Download Muscles - Drdodgeod.com

Muscles
Skeletal Muscle Anatomy

Skeletal Cells
o Skeletal muscle cells generally makes up 40-45% of the total body weight.
o Here, the cells are long, straight, seldom-branching cylinders. They are 10100mm in diameter and up to 4cm in length. This is among the largest cells in
the body.
o The organelles include long mitochondria with multiple, peripheral nuclei, a
cell membrane called the sarcolemma, and cell cytoplasm called the
sarcoplasm.


The neural muscular junction
o Also known as the motor endplate, the neuromusclular junction is the point of
communication between the terminal branches of alpha motor neurons and the
sarcolemma of the skeletal muscle fibers that they innervate.
 It is the alpha motor neurons that control the neuromuscular junction.
 The endplate is an enlargement of the sarcoplasm of the muscle fibers
at the neuromuscular junction. Depolarization occurs here giving rise
to the endplate potential.
 The sarcolemma is the cell membrane of a muscle fiber. This accepts
the endfoot and has folds called palisades that give the impression of
having an indentation and being thickened.
o Schwann cells insulate this junction.
Tissue Organization
o Connective tissues



Epimysium- surrounds the entire muscle and is continuous with the
tendon.
Perimysium- surrounds individual fascicles
Endomysium- surrounds each fiber
o Each muscle is a family of cells with each cell generally the length of the
muscle surrounded by connective tissue and attached to bones by bundles of
collagen known as tendons.
o The cellular level of organization is the muscle fiber. These are single muscle
cells that are organized into fascicles. Within a muscle, there are twenty or
more fascicles composed of a number of muscle fibers.
o Myofibrils (aka fibrils) are the subunits within fibers, containing filaments.
This is surrounded by other cellular constituents, such as the sarcoplasmic
reticulum. The major protein components of the myofibril are actin and
myosin. The striated patterns formed by these filaments are sarcomeres.
o This is further broken down into long protein molecules called filaments.
They can be classified as actin, which is thin, or myosin, which is thicker.

Sarcomere
o Every fibril is composed of repeated units called a sarcomere, the histological
and function unit of the muscle. The striated structure is complicated, formed
by repeating units of actin and myosin filaments
o There are 20,000 sarcomeres in an average muscle and they vary in size
tremendously.
o The sarcolemma is the cell membrane, not a layer of connective tissue. .
o The sarcoplasmic reticulum is a membranous, tube-like network surrounding
each individual myofibril within the muscle fiber. It is analogous to the
endoplasmic reticulum found in the muscle cell. The space in the sarcoplasmic
reticulum is separate from the rest of the fibril. Therefore it is an entity unto
itself surrounding the fibril.
o Myosin
 Myosin is an asymmetric hexamer with a molecular weight of
460,000. It contributes 55% of muscle protein by weight and forms the
thick filaments.




o Actin
Myofibrils are composed of many repeating units of myosin
molecules. The filaments are arranged in parallel arrays by an
antiparallel arrangement of myosin molecules in such a way that the
smooth central region of the filament is occupied only by the rod-like
parts of the molecules with the globular heads projecting outward
nearer the ends of the fibrils.
Myosin consists of one pair of heavy chains and two pairs of light
chains. It has a fibrous portion consisting of two intertwined alpha
helices, each terminating in a globular head portion attached at one
end. The head serves as the binding site for actin and ATP.
Sticking out of the core will be six cross bridges coming out at
different angles. Each cross bridge attaches to an actin filament.
Having the ability to change shape, it can go from an angled position
to perpendicular to the axis of the core, which is important in the
contraction of the muscle.
Skeletal muscle myosin exhibits ATP-hydroxylating (ATPase)
activity. Different types of myosin ATPases exist that determine the
different types of muscle functions.

On each actin molecule there is a myosin binding site where the
myosin can bind.
 Actin filaments are composed of:
 F-actin
o This is the filamentous portion of the actin filament. It
appears similar to a strand of pearls. Each actin filament
is composed of two F-actin strands in an alpha helical
configuration.
 G-actin
o This monomeric, globular portion of actin is a 43,000
MW globular protein and comprises 25% of muscle
protein by weight.
o Each pearl on the strand of F-actin is a G-actin. At
physiologic ionic strength, and in the presence of
magnesium, G-actin polymerizes noncovalently to form
an insoluble double helical filament that is F-actin.
 2 complex proteins associated with actin are crucial to
contraction of skeletal muscle.
o Tropomyosin
 This is another filamentous portion that lies
between the grooves of the F-actin strands. It
consists of two chains, alpha and beta, that
attach to the F-actin in the groove between the
two polymers. This is present in all muscle and
muscle-like structures.
 In the relaxed state, troponin holds tropomyosin
in position to block myosin-binding sites on
actin. This forms the H-band.
o Troponin
 This is unique to striated muscle. It is
\composed of three different subunits found for
every turn of the actin filament.
 C subunit (TpC)
 High affinity binding site for calcium
 T subunit (TpT)
 High affinity binding site for
tropomyosin
 I subunit (TpI)
 High affinity binding site for actin,
inhibiting the F-actin-myosin interaction
o Defined areas of the Sarcomere
 Z-line
 The bounds of the sarcomere are called Z-lines or Z-discs.
These are the anchoring points of actin. Myosin filaments are
arranged such that the ends of the myosin are at a distance from
the Z-line in a relaxed configuration.




I-band
 This is a light band of actin filaments alone.
A-band
 This is a dark band area containing myosin. It includes the Hband (myosin only) and the zone of overlap (actin and myosin).
T (transverse) tubules
 There are two transverse tubules per sarcomere.
 These are invaginations of the sarcolemma that pass into the
interior of the fiber. Here the interior is continuous with the
exterior of the cell. Extra-cellular fluid fills the T-tubule
 It enables myofibrils at the center of a muscle fiber to contract
simultaneously with those at the surface that are adjacent to the
excitatory action potential.
 Bare Zone
o This is an area where there is no cross bridges found
down the center of the myosin filaments.
Lateral (Terminal) Cisternae
 These are expansions of the sarcoplasmic reticulum that abut
the T-tubule.



Calsequestrin
o The protein calsequestrin stores or sequesters calcium
within the terminal cisternae, causing the calcium
concentration to continually increase. The calcium
bound to the calsequestrin does not contribute to the
“free calcium concentration,” increasing until the next
action potential comes along.
Innervation
o Voluntary
o Motor unit = a single nerve and all the muscle fivers it supplies. Motor end
plates are the sites at which a nerve axon terminates.
Different Muscle Fiber Types
o All muscles have a mixture of Type I and II, but some muscles tend to
predominantly have one type or the other.
o The ocular muscles tend to be predominantly Type II.
Type I Red
Duration of
contraction

~70ms
Type II (Fast Twitch)White
 Ocular muscle:10ms
Mechanism by
which ATP is
synthesized
Mitochondria




Blood


Color

Primary substrate
for energy
production
Diameter
SLOW TWITCH
High (primary)
oxidative fibers
Aerobic (ox phos)
More mitochondria to
support oxidative
metabolism
Fatigue resistant
More extensive blood
vessels and capillaries
“Redder” due to
myoglobin, an oxygen
binding pigment.


Soleus: 200ms
FAST TWITCH

Low oxidative fibers


Primarily anaerobic
Less mitochondria

Fatigable

Less extensive blood
supply
“White appearance.”
Less myoglobin, but a
more extensive
sarcoplasmic reticulum
“White meat”
Uses glycogen, lower
fat content and higher
caloric content
Larger diameter



“Dark meat”
Uses fat, higher fat
content



Smaller diameter

o Marathon runners have legs with muscles heavily weighted towards Type I
muscle. Sprinters will have more Type II. Some argue that the muscles in the
body can be trained or changed from one type to the next. This has been
demonstrated when a Type I muscle has been put into a cast without any
movement for a period of time. The same situation occurs with astronauts
after long-term space dwelling. One does not get complete conversion of
muscle fibers but similarities between fibers.
o The difference between the two fibers is generally due to the type of myosin
ATPase found in the head of the myosin filament. There are at least six
different forms of the enzyme, differing in the amount of time that the ATP is
cleaved. The types can be trained to be more like the other. Type I does not
hypertrophy to the same degree as Type II does.
Histogenesis

Myoblast differentiation and migration
o Skeletal, smooth, and cardiac muscle all differentiate from myoblasts which
are derived from mesenchymal cells.
o Striated Muscular Tissue
 The myoblasts have large nuclei with prominent nucleoli, and
cytoplasm rich in ribosomes contain scattered myofilaments. The
endoplasmic reticulum is poorly developed. These cells can be found
in the process of fusing with one another or with muscle fibers in more
advanced states of differentiation. As development progresses, the
thick and thin filaments become associated to form myofilaments. This
occurs early, around the time of myoblast differentiation. Then new
filaments are added to the lateral surfaces and distal ends of existing
myofibrils. With the appearance of myofibrils is the gradual
development of the characteristic cross striations.
o Smooth muscle
 Smooth muscle formation begins about the fifth week of development.
In blood vessels, mesenchymal cells are arranged at regular intervals
alongside the vessel. These mesenchymal cells differentiate into
myoblasts capable of mitosis, enlargement, and elongation. Myoblasts
then come in contact with one another laterally and a continuous layer
of smooth muscle is produced.
 The differentiated muscle fiber is spindle shaped with a central
nucleus. These mesenchymal cells are stretched out, with elongated
nuclei, and myofilaments in the cytoplasm.
 Note that not all smooth muscle is mesodermal in origin. For example,
the smooth muscle of the iris is ectodermally derived.
o Skeletal muscle
 This develops from two sources
 Paraxial somites
 Mesenchyme of the brachial arches
 Early in development, the somites thicken and myoblasts are formed.
The myoblasts undergo mitotic division, creating a mass of cells with
apparent syncytial formation which goes onto form myotubules.
Nuclei at this point are centrally located.
 Myofilaments begin to form into parallel arrangements in about the
third month of development, and gradually striations become visible as
myofibrils form. The nuclei are pushed to the fiber periphery by the
continued growth of the filaments throughout fetal development
(growth by myoblast differentiation, or possibly longitudinal splitting
of the fibers (Arey). After the late fetal stages, muscle enlargement is
due to increased individual fiber sizes. The development of muscle
from the branchial arches follows a similar process.
Skeletal Muscle Physiology

Muscles can shorten and contract, but cannot be lengthened. Typically, a muscle fiber
is 2/3 the length of the entire muscle. The connective tissue joins each fiber to each
point of origin and insertion of the muscle that makes up the other 1/3. When a
skeletal muscle contracts completely, it shortens about 1/3 of its initial length, i.e. a
3cm muscle contracts to 2cm.
Muscle Contraction
 The Motor Unit



o Muscles are controlled by the nervous system. The process begins at the
motor cortex, then sent to the ventral (anterior) horn of the spinal cord, to the
alpha motor neurons which originate at the ventral horn of the spinal cord.
Action potentials are elicited at the alpha motor neurons, then transmitted to
the muscle fibers which reside in the motor unit.
o The motor unit composition
 Alpha motor neurons
 Muscle fibers it innervates.
o These units differ in size.
 The smallest motor unit is found in the laryngeal muscles. They have
as few as two muscle fibers per nerve fiber. The eye muscles average
about twelve muscle fibers per nerve fiber. These are both considered
small motor units.
 This is an anomaly since ultra small motor units have a
predominance of type II fibers (fast twitch). Generally type II
fibers innervate more fibers, and type I less.
 Typically larger muscles have 100-5000 muscle fibers per nerve fiber.
The Somatic Nervous System
o The somatic nervous system is the efferent division of the peripheral nervous
system which innervates skeletal muscle. It is partially under multi-neuronal
voluntary control, while its simplest reflex arcs include only one sensory and
one motor neuron.
Proposed in the mid-1950s by Jean Hanson and Hugh Huxley and known as the
sliding filament model (myosin “walks” along the actin molecule in the sarcomere
structure and the Z lines are drawn closer). Sequence of events involved in the
excitation and contraction of a muscle fiber:
Spread of the Action Potential
o Motor neurons are activated by local reflex mechanisms at the level of the
spinal cord or brain stem, or by higher brain center pathways under conscious
and non-conscious control.
o A resting muscle fiber is polarized with the inner portion being negatively
charged. Because the muscle cell membrane contains voltage gated channels,
muscles are electrically excitable.
o As a result of a nerve impulse, an action potential will travel down the alpha
motor neuron and cause release of acetylcholine, a stimulatory transmitter,
from the endfoot. Acetylcholine will traverse the synaptic cleft and attach to
receptors on the endplate. The receptors on the endplate are nicotinic. When
the acetylcholine binds to the nicotinic receptors, channels open allowing an
influx of sodium across the end plate. That produces a potential called the end
plate potential (EPP). This is a momentary reduction of the polarization, i.e.,
depolarization. If depolarization reaches threshold level, an impulse or action
potential is triggered and runs along the muscle’s plasma membrane and along
the transverse tubules.
o The EPP acts a lot like an EPSP, except that it is at the end plate. An EPP has
a magnitude of 45-70mV and the threshold of a muscle fiber is about 15mV,
o
o
o
o
o
o
o
so the EPP is 3-4X greater than what is necessary to cause an AP in the
muscle fiber. Therefore, no summation is needed.
In a muscle fiber, each muscle fiber has one neuromuscular junction located in
the middle of the muscle fiber. During development, each muscle fiber has as
many as 50 neuromuscular junctions before birth. By the time birth occurs, it
has been brought down to a single neuromuscular junction. At the NMJ, there
are no voltage-gated sodium channels. But there are voltage-gated sodium
channels adjacent to the junction. So the currents cause by the EPP will spread
to the area that have the EPPs and will cause APs that will travel in every
direction from the NMJ.
The depolarization phase of the action potential causes an inward flux of
sodium through “fast” opening sodium channels. Then there is a
repolarization phase of the action potential, which is an outward flow of
potassium through “slow” opening potassium channels.
As the action potential depolarizes along the outside of the sarcolemma, it
dips into the T-tubule and terminal cisternae, opening the voltage gated
calcium channels and releasing the sequestered calcium into the sarcoplasm.
The concentration of calcium within the terminal cisternae is 1000x greater
than the concentration in the fibril. So the calcium diffuses from the terminal
cisternae out into the fibril.
The calcium uptake stimulates the release of acetylcholine into the
neuromuscular junction. Acetylcholinesterase immediately begins to
breakdown the acetylcholine, however some diffuses across the junction to
attach to receptor proteins located on the sarcolemma.
The binding of Ach causes the membrane to become leaky to sodium ions and
causes a depolarization which stimulates adjacent sodium and potassium gates
to open, thus starting an action potential in the muscle cell.
The action potential propagates in both directions from this initial point along
the sarcolemma and it will come into close proximity to the sarcoplasmic
reticulum inside the cell.
Calcium will be pumped by primary active transport out of the interior of the
fibrils into the sarcoplasmic reticulum.

The Power Stroke
o In the relaxed state, troponin holds tropomyosin in position to block myosin
binding sites. Binding between actin and myosin occurs when increased levels
of calcium are present surrounding the myofibrils. Calcium binds to the C-unit
of troponin, which produces a conformational change in the shape of the
troponin. This also causes a change in the shape of tropomyosin such that it
sinks deeper within the groove of the two F-action strands and uncovers the
myosin-binding sites on actin.
o The myosin, which is capable of ATP-ase activity, has ADP and Pi bound to
it. The myosin-ADP-Pi complex has a high level of free energy. It also has
great affinity for actin and binds to it when able.
o Once actin is attached, the high-energy myosin releases the ADP and Pi and
becomes low energy. The release of free energy allows the myosin to undergo
a conformational change such that the myosin filament advances along the
thin filament.
o During contraction, the angle of cross bridges will point toward the Z-line,
attach and pull the actin towards the center of the sarcomere. The actin slides
past the myosin, diminishing the space between the end of myosin and the Zline. It is not the filaments, but the sarcomeres that decrease in length. With so
many sarcomeres, this means that the muscle decreases from its total length to
two-thirds its initial length.
o The cross bridges act asynchronously, such that some are attached while
others are unattached, so that they are in different parts of the cycle. The
muscle will contract until the myosin abuts the Z-line and limits how short a
muscle can become. The muscle will remain in the contracted position until
something causes it to stretch out. The action of the antagonist will cause the
shortened muscle to stretch out. Muscles tend to work in antagonistic groups
such that the muscle that causes the flexion is antagonized by different sets of
muscle that cause extension.

Re-loading
o After the power stroke, there is an exposure of the binding sites for ATP at the
myosin cross bridge. This allows ATP to bind to the myosin head. When this
happens, the affinity of actin for myosin diminishes, and they uncouple.
 If ATP is not available, and there is no binding, myosin cannot
dissociate, and the muscle will stay in a fixed position called rigor. In
death, there is a lack of ATP, so the body gets really stiff in a state
called rigor mortis. The muscles last in this state of rigidity about 24
hours at which time tissues begin to disintegrate.
o The dissociation activates myosin ATPase.
o Internal hydrolysis of the bound ATP is split into ADP and phosphate, again
producing high energy myosin by “re-cocking” it. This allows the steps listed
above to once again be repeated, and several repetitions cause a significant
movement. This repeats as long as calcium ions are bound to troponin.
Calcium ions return to the lateral sacs of the sarcoplasmic reticulum resulting
in tropomyosin moving back to its blocking position, preventing further
interaction between high energy myosin and actin subunits. This results in
ceasing the contraction and relaxing the muscle fiber. As soon as the calcium
is released from the terminal cisternae, there are primary transport
mechanisms that pump the calcium back into the sarcoplasmic reticulum.
o At full contraction the myosin is still trying to pull on the actin and ATP is
still used.
Types of Contraction
 Treppe
o When a single suprathreshold action potential is delivered to a single skeletal
muscle fiber, the strength of the contraction can be measured. After complete
relaxation of the muscle, a second stimulus can be delivered with a response
greater in magnitude than the first. A few milliseconds later, after complete
relaxation, another stimulus is delivered with a response of greater magnitude
than the previous. The stimulus strength delivered in each case is the same,
but each consecutive muscle contraction is greater in magnitude than the
previous. This situation is either referred to as Treppe, the Warm-Up Effect,
or the Bowditch Effect.


o When the muscle is at rest for a period of time, there is a maximum amount of
calcium that can be pumped into the terminal cisternae. In response to a single
action potential, the amount of calcium does not saturate every available
binding site, resulting in some cross bridges remaining inactive. Following the
first event, calcium will be pumped out, but before all calcium is pumped out,
another stimulus is delivered. The residual calcium from the first stimulus,
plus the second dose of calcium being released from the terminal cisternae
together results in a greater intracellular calcium concentration which affects
more cross bridges and an even stronger contraction. This continues for a
sequence of events until the amount of calcium is sufficient to saturate the
calcium binding sites for every event. Following this, the amount of calcium
in the fibril in response to the action potential is sufficient to saturate all of the
binding sites.
o In resistance exercise, the amount of weight that can be lifted towards the end
of the training is approximately 1/3 greater than in the beginning.
o Muscle fibers respond all or none past treppe, because the amount of calcium
is elevated for a longer period of time, meaning more crossbridges are
activated for a longer period of time.
Twitch
o A single action potential is produced if threshold is reached. If the stimulus
intensity is increased, there is an increase in the strength of the contraction,
similar to Treppe. This increase in strength of contraction occurs because the
number of motor neurons recruited is increased.
o This situation in which a single stimulus response is delivered is referred to as
twitch. In this situation, there is a collection of cell bodies within the nervous
system called a nucleus. The cell body that is associated with small motor
neurons has a resting membrane potential closest to threshold, so that the
descending stimulus signal from the central nervous system recruits these cell
bodies first.
o Using a muscle to the smallest degree of its capability requires control. The
recruitment of smaller motor muscles requires smaller increments of
movement of the muscle, i.e. more control. Therefore, small motor neurons
are recruited first. This gives control and at the same time, these Type I
muscles are fatigue resistant. Later, more and more muscle units are recruited
until all the motor units present are recruited.
Tetanus
o The contraction/relaxation cycle in skeletal muscle does not have a refractory
period. The action potential has a refractory period, but not the muscle.
o Stimulating 1 muscle/second allows contraction and relaxation, as does 5
muscles/second. But increasing the frequency to 10 muscles/second, does not
allow the muscle to completely contract, and relaxation is prevented. This is
called fusion of response or incomplete tetanus.
o Complete tetanus is an increase in frequency with absolutely no relaxation.
There is a minimum frequency that elicits a complete tetanus, called the
critical frequency.
 Type I: 15 muscles/sec


 Type II: 60 muscles/sec
o Muscle Contraction
 Alpha motor neurons are stimulated with a burst of stimulus, not with
a single twitch. This typically causing incomplete tetanus, but bodily
movements are not jerky. They are smooth so that contraction can be
maintained. The muscle stays in a fixed position, because the fibers are
recruited in an asynchronous fashion.
 Muscle is generally never recruited at complete tetanus. This can only
happen with a highly trained athlete. Complete tetanus is avoided since
it could cause a broken bone or a torn muscle.
Eccentric vs. Concentric Contraction
o Concentric Contraction
 This type of contraction is the normal contraction that is thought of
where a muscle shortens, i.e., with a flexing arm.
o Eccentric contraction
 This is a lengthening contraction, where resistance to the muscle
lengthening is opposed.
 Eccentric contraction is capable of developing 30% more force than a
concentric contraction. In theory, if one could curl 100 lbs, they would
be able to resist lengthening with 130lbs. This is due to the fact that
concentric contractions are only due to the power stroke. In terms of
lengthening a muscle, both the power stroke of the cross bridge and
the bond between actin and myosin is in effect.
Isometric vs. Isotonic
o Isometric
 Isometric contraction of a muscle is a movement in which it does not
shorten. The muscle has a constant length. The energy derived from
the chemical reactions is release as heat and produces tension of the
muscle.
o Isotonic
 Isotonic contraction is a shortening of the muscle while the tension
generated remains relatively constant. As the muscle shortens, it
moves a load of certain distance, and work is done.
Contraction Strength
 The strength of the muscle contraction primarily depends on the number of cross
bridge interactions that occur. Increasing the cross sectional area of a muscle fiber
increases the number of myofilaments present and consequently increases the strength
that the fiber can develop, as long as there is not a significant fat deposition in
between the fibrils and the fibers of that muscle. Fat can contribute to the cross
sectional area of the muscle, but it does not contribute to the strength of contraction.
There is an increased amount of fat in between muscle fibers as one ages. So the cross
sectional area is no longer just lean tissue.
 The strength of contraction for a skeletal muscle is about 3.5kg per cm2 or 50lb. per
in2. The capacity of muscles is never utilized to their fullest. If they were, there is a
possibility of ripping muscle out of the bone. Multiple safety mechanisms are built-in
that prevent this.
 The signal coming out of the brain is important in determining the maximum strength
of contraction. An untrained individual only recruits about 50% of his available motor
units. After a short while, the strength can be increased, because more motor units
have been trained to be recruited. This is seen in instances such as cross-training
without any measurable increase in muscle. This phenomena occurs in the motor
cortex.
o Focus and visualizing performance can also be very important to an individual
trying to perform a task. Experiments have been performed in which an
athlete only trains the right side, but both sides increase in performance. This
is accomplished by “training the brain.”
 Training muscle to increase in endurance and strength
o To increase in muscle endurance, low resistance /high repetition exercises
should be performed.
o An increase in strength is accomplished with high resistance and low
repetition exercises.
o Muscles can also be trained to increase in strength and endurance at the same
time.
o When exercising, muscles increase in size due to an increase in the number of
myofilaments. This is called hypertrophy.
o It atrophies with disuse.
 DOMS- Delayed Muscle Onset Soreness
o This occurs when muscles are exercised excessively. It occurs 24-48 hours
after exercising. This is due to microtrauma damage to the muscle fiber, not
lactic acid buildup. Examining the muscle histologically reveals many
aberrations, including Z-band streaming in which the Z bands are pulled out
of alignment and sit at an angle. DOMS can also initiate the inflammatory
response.
o Hyperbaric oxygen has no effect on healing.
o An eccentric contraction would be more apt to cause this.
Length-Strength Relationship


In a typical resting situation (B and C) there is a maximum overlap of myosin and
actin. The muscle fiber is at a length that will result in the greatest degree of
stimulation. If the length is decreased or increased, this will diminish the strength of
contraction that can be developed by that muscle fiber. This is called the length-stress
relationship, and it has to do with the number of cross bridge interactions, as well as
the total time of actin and myosin interaction.
Point A represents an overlap of actin, reducing the number of cross bridges binding
that can occur. Point D allows no binding for the cross bridge, resulting in a small
strength of contraction.
Load to Velocity Relationship

The more load placed on a muscle, the slower the muscle contracts. This is due to the
number of cross bridge interactions occurring. If the muscle is contracting rapidly,
few cross bridges are required to do the task. If the load is great, then every one of the
cross bridges will have to bind numerous times in order to develop the necessary
force to overcome the event to occur. With greater force, the contraction occurs
slower.
Fatigue



This is a decrease in the ability of a muscle to perform a task. At this moment it is
poorly understood, and the cause is unknown. Some suggest that it is due to an
inadequate amount of oxygen in the blood.
When certain motor units begin to fatigue, other motor units are brought in with more
weight. This causes less of a rotation between the muscles, because there are no more
“back-ups.”
Central Fatigue is a phenomenon that occurs in the motor control centers of the brain.
It has nothing to do with the muscle fiber itself. Part of the inability to perform a task
has to do with glycogen depletion normally stored in the liver and skeletal muscle.
Reflex Arc
 A reflex is a stereotyped motor response.
 Stretch reflexes involve two neurons- sensory and motor
o In the stretch reflex, the stretching of the muscle results in an increased
frequency of nerve impulses in the afferent neurons associated with the
muscle spindles. Within the spinal cord, the afferent neurons synapse with
efferent neurons called alpha motor neurons that supply the extrafusal fibers
of the muscle.
o As a result of the increased frequency of nerve impulses in the afferent
neurons increasing the stimulation of the alpha motor neurons, the muscle
contracts to resist the stretch of the muscle.
 Simple reflex arc- 5 components

o Sensory receptor
o Sensory neuron- in dorsal ganglion just outside the spinal cord.
o Interneuron- in gray matter of the spinal cord
o Motor neuron (alpha motor neuron) in the ventral horn of the spinal cord.
o Effector- the muscle fiber that is stimulated.
Golgi Tendon Organ
o These are specialized muscle spindles and neurotendinous end organs capable
of testing the degree of stretch in a muscle or at the junction of a muscule with
its tendon. These receptors are stimulated when the antagonistic muscles
shorten. Presynaptic inhibition of the motor neuron, maintains relaxation of
the muscle despite the stretch upon it, for instance, when the antagonistic
muscle is contracting, the flexor in this case.
Pathology of Skeletal Muscle



Muscle Atrophy
o Decrease in muscle size
o Causes
 Disuse
 Disuse atrophy occurs when the muscle is not used.
 Neurogenic (ex, carpal tunnel)
 Denervation atrophy occurs when the nerve going to the
skeletal muscle is severed. This is much more severe than
disuse since there is some permanent loss of function,
where only about 80% is usually recovered.
 Ischemic
 Iatrogenic (glucocorticoids)
 Idiopathic
o If atrophy is maintained for a significant amount of time, genes are
activated which result in a decrease in the number of myofilaments, which
causes a decrease in the number of muscle fibers.
Myasthenia Gravis
o Autoimmune disorder
o Post-synaptic acetylchoine receptors decreased binding.
o Muscular weakness (facial, limb, trunk). Fatigue, ptosis, diplopia,
dysphagia
o Symptoms often fluctuating, may be spontaneous or dependent on activity
o 90% ptosis or EOM paresis
o 90% anti-acetylcholine receptor antibody
o Tensilon (edrophonium) test
o Females>males
o Thymomas- tumors of thymus gland- diagnosed with chest x-ray.
Inflammatory myopathies
o Diffuse, idiopathic
o Polymyositis
 Muscle inflammatory disease
o Dermatomyositis
 With rash
o Inclusion body myositis
 Extensor muscles
 Inclusion bodies in muscle
 Acquired: weakness in proximal and distal muscles
o History with PM and/or DM
 Symmetric proximal muscle pain and weakness
 Muscle pain at rest or with use
 Symptoms develop over weeks to months


Dysphagia (30%)
 Difficulty swallowing
 Arthralgias- joint pain
 Difficulty kneeling, climbing, or descending stairs, raising arms,
and arising from a sitting or lying position
 Joint pain
 Rash over the face, chest, and hands
 Heliotrope rash on sun-exposed areas
 Increased muscle enzymes like CPK
Muscular Dystrophies
o Inherited and characterized via gene location
o Progressive muscle waste and weakness
o Duchenne’s Muscular Dystrophy
 Most common form of dystrophy
 X-linked recessive trait and therefore predominantly affects boys
 Progressive muscle wasting and weakness
 Most boys start using wheelchairs by age 12 and to die in their 20s.
o Becker’s Muscular Dystrophy
 Clinically similar to Duchenne’s
 Milder, onset in teenage years
 Less progression.
o Myotonic Dystrophy
o Facioscapulohumeral Dystrophy
o Limb-girdle Dystrophy
o Treatment: Prevention
Smooth Muscle
Anatomy
 This is an involuntary, nonstriated muscle found in the walls of the internal organs,
digestive tract, respiratory passages, urinary and genital ducts, bladder, gallbladder,
arteries, and the iris and ciliary body of the eye.
 Smooth muscle cells are spindle-shaped, with an elongated, oval nucleus that is
smaller than skeletal muscle fibers. It is about 5microns in diameter and 2050microns in length.
 Tissue Organization
o Cells form sheets or layers of tissue that constitute parts of the walls of the
hollow viscera and vessels of the body. They are intimately associated with
connective tissue. Groups of cells are enveloped in fine fibroelastic tissue.
They are closely packed, and individual cell boundaries cannot be seen.
o Fibers stimulate adjacent fibers and are joined in branching for sciculi.
Smooth muscle fibers are connected by white, elastic, and reticular fibers.


Organelles include a single central nucleus with several nucleoli, (less) mitochondria,
a pair of centrioles, free ribosomes, rough endoplasmic reticulum, Golgi bodies, and
sarcoplasmic reticulum.
Smooth muscle fibers possess thick filaments that contain myosin and thin filaments
that contain actin and tropomyosin, but their arrangement is such that striations are
not present. The filaments are not organized into regularly ordered sarcomeres.
Smooth muscle has dense bodies which are similar to Z-lines. The structure of
smooth muscle is similar to skeletal muscle, but it lines up diagonally. This is why the
cells do not appear striated.
o Smooth muscle does not contain troponin, however it does contain the protein
calmodulin which is structurally similar to troponin. Calcium activates
calmodulin to allow the binding of myosin to actin via phosphorylation of
myosin, resulting in contraction.
Physiology
 Control
o It is not under conscious control. It is innervated by sympathetic and
parasympathetic nerve fibers. Smooth muscle does not contract as rapidly as
skeletal muscle, because there is no myelin, but it can remain contracted
longer. In smooth muscle contraction, relaxation cycle is mush slower (23sec) than in skeletal muscle (10-200ms)
o There is slow contraction, and it is slow to fatigue. Thus, it can function for
long periods of time such as in digestion.
 Two Main Types
o Single-unit
 Most of the smooth muscle in the body is single-unit. They are found
in the walls of hollow organs, ducts, blood vessels, and in the walls of
the intestine. Pacemaker activity contributes greatly to intestinal
motility.
 In this type, there are connections between adjacent cells called gap
junctions. These are sites of endoplasmic continuity which electrically
connects all of the cells in the unit. They are also sites of reduced
resistance to electric current flow. This allows calcium to flow freely
from one cell to another so that all cells can contracts as one unit.
 These can be influenced by the nervous system, but it can act
autonomously. This is the function of the pacemaker function in the
cells. There is an oscillation of the membrane potential so the
membrane potential will continuously repolarize and depolarize.
Frequently, at the apex of the oscillation the depolarization will have
reached threshold and an action potential will result.
 Going from depolarization → action potential → action potential →
repolarization is called a pacemaker potential. This is primarily a
function of the sodium pump. The pump is inactive during
depolarization, then activated by an action potential. It repolarizes as
sodium is pumped out.



The action potentials are a little different here in the fact that they are
due to an influx of calcium instead of sodium. The pacemaker
potential is due to an influx of sodium, but when threshold is achieved,
voltage-gated calcium channels open and the action potential is a
function of the influx of calcium and efflux of potassium.
o Multi-unit
 These are found in some large arteries and the ciliary muscles of the
eye. No gap junctions are present here. The fibers work independently.
They are primarily controlled by the nervous system. Without neural
control these muscles are quiet.
 Small structures called variscosities contain neurotransmitters which
are released and will alter the activity of smooth muscle. The release
of neurotransmitters, if stimulatory, will open ligand-gated calcium
channels and there is a calcium influx and a depolarization, but no
action potential takes place.
Cross Bridge Cycling
o Cross bridge cycling cause the fiber to shorten, but the activation of cross
bridge cycling in smooth muscle is very different than in skeletal muscle. In
smooth muscle, the influx of calcium is going to stimulate the process, as was
the case in skeletal, but the calcium is going to bind to calmodulin. The
calcium-calmodulin complex is formed and activates myosin kinase, which
then phosphorylates the myosin. This allows ATP to bind to the myosin and
be converted to ADP, which leads to the cross bridge cycling. When calcium
is removed, the myosin kinase is turned off, and myosin phosphatase will
phosphorylate the myosin. This terminates the cross bridge cycling.
o Nature of shortening
 In skeletal muscle when a sarcomere is shortened, it is similar to
pushing a telescope down. In smooth muscle, the arrangement is
elliptical around the cell so when the actin and myosin slide past each
other, the cell attains a helical configuration so it twists around itself
like a corkscrew. When it twists this way, it shortens the entire fiber.
This was determined via experiments with fluorescence and
antibodies.
Force
o Force developed in smooth muscle (6kg/cm2) is much greater than in skeletal
muscle (3.5kg/cm2).
o In smooth muscle, there is a process where actin and myosin can stay
associated without using ATP. This is called latching. This means that a
smooth muscle can maintain a shortened condition using much less energy
than a skeletal muscle fiber.
Cardiac Muscle
Anatomy
 Cell shape





o Similar to skeletal muscle, except smaller and frequently branched
Size
o 15 microns in diameter and 100 microns in length.
Organelles
o Single, oval nucleus, centrally located and possibly binucleated.
Tissue Organization
o Branching, anastomosing fibers produce a continuous network.
o Functionally similar to smooth muscle
o Some muscle fibers overlap.
Fine Structure
o Muscle cells are joined end to end by intercalated discs and are
mechanically coupled by fascia adherens.
o Sarcoplasmic reticulum is less developed than in skeletal muscle.
o The intercalated discs appear as dark-staining bands oriented transversely
to the long axis of the fibers.
o T tubules are less frequent and only at Z lines.
Innervation
o Involuntary
o Difficult to fatigue
o Specialized muscle fibers in SA and AV nodes and Purkinje fibers in the
Bundle of His regulate contraction.
Pharmacology
Anticonvulsants
 Convulsions are involuntary, general paroxysms of muscular contractions. A
frequent etiology for convulsions is neuronal defects grouped under the collective
term epilepsy. Seizures can also be brought on by fever or hypoglycemia. Status
epilepticus can be brought on by head injury, certain poisons, or an abrupt
withdrawal from CNS depressant drugs.
 Epilepsies are categorized for purpose of therapeutic management even though
epilepsy is a symptom more than it is a specific disease. Classification of
epilepsies is as follows.
o Partial (Focal)
 These are characterized by localized EEG abnormalities.
 Types
 Simple (Jacksonian type)
o The consciousness is unaltered.
 Temporal limbic (Psychomotor type)
o This can either be a simple sensory disturbance, of
either the visual, auditory, olfactory, or autonomic
sense. They could also be complex where the
consciousness is impaired or lost. Here the patient
can have intense emotions or psychic experiences.
 Focal has the capability to become generalized.


o Generalized seizures
 Absence seizures (Petit Mal)
 These are usually seen in kids and are generally outgrown.
 Here there is a loss of consciousness. The patient might not
collapse, but the patient could stare or have an absence of
reactions. There are no motor signs.
 Tonic-clonic Seizure (Grand Mal)
 This generally starts with an aura. Other signs can include
muscle tonicity (rigidity), clonic activity (twitching),
postictal CNS Depression, and unconsciousness.
 Myoclonic attacks
 These are rhythmic body jerks without loss of
consciousness.
The modes of action of most antiepileptic drugs are unknown. The spread of
seizure discharge is decreased by phenytoin, Phenobarbital, and primidone. It is
thought that the effects of anticonvulsants on threshold and spread are the result
of membrane stabilization. Convulsive threshold is elevated by most drugs in this
class. Events thought to enhance stability include altering the activity of
(Na/K)ATPase, shifting the production of cyclic nucleotides, and interfering with
protein phosphorylation.
Agents Used in Treating Partial Seizures
o Carbmazepine (Tegretol)
 Mechanism: reduces repetitive firing of neurons by partially
blocking Na+ channels.
 Can also treat trigeminal neuralgia and bipolarity.
 May also retard seizure irritation
 Adverse effects
 Nausea
 Diplopia, blurred vision
 Bone marrow depression (aplastic anemia)
o Phenytoin (Dilantin)
 Mechanism: reduces repetitive firing of neurons by blocking NA+
channels.
 Zero-order kinetics at high concentrations
 Adverse effects
 Rash
 Drowsiness, nystagmus
 Gingival hyperplasia
 Tolerance and cross-tolerance
o Phenobarbital (Luminal, etc)
 Mechanism: enhances GABA binding, delaying closure of chloride
channels.
 Induction of hepatic drug-metabolizing enzymes (like other longlasting barbiturates).
 Adverse effects
 Drowsiness

 Emotional depression
o Primidone (Mysoline)
 Effects are similar to those of Phenobarbital.
 Metabolized to phenylethylmalonamide (another anti-convulsant)
o Topiramate (Topamax)
 For patients as young as 2 years
 Blocks sodium channels and enhances GABA.
 Also a treatment for migraines
 Adverse effects
 Drowsiness
 Anorexia
 Mental slowing
o Felbamate (Felbatol)
 Mechanism unknown
 Adverse effects
 Aplastic anemia
 Hepatic failure
o Gabapentin (Neurontin)
 For adjunctive use only. (Used only with other agents)
o Lamotrigine (Lamictal)
 For adjunctive use only.
o Tiagabine (Gabitril)
 For adjunctive use only
 Used only if >12 yr.
 Mechanism: inhibition of GABA reuptake
 Adverse effects
 Dizziness
 HA
 Mental slowing
o Viabatrin (Sabril)
 Mechanism: enhancement of GABA release by inhibition of
GABA aminotransferase (metabolism)
 Adverse effects
 Drowsiness
 Dizziness
 Weight gain
 Relative contraindication: mental illness
o Levetiracetam (Keppra)
Agents used in treating Absence Seizures (Nonconvulsive)
o Ethosuximide (Zarontin)
 Probable mechanism: reduce calcium currents in thalamic neurons
 Adverse effects
 Gastric distress, vomiting
 Hiccups
o Valproate (Depakene) = Valproic Acid






Mechanism: prolongs recovery of voltage-activated NA+ Channels
from inactivation
 Adverse effect
 N, V
 Lethargy
 Tremors
 Hair loss
 Weight gain
o Clonazepam (Klonopin)
 A benzodiazepine
o Trimethadione (Tridione)
 Adverse effect: Hemeralopia- fuzziness in bright lights (vs.
Nichteralopia)
Agents Used in treating generalized tonic-clonic seizures (Convulsive)
o Carbamazepine (Tegretol)
o Phenytoin (Dilantin)
 Aura may persist
 Prevents the spread of seizures from focus.
 Blocks sodium channels.
o Valproate (Depakene)
 Valproic Acid. Also comes in “Valproate sprinkles”
o Phenobarbital (Luminal)
 Enhances GABA binding.
o Mephobarbital (mebaral)
o Primidone (Mysoline)
o Diazepam
Drugs Used in Treating Status Epilepticus
o Chronic Grand Mal seizures. Very dangerous.
o Diazepam (Valium)
o Lorazepam (Ativan)- more effective; shorter acting
o Phenytoin (Dilantin)
o Phenobarbital (Luminal)
Adverse effects
o These tend to be GI, neurologic, cutaneous, mental, hematopoietic, and
renal. Drowsiness and ataxia are common side effects.
Agents Used in Hyperkinetic Disorders
o Tics: Chlorpromazine (Thorazine)
o Essential tremor: Propranolol (Inderal) and benzodiazepines
o Dystonias- activation of opposing muscle groups
 Atropine- blocks cholinergic receptors
 Botulinum toxin: prevents Ach release.
Agents Used in Treating Spasticity
o Baclofen (Lioresal): An agonist of GABAB receptors, found only in the
spinal cord.
o Benzodiazepines
 Agents
 Diazepam (Valium)
 Chlordiazepoxide (Librium)
 Mechanism: bind to GABAA receptors, which enhances binding of
GABA (relaxing the muscles)
o Dantrolene (Dantrium): prevents release of calcium from sarcoplasmic
reticulum.
 Also treats malignant hyperthermia and chronic spastic disorders
 Adverse effect
 Drowsiness
Skeletal Muscle Relaxants
Neuromuscular Blocking Agents
 Nondepolarizing Agents- prevent depolarization in NMJ
o Agents
 d-Tubocurarine (Curare)
 Used on arrow tips in the old days. This is destroyed in the
stomach, so only works if injected.
 Atracurium (Tracrium)
 Pancuronium (Pavulon)
 Mivacurium (Mivacron)
 Vecuronmium (Norcuron)
 Doxacurium (Nuromax)
 Pipecuronium (Arduan)
 Triacruine
o Action: relax skeletal muscles. They work in the brain, NMJ, or in the
muscle cells
o Use: relaxation for surgery
o Mechanism: Blockade of Nm receptors on motor end plates (nicotinic)
 Competitive blockade- analogous to atropine
 Reversible
o Durations of action
 d-Tubocurarine- 3-120 min (longest)
 Atracurium- 15-30 min
 Pancuronium- 30-120 min
 Mivacurium- 10-15 min
 Vecuronium- 15-30 min
 Doxacurium- 30-120 min
 Pipecuronium- 30-120 min
o Adverse Effects
 Apnea
 Histamine release (decreases blood pressure)
 Relaxation of respiratory muscles






 Treatment: reversible cholinesterase inhibitor (ex. Neostigmine)
Depolarizing Agents: Succinylcholine (Anectine)
o Action: relaxes skeletal muscles. This is 2 Ach together, so it acts on the
same receptors and stays on longer.
o Mechanism: maintains depolarization of motor end plates/blockade of Ach
receptors on motor end plate when infused via IV.
o Metabolized by plasma cholinesterase (pseudocholinesterase,
butyrylcholinesterase), not by true cholinesterase (in red blood cells)
o After about 2 hours, blockade becomes partially competitive, due to the
formation of monocholine, a nondepolarizing blocker.
o Duration of action: 5-10 minutes, so only use it for short procedures
o Uses: relaxation for surgery
o Adverse effects
 Fasciculation, apnea
 Histamine release
 Relaxation of respiratory muscles
Dantrolene (Dantrium)
o This is not really a neuromuscular blocker. It is located in the muscle cells.
o Mechanisms: suppress release of calcium from the sarcoplasmic
reticulum.
o Uses
 Treat malignant hyperthermia. If the body temperature rises too
much, it could be fatal.
 Chronic spastic disorders
Hexofluorenium
o Inhibition of acetylcholinesterase, prolonging the action of
succinylcholine.
o Prevent fasciculation caused by succinylcholine.
Centrally-Acting Agents
o Used for muscle spasm due to anxiety, muscle spasm due to injury, and
counteract convulsions due to CNS stimulants.
o Baclofen; diazepam (Valium)
o Adverse effects
 Drowsiness, paralysis, apnea, nystagmus, diplopia.
Halothane
o Causes calcium release therefore it increases the body temperature. Use
ice packs with this to keep the body cool.
Botulinus Toxin
Myology (Muscle Action)
Definitions
 Origin
o Stable attachment of a muscle to bone.
 Insertion
o Mobile attachment of a muscle





















Innervation
o The nerve that stimulates the muscle to contract
Tendon
o How muscles attach to bones (cordlike)
Aponeurosis
o A flat sheet of connective tissue connecting muscles.
Flexion
o Decrease in angle between two bones
Extension
o Increase in angle between 2 bones
Abduction
o Movement away from the midline of the body.
Adduction
o Movement towards the midline of the body.
Circumduction
o Rotation, flexion, and extension all at once. This makes a circle.
Rotation
o
Pronation
o “Palm up to down”
Supination
o “Palm down to up”
Plantar flexion
Dorsiflexion
Lateral flexion
o Decreasing angle along axis (to side)
Medial/internal rotation
o Rotation forward with arm on hip
Lateral/external rotation
o Rotation back
Inversion
o Moves soles towards each other
Eversion
o Move soles out
Elevation
o Move up
Depression
o Move down
Hyperextension
o Increasing an angle beyond 180º of anatomical position
Muscles of Facial Expression and Mastication
 Muscles of facial expression are innervated by CN VII and those of mastication
are innervated by CN V.
Muscle
Occipital frontalisGala aponeurotica
Frontalis
Origin
Occipital bone and
mastoid
Gala aponeurotica
Insertion
Gala aponeurotica
Medial palpebral
ligament
Lateral palpebral
ligament
Muscles of the
superior orbit
Corrugator
supercilii
Orbicularis oculi
Nasalis
Frontal process of
maxilla
Upper lip muscles,
lip cartilage
Depresses nose
cartilage
Draws medial
eyebrow downward
Enlarges the nares
in hard breathing
and anger
Constricts nares
Raises lip and
dilates nares
Infraorbital margin
Upper lip muscles
Raises upper lip
Procerus
Anterior and
posterior dilator
nares
Depressor septi nasi
Levator labii
superioris alaeque
nasi
Levator labii
superioris
Auricularis anterior
Action
Aids action of
frontalis
Raises brow and
wrinkles forehead as
in surprise
Draws eyebrow
down and medially
as in a frown
Closes eyelid
Draws ear up and
Superior auricular
Posterior auricular
Zygomaticus minor
Zygomatic bone
Skin of upper lip
Anterior to
zygomaticotemporal suture
Maxilla, inferior to
infraorbital foramen
Maxilla and
mandible
Angle of mouth
Maxilla and cheek
muscles
Mandible
Around mouth
Mandible
Skin of lower lip
Masseter
Squamous portion
of temporal bone
Zygomatic arch
Coronoid process of
mandible
Lower ramus and
angle of mandible
Lateral pterygoid
Sphenoid bone
Mandible
Medial pterygoid
Lateral pterygoid
plate of phenoid
Mandible
Zygomaticus major
Levator anguli oris
Buccinator
Angle of mouth
Angle of mouth
Risorius
Orbicularis oris
Depressor anguli
oris
Depressor labii
inferioris
Mentalis
Temporalis fascia
Temporalis
Muscles of the Neck
Angle of mouth
forward
Draws ear up
Draws ear back
Forms nasolabial
furrow and elevates
upper lip
Draws angle of
mouth up and back,
as in smiling
Expresses contempt
or disdain
Compresses cheek
(whistling)
Retracts corner of
mouth and tenses
lips
Closes and
protrudes the mouth
Depresses angle of
mouth, as in
frowning
Draws lip down and
back, as in pouting
Raises and
protrudes upper lip,
as well as wrinkles
the chin
Elevates the
mandible, chewing
Elevates jaw and
prime mover of jaw
closure
Moves jaw from
side to side,
depresses jaw, and
protrudes jaw
Synergist of
temperalis. Elevates
mandible.
Muscle
Platysma
Origin
Pectoralis
fascia and
Deltoid
Sternocleidomastoid Sternum and
Clavicle
Insertion
Mandible and
lower face
Trapezius
Clavicle and
Scapula
Occipital and
Vertebrae
Mastoid
process
Action
Opens jaw and
depresses the lower
lip
Draws head to side,
flexes back, flexes
head on chest,
elevates chin, and
rotates head.
Draws head back,
rotates scapula,
draws head to side,
braces shoulder, and
adducts scapula
Nerve
VII
XI
XI
Digastic
Opens the jaw and
moves the hyaloid
Draws hyoid up and
back
Raises hyoid
Draws hyoid and
tongue forward
Depresses hyoid
Depresses hyoid
Stylohyoid
Mylohyoid
Geniohyoid
Sternohyoid
Omohyoid
V and
VII
VII
V
XII
XII
XII
Muscles of Thorax and Abdomen
Anterior
Muscle
Pectoralis Major
Pectoralis minor
Serratus anterior
External Intercostals
Origin
Insertion
Coracoid process
of the scapula
Action
Horizontal adduction of
humorus
Forward movement of
shoulder. “Putting on a
jacket.”
Abduction of scapula.
“Punching, hugging.”
Pull ribs up to expand
thorax during
inspiration.
Deltoids
Subscapularis
Rectus abdominis
External abdominal
obliques
Internal abdominal
obliques
Transverses abdominus
Rectus sheath
Linea alba
Tendinous inscriptions
Inguinal ligament
Posterior
Clavicle/spine of
scapula
Deltoid
tuberosity
Abduction of humorus
and scapula
Medial/internal rotator
of humerus.
Flexion of vertebral
column and
compression of
abdominal contents.
Allow rotation of
vertebral column and
lateral flexion.
“
Covers the abdominal
muscles
Line separating the
rectus abdominus
Connective tissue
between the 6 pack
Contains many canals
going to the
reproductive
equipment. Larger in
males, therefore more
prone to hernias.
Muscle
Erector Spinae Group
Trapezius
Latissimus dorsi
Levator scapulae
Rhomboids
Supraspinatus
Infraspinatus
Action
Keeps the spine erect. Giving good posture.
Rotation of scapula to raise hand, extends
head and neck, elevates shoulders, scapula
adduction. Attaches at occipital bone,
vertebral column, and scapula.
Pulls arm down if raised. “Swimmer’s
muscle” Attaches to anterior humerus.
Elevates scapula
Adducts scapula. Attach to scapula and
vertebral column.
Abduction of humerous. Crosses the
superior scapula and ends at the tuberacle
of the humerus.
Lateral/external rotation of humerus at
shoulder. Below the spine of scapula to the
posterior humerous.
Lateral/ external rotation of humerus. From
scapula to posterior humerus.
Medial/ internal rotation of humerus.
Inserts at anterior humerous.
Extends femur at hip when running.
Externally rotates the femur.
Abduction of femur. (Larger in male dogs)
Abduction of femur
Largest nerve in the body
Teres minor
Teres major
Gluteus maximus
Gluteus medius
Gluteus minimus
Sciatic nerve
Muscles of the Upper Extremity
Muscle
Anterior
Biceps brachii
Brachialis
Brachioradialis
Pronator teres
Flexor carpi radialis
Palmaris longus
Flexor carpi ulnaris
Flexor digitorum
superficialis
Origin
Insertion
Action
Coracoid process
Radial tuberosity
Coranoid process of
ulna
Styloid process of
elbow
Suppinates forearm
Flexion of elbow
Flexion at the elbow
Pronates forearm
Flexes wrist
Flexes wrist
Flexes wrist
Flexes digits
Flexor digitorum
profundus
Posterior
Triceps brachii
Extensor carpi
radialis longus
Extensor carpi
brevis
Extensor digitorum
Extensor carpi
ulnaris
Muscles of the Lower Extremities
Flexes digits
Olecranon of ulna
Extension at elbow
Extend wrist
Extend wrist
Extend digits
Extend wrist
Muscle
ANTERIOR/ MED
Quadriceps femoris
(rectus femoris,
vastus lateralis,
vastus medialis,
vastus intermedius)
Sartorius
Origin
Insertion
Action
Tibial tuberosity
Extension at the
knee
Lateral 4 digits
Flex femur at the
hip, externally
rotating it. “Allows
you to sit crosslegged on the floor”
Adducts femur at
hip
Adducts femur and
flexes knee
Blood vessel in
coronary
transplants.
Dorsiflexion foot at
ankle
Extend lateral 4 toes
Distal phalynx
Extends great toe.
Adductor longus
Gracilis
Great saphenous
vein
Tibialis anterior
Extensor digitorum
longus
Extensor hallucis
longus
POSTERIOR/ LAT
Hamstrings (biceps
femoris,
semitendinosus,
semimembranosus)
Gastrocnemius
Soleus
Flexor digitorum
longus
Flexor hallucis
longus
Fibularis (peroneus)
longus
Fibularis (peroneus)
brevis
Extend the femur at
hip and flexion at
the knee.
Femur
Calcaneus
4 lateral phalanges
Distal phalynx
Plantarflexor feet
Plantarflexor of foot
at ankle
Extends 4 lateral
toes
Extends great toe
Plantarflex foot at
angle
Evert feet