MUSCLE

TISSUES
Mrs. OFELIA SOLANO
SALUDAR
Department of Natural Sciences
University of St. La Salle
MUSCLE TISSUE- cells contain contractile proteins which generate
the forces necessary for cellular contraction, and drives movement
within organs and the body as a whole.
 The cellular structure is organized in long units referred to as muscle
fibers, which is an adaptation to its function of contraction.
 The sarcoplasm appears fibrillar due to its contents of myofibrils.
The staining is acidophilic or pinkish due to its affinity to acid stains.
 The cells and fibers are bound together by varying amounts of
areolar CT containing blood vessels and nerves. Their arrangement
allows groups to act together or separately, generating contractile
forces of varying strength.
 Arises from mesodermal mesenchyme through accumulation of
myofilaments & development of special membranous channels &
compartments in the cytoplasm. Exception: iris smooth muscle cells
are ectodermal.
Terminology associated with muscle tissue:
1. Sarcoplasm- acidophilic cytoplasm of muscle cells
and fibers
2. Sarcolemma- cell membrane complex consisting of
an external coating of protein polysaccharide over the
sarcolemma.
3. Sarcosome- granules in the sarcoplasm which is
actually a mitochondrion under EM.
4. Myofibrils- fine threadlike structures in the
sarcoplasm which are responsible for contraction.
Under EM, each myofibril is composed of finer
myofilaments.
5. Sarcomere- a linear unit of muscle contraction
6. Sarcoplasmic reticulum- refers to the ER.
 STRIATED or SKELETAL MUSCLE
DISTRIBUTION: comprise most of the entire musculature of the
body and are attached to the skeletal system.
 Exceptions:
tongue and
the upper
portion of the
esophagus
(striated, but
involuntary
in nature),
 The contrac-
tion is quick,
forceful and
usually under
voluntary control.
ORGANIZATIONAL LEVELS OF SKELETAL MUSCLE
 HISTOLOGICAL VARIANTS

1. The skeletal muscle fiber is the biggest among the 3 types, and
does not branch except in the muscles of the tongue. It has
abundant areolar CT containing blood vessels intervening
between sections of muscle fibers.
2. Fibers making up a single muscle are not uniform in cytological
characteristics, becoming evident only in histochemical
methods:
a. Red muscle (slow fibers)- small dark fibers with relatively
abundant sarcoplasm, fewer myofibrils, rich in mitochondria
and myoglobin, possess a richer blood supply, thicker Z-
lines, and complex profiles of sarcoplasmic reticulum;
contraction is slow and steady; predominant in postural
muscles and limbs.
b. White muscle (fast fibers)- paler fibers of large diameter, abundant
myofibrils, granular sarcoplasm sparse, relatively narrow Z-lines,
simple sarcoplasmic reticulum and sparse mitochondria. They react
with quick, forceful contractions that cannot be sustained for long
periods; predominate in extraocular muscles.
c. Intermediate muscles- dispersed among red and white muscles where
either type predominates.
 The histological criteria to differentiate skeletal muscle from
other fibers are their numerous nuclei located peripherally just
beneath the sarcolemma.
 The sarcolemma has a protein (dystrophin) external coating
with a delicate network of reticular fibers.
 In Duchenne muscular dystrophy, this protein is lacking,
resulting to structural weakness of the sarcolemma; damaged
muscle fibers are replaced by CT and adipose tissue, that
renders patients unable to walk by age 12.
 The sarcoplasm consists of a typical cytoplasmic matrix, the usual
cell organelles and myofibrils characteristic of muscle tissue.
 Due to the high energy demands of contraction, there are abundant,
large mitochondria distributed in longitudinal rows between
myofibrils.
 Lipid droplets, glycogen (depot of energy mobilized during
contraction), and the oxygen-binding protein myoglobin
(necessary for the high oxidative phosphorylation level of the
tissue) are inclusions of the sarcoplasm.
 The interior is occupied by myofibrils, seen as fine dots uniformly
distributed or grouped as polygonal shrinkage artifacts called
Conheim’s area or field.
 Bundles of myofibrils are arranged in characteristic Kollicker’s
columns. They are so placed that the corresponding bands appear
on the same transverse plane across the fiber.
 This arrangement results
in the appearance of
alternating dark (A-
band) and light bands (I-
band) on the fiber.
 The I-band is dissected
by a dark transverse Z-
line or telophragma; the
segment between 2
succeeding Z-lines is
termed a sarcomere
(includes an A-band and
half I-bands on either
side).
 A paler zone, the H-band
(also called intermediate
disk of Hensen)
traverses the center of the
A band.
 In the center of this H-band is a narrow dark line, the M-line or
mesophragma. The major protein of the M-line is creatine kinase
which forms phosphocreatinine required for ATP
synthesis.

 EM reveals that
myofibrils are
composed of
units termed
myo-filaments
responsible for
the observed
cross-striations.
MYOFILAMENTS
Myosin resembles a golf club: its thin shaft is composed of the
LMM (light meromyosin) chain; the heavier head chain
(HMM) has actin and ATP-binding sites for contraction.
 In addition to actin and myosin, 2 other proteins are known to
compose myofilaments: tropomyosin, and troponin.
 Tropomyosin form filaments that run over the actin subunits
alongside the outer edges of the groove between the 2 twisted
actin strands. Troponin is a complex of 3 subunits: TnC binds
calcium ions; TnT strongly attaches to tropomyosin; TnI inhibits
actin-myosin interaction.
The spatial configuration of the 3 troponin subunits on F-actin hides
the binding site of myosin heads
to actin in the uncontracted muscle.
 Independent of the action of actin and myosin are other associated
proteins (nebulin, tropomodulin, myomesin).
 Titin is a third type of filament spanning the distance from the M-
line of the A-band to the Z-disc.
 They are responsible for myofibrillar passive elasticity, and
maintain the central position of thick filaments in the sarcomere.
 The A-band is composed of thick myosin filaments held
together in alignment by slender cross connections at the
middle of the A-band, giving rise to the M-line.
 The thinner actin filaments extend to either direction from the
Z-line, constituting the I-band. They also extend some distance
into the A-band.
 The distance
between their ends
determine the length
of the H-band
which has no actin
filaments (in the
contracted state, the
H-band is almost
absent).
When a muscle contracts, the thin
filaments slide past between the
myosin filaments in the A-band

H-band is narrowed and the Z-

line is drawn closer to the A-
bands which shortens the
myofibril.
 The sarcoplasmic reticulum is the sER of striated muscle cells,
specialized to sequester Ca+2 ions.
 It is a continuous system of membrane-limited sarcotubules extending
throughout the sarcoplasm, forming a close-meshed canalicular network
around each myofibril. It exhibits a repeating pattern of local
differentiation in the sarcomere.
 Longitudinal sarcotubules
over the A and I junctions
are confluent at regular
intervals with pairs of
transverse channels
called terminal cisternae;
pairs of these cisternae
run transversely close to
invaginations of the
sarcolemma, the slender
intermediate T-tubule.
 These 3 tubules form the triads of skeletal muscle. In mammalian
muscle there are 2 triads per sarcomere, situated at the junctions
of each A-band with I-bands.
 The sarcoplasmic reticulum
and the triads of each Z-line
are the submicroscopic
structures involved in the
inward spread of activation.
 Two proteins have been
isolated that are involved in
signal transduction: an
1800kD protein binds
ryanodine, a plant alkaloid
that release calcium from the
sarcoplasmic reticulum; a
212kD protein binds 1,4
dihydroxypyridine, a voltage
dependent blocker of Ca+2
channels.
 PHYSIOLOGY OF SKELETAL MUSCLE
CONTRACTION
 When a muscle is stimulated, the sarcoplasmic reticulum
releases calcium ions which changes the configuration of
the actin-troponin-tropomyosin complex, exposing the
myosin-binding site on actin.
 The bending of the myosin head pulls the actin past the
myosin filament.
 The force responsible for this sliding filament theory of
contraction is the breakdown of ATP by myosin ATPase
localized in the cross bridges.
 When ATP is not available, actin-myosin binding
becomes stabilized (rigor mortis is the muscular rigidity
that occurs shortly after death).
http://highered.mcgraw-hill.c
om/olc/dl/120104/bio_b.swf
 INNERVATION

1. Motor (efferent)- the axons of motor neurons whose cell bodies

lie in the spinal cord, branch and form myoneural junctions
(motor-end plate) with several muscle fibers.
 Motor unit consists of one motor neuron and all the muscle
fibers it innervates. The number and size of motor units, as
well as the control of the firing frequency of the activated
units determine the intensity of a muscle contraction.
 Motor-end plate appears as an arborization of the axon
terminal closely apposed to the muscle fiber surface. In EM,
each small axon lies in a groove on the surface of the muscle
fiber showing a profuse folding of the sarcolemma.

http://highered.mcgraw-hill.com/olc/dl/120107/bio_c.swf
 The specialization beneath the axon terminal is termed the
subneural apparatus.
 Within the axon terminal are seen the synaptic vesicles (source of
neurotransmitters, e.g. acetylcholine), and abundant mitochondria.
 The depolarization at the motor-end plate is propagated into the
fibers via the transverse tubule system.
 At each triad, the depolarization causes the release of Ca +2, which
initiates the contraction cycle.
 When it ceases, calcium is actively transported back to the
sarcoplasmic reticulum cisterna, TnC returns the TnI to a position in
which it inhibits binding of the myosin head to actin, and the
muscle relaxes.
 Myasthenia gravis or muscular dystrophy is a progressive
muscular weakness caused by a reduction in acetylcholine receptors
in the myoneural junction.
2. Sensory (afferent)- the sensory end organ is a neuro-muscular
spindle lying in the perimysium, closely attached to a fasciculus,
and running parallel to the surface.
 It consists of a CT capsule within which lie striated intrafusal
muscle fibers. The main afferent annulo-spiral nerve endings
coil around these fibers. Intrafusal fibers, which function as stretch
or proprioreceptors, also receive motor input from gamma
afferents.
 Some muscles taper off at their
extremities, where a myotendinous
junction is formed. In this region,
collagen fibers of the tendon insert
themselves into complex infoldings
of the plasmalemma of the muscle
fibers.
 The nerve endings supplying the
junction are the encapsulated
tendon organs or Golgi tendon
organs which detect changes in
muscle tension. An intense response
of the tendon organ inhibits muscle
contraction that can develop into
potentially destructive excessive
tension.
 REGENERATION

 Skeletal muscle increases in volume

(hypertrophy) by enlargement of existing
fibers through an increase in the amount of
sarcoplasm but not in the number of fibrils
(hyperplasia); atrophy of disuse results to
thinner fibers.
 After destruction, myoblast-like stem cells
form new myofibrils from normally
quiescent satellite cells which are apposed
with the surface of mature muscle fibers.
Large defects are replaced by a CT scar.
 For successful regeneration, connection
with motor nerves is necessary.
 CARDIAC MUSCLE
DISTRIBUTION- found only in the myocardium of
the heart, and in the walls of the large vessels joining
the heart like the aorta, vena cava and the pulmonary
vessels. Contraction is involuntary, vigorous and
rhythmic.
 HISTOLOGICAL CHARACTERISTICS
 In l.s., cardiac muscle fiber is long and branching, smaller than
skeletal muscle, but also appears to be cross-striated.
 The dark stripe (A or Q-band) is anisotropic; the light band (I or
J-
band) is
clear and
isotropic.

 Each
myofibril
contains
actin and
myosin
filaments.
 The myofibrils diverge around the single, centrally placed
nucleus in the interior of the cell.
 They are arranged in parallel bundles; a small amount of
sarcoplasm separates each bundle.
 Unlike skeletal
muscle, there
are lesser
amounts of
areolar CT,
though richly
supplied
with
small blood
vessels and
nerve
plexuses.
 The fibers are not syncytial but are made up of separate
cellular units joined by the intercalated discs, a unique
characteristic of cardiac muscle. They occupy the Z-line of
the I-band.
 These discs are heavy, step-like transverse lines as seen in
iron-hematoxylin stains. EM studies show that they
are junctional
complexes
(desmosomes,
zonula adherens/
zonula
occludens,

gap junctions) of
apposing
plasmalemma.
 They are anchoring sites for actin filaments and bind
cardiac cells together to prevent their separation during
contraction cycles.
 Gap junctions permit a rapid spread of excitation from
cell to cell, hence cardiac muscle appear to function as a
syncytium.
 The sarcoplasm has interstitial granules or granules of Kollicker
seen under LM as muscle granules of glycogen, fat, albumin,
lipofuscin, pigment and mitochondria.
 The latter contain closely-packed cristae with a zig-zag appearance.
It is richer in glycogen than that of skeletal muscle.
 The sarcoplasmic reticulum is not as highly developed but more
numerous and larger than those in skeletal muscle.
 Instead of triads, these simple plexiform arrangement of tubular
elements with no terminal cisternae are composed only of dyads
(T-tubule and 1 sarcoplasmic reticulum).
 Aside from their role of coupling excitation to contraction, these
channels are additional surfaces for exchange of metabolites
between muscle and extracellular space.
 The TATS
(transverse-
axial-tubular)
system occur
only over the Z-
lines of the ends
of sarcomeres.
 They wander
irregularly
through the
myofilaments,
hence discrete
bundles are not
present.
 Despite differences in structure, the composition and arrangement
of myofilaments are similar in skeletal and cardiac muscle; hence
their contraction are essentially
the same at the cellular level.
 Atrial muscle has fewer T-tubules
than ventricular muscles.
 Membrane-limited granules are
found in the atria, containing
precursors of cardiodilatins (CDD)
or atrial natriuretic polypeptides
(auriculin or atriopeptin).
 This hormone causes vaso-
dilatation, lowering blood pressure
and decreased blood volume; EM of an atrial muscle cell
opposes the sodium and water showing the presence of
conservation actions of natriuretic granules
aggregated at the nuclear
aldosterone and ADH.
pole.
 SPECIALIZED CONDUCTING TISSUE OF THE HEART
Lesions in the following may
cause asychrony in the timing of
atrial & ventricular contraction
resulting in impaired efficiency of
the heart.
1. Sinoatrial node (node of
Keith
and Flack or “pace- maker”)-
located beneath
the
epicardium at the junction of
the superior vena cava and the
right atrium. These are striated,
slender, fusiform fibers that are
continuous with atrial muscle
fibers.
2.Internodal tracts- connect
the sinoatrial and
atrioventricular nodes
3.Atrioventricular node-
situated in the lower part of
the interatrial septum

A merry
heart doeth
good like a
medicine.
4.Atrioventricular bundle
(neuromuscular bundle or
bundle of His)- located
beneath the pericardium and
composed of muscular
elements called Purkinje
fibers.
 They penetrate the ventricular
myocardium and come in
contact with ordinary muscle
fibers at their ends, where
they appear to lose their
specific cytological features.
 They are bigger, shorter, less branched with fewer nuclei,
myofibrils, stripes, and a relatively greater amount of
sarcoplasm which has abundant glycogen and mitochondria.
 Few intercalated discs are found, but there are numerous
desmosomes and gap junctions.
INNERVATION- heartbeat is myogenic, but modulated by ANS. Heart
rate is slowed by the parasympathetic vagus nerve, and accelerated by
sympathetic nerve stimulation.
REGENERATION- cardiac muscle is more resistant to injuries, but
shows very little evidence of regeneration after injury.
 The coronary arteries supplying blood to the heart are anatomical end
arteries and lack collaterals.
 In the event of blockage of coronary arteries (as a result of a blood clot
or atherosclerotic blockage), the cardiac myocytes vascularized by the
coronaries cannot receive essential oxygen and the result is infarct.
 Following infarcts, the remaining heart muscle undergoes
compensatory hypertrophy, with subsequent enlargement of the heart.
 Hypertrophied hearts are commonly an indication of underlying
pathological disorders, though they may develop in specific cases of
training and overload as in athletes. 
 Stem cell technology holds promise for damaged hearts.
 SMOOTH MUSCLE

DISTRIBUTION:
 Forms the contractile portion of the walls of the digestive tract from the
middle of the esophagus to the internal sphincter of the anus.
 Walls of ducts in glands associated with the alimentary canal.
 Walls of the respiratory passages from the trachea to the alveolar ducts;
in the urinary and genital ducts.
 Walls of the arteries, veins and larger lymphatic vessels.
 Capsules of certain organs like the spleen.
 Arrectores pilorum muscles in the skin responsible for the so-called
“goose flesh”
 Iris and ciliary body of the eyes concerned with accommodation and
with constriction and dilation of the pupil.
 Areola of the mammary gland and in the subcutaneous tissue of the
scrotum.
HISTOLOGICAL CHARACTERISTICS:
 Smooth muscle fibers form smaller fascicles with meager perimysium.
They are classified according to developmental, biochemical and
functional differences:
1. Visceral smooth muscle- derived from splanchnopleural mesenchyme
and found in walls of thoracic, abdominal and pelvic organs of the
respiratory digestive and urogenital systems; contains actin, myosin
and desmin; poor nerve supply; unitary muscle exhibits
autorhythmicity via gap junctions; contraction is slow and in waves.
2. Vascular smooth muscle- differentiate in situ from mesenchyme
around blood vessels; contains desmin and vimentin; also unitary
muscle; contraction are not sustained and localized.
3. Smooth (sphincter and dilator) muscles of the iris- derived from
ectoderm and has a rich nerve supply; multiunit muscle because cells
can contract individually; capable of precise and graded contractions.
 Appears in l.s. as fusiform or spindle shaped cells with fine tapering
ends and a wider central region in which the oval nucleus is situated.
 The surface of each cell is invested by a thick extracellular coating
which corresponds to the basal lamina of epithelia and containing
collagenous, elastic and reticular fibers.
 This is responsible for its positive response to the PAS reaction, and
favors the transmission of the pull of contraction
to neigh-
boring cells
since

reticular
fibers
continue
into
surrounding
tissue.
 In x.s. smooth muscle appear like a mosaic of rounded or
irregularly polygonal structures of varying diameters. Only the
biggest fibers show the nucleus.
 A scanty amount of areolar CT containing blood vessels is seen
between units; it is
not as vascular
as either skeletal or cardiac
muscle.
 Irregular dark staining areas
traversing muscle cells are
called contraction nodes/
bands believed to be
the result
of movement of
electrolytes and granules
within the muscle cell during
contraction.
 The plasmalemma between sites of attachment of myofilament
has gap junctions or nexuses, and vesicular pinocytic inpocketings
similar to those found in endothelial cells.
 After maceration in
nitric acid, myofibrils
appear arranged
parallel to the long
axis of the muscle
cell.
 These contractile
elements are double refractile under the polarizing microscope,
but do not show the alternating isotropic
and anisotropic birefringent)
transverse bands of
striated muscle fibers.
 There are slender mitochondria, scanty ribosomes and rER in the
sarcoplasm.
 Thin, parallel myofilaments containing actin and
myosin are associated in bundles, and overlap
much more than striated muscle. This accounts
for lack of striations, and permits greater
contraction.
 Myosin have heads along most of their length, are
less stable in the cytoplasm, and interact with
actin only when the HMM is phosphorylated in
response to a contractile stimulus.
 Since the tropomyosin complex of skeletal
muscle is absent, Ca+2 complexes with the
calcium-binding protein calmodulin, also
involved in the contraction of non-muscle cells.
 A rudimentary sarcoplasmic reticulum is present;
T–tubules, dyads/triads are absent. Membrane-
limited vesicles called caveolae aid in Ca+2
uptake and release.
Action of hormones, neurotransmitters (ACh) or deformation of the epithelial cell by flow
of blood can trigger reactions which can stimulate or inhibit associated smooth muscle
beds. These effects may operate via 2nd messenger systems such as phospholipase A2
(PLA2) which may in turn activate cyclo-oxygenase (COX) / prostacyclin synthase (PCS)
enzyme systems to produce prostaglandins (PGI2) which diffuse readily through the tissue
fluids to act on the smooth muscle cells. 

Activation of nitric
oxide synthase (L-
arginase) (NOS) may
result in production of
gaseous
"neurotransmitter" NO. 
These paracrine agents
act on the smooth
muscle cells either
through G-protein
systems or directly on
ion channels.
 Abundant in smooth muscle are the intermediate filaments
desmin (skeletin) and vimentin.
 Two dense bodies that contain -actinin of Z-lines of striated
muscle are also present. They transmit contractile force to
adjacent cells.
 The force of slow, wave-like contraction is transmitted through
their investment of reticular fibers to the interstitial CT. It is
under involuntary control from the ANS: a sympathetic
innervation from the thoracic autonomic nerves and a
parasympathetic innervation from the cranial and pelvic
autonomic nerves.
 Elaborate neuromuscular junctions are not present.
 Autonomic nerve axons terminate in a series of dilatations in
endomysial CT.
 Smooth muscles maintain a state of partial contraction called
tonus, subject to modulation by blood-borne hormones:
norepinephrine, angiotensin and vasopressin, resulting in
vasoconstriction; circulating estrogens also affect uterine
smooth muscles.
 VARIATIONS OF SMOOTH MUSCLE CELLS

 Pericytes found on surface of capillaries and post-capilary venules are

assumed to be capable of contraction and influence blood flow.
 Myoepithelial cells are smooth muscle cells that lie between the
glandular epithelial cells and the basal lamina of glandular acini of
salivary, sweat, lacrimal or mammary glands (also referred to as
“basket/basal” cells due to their branching, stellate shape, or their
location at the base of alveolus). They expel secretion from the acini to
the ducts of the glands by contraction.
 REGENERATION

 It may divide by mitosis, but this capacity is limited.

 Defects in smooth muscle heal by scar formation
developed from perivascular mesenchymal cells.
 In the uterus, cells are capable of hyperplasia in the event
of pregnancy. After delivery, hypertrophied cells return to
their normal size, with the excess number undergoing fatty
degeneration.
 An abnormal proliferation of smooth muscle cells and
their excess collagen contribute to artherosclerotic plaques
in aging aorta and coronary arteries.
QUESTIONS?