cytosolic Ca2+.
• Each smooth muscle belongs to one class of each category
• Phasic smooth muscle (most abundant in walls of hollow
organs) contracts in bursts, triggered by action potentials that
lead to increased cytosolic Ca2+. E.g digestive tract
• Two Ca2+ sources: ECF and SR stores
• Tonic smooth muscles are partially contracted at all times
(toned). Has low resting potential. E.g walls of arterioles
• Relaxation achieved by removal of Ca2+ leading to
dephosphorylation of myosin.
• Multiunit and single-unit differentiated by number of excited
muscle fibers
30. Multiunit smooth muscle is neurogenic
(nerve produced).
• It has properties partway between skeletal muscle and single-unit
smooth muscle.
• Smooth muscle is supplied by the involuntary autonomic nervous
system.
• Multiunit smooth muscle (phasic) consists of multiple discrete
units
• 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 functional syncytium is a group of interconnected cells that
function mechanically and electrically, e.g uterine wall. When an
action potential develops in one cell, it quickly spreads to other
cells.
• Therefore, the cells in a syncytium contract as a single,
coordinated unit.
31. 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.
• the self-excitable cells of single-unit smooth muscle do not
maintain a constant resting potential.
• Types of spontaneous depolarizations: pacemaker potentials and
slow-wave potentials (HW)
• 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.
32. Single-unit smooth muscle can produce
gradations of contraction.
• It differs from the mechanism for producing the gradations of
skeletal muscle contraction.
• In single-unit smooth muscle, gap junctions ensure that an entire
smooth muscle mass contracts as a single unit
• Only the tension of the fibers can be modified to achieve varying
strengths of contraction of the whole organ
• 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 self-
induced, 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.
33. Smooth muscle can develop tension when it
is stretched significantly. It inherently
relaxes when stretched.
• This ability allows smooth muscle to stretch as the volume of
the organ’s contents expand, and also contract to allow
emptying of the organ, e.g., urinary bladder or uterus
• Its contraction is slow (e.g., uterus) and energy-efficient.
• 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.
• Smooth muscle also relaxes more slowly because of slower Ca2+
removal.
34. 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.
• As in smooth muscle, Ca2+ enters the cytosol from both the
ECF and the sarcoplasmic reticulum during cardiac excitation.
• The heart displays pacemaker (but not slow-wave) activity.
• The heart is innervated by the autonomic nervous system,
which, along with certain hormones and local factors, can
modify the rate and strength of contraction