Muscle Physiology • I bands : light bands contain only actin

filaments
SKELETAL MUSCLE FIBER • isotropic to polarized light
Skeletal muscle: 40 % of the body • A bands: dark bands contain myosin
smooth & cardiac muscle: 10%. filaments, as well as the ends of the actin
filaments where they overlap the myosin
• anisotropic to polarized light.
• cross-bridges: It is the interaction between
these cross-bridges and the actin filaments that
causes contraction

Sarcolemma
• Thin Membrane Enclosing a Skeletal Muscle
Fiber • Z disk: where the ends of the actin filaments
• consists of a plasma membrane, and an outer are attached to
coat made up of a thin layer of polysaccharide • Filaments extend in both directions to
material that contains numerous thin collagen interdigitate with the myosin filaments
fibrils. • These bands give skeletal and cardiac muscle
• At each end of the muscle fiber, this surface their striated appearance
layer of the sarcolemma fuses with a tendon
fiber. • sarcomere
• The tendon fibers in turn collect into bundles • The portion of the myofibril (or of the whole
to form the muscle tendons that then connect muscle fiber) that lies between two successive Z
the muscles to the bones. disks
• contracted muscle fiber, length of the
Myofibrils sarcomere: 2 micrometers.
• Are Composed of Actin and Myosin
• At this length, the actin filaments completely
Filaments.
overlap the myosin filaments,
• muscle fiber : several hundred to several
and the tips of the actin filaments are just
thousand myofibrils
beginning to overlap one another.
• Myofibril : about 1500 adjacent myosin
• at this length the muscle is capable of
filaments and 3000 actin filaments, which are
generating its greatest force of contraction.
large polymerized protein molecules that are
responsible for the actual muscle contraction.,
• thick filaments: myosin
• thin filaments: actin

Titin Filamentous Molecules
• Keep the myosin and actin filaments in place.
• The side-by-side relationship between the
myosin and actin filaments
is maintained by a large number of filamentous
protein molecules
• has a molecular weight of about 3 million
• which makes it one of the largest
protein molecules in the body.
• because it is filamentous, it is very
springy
Sarcoplasm
• intracellular fluid between myofibrils.
• containing large quantities of potassium,
magnesium, and phosphate,
plus multiple protein enzymes.
• tremendous numbers of mitochondria that lie
parallel to the myofibrils.
• Mitochondria: supply large amounts ATP
Sarcoplasmic Reticulum
• Is a specialized endoplasmic reticulum of
skeletal muscle.
• important in regulating calcium storage,
release, and reuptake and therefore muscle
contraction
GENERAL MECHANISM OF MUSCLE
CONTRACTION

titin molecule
• act as a framework that holds the myosin and
actin filaments in place so that the contractile
machinery of the sarcomere will work.
• One end is elastic and is attached to the Z disk,
acting as a spring and changing length as the
sarcomere contracts and relaxes.
• The other part tethers it to the myosin thick
filament.
• act as a template for initial formation of
portions of the contractile filaments of the
sarcomere, especially the myosin filaments.

Poten
Muscle Contraction Occurs by a
Sliding Filament Mechanism
• relaxed state: ends of the actin filaments
barely overlap one another
• contracted state: actin filaments have been
pulled inward among the myosin filaments, so
their ends overlap one another
• Z disks: pulled by the actin filaments up to the
ends of the myosin filaments.
• But what causes the actin filaments to slide
inward among the myosin filaments?
• interaction of the cross-bridges from the
myosin with the actin filaments.
• AP - SR release large quantities of calcium ions
- activate the forces between the myosin and
actin filaments - contraction begins
Myosin Filaments Are Composed of Multiple
Myosin Molecules
• molecular weight: 480,000.
• is composed of six polypeptide chains
• 2 heavy chains, MW: 200,000
• 4 light chains, MW: 20,000 each
• two heavy chains wrap spirally around each
other to form a double helix, which is called the
tail of the myosin molecule
• One end of each of these chains is folded
bilaterally into a globular polypeptide structure
called a myosin head
• two free heads at one end of the double-helix
myosin molecule.
• four light chains are also part of the myosin
head, two to each head.
• light chains help control the function of the
head during muscle contraction
myosin filament : ≥ 200 individual myosin
molecules.
• central portion: the tails of the myosin
molecules bundled together to form the body
of the filament, while many heads of the
molecules hang outward to the sides of the
body.
• part of the body of each myosin molecule
hangs to the side along with the head, thus
providing an arm that extends the head
outward from the body
* The protruding arms and heads together are
called cross-bridges
* Each cross-bridge is flexible at two points
called hinges—1) arm leaves the body of the
myosin and 2) the head attaches to the arm
Adenosine Triphosphatase Activity of the
Myosin Head
• Another feature of the myosin head that is
essential for muscle contraction is that it
functions as an adenosine triphosphatase
(ATPase) enzyme.
• the head to cleave ATP and use the energy
derived from the ATP’s high-energy phosphate
bond to energize the contraction process.
Tropomyosin Molecules
• Found in the actin filament
Actin Filaments Are Composed of Actin, • MW: 70,000 length: 40
Tropomyosin, and Troponin
nanometers
• The backbone of the actin filament is a
• Wrapped spirally around the sides of the F-
double-stranded F-actin protein molecule
actin helix
• The two strands are wound in a helix
• Resting state: lie on top of the active sites of
• Each strand of the double F-actin helix is
the actin strands so that attraction cannot occur
composed of polymerized G-actin molecules,
between the actin and myosin filaments to
each having a molecular weight of about
cause contraction.
42,000.

• Attached to each one of the G-actin

molecules is one molecule of ADP.
• ADP : active sites on the actin filaments with
which the cross-bridges of the myosin filaments
interact to cause muscle contraction.
• The active sites on the two F-actin strands of
the double helix are staggered, giving one
active site on the overall actin filament about
every 2.7 nanometers.
• Length of actin filament: 1 micrometer
• The bases of the actin filaments are inserted
strongly into the Z disks; the ends of the
filaments protrude in both directions to lie in
the spaces between the myosin molecules.
Troponin and Its Role in Muscle Contraction
• Attached intermittently along the sides of the
tropomyosin molecules
• complexes of three loosely bound protein
subunits
• troponin I : strong affinity for actin
• troponin T: tropomyosin,
• troponin C: calcium ions
• This complex is believed to attach the
tropomyosin to the actin.
• The strong affinity of the troponin for calcium
ions is believed to initiate the contraction
process
Inhibition of the Actin Filament by the
Troponin- Tropomyosin Complex
• A pure actin filament without the presence of
the troponintropomyosin complex (but in the
presence of magnesium ions and ATP) binds
instantly and strongly with the heads of the
myosin molecules.
• Then, if the troponin-tropomyosin complex is
added to the actin filament, the binding
between myosin and actin does not take place.
• Before contraction can take place, the
inhibitory effect of the troponin-tropomyosin
complex must itself be inhibited
Activation of the Actin Filament by Calcium
Ions
• large amounts of calcium ions --- inhibitory
effect of the troponin-tropomyosin on the actin
filaments is itself inhibited.
C Binds up to 4 mo
re
Interaction of “Activated” Actin Filament & the
Myosin Cross-Bridges— The “Walk-Along”
Theory of Contraction or “Ratchet”
• actin filament is activated by the calcium ions
----- heads of the crossbridges from the myosin
filaments become attracted to the active
sites of the actin filament --- contraction occurs
h an
ATP as the Energy Source for Contraction—
Chemical Events in the Motion of the Myosin
Heads
• Large amounts of ATP are cleaved to form ADP
during the contraction process
• the greater the amount of work performed by
the muscle, the greater the amount of ATP that
is cleaved (Fenn effect)
• The following sequence of events is believed
to be the means by which this effect occurs:
• 1. Before contraction begins:
• the heads of the cross bridges bind with
ATP.
• ATPase activity of the myosin head
immediately cleaves the ATP but leaves
the cleavage products, ADP plus phosphate ion,
bound to the head.
• In this state, the conformation of the
head is such that it extends
perpendicularly toward the actin filament but is
not yet attached to the actin.
• 2. When the troponin-tropomyosin complex
binds with calcium ions
• active sites on the actin filament are
uncovered
• myosin heads then bind with these sites
3. The bond between the head of the cross- THE AMOUNT OF ACTIN AND MYOSIN
bridge and the active site of the actin filament FILAMENT OVERLAP
DETERMINESTENSION DEVELOPED BY
causes a conformational change in the head,
THE CONTRACTING MS
prompting the head to tilt toward the arm of
the cross-bridge and providing the power stroke
for pulling the actin filament.
• The energy that activates the power
stroke is the energy already stored, like a
“cocked” spring, by the conformational change
that occurred in the head when the ATP
molecule was cleaved earlier
4. Once the head of the cross-bridge tilts,
release of the ADP and phosphate ion that were
previously attached to the head is allowed.
• At the site of release of the ADP, a new Effect of Muscle Length on Force of Contraction
molecule of ATP binds. in the Whole Intact Muscle
• This binding of new ATP causes
detachment of the head from the actin Resting ms length: 2um
5. After the head has detached from the actin,
the new molecule of
ATP is cleaved to begin the next cycle, leading
to a new power stroke.
• the energy again “cocks” the head back
to its perpendicular condition, ready
to begin the new power stroke cycle.

6. When the cocked head (with its stored

energy derived from the cleaved ATP) binds
with a new active site on the actin filament, it
becomes un-cocked and once again provides a
new power stroke. THREE SOURCES OF ENERGY FOR
• Thus, the process proceeds again and MUSCLE CONTRACTION
again until the actin filaments pull the Z
PHOSPHOCREATINE
membrane up against the ends of the myosin
filaments or until the load on the muscle • Carries a high-energy phosphate bond
becomes too great for further pulling to occur.
• is instantly cleaved, and its released energy
causes bonding of a new phosphate ion to ADP
to reconstitute the ATP

• the total amount of phosphocreatine in the

muscle fiber is also small— only about five
times as great as the ATP.

• the combined energy of both the stored ATP

and the phosphocreatine in the muscle is
capable of causing maximal muscle contraction
for only 5 to 8 seconds

GLYCOLY

• glycogen previously stored in the muscle cells.

• Rapid enzymatic breakdown of the glycogen

to pyruvic acid and lactic acid liberates energy
that is used to convert ADP to ATP; the ATP can
Characteristics of Isometric Twitches
then be used directly to energize additional Recorded from Different Muscles
muscle contraction and also to reform the • ocular muscle: < 1/50 second
stores of phosphocreatine. • Gastrocnemius: 1/15 second
• Soleus: 1/5 sec
THREE SOURCES OF ENERGY
FOR MUSCLE CONTRACTION
• (1) glycolytic reactions can occur even in the
absence of oxygen, so muscle contraction can
be sustained for many seconds and sometimes
up to more than a minute, even when oxygen
delivery from the blood is not available.
• (2) the rate of formation of ATP by the
glycolytic process is about 2.5
times as rapid as ATP formation in response to
cellular foodstuffs reacting with oxygen.

Fast Versus Slow Muscle Fibers

OXIDATIVE METABOLISM
• combining oxygen with the end products of
glycolysis and with various other cellular
foodstuffs to liberate ATP.
• More than 95 percent of all energy used by the
muscles for sustained, long-term contraction is
derived from oxidative metabolism.
CHARACTERISTICS OF WHOLE
MUSCLE CONTRACTION
Isometric Contractions Do Not Shorten
Muscle, Whereas Isotonic Contractions
Shorten Muscle at a Constant Tension.
• Isometric: muscle does not shorten during
contraction
• Isotonic: ms shorten but tension remains
constant throughout contraction
SLOW FIBERS (TYPE 1, RED MUSCLE)
• 1. smaller
• 2. innervated by smaller nerve fibers.
• 3. more extensive blood vessel to supply extra
amounts of oxygen.
• 4. greatly increased numbers of mitochondria
to support high levels of oxidative metabolism.
• 5. contain large amounts of myoglobin, an
iron-containing protein similar to hemoglobin in
red blood cells.
• Myoglobin combines with oxygen and stores it
until needed, which also greatly speeds oxygen
transport to the mitochondria
Fast Fibers (Type II, White Muscle)
• 1. large for great strength of contraction.
• 2. An extensive sarcoplasmic reticulum is
present for rapid release of calcium ions to
initiate contraction.
• 3. Large amounts of glycolytic enzymes are
present for rapid release of energy by the
glycolytic process.
• 4. have a less extensive blood supply
• because oxidative metabolism is of
secondary importance.
• 5. fewer mitochondria
• because oxidative metabolism is
secondary
Motor Unit—All the Muscle Fibers
Innervated by a Single Nerve Fiber
• All the muscle fibers innervated by a single
nerve fiber (motor unit)
• small muscles that react rapidly and whose
control must be exact have more nerve fibers
for fewer muscle fibers
• large muscles that do not require fine control
may have several hundred muscle fibers in a
motor unit.
• Average: 80 to 100 muscle fibers to a motor
unit.
Muscle Contractions of Different Force—
Force Summation
SUMMATION
• adding together of individual twitch
contractions to increase the intensity of overall
muscle contraction.
• occurs in two ways:
• (1) by increasing the number of motor units
contracting simultaneously (multiple fiber
summation)
• (2) by increasing the frequency of contraction
(frequency summation) and can lead to
tetanization.
Multiple Fiber Summation
• CNS sends a weak signal to contract a muscle -
-- smaller motor units may be stimulated in
preference to the larger motor units.
• strength of the signal increases --- larger and
larger motor units begin to be excited
• size principle
• smaller motor units are driven by small motor
nerve fibers
• small motoneurons in the spinal cord are
more excitable than the larger ones
• different motor units are driven
asynchronously by the spinal cord
• contraction alternates among motor units one
after the other, thus providing smooth
contraction even at low frequencies of nerve
signals
T E TA N I Z AT I O N
•frequency reaches a critical level --- successive
contractions eventually become so rapid fuse
together ---- whole muscle contraction appears
to be completely smooth and continuous
T E TA N Y
•enough calcium ions are maintained in the
muscle sarcoplasm, even between action
potentials, so that full contractile state is
sustained without allowing any relaxation
between the action potentials
Maximum Strength of Contraction
• max strength of tetanic contraction of a
muscle: 3 and 4 kilograms per square
centimeter, or 50 pounds per square inch.
• Quadriceps: up to 16 square inches of muscle
belly, as much as 800 pounds of tension may be
applied to the patellar tendon.
• it is possible for muscles to pull their tendons
out of their insertions in bone.
S TA I R C A S E E F F E C T or T R E P P E
• strength of contraction increases to a plateau
• muscle contract after a long period of rest ----
initial strength of contraction may be as little as
one half its strength 10 to 50 muscle twitches
later.
• Cause: increasing Ca++ in the cytosol because
of the release of more and more ions from the
SR with each successive muscle action potential
and failure of the sarcoplasm to recapture the
ions immediately.
Skeletal Muscle Tone
•amount of tautness that remains in a muscle
at rest
•results entirely from a low rate of nerve
impulses coming from the spinal cord or ms
spindle
Muscle Fatigue
•Prolonged and strong contraction of a muscle
•increases in almost direct proportion to the
rate of depletion of muscle glycogen.
•inability of the contractile and metabolic
processes of the muscle fibers to continue
supplying the same work output.
Muscle Fatigue
• transmission of the nerve signal through the
NMJ diminish at least a small amount after
intense prolonged muscle activity, thus further
diminishing muscle contraction.
• Interruption of blood flow through a
contracting muscle leads to almost complete
muscle fatigue within 1 or 2 minutes because of
the loss of nutrient supply, especially the loss of
oxygen.
Muscle Hypertrophy and Muscle Atrophy
Muscle Atrophy
• rate of degradation of the contractile proteins
is more rapid than the rate of replacement
• ATP-dependent ubiquitin-proteasome
pathway
• Proteasomes -- large protein complexes that
degrade damaged or unneeded proteins by
proteolysis, a chemical reaction that breaks
peptide bonds.
• Ubiquitin is a regulatory protein that basically
labels which cells will be targeted for
proteosomal degradation.

Adjustment of Muscle Length
• Another type of hypertrophy occurs when
muscles are stretched to greater than normal
length.
• stretching --- new sarcomeres added at the
ends of the muscle fibers, where they attach to
the tendons.
• muscle remains shortened to less than its
normal length, sarcomeres at the ends of the
muscle fibers can actually disappear.
• It is by these processes that muscles are
continually remodeled to have the appropriate
length for proper muscle contraction.
Muscle Denervation Causes Rapid Atrophy
• When a muscle loses its nerve supply, it no
longer receives the contractile signals that are
required to maintain normal muscle size.
• Therefore, atrophy begins almost
immediately.
• After about 2 months, degenerative changes
also begin to appear in the muscle fibers.
• If the nerve supply to the muscle grows back
rapidly, full return of function can occur in as
little as 3 months, but from that time
onward, the capability of functional return
becomes less and less, with no further return of
function after 1 to 2 years
• In the final stage of denervation atrophy, most
of the muscle fibers are destroyed and replaced
by fibrous and fatty tissue.
• The fibers that do remain are composed of a
long cell membrane with a lineup of muscle cell
nuclei but with few or no contractile properties
and little or no capability of regenerating
myofibrils if a nerve does regrow.
• The fibrous tissue that replaces the muscle
fibers during denervation atrophy also has a
tendency to continue shortening for many
months, which is called contracture
Recovery of Muscle Contraction in
Poliomyelitis
• Poliomyelitis: some nerve fibers to a muscle
are destroyed---remaining nerve fibers branch
off to form new axons that then innervate many
of the paralyzed muscle fibers --- in large motor
units (macromotor units) -- can contain as
many as five times the normal number of
muscle fibers for each motoneuron coming
from the spinal cord.
• The formation of large motor units decreases
the fineness of control one has over the
muscles but does allow the muscles to regain
varying degrees of strength.
Rigor Mortis
• all the muscles of the body go into a state of
contracture several hours after death
• muscles contract and become rigid, even
without action potentials.
• results from loss of all the ATP, which is
required to cause separation of the cross-
bridges from the actin filaments during the
relaxation process.
• The muscles remain in rigor until the muscle
proteins deteriorate about 15 to 25 hours later,
which presumably results from autolysis
caused by enzymes released from lysosomes.
• All these events occur more rapidly athigher
temperatures.
Muscular Dystrophy
• inherited disorders that cause progressive
weakness and degeneration of muscle fibers,
which are replaced by fatty tissue and collagen.
• Duchenne muscular dystrophy (DMD)
• only males because it is transmitted as an
X-linked recessive trait and is caused by a
mutation of the gene that encodes for a protein
called dystrophin, which links actins to proteins
in the muscle cell membrane
• Dystrophin and associated proteins form
an interface between the intracellular
contractile apparatus and the extracellular
connective matrix
Lack of Dystrophin
• muscle cell membrane destabilization
• altered intracellular calcium handling
• impaired membrane repair after injury
• increase in membrane permeability to calcium
--- extracellular calcium ions to enter the
muscle fiber ----- initiate changes in
intracellular enzymes ---- lead to proteolysis and
muscle fiber breakdown

Symptoms of DMD
• muscle weakness: begins in early childhood
and rapidly progresses ---- patients are usually
in wheelchairs by age 12 years -----die of
respiratory failure before age 30 years.

Becker muscular dystrophy (BMD)

• milder form
• mutations of the gene that encodes for
dystrophin
• has a later onset and longer survival
• It is estimated that DMD and BMD affect 1 of
every 5,600 to 7,700 males between the ages of
5 through 24 years.
MUSCLE TISSUE other so that the entire heart contracts as one
unit (called a SYNCYTIUM)
• types of muscle tissue: • smooth ms: single nucleus, has a uniform,
• skeletal, cardiac, and smooth nonstriated

• EXCITABILITY
• plasma membranes can change SKELETAL MUSCLE
their electrical states (from polarized • hold a body upright or balanced in any
to depolarized) position
• keep joints stable
• send an electrical wave called an • protect internal organs
ACTION POTENTIAL • maintenance of homeostasis in the body by
generating heat

• nervous system: influence the excitability of

cardiac and smooth muscle to some degree
• skeletal muscle completely depends on
signaling from the nervous system
• cardiac muscle and smooth muscle can
respond to other stimuli, such as hormones and
local stimuli
• Muscle contraction (shortening) when actin is
pulled myosin
• In striated muscle: exposure of actin binding
sites due to the interaction between calcium
ions (Ca++) and (troponin and tropomyosin)
that “shield” the actin binding sites
• Ca++ : required for the contraction of smooth
muscle
• Ca++ : activate myosin heads
THREE LAYERS OF CONNECTIVE TISSUE
EPIMYSIUM
• sheath of dense, irregular connective tissue
wrapping each ms
• allows a muscle to contract and move
powerfully while maintaining its structural
integrity
PERIMYSIUM
• middle layer of connective tissue enveloping a
muscle fascicle (individual muscle fiber bundles)
ENDOMYSIUM
• encloses each muscle fiber inside each fascicle

• muscles require ATP for contraction, and relax

when Ca++ is removed and the actin-binding
sites are re-shielded.
• muscle can return to its original length when
relaxed : ELASTICITY
• 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
SKELETAL MUSCLE FIBERS
• Greek sarco, which means “flesh.”
• SARCOLEMMA : plasma membrane of muscle
fibers
• SARCOPLASM: cytoplasm
• SARCOPLASMIC RETICULUM : specialized
smooth endoplasmic reticulum, which stores,
releases, and retrieves calcium ions (Ca++)
SARCOMERE
• functional unit of a skeletal muscle fiber
• contractile myofilaments actin (thin filament)
and myosin
(thick filament), along with other support
proteins
• The striated appearance of skeletal muscle
fibers is due to the arrangement of the
myofilaments of actin and myosin in sequential
order from one end of the muscle fiber to the
other
SARCOMERE
• microfilaments and their regulatory proteins,
troponin and tropomyosin
• Z-discs / Z-lines -- actin myofilaments are
anchored; border of the sarcomere
• periodic invaginations in the sarcolemma,
called T-tubules
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
EXCITATION-CONTRACTION COUPLING
• External stimuli --- excite the sarcolemma ---
release of Ca in SR ---- Ca opens actin binding
sites --- myosin heads attach to the actin
binding sites ----- myosin then pulls the actin
filaments toward the center ---- shortening the
muscle fiber ---- action potential
• action potential travels along the axon of a
motor neuron
• Terminate at the NMJ
• axon terminal releases acetylcholine
• ACh diffuse the synaptic cleft
• ACh bind to ACh receptors in the motor end-
plate
• ACh receptor opens and positively charged
ions can pass causing it to depolarize
• voltage-gated sodium channels are triggered
to open
• Sodium ions enter the muscle fiber, and an
action potential rapidly spreads
• it repolarizes, re-establishing the negative
membrane potential
• AChE degrades ACh
 action potential travels along a motor nerve
to its endings on muscle fibers.
 At each ending, the nerve secretes a small
amount of the neurotransmitter substance
acetylcholine
 acetylcholine acts on a local area of the
muscle fiber membrane to open
“acetylcholine gated” cation channels
through protein molecules floating in the
membrane.
 large quantities of sodium ions to diffuse to
the interior of the muscle fiber membrane.
This action causes a local depolarization
that in turn leads to opening of
voltagegated sodium channels, which
initiates an action potential at the
membrane
 AP travels along the muscle fiber
membrane
 AP depolarizes the muscle membrane, and
much of the action potential electricity
flows through the center of the muscle
fiber. Here it causes the sarcoplasmic
reticulum to release large quantities of
calcium ions that have been stored within
this reticulum.
 calcium ions initiate attractive forces
between the actin and myosin filaments,
causing them to slide alongside each other,
which is the contractile process.
 calcium ions are pumped back into the
sarcoplasmic reticulum by a Ca++
membrane pump and remain stored in the
reticulum until a new muscle action
potential comes along
• 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
• T-tubules ---
• carry the action potential into the interior of
the cell ----
• triggers the opening of calcium channels in
the membrane of the adjacent SR ----
• causing Ca++ to diffuse out of the SR and into
the sarcoplasm.
• the arrival of Ca++ in the sarcoplasm ----
• initiates contraction of the muscle fiber
MUSCLE FIBER CONTRACTION AND
RELAXATION
• Ach is released from the motor neuron
• local membrane will depolarize (Na+ enter ----
action potential)
• Depolarize the rest of the membrane
including the T-tubules.
• release of Ca++ from storage in the
sarcoplasmic reticulum (SR).
• The Ca++ then initiates contraction, which is
sustained by ATP

• Muscle contraction stops
• repolarizes the sarcolemma and T-tubules
• closes the voltage-gated calcium channels in
the SR.
• Ca++ ions are then pumped back into the SR
• tropomyosin to reshield (or re-cover) the
binding sites on the actin strands.
• A muscle also can stop contracting when it
runs out of ATP and becomes fatigued
• 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.
• A myofibril is composed of many sarcomeres
running along its length; thus, myofibrils and
muscle cells contract as the sarcomeres
contract.
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.
• TROPOMYOSIN
• protein that winds around the chains
of the actin filament and covers the myosin-
binding sites to prevent actin from binding to
myosin.
• 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 sothat tropomyosin
can slide away from the binding sites on the
actin strands.
• This allows the myosin heads to bind to these
exposed binding sites and form cross-bridges.
• The thin filaments are then pulled by the
myosin heads to slide past the thick
filaments toward the center of the sarcomere.
• But each head can only pull a very short
distance before it has reached its
limit and must be “re-cocked” before it can pull
again, a step that requires ATP.
ATP AND MUSCLE CONTRACTION
• For thin filaments to
continue to slide past
thick filaments during
muscle contraction,
myosin heads must
pull the actin at the
binding sites, detach,
re-cock, attach to more
binding sites, pull,
detach, re-cock, etc.
• This repeated movement
is known as the
cross-bridge cycle
• Cross-bridge formation occurs when the
myosin head attaches to the actin while
adenosine diphosphate (ADP) and inorganic
phosphate (Pi) are still bound to myosin
• Pi is then released, causing myosin to form a
stronger attachment to the actin, after which
the myosin head moves toward the M-line,
pulling the actin along with it.
• As actin is pulled, the filaments move
approximately 10 nm toward the Mline. This
movement is called the power stroke, as
movement of the thin filament occurs at this
step
• In the absence of ATP, the myosin head will
not detach from actin.
• One part of the myosin head attaches to the
binding site on the actin, but the head has
another binding site for ATP.
• ATP binding causes the myosin head to detach
from the actin
• After this occurs, ATP is converted to ADP and
Pi by the intrinsic ATPase activity of myosin.
• The energy released during ATP hydrolysis
changes the angle of the myosin head into a
cocked position
• The myosin head is now in position for further
movement.
• When the myosin head is cocked, myosin is in
a high-energy configuration.
• 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
lowenergy 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.
• 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 replacedquickly to allow for
sustained contraction.
• There are three mechanisms by which ATP
can be regenerated:
• creatine phosphate metabolism,
• anaerobic glycolysis, and
fermentation
• aerobic respiration.
• Creatine phosphate
• is a molecule that can store energy in its
phosphate bonds.
• In a resting muscle, excess ATP transfers its
energy to creatine, producing ADP and creatine
phosphate.
• This acts as an energy reserve that can be
used to quickly create more ATP.
• When the muscle starts to contract and needs
energy, creatine phosphate transfers
its phosphate back to ADP to form ATP and
creatine
• This reaction is catalyzed by the enzyme
creatine kinase and occurs very quickly;
thus, creatine phosphate-derived ATP powers
the first few seconds of muscle contraction.
• However, creatine phosphate can only
provide approximately 15 seconds worth of
energy, at which point another energy source
has to be used
• As the ATP produced by creatine phosphate is
depleted, muscles turn to glycolysis as an ATP
source
• Glycolysis
• is an anaerobic (non-oxygen-dependent)
process that breaks down glucose (sugar) to
produce ATP; however, glycolysis cannot
generate ATP as quickly as creatine phosphate.
• Thus, the switch to glycolysis results in a
slower rate of ATP availability to the muscle.
• The sugar used in glycolysis can be provided
by `or by metabolizing glycogen that is stored in
the muscle
• The breakdown of one glucose molecule
produces two ATP and two molecules of pyruvic
acid, which can be used in aerobic respiration or
when oxygen levels are low, converted to lactic
acid
• If oxygen is available, pyruvic acid is used in
aerobic respiration.
• However, if oxygen is not available, pyruvic
acid is converted to lactic acid, which may
contribute to muscle fatigue.
• This conversion allows the recycling of the
enzyme NAD+ from NADH, which is needed for
glycolysis to continue
• This occurs during strenuous exercise when
high amounts of energy are needed but oxygen
cannot be sufficiently delivered to muscle.
• Glycolysis itself cannot be sustained for very
long (approximately 1 minute of muscle
activity), but it is useful in facilitating short
bursts of high-intensity output.
• This is because glycolysis does not utilize
glucose very efficiently, producing a net gain of
two ATPs per molecule of glucose, and the end
product of lactic acid, which may contribute to
muscle fatigue as it accumulates
AEROBIC RESPIRATION
• is the breakdown of glucose or other nutrients
in the presence of oxygen
(O2) to produce carbon dioxide, water, and ATP.
• Approximately 95 percent of the ATP required
for resting or moderately active muscles is
provided by aerobic respiration, which takes
place in mitochondria.
• The inputs for aerobic respiration include
glucose circulating in the bloodstream, pyruvic
acid, and fatty acids
• is much more efficient than anaerobic
glycolysis, producing approximately
36 ATPs per molecule of glucose versus four
from glycolysis.
• Cannot be sustained without a steady supply
of O2 to the skeletal muscle and is much slower
• 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.
• Imbalances in Na+ and K+ levels as a result of
membrane depolarization may disrupt Ca++
flow out of the SR.
• Long periods of sustained exercise may
damage the SR and the sarcolemma, resulting in
impaired Ca++ regulation.
• Intense muscle activity results in an oxygen
debt, which is the amount of oxygen needed to
compensate for ATP produced without oxygen
during muscle contraction.
• Oxygen is required to restore ATP and
creatine phosphate levels, convert lactic acid to
pyruvic acid, and, in the liver, to convert lactic
acid into glucose or glycogen.
• Other systems used during exercise also
require oxygen, and all of these combined
processes result in the increased breathing rate
that occurs after exercise.
• Until the oxygen debt has been met, oxygen
intake is elevated, even after exercise has
stopped
RELAXATION OF A SKELETAL MUSCLE
• Relaxing skeletal muscle fibers, and
ultimately, the skeletal muscle, begins with the
motor neuron, which stops releasing its
chemical signal, ACh, into the synapse at the
NMJ.
• The muscle fiber will repolarize, which closes
the gates in the SR where Ca++ was being
released.
• ATP-driven pumps will move Ca++ out of the
sarcoplasm back into the SR.
• This results in the “reshielding” of the actin-
binding sites on the thin filaments.
• Without the ability to form cross-bridges
between the thin and thick filaments, the
muscle fiber loses its tension and relaxes.
MUSCLE STRENGTH
• Muscle strength is directly related to the
amount of myofibrils and sarcomeres within
each fiber.
• Factors, such as hormones and stress (and
artificial anabolic steroids), acting on the muscle
can increase the production of sarcomeres and
myofibrils within the muscle fibers, a change
called hypertrophy, which results in the
increased mass and bulk in a skeletal muscle
• decreased use of a skeletal muscle results in
atrophy, where the number of sarcomeres and
myofibrils disappear (but not the number of
muscle fibers).
• 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: isotonic
contractions and isometric contractions.
• isometric contraction
• occurs as the muscle produces tension
without changing the angle of a skeletal joint.
• involve sarcomere shortening and increasing
muscle tension, but do not move a load, as the
force produced cannot overcome the resistance
provided by the load.
• For example, if one attempts to lift a hand
weight that is too heavy, there will be
sarcomere activation and shortening to a point,
and ever-increasing muscle tension, but no
change in the angle of the elbow joint.

• isotonic contractions
• tension in the muscle stays constant
• a load is moved as the length of the
muscle changes (shortens).
• two types of isotonic contractions:
concentric and eccentric.
• concentric contraction
• involves the muscle shortening to
move a load.
• An example of this is the biceps
brachii muscle contracting when a hand weight
is brought upward with increasing muscle
tension.
• As the biceps brachii contract, the
angle of the elbow joint decreases as the
forearmis brought toward the body.
• Here, the biceps brachii contracts as
sarcomeres in its muscle fibers are shortening MOTOR UNITS
and cross-bridges form; the myosin heads pull • The actual group of muscle fibers in a muscle
the actin innervated by a single motor
neuron
• eccentric contraction • SMALL MOTOR UNIT
• occurs as the muscle tension diminishes and • a single motor neuron supplies a small
the muscle lengthens. number of muscle fibers in a muscle.
• In this case, the hand weight is lowered in a • permit very fine motor control of the
slow and controlled manner as the amount of muscle
crossbridges being activated by nervous system • Ex: extraocular eye muscles that move
stimulation decreases. the eyeballs
• In this case, as tension is released from the
biceps brachii, the angle of the elbow joint LARG E MO TOR UNI T
increases. Eccentric contractions are also used • is an arrangement where a single motor
for movement and balance of the body neuron supplies a large number of muscle fibers
in a muscle.
• Large motor units are concerned with simple,
or “gross,” movements, such as powerfully
extending the knee joint.
• Ex: thigh muscles or back muscles
cross-bridges can be formed, and no tension is
produced in that sarcomere.
• This amount of stretching does not usually
occur, as accessory proteins and connective
tissue oppose extreme stretching.

• R ECRUI TM EN T
• This increasing activation of motor units
produces an increase in muscle contraction
• As more motor units are recruited, the muscle
contraction grows progressively stronger.

THE LENGTH-TENSION RANGE OF A

SARCOMERE
• When a skeletal muscle fiber contracts,
myosin heads attach to actin to form cross-
bridges followed by the thin filaments sliding THE FREQUENCY OF MOTOR NEURON
over the thick filaments as the heads pull the STIMULATION
actin, and this results in sarcomere shortening, TWITCH
creating the tension of the muscle contraction. • A single action potential from a motor neuron
• The cross-bridges can only form where thin will produce a single contraction in the muscle
and thick filaments already overlap, so that the fibers of its motor unit.
length of the sarcomere has a direct influence • Myogram: an instrument that measures the
on the force generated when the sarcomere amount of tension produced over time
shortens
• The ideal length of a sarcomere to produce THREE PHASES OF MS TWITCH
maximal tension occurs at 80 percent to 120
percent of its resting length, with 100 percent
being the state where the medial edges of the
thin filaments are just at the most-medial
myosin heads of the thick filaments
• This length maximizes the overlap of actin-
binding sites and myosin heads.
• 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
GRADED MUSCLE RESPONSE
• Normal muscle contraction is more sustained,
and it 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 while a previous
twitch is still occurring, the second twitch will
be stronger.
• because the excitation-contraction coupling
effects of successive motor neuron signaling is
summed, or added together
INCOMPLETE TETANUS
• If the frequency of motor neuron signaling
increases, summation and subsequent muscle
tension in the motor unit continues to rise until
it reaches a peak point
• The tension at this point is about three to four
times greater than the tension of a single twitch
• muscle goes through quick cycles of
contraction with a short relaxation phase for
each.
TETANUS
• If the stimulus frequency is so high that the
relaxation phase disappears completely,
contractions become continuous
• the concentration of Ca++ ions in the
sarcoplasm allows virtually all of the sarcomeres
to form crossbridges and shorten, so that a
contraction can continue uninterrupted (until
the muscle fatigues and can no longer produce
tension).
TREPPE
• When a skeletal muscle has been dormant for
an extended period and then activated to
contract, with all other things being equal, the
initial contractions generate about one-half the
force of later contractions.
• muscle tension increases in a graded manner
that to some looks like a set of stairs.
• muscle contractions become more efficient
• results from a higher concentration of Ca++ in
the sarcoplasm resulting from the steady
stream of signals from the motor neuron. It can
only be maintained with adequate ATP
MUSCLE TONE
- Skeletal muscles are rarely completely
relaxed, or flaccid.
- Even if a muscle is not producing
movement, it is contracted a small
amount to maintain its contractile
proteins
- The tension produced by muscle tone
allows muscles to continually stabilize
joints and maintain posture.
HYPOTONIA
•absence of the low-level contractions that lead
to muscle tone
•Cause: damage to CNS, such as the
cerebellum, or from poliomyelitis.
•flaccid appearance
•functional impairments, like weak reflexes
HYPERTONIA
•excessive muscle tone
•accompanied by hyperreflexia
•damage to upper motor neurons in the CNS
•muscle rigidity (as seen in Parkinson’s disease)
or spasticity, a phasic change in muscle tone,
where a limb will “snap” back from passive
stretching (as seen in some strokes)
TYPES OF MUSCLE FIBERS
FAST GLYCOLYTIC (FG) FIBERS
•have fast contractions
•primarily use anaerobic glycolysis
•fatigue more quickly than the others
- Most skeletal muscles in a human
contain(s) all three types, although in
varying proportions.
- The speed of contraction is dependent
on how quickly myosin’s ATPase
hydrolyzes ATP to produce cross-bridge
action.
- Fast fibers hydrolyze ATP approximately
twice as quickly as slow fibers, resulting
in much quicker cross-bridge cycling
(which pulls the thin filaments toward
the center of the sarcomeres at a faster
rate).
The primary metabolic pathway used by a
muscle fiber determines whether the fiber is
classified as oxidative or glycolytic.
If a fiber primarily produces ATP through
aerobic pathways it is oxidative.
•More ATP can be produced during each
metabolic cycle, making the fiber more
resistant to fatigue.
Glycolytic fibers primarily create ATP through
anaerobic glycolysis, which produces less ATP
per cycle.
•As a result, glycolytic fibers fatigue at a
quicker rate
OXIDATIVEFIBERS
• contain more mitochondria than the glycolytic
fibers
• aerobic metabolism, uses O2,occurs in the
mitochondria
• SO fibers -- capable of contracting for longer
periods
• large amount of ATP produced
• small diameter &don’t produce large amount
of tension
• SO fibers -- supplied with blood capillaries to
supply O2 from the red blood cells in the
bloodstream.
• SO fibers -- myoglobin, an O2-carrying
molecule similar to
O2-carrying hemoglobin in the red blood cells
SO Fibers
•can function for long periods without fatiguing
•maintaining posture
•producing isometric contractions
•stabilizing bones and joints
•making small movements that happen often
but do not require large amounts of energy
•do not produce high tension
•not used for powerful, fast movements that
require high amounts of energy and rapid cross-
bridge cycling
FO fibers
•intermediate fibers
• characteristics intermediate between fast
fibers and slow fibers
•produce ATP relatively quickly
•produce high amounts of tension.
•produce ATP aerobically
•possess high amounts of mitochondria
•do not fatigue quickly
FO fibers
•do not possess significant myoglobin
•lighter color than the red SO fibers.
•used primarily for movements
•walking
•produce more tension than SO fibers
•more fatigue-resistant than FG fibers.
Fast glycolytic fibers
•primarily use anaerobic glycolysis as their ATP
source
•large diameter
•possess high amounts of glycogen
•used in glycolysis to generate ATP quickly to
produce high levels of tension
Fast glycolytic fibers
•do not primarily use aerobic metabolism
•do not possess substantial numbers of
mitochondria or significant amounts of
myoglobin
•white color
•produce rapid, forceful contractions to make
quick, powerful movements.
•fatigue quickly, permitting them to only be
used for short period
ENDURANCE EXERCISE
- Slow fibers are predominantly used –
- require little force but involve
numerous repetitions
- aerobic metabolism used by slow-
twitch fibers allows them to maintain
contractions over long periods.
- Endurance exercise can also increase
the amount of myoglobin in a cell, as
increased aerobic respiration increases
the need for oxygen
- Myoglobin is found in the sarcoplasm
and acts as an oxygen storage supply
for the mitochondria.
- The training can trigger the formation
of more extensive capillary networks
around the fiber, a process called
ANGIOGENESIS, to supply oxygen and
remove metabolic waste.
- To allow these capillary networks to
supply the deep portions of the muscle,
muscle mass does not greatly increase
in order to maintain a smaller area for
the diffusion of nutrients and gases
- All of these cellular changes result in
the ability to sustain low levels of
muscle contractions for greater periods
without fatiguing.
- The proportion of SO muscle fibers in
muscle determines the suitability of
that muscle for endurance, and may
benefit those participating in endurance
activities.
- Postural muscles have a large number
of SO fibers and relatively few FO and
FG fibers, to keep the back straight
RESISTANCE EXERCISE
- require large amounts of FG fibers to
produce short, powerful movements
that are not repeated over long periods.
- The high rates of ATP hydrolysis and
cross-bridge formation in FG fibers
result in powerful muscle contractions.
- Muscles used for power have a higher
ratio of FG to 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 the addition of structural
 proteins, athletes trying to build muscle
mass often ingest large amounts of
protein.
PERFORMANCE-ENHANCING
SUBSTANCES
ANABOLIC STEROIDS
•boost muscle mass and increase power output
•TESTOSTERONE
•male sex hormone
•stimulates muscle formation
•increased muscle mass
ERYTHROPOIETIN (EPO)
• boost the availability of oxygen to muscles to
increase aerobic respiration
• produced in the kidneys
• triggers the production of red blood cells
• The extra oxygen carried by these blood cells
can then be used by muscles for aerobic
respiration
HUMAN GROWTH HORMONE (hGH)
• it can facilitate building muscle mass
• main role is to promote the healing of muscle
and other tissues after strenuous exercise.
• allow for faster recovery after muscle damage
• reducing the rest required after exercise
• allowing for more sustained high-level
performance.
CREATINE PHOSPHATE
• provides quick bursts of ATP to muscles in the
initial stages of contraction.
• produce more
• increase explosive power output
• its effectiveness as a supplement has been
questioned
CARDIAC MUSCLE TISSUE
- pump blood into the vessels of the
circulatory system.
- striated and organized into sarcomeres
- shorter than skeletal muscle fibers
- usually contain only one centrally
located nucleus
- possess many mitochondria and
myoglobin
- ATP is produced primarily through
aerobic metabolism
INTERCALATED DISC
• allows the cardiac muscle cells to
contract in a wavelike pattern so that
the heart can work as a pump
• Connects one cardiac ms fiber to
another
• are part of the sarcolemma
• contain two structures important in
cardiac muscle contraction: gap
junctions and desmosomes
GAP JUNCTION
• forms channels between adjacent
cardiac muscle fibers
• allow the depolarizing current to flow
from one cardiac muscle cell to the next
• This joining is called electric coupling
• allows the quick transmission of
action potentials and the coordinated
contraction of the entire heart
• This network of electrically connected
cardiac muscle cells creates a functional
unit of contraction called a
SYNCYTIUM
DESMOSOMES
•anchors the ends of cardiac muscle fibers
together
•cells do not pull apart during the stress of
individual fibers contracting
PACEMAKER CELLS
•specialized cardiac muscle cells
•directly control heart rate.
•respond to signals from the autonomic
nervous system (ANS) to speed up or slow down
the heart rate.
•can also respond to various hormones that
modulate heart rate to control blood pressure
Plateau
•is produced by Ca++ entry though voltage-
gated calcium channels in the sarcolemma of
cardiac muscle fibers.
•provides for a longer contraction than is
produced by an action potential in skeletal
muscle.
•Unlike skeletal muscle, a large percentage of
the
Ca++ that initiates contraction in cardiac
muscles comes from outside the cell rather than
from the SR.
SMOOTH MUSCLE
- cells do not have striations
- Walls of hollow organs: urinary bladder,
uterus, stomach, intestines
- walls of passageways: arteries and veins
- tracts of the respiratory, urinary, and
reproductive systems
- Eyes: functions to change the size of the
iris and alter the shape of the lens
- Skin: hair to stand erect in response to
cold temperature or fear
Smooth muscle fibers
•spindle-shaped
•single nucleus
•Size: 30 to 200 μm
•produce their own connective tissue,
endomysium
•do not have striations and sarcomeres
DENSE BODY
•is analogous to the Z-discs of skeletal and
cardiac muscle fibers
•is fastened to the sarcolemma
•Ca++ are supplied by the SR in the fibers and
by sequestration from the extracellular fluid
through membrane indentations called
CALVEOLI
CALMODULIN
•regulatory protein
•smooth muscle cells do not contain troponin
•cross-bridge formation is not regulated by the
troponin-tropomyosin complex
•external Ca++ ions passing through opened
calcium channels in the sarcolemma, and
additional Ca++ released from SR, bind to
calmodulin.
- The Ca++-calmodulin complex then
activates an enzyme called myosin (light
chain) kinase, which, in turn, activates
the myosin heads by phosphorylating
them (converting ATP to ADP and Pi,
with the Pi attaching to the head).
- The heads can then attach to actin-
binding sites and pull on the thin
filaments.
DENSE BODIES
•where thin filaments are anchored
•the structures invested in the inner membrane
of the sarcolemma (at adherens junctions) that
also have cord-like intermediate filaments
attached to them.
•When the thin filaments slide past the thick
filaments, they pull on the dense bodies,
structures tethered to the sarcolemma, which
then pull on the intermediate filaments
networks throughout the sarcoplasm.
•This arrangement causes the entire muscle
fiber to contract in a manner whereby the ends
are pulled toward the center, causing the
midsection to bulge in a corkscrew motion
• smooth muscle contraction relies on the
presence of Ca++ ions, smooth muscle fibers
have a much smaller diameter than skeletal
muscle cells.
• T-tubules are not required to reach the
interior of the cell and therefore not necessary
to transmit an action potential deep into the
fiber.
• Smooth muscle fibers have a limited calcium-
storing SR 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.
• However, a low concentration of calcium
remains in the sarcoplasm to maintain muscle
tone.
• This remaining calcium keeps the muscle
slightly contracted, which is important in certain
tracts and around blood vessels.
• Because most smooth muscles must function
for long periods without rest, their power
output is relatively low, but contractions can
continue without using large amounts of
energy.
• Some smooth muscle can also maintain
contractions even as Ca++ is removed and
myosin kinase is inactivated/dephosphorylated.
• This can happen as a subset of cross-bridges
between myosin heads and actin, called latch-
bridges
• keep the thick and thin filaments linked
together for a prolonged period, and without
the need for ATP.
• maintaining of muscle “tone” in smooth
muscle that lines arterioles and other visceral
organs with very little energy expenditure.
• Smooth muscle is not under voluntary control;
thus, it is called involuntary muscle.
Smooth muscle is organized in two ways:
- single-unit smooth muscle
•more common
- Multiunit smooth muscle
Single-unit muscle
• muscle fibers joined by gap junctions
• muscle contracts as a single unit.
• found in the walls of all visceral organs except
the heart
• 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
contents prematurely
• produces slow, steady contractions that allow
substances, such as food in the digestive tract,
to move through the body
Multiunit smooth muscle cells
•rarely possess gap junctions
•are not electrically coupled.
•contraction does not spread from one cell to
the next
•confined to the cell that was originally
stimulated.
•Stimuli for multiunit smooth muscles come
from autonomic nerves or hormones but not
from stretching.
•This type of tissue is found around large blood
vessels, in the respiratory airways, and in the
eyes.
HYPERPLASIA IN SMOOTH MUSCLE
- smooth muscle can undergo
hypertrophy to increase in size
- smooth muscle can also divide to
produce more cells (HYPERPLASIA)
- uterus at puberty -- responds to
increased estrogen levels by producing
more uterine smooth muscle fibers, and
greatly increases the size of the
myometrium
DEVELOPMENT AND REGENERATION OF
MUSCLE TISSUE
- Origin: embryonic mesoderm
- Skeletal ms, excluding those of the head
and limbs: mesodermal somites
- skeletal ms in the head and limbs
develop from general mesoderm
MYOTUBE
•is formed from many different myoblast cells
•it contains many nuclei, but has a continuous
cytoplasm
•skeletal ms cells: multinucleate
•the nucleus of myoblast remains intact
•cardiac and smooth muscle cells are not=
multinucleate because the myoblasts that form
their cells do not fuse

SATELLITE CELL
•similar to a myoblast
•because it is a type of stem cell
•are incorporated into muscle cells
•facilitate the protein synthesis required for
repair and growth
•located outside the sarcolemma
•stimulated to grow and fuse with muscle cells
by growth factors that are released by muscle
fibers under certain forms of stress
•can regenerate muscle fibers to a very limited
extent
•primarily help to repair damage in living cells
•If a cell is damaged to a greater extent than
can be repaired by satellite cells, the muscle
fibers are replaced by scar tissue in a process
called fibrosis.
•scar tissue cannot contract, muscle that has
sustained significant damage loses strength and
cannot produce the same amount of power or
endurance as it could before being damaged

PERICYTE
•found in some small blood vessels
•allow smooth muscle cells to regenerate
•cardiac muscle does not regenerate to a great
extent
•Dead cardiac muscle tissue is replaced by scar
tissue, which cannot contract
•As scar tissue accumulates, the heart loses its
ability to pump because of the loss of
contractile power.
MUSCULAR SYSTEM 1 ◦ Widespread expansion over a sizable area, but
then te fascicles come to a single,
• Tendons - strong bands of dense, regular common attachment point
connective tissue that connect muscles to • Pennate muscles
bones ◦ Like a feather
• Insertion - moveable end of the muscle, ◦ Blend into a tendon that uns through the
example biceps brachii central region of the muscle for its whole
• Origin - fixed (stabilized) end, ex: head of length,
humerus • Unipennate muscle
Roles of Muscles ◦ Fascicles are located on one side of the tendon
• Prime Mover/ Agonist • Bipennate muscle
- main muscle responsible for producing a ◦ 2 pennate muscles
specific movement of the body • Multipennate
- principal muscle involved ◦ More than 2• Flat muscles
• Antagonist ◦ Parallel fibers often with an aponeurosis
- muscle tat opposes the action of another ◦ External oblique (broad flat muscle)
muscle ◦ Sartorius is a narrow flat muscle with parallel
- roles: fibers
- maintain body o limb position • Pennate muscles
- control rapid movement or the ability to ◦ Feather-like
• Fixator ◦ Extensor digitorum longus (unipennate)
- steadies the proximal parts of a limb through ◦ Recluse femur is (bipennate)
isometric contraction while movement ◦ Deltoid (multipennate)
• Synergist • Fusiform
- assist the prime mover ◦ Spindle-shaped w/ a round, thick belly and
MS tissue tapered ends
• Epimysium ◦ Biceps brachii
- covers the entire muscle • Convergent
• Perimysium ◦ Arise from a broad area and converge to form
- covers the muscle fascicle group of bundled a single tendon
• Endomysium ◦ Pectoralis major
- innermost • Quadrate muscles
Muscle Shape & Fiber Arrangement ◦ Have four equal sides
• Parallel muscles ◦ Rectus abdominis
◦ Fascicles arranged in te same direction as the • Circular or sphincteral muscles
long axis of te muscle ◦ Surround a body opening or orifice,
• Belly constricting it when contracted
◦ Plump large mass of tissue in te middle of the ◦ Orbicularis oculi
muscle • Multiheaded or multibellied
• Fusiform ◦ More than one head of attachment
◦ Has a central large belly that is spindle-shaped ◦ Biceps muscles have two heads (biceps
• Circular muscles (sphincters) brachii)
◦ Surround the oraphyses ◦ Triceps muscles have tree heads (triceps
◦ Relax: increase the size of the opening brachii)
◦ Contract: size of the opening shrinks to the ◦ Digastric and gastrocnemius have two bellies
point of closure Muscle of Facial Expression
• Convergent • orbicularis oris - circular, mouth (act as a
sphincter)
• Orbicularis oculi - • Genioglossus - from genial tubercle of
• Occipitofrontalis - has two bellies; mov the mandible
forehead back and forth • Styloglossus - coming from the styloid process
◦ Epicranial aponeurosis or galea aponeurotica/ • Hyoglossus - from hyoid bone
aponeurosis • Palatoglossus - attaches to the soft palate
• buccinator - whistle, blow, suck Intrinsic
• Corrugator supercilii - prime mover of the • Superior longitudinal
eyebrows, surprised and frowning • Inferior longitudinal
• Risorius muscle - fake smile • Transverse
• Zygomaticus major muscle - true smile • Vertical
• Mentalis muscle - pouting MS of the Anterior Neck
• All muscles done(?) by the cranial nerve • Sternocleidomasteoid - boundary sa triangle
• Platysma - tension • Platysma
MS which surrounds the eyes • Inferior belly of omohyoid - divides the
• Levator palpebrae superioris - open or close occipital triangle
eyelids • Digastric triangle
• Superior oblique - attach to the trochlea MS that move the head
(pulley) • Romboid major
• Lateral rectus - • Romboid minor
• Inferior rectus - • Levator scapulae - attach to the scapula
• Medial rectus - near to the nose • Splenius capitis - attach to the occipital area
• Extrinsic muscle of the eye - supplied by the • Splenius cervicis - attach to the neck
oculomotor nerve except superior oblique • Sternocleidomastoid
muscle & lateral rectus muscle • Semispinalis capitis - rotate the end
• (LAST) lateral rectus = abducens ; Superior • Splenius capitis
oblique muscle trochleaMS that move the lower • Longissimus capitisMS of the posterior neck &
jaw back
Muscles of mastication (chewing) • Erector spinae (ILS)
• Masseter - lower the temporalis ◦ Iliocostalis lumborum -
• Temporalis - covering the temporal bone ; ◦ Longissimus thoracis
convergence muscle ◦ Spinalis thoracis - median group
• Lateral pterygoid - • Multifidus -
• Medial pterygoid - bigger MS of the Abdomen
MS of the neck • External obliques - fibers are going
Suprahyoid - presence/ attach the upper of downwards / inward
hyoid bone ; upper part • Internal obliques - pointing up / outward
• Digastric - has two; anterior and posterior • Transversus abdominus - straight
• Stylohyoid • Rectus abdominus - form the packs
• Mylohyoid • Tendinous intersection - divide
• Geniohyoid
Infrahyoid
• Thyrohyoid
• Omohyoid (upper belly)
• Sternohyoid
• Sternothyroid
MS that move the tongue (glossus)
Extrinsic
MUSCULAR SYSTEM 2 • Latissimus dorsi - fibers fan out then to be
Muscles of the Thoracic wall inserted to the humerus
• Serratus posterior superior -superficial Deep
• Serratus posterior inferior - superficial • levator scapulae - superior to the rhomboid ;
• Levator costarum - to elevate the ribs esp origin superior angle of scapula
during respiration • Rhomboid - spine of scapula divides
• External intercostal - most superficial, going ◦ Rhomboid minor - more superior
down fibers, until lateral and not go beyond the ◦ Rhomboid major - attaches to the spinous
costal cartilage process• Supraspinatus - above the spine of the
• Internal intercostal - fibers going up scapula
• Innermost intercostal - vertical fibers • Infraspinatus - below the spine
• Subcostal • Teres minor
• Transversus thoracis - ms traverses • Teres major - lower boarder
horizontally • Subscpularis
• diaphragm - major muscle for respiration Intrinsic shoulder ms
◦ Respiratory diaphragm - dome-shaped, • Deltoid - produces the concavity of the
separates abominal cavity from respiratory shoulder
-3 opening: • Supraspinatus
- t (8) • Infraspinatus
- e (10 • Teres minor - inferior to the
- a (12) • teres major - origin: inferior angle of the
◦ pelvic diaphragm - scapula then attach to the humerus
MS of te Pelvic Floor • Subscapularis
• Obturator intermus - lateral wall Rotator cuff muscles (SITS)
• Piriformis - posterior-superior wall • Supraspinatus
• Coccygeus - floor • Infraspinatus
• Levator - floor • Teres minor
◦ Pubococcygeus • Subscapularis
◦ Iliococcygeus MS that positions the pectoral girdle
◦ • Serratus anterior
• Pelvic diaphragm = Levator ani + Coccygeus • Pectoralis minor
• Levator ani = Pubococcygeus + Iliococcygeus • Trapezius
• Pubococcygeus = Puborectalis + Pubovaginalis • Rhomboids minor &major
(female) • Subclavius
• Pubococcygeus = Puborectalis + MS that move the humerus
Puboprostaticus (male) • pectoralis major
Anterior axio-appendicular MS - attach • Latissimus dorsi
• Pectoralis Major - originate in the clavicle, fan- • Deltoid
like • Subscapularis
• Pectoralis Minor - origin in coracoid process of • Supraspinatus
scapula • Infraspinatus
• Subclavicus - underneath the clavicle • Teres major
attaching the first rib • Teres minor
• Serratus anterior - • Coracobra chialis
Posterior axio-appendicular ms MS that move the forearm (antebrachium)
&scapulohumeral -significance of palmaris longus
Superficial • Brachioradialis - most lateral muscles
• Trapezius •
• common flexor tendon • Thenar muscles - forms the muscle group in
◦ Pronator teres the hand
◦ Flexor carpi radials ◦ Opponens pollicis
◦ Palmaris longus ◦ Abductor pollicis brevis◦ Flexor pollicis brevis
◦ Flexor carpi ulnaris ◦ Superficial head
Superficial ◦ Deep head
• Pronator• Flexor carpi radialis ◦ Adductor pollicis
• Palmaris longus • Hypothenar - inferior to the little finger
• Flexor ◦ Abductor digiti minimi
Intermediate ◦ Flexor digiti minimi brevis
• Flexor digitorum superficialis ◦ Opponens digiti
Deep • Short muscles
• FDP ◦ Lumbricals
• FPL ‣1 - come from the medial part of the tendon
• Quadrants ‣2
MS OF POSTERIOR COMPARTMENT ‣3 - come from the medial and lateral
Superficial ‣4
• Brchioradialis ◦ Dorsal intercossei (4) - bipennate; adjacent to
• Extensor carp radialis longus two metacarpals
• Extensor carpi radialis brevis ◦ Palmar intercossei (3) - unipennate
• Abductor policies longus MS in te lower limb
Deep Anterior Thigh MS : Flexors of the hip joint
• Supinator • Pectineus
• Extensor pollicis brevis • Iliopsoas - found i the pelvic cavity
• Abductor pollicis ◦ Psoas major - bulkier
= mini - fingers ◦ Psoas minor - on top of psoas major, small or
= pollicis - thumb thin belly,
MS of Arm • illiacus -
Anterior - flexion • Sartorius - tailor’s ms, come from anterior-
• Biceps brachii - inferior spine then inserted to the tibia
◦ Long head - lateral Anterior
◦ Short head - medial Extensors of te knee joint
• Coracobrabrachialis - • Quadriceps femoris
• Brachialis - found under the cover of biceps ◦ Rectus femoris - most superficial, straight ms
brachii ◦ Vastus lateralis -
Posterior - extension ◦ Vastus medialis - under the vastus intermedius
• Triceps brachii ◦ Vastus intermedius - under the rectus femoris
◦ Medial Adductors of the thigh
◦ Lateral • Adductus longus - longer
◦ Long-head • Adductor brevis
• Anconeus - not part of the arm • Adductor magnus - most superficial
Posterior : ◦ Hamstring part
• biceps brachii ◦ Adductor part
• Coraco • Gracilis - lines the medial aspect of the thigh,
• Brachialis starts at the pubis then to be inserted to the
MS that move the wrist, hand fingers tibia
Intrinsic MS of the hand • Obturator externus
• Pes anserinus - be seen like the web of the Deep MS: posterior compartment of the leg
goose, made up of: • Popliteus - below the knee caps
◦ Sartorius • flexor hallucis longus
◦ Semitendinosus • Flexor digitorum longus
◦ Gracilis • Tibialis posterior
Gluteal and posterior thigh region
Gluteal region: - abduct and rotate the thigh
area• Gluteus Maximus - big, powerful ms
• Gluteus Medius - underneath the gluteus
Maximus
• Gluteus minimus - innermost gluteal muscle
• tensor fascia
• Piriformis - cyatic nerve can be found, found
inferior to the gluteus minimus
◦ Piriformis syndrome
• Obturator internus
• Inferior gemellus
• Superior gemellus
• Tensor fasciae Latae
• Iliotibial tract - tendon of the tensor fasciae
latae
MS of posterior thigh area: extensors of hip and
flexors of knee
hamstring muscles: posterior part of thigh area
• Semitendinosus - most superficial, tendons
can be found
• Semimembranosus - underneath the
semitendinosus, most muscular
• Biceps femoris - lateral aspect of te posterior
part of te thigh
MS of the anterior & lateral of the leg
lateral compartment:
• Fibularis longus -
• Fibularis brevis - underneath the fibularis
longus
Anterior compartment
• Tibialis anterior - palpate for the shin,
responsible for cramps if you’re untrained
• extensor digitorum longus
• Fibularis tertius - attaches to foot
• tensor hallucis longus
Superficial MS
• Gastrocnemius - taper down and then
inserted to the heel bone, calcaneal tendon
◦ Medial head
◦ lateral head
• Soleus - underneath the gastrocnemius
• Plantaris - plantaris tendon (freshmen nerve)