LE11 HUMAN HISTOLOGY

SY 2020-2021
2ND SEMESTER
BS-MLS
PROF. ETHEL MANGADA, RMT

MUSCULAR TISSUE
X Events of muscle contraction
OUTLINE A Sliding filaments and sarcomere shortening in
I Muscular Tissue contraction
II Types of Muscle Tissue B Motor innervation
A Skeletal Muscle C Sensory innervation
B Cardiac Muscle XI Cardiac Muscle
C Smooth Muscle XII Smooth Muscle
III Terminologies A Thick and Thin filament
IV Skeletal Muscle B Intermediate Filament
A Development of Skeletal Muscle C Dense bodies and myofilaments
B Clinical Siginificance XIII Contraction of Smooth Muscles
C Organization A Renewal, Repair and Differentiation
V A and I Banding Pattern XIV Regeneration of Muscle
A A band
B I band
VI Thin filamen
VII Thick filament
VIII Structure that play important role in muscle contraction
IX Events of leading to muscle contraction

MUSCULAR TISSUE  Myofilament is responsible for muscle cell contraction

Thin filaments
FUNCTIONS
o

6 to 8 nm in diameter, 1.0 m long) are

 Is the primary tissue of motion


composed primarily of the protein actin

 Responsible for locomotion and movement of the


Thick filaments
different parts of the body (ex. Blinking)
o

5 nm in diameter, 1.5 m long) are

 Maintain an erect or seated position, or posture


composed of the protein myosin II

(through generating contractile force)


 Convert chemical energy to mechanical energy TYPES OF MUSCLE TISSUE

 Produce heat in the body – maintain temperature  Skeletal muscle
hemostasis in the body  Cardiac muscle
 Smooth muscle
GENERAL CHARACTERISTICS
 Contractility is the tendency of muscle cells to shorten SKELETAL MUSCLE
significantly.  is composed of bundles of very long, cylindrical,
o Ex: Flexing the elbow multinucleated cells that show cross-striations
 Extensibility is a muscle's capacity to extend. o Nucleus are found near the sarcolemma
 Elasticity is the tendency to rebound upon o Contraction: quick, forceful, and usually under
contracting. voluntary control
 Excitability is the ability to react to a stimulation that a
hormone or motor neuron may deliver.
 The unit structure is elongated in shape which is an
adaptation to its function of contraction
 Sarcoplasm appears fibrillar due to its contents of
myofibrils
o Sarcoplasm is the cytoplasm of the muscle tissues
 Staining is acidophilic or pinkish
o Because of their cytoplasmic filaments or their
myofilaments (thick and thin)
 Cells are bound together by varying amounts of
areolar connective tissue containing blood vessels
and nerves
o Connective tissue covering the inside of individual
muscle fiber, myocyte or muscle cell
o Connective tissue covering bundles of muscle
fibers called fascicles
o Connective tissue covering the whole muscle CARDIAC MUSCLES
tissue – outer covering  has cross-striations (due to organization of filaments;
due to dark and light bonding of myofilaments) and is

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composed of elongated, branched individual cells o Distance between 2 Z lines

that lie parallel to each other o Z line – looking closer at myofibril, it has
 Nucleus is usually single and is usually found on the alternating dark and light bonds due to
center of the muscle cell arrangement of thick and thin filaments, there, z
o Contraction: involuntary, vigorous, and rhythmic line is observed
 Sarcoplasmic reticulum – refers to endoplasmic
reticulum
o Also important in muscle cell contraction
initiation
o Responsible for sequestration of calcium
necessary for muscle cell contraction initiation

SKELETAL MUSCLE

 Skeletal muscle consists of muscle fibers, which are

long, cylindrical multinucleated cells with diameters
of 10–100 um displaying cross-striations
o Contraction: quick, forceful, and usually under
voluntary control
 long oval nuclei are usually found at the periphery of
the cell under the cell membrane
o helpful in discriminating skeletal muscle from
cardiac and smooth muscle

SMOOTH MUSCLE DEVELOPMENT OF SKELETAL MUSCLE

 Consists of collections of fusiform cells that do not MYOBLASTS

show striations
 Mesenchymal cells derived from a self-renewing
o Contraction: process is slow and not subject to
population of multipotential myogenic cells that
voluntary control
originate in the embryo
o Smooth because non-striated due to unique
 Early in embryonic development, these cells express
arrangement of thick and thin filaments –
MyoD transcription factor, which, along with other
arranged in an oblique manner
myogenic regulatory factors (MRFs), plays a key role in
 Appear fusiform and tapered at the ends
activation of muscle-specific gene expression and
 Similar with cardiac muscle having 1 or 2 nuclei (often
differentiation of all skeletal muscle lineages
single nuclei) which is centrally located
 During development, skeletal muscle begins to
differentiate and form when myoblasts align and fuse
together to make longer, multinucleated tubes called
myotubes (immature, undifferentiated skeletal muscle
fibers)

MYOTUBES
 Myotubes continue differentiating to form functional
myofilaments and the nuclei are displaced
against the sarcolemma
TERMINOLOGIES  Fuse together to form the muscle fiber
 Sarcoplasm –the cytoplasm of muscle cells and fibers
which is acid in staining SATELLITE CELLS
o Appear pinkish due to the presence of  Satellite cells are unfused myeloblasts population
cytoplasmic filaments that contain proteins that located on the external surface of muscle fibers inside
are basic (have affinity to acidic states) the developing external lamina
 Sarcolemma- cell membrane complex o these cells proliferate and produce new muscle
o Have significance in muscle cell contraction fibers following muscle injury - important in muscle
initiation regeneration
o Derived from “plasmalemma”
 Sarcosome – granules in the cytoplasm which under DEVELOPING EMBRYO CONTAINS 2 TYPES OF
the electron microscope is actually mitochondrion MYOBLASTS
o on different muscle fiber types
 Myofibrils- fine threadlike structures in the sarcoplasm
EARLY MYOBLASTS
which is responsible for muscle contraction
o Contain the myofilaments (thick and thin  responsible for the formation of primary myotubes,
filaments) chainlike structures stretching between tendons of the
 Sarcomere – a linear unit for muscle contraction developing muscle

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 Primary myotubes are formed by nearly synchronous o Through the light microscope, the cytoplasm
fusion of early myoblasts usually blends in with the sarcoplasm of the
o Elongated myotubes muscle cell, making them difficult to identify
 Myotubes undergo further differentiation into mature  Each satellite cell has a single nucleus with a
skeletal muscle fibers chromatin network denser and coarser than the nuclei
 Primary myotubes observed in the light microscope of muscle cells
exhibit a chain of multiple central nuclei surrounded o These cells are responsible for the ability of
by microfilaments skeletal muscle to regenerate but their
potential for regeneration is minimal
LATE MYOBLASTS  Myogenic precursors of muscle cells are usually
 allow secondary myotubes to grow in the innervated quiescent and do not express myogenic regulatory
region of muscle growth where the myotubes have factors.
close contact with nerve terminals.  Some satellite cells are activated after muscle tissue
 Secondary myotubes continue to be formed by damage, re-enter the cell, and begin to express MRFs
sequential fusion of myoblasts into the already-formed o They are proliferating and producing new
secondary myotubes at random positions along their myoblasts
length  As long as the outer lamina remains intact, the
o Secondary myotubes fuse to form new myoblasts fuse to form myotubes within the outer
secondary myotubes lamina, and then develop a new fiber
 Secondary myotubes have a reduced diameter, more  If the external lamina becomes damaged, fibroblasts
widely spaced nuclei, and increased number of heal the injured site with eventual development of
myofilaments scar tissue.
 The nuclei are located in the superficial sarcoplasm,
just within the plasma membrane, in the mature CLINICAL SIGNIFICANCE
nucleated muscle fiber  The increase in muscle is caused by formation of new
o Widely spaced nuclei in the sarcolemma is myofibrils and a pronounced growth in the diameter
similar with that of mature muscle fiber of individual muscle fibers.
(multinucleated and found at the periphery)
HYPERTROPHY
 increase cell volume
 enlargement of skeletal musculature through exercise
is caused by the formation of new myofibrils and a
pronounced growth in the diameter of individual
muscle fibers
o Example: biceps during strenuous physical
exercises

HYPERPLASIA
 increase number of cells
 growth of tissues in most smooth muscle
 Physiologic hyperplasia
o Example: uterus of pregnant woman (enlarges
as the pregnancy progresses)
 Pathologic hyperplasia
o Example: Payer’s patches (example of
lymphatic tissues) in patients with typhoid fever
 Myotubes synthesize the proteins to form myofilaments
- because of infection with salmonella, it
and gradually begin to demonstrate cross-striations by
caused hyplerplastic changes in Payer’s
light microscopy
patches
 Myotubes continue differentiating to form functional
myofilaments and the nuclei towards the sarcolemma
ORGANIZATION
 The connective tissue covering both individual muscle
are displaced.
fibers and muscle fiber bundles is important for the
 The mature multinucleated muscle fiber reveals a
transduction of energy or signal transduction
polygonal shape with a diameter of 10 to 100 µm
 At the end of the muscle, the connective tissue
when viewed in cross section.
continues as a tendon or some other arrangement of
 Their length ranges from nearly a meter, as in the lower
collagen fibers that attaches the muscle, usually to
limb’s sartorius muscle, to only a few millimeters in the
bone.
middle ear’s stapedius muscle
 A vast supply of blood vessels and nerves flows in the
 On the external surface of muscle fibers inside the
connective tissue.
developing external lamina, a group of mesenchymal
cells with scant cytoplasm, called muscle satellite cells
do not fuse and differentiate

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THE MUSCLE BASED CONNECTIVE TISSUE IS NAMED

ACCORDING TO ITS ASSOCIATION WITH THE MUSCLE
FIBERS:

EPIMYSIUM
 Sheath of dense connective tissue that enclosed the
entire skeletal muscle consisting of a collection of
fascicles (bundles of muscle cells/fibers or myocytes)
 The major vascular and nerve supply of the muscle
penetrates the epimysium

PERIMYSIUM
 Wraps each fascicle of muscle fibers BASIS OF MUSCLE FIBER TYPES CLASSIFICATION
 Thicker connective tissue layer, extending inward from  Classification of muscle based on color, appearance,
the epimysium and pathway they utilized in generating atp.
 Surrounds a group of fibers to form a bundle or fascicle  Categorized based on physiologic, biochemical, and
 Fascicles – functional units of muscle fibers that tend chemical caharcteristics
to work together to perform a specific function 1. Contractile speed defines how easily fiber can contract
 Larger blood vessels and nerves travel in the and relax.
perimysium o Speed of contraction of muscle cell
1. Velocity of the myosin ATPase reaction determines the
ENDOMYSIUM rate at which this enzyme will break down ATP
molecules during the contraction process.
 Delicate layer which surrounds individual muscle fibers
o Whether fast or slow muscle
(elongated multinuclear cells)
o Will tell if the reaction of myosin ATPase in breaking
 More delicately layer of connective tissue
down ATP
 Surrounds individual muscle fibers
o For contraction to occur, there is hydrolysis of ATP
 Composed of basal lamina synthesized by the
and organic phosphate that will lead to power
multinucleated fibers themselves as well as reticular
stroke or sliding of thin and thick filaments
fibers and fibroblasts
2. Metabolic profile reveals the ability of the oxidative
 Within each fiber, the nuclei are displaced
peripherally against the sarcolemma phosphorylation or glycolysis to generate ATP
 Only small-diameter blood vessels and the finest o Describes the concentration of myoglobin and
neuronal branches are present within the mitochondrion
endomysium, running parallel to the muscle fibers  More abundant myoglobin, the redder the
muscle color
 The scantier the myoglobin, the paler of
muscle fiber type.
o What type of respiration the muscle is using in
generating ATP
 if it is oxidative phosphorylation/ aerobic
respiration of glycolysis/ anerobic respiration

MUSCLE FIBER TYPES

TYPE I OR SLOW, RED OXIDATIVE FIBERS
 Metabolic profile.
o contain many mitochondria and abundant
myoglobin and cytochrome complexes. Red
fibers derive energy primarily from aerobic
oxidative phosphorylation of fatty acids
o has the most abundant myoglobin thus, has the
reddest color
o oxidative fiber because of aerobic oxidative
phosphorylation
 Contractile speed.
o are slow-twitch, fatigue-resistant motor units (a
twitch is a single, brief contraction of the
muscle). These fibers have great resistance to
fatigue but generate less tension than other
fibers.
o Adapted for long period of contractions
o Can be seen in marathon runners

 Velocity of the myosin ATPase reaction

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o is the slowest of all muscle fiber types o Contains myofilaments.

o slowest conversion of ATP to ADP and organic  Myofilaments- are the single filamentous polymers of
phosphate myosin II (thick filaments) and actin (thin filaments)
TYPE IIA OR FAST, INTERMEDIATE OXIDATIVE- and its related proteins. Myofilaments are themselves
GLYCOLYTIC FIBERS the contractile elements of the striated muscle.
 Sarcoplasmic reticulum- covers the bundles of
 are medium in size and are adapted for rapid
myofilaments. Within the myofibrils are also SER-
contractions and short bursts of activity
associated concentrations of mitochondria and
 for short burst activities ex: swimmers, sprinters
glycogen.
 intermediate – intermediate to type I and type IIb
 has combination of type I and type IIb MYOFIBRILS
o ex is the pathway it utilizes = both oxidative A BANDS
metabolism/aerobic respiration and anaerobic  darker bands (anisotropic)
glycolysis I BANDS
 color is light red to pink  lighter bands (isotropic)
 Metabolic profile.
Z LINE
o have many mitochondria and much
myoglobin. In contrast to type I fibers, type IIa  dark transverse line that bisects the I band
contain considerable glycogen. They are  the sarcomere ( contractile unit of the muscle tissue),
capable of both oxidative metabolism and extends from Z line to Z line about 2.5 m long in resting
anaerobic glycolysis muscle
 Contractile speed. A AND I BANDING PATTERN
o muscle fibers make up fast-twitch, fatigue-
resistant motor units that generate high peak
muscle tension.
o Same with type IIb with speed but is also fatigue-
resistant that is the same with type I
 Velocity of the myosin ATPase is intermediate
TYPE IIB OR FAST, WHITE GLYCOLYTIC FIBERS
 are typically small muscles adapted for rapid
contraction with a relatively large number of
neuromuscular junctions allowing precise, fine
movements
 color is white because it has the least amount of
myoglobin  Inside muscle fiber is the myofibril.
 Most abundant glycogen among the three that is why  Transverse section is fibrilar.
it is called Glycolytic fiber  Cross section is speckled.
 Metabolic profile.  Inside one myofibril:
o fibers have fewer mitochondria and less o Alternating dark and light bands,
myoglobin making them to appear light pink in o Dark band is A band
fresh specimen. However, they have abundant  One dark band to another dark band
glycogen.  Light portion between the dark bands is
o Only uses anaerobic glycolysis called the H zone
 Contractile speed.  Traversing the H zone is the M line
o are fast-twitch and generate high peak muscle  Best demmonstrated by electron
tension. However, they are fatigue-prone motor micrographs.
units unlike type IIa fibers  Ideal also in H&E preparation for light
o also for short burst activities microscope.
o same speed with type IIa but is fatigue-prone o Light band is the I band
 Velocity of the myosin is the fastest of all the fibers.  Z line or Z disc traverses the light band
MYOFIBRILS AND MYOFILAMENTS  Distance from one Z disc to another Z disc is
 Muscle fibers- long, multi-nucleated, cylindrical with a called the sarcomere.
diameter of 10–100 um and packed with longitudinally  Sarcomere can extend up to 2.5 meters long
organized structural subunits, myofibrils. in resting muscle.
 Myofibrils- are evident in favorable histological  Light band and dark band creates adjacent
preparations and are better seen in muscle fiber cross- sarcomeres
sections that give it a speckled appearance. Myofibrils  Sarcoplasm has little RER and is filled by long
extend the entire length of the muscle cell. Myofibrils cylindrical filamentous bundles of myofibrils running
have a diameter of 1–2 um and are made of parallel to the long axis.
myofilament tubes.  A and I banding pattern is the dark and light banding
o Cross striated because of the presence of pattern of the skeletal muscle tissue. It gives the cross
banding pattern. striated appearance.
o Gives the fibrillar appearance in transverse
section.

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o binding of calcium leads to muscle contractin

 TnI
o which inhibits the actin-myosin interaction

o Appearance of sarcomere if the muscle is in the

relaxed state. THICK FILAMENTS
A BAND/ DARK BAND  Thick filaments consist primarily of myosin.
H ZONE o Myosin is a large complex: into two identical
 It contains the rods of the thick filaments. heavy chains and two pairs of light chains
 Lighter because only the rods are seen in the area  Myosin heavy chains- are thin, rod-like molecules
 The side of the H zone are darker areas because it made up of two heavy chains twisted together as
contains overlapping actin and myosin heads. myosin tails the heads, which have ATP binding sites as
well as ATPase activity and the ability to bind actin
M LINE
 The heads are the one rubbing or associating with
 Traverses the H zone actin of the thin filament active site. It causes the
 M line is where lateral connections are made between sliding motion.
adjacent thick filaments.  The four light chains are associated with the head. It
 Major filament of the M line region is are the contains:
myomesin, hold thick filaments in place, and the o 2 essential light chains
creatinine kinase, that catalyzes the transfer of o 2 regulatory light chains
phosphate groups from phospocreatenine(storage o This is where the enzyme myosin light chain kinase
form of high energy phosphate group) to adenosine is attached.
diphosphate(ADP) thereby helping to supply
adenosine triphosphate for muscle contraction.
I BAND/ LIGHT BAND
 Light because it only contains the thin filaments
 No overlapping thick and thin filament

THIN FILAMENTS
COMPONENTS
F-ACTIN
 , associated with tropomyosin, which also forms a long
fine polymer, and troponin, a globular complex of NOTE:
three subunits To preserve performance and speed of muscle
 Primary protein in thin filament contraction both thin and thick filaments in each
 Formed by the polymerization of G actin myofibril must be aligned precisely and held at
 G actin molecules are asymmetric, each containing a optimum distance.
binding site from myosin
 Alpha actinin binds the plus end of each filament to
the Z line; minus end extends to the M line, and is  Proteins that are essential for regulation of
protected by an actin capping protein. myofilament spacing, attachment and alignment are
TROPOMYOSIN titin, alpha-actinin, nebulin, tropomodulin, desmin,
myomesin, c protein and dystrophin.
 is a long, thin molecule about 40 nm in length
containing two polypeptide chains, which assembles
to form a long polymer located in the groove CLINICAL CORRELATION
between the two twisted actin strands DUCHENNE’S MUSCULAR DYSTROPHY
 Covers the active sites  Genetic condition characterized by progressive
muscular weakness
TROPONIN COMPLEX  Assciated with the absence of dystrophin protein.
 TnT  Dystrophin is encoded on the X chromosome which
o which attaches to tropomyosin explains why boys suffer from DMD.
o anchor the whole troponin complex to
tropomyosin
 TnC
o which binds calcium ions

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STRUCTURE THAT PLAY IMPORTANT ROLE IN MUSCLE  Diagram indicating key features of a typical
CONTRACTION neuromuscular junction: synaptic vesicles of
acetylcholine (ACh), a synaptic cleft, and a
postsynaptic membrane. This membrane, the
sarcolemma, is highly folded to increase the number
of Ach receptors at the NMJ. Receptor binding
initiates muscle fiber depolarization, which is carried to
the deeper myofibrils by the T tubules.
 Neuromuscular junction
 Axon teminal(white structure) is unmyelinated but it is
surrounded by schwann cells.
o Contains mitochondria and synaptic
vesicles(blue)
o Synaptic vesicles contain the acetylcholine that is
essential in the spread of nerve impulse in the
sarcolemma to T-tubules.
 Synaptic cleft is where axon terminal meets the
 Diagram above is the muscle fiber sarcolemma
 Red structures are myofibrils  There are acetylcholine receptors in the sarcolemma
 Dark blue are the sarcoplasmic reticulum that forms that bind acetylcholine that is released from the
the terminal cisternae of the sarcoplasmic reticulum synaptic vesicles of the axon terminal
which is important in the delivery of calcium to initiate o The binding of acetylcholine to the receptor will
contraction. initiate muscle impulse in the sarcolemma. It will
o Extends from one A-I band junction to another. move to T tubules that will result in the release of
o Calcium is delivered to the sarcoplasm of the calcium ions in the sarcoplasmic reticulum to
muscle fiber sarcoplasm.
o After contraction calcium must be removed.
 Sarcolemma is the plasma membrane of the muscle EVENTS OF LEADING TO MUSCLE CONTRACTION
fiber. It has invagination (light blue) called the
transverse(T) tubule
o Transverse tubule is important in the spread of
stimulus
o The stimulus initiate spread of calcium from the
sarcoplasmic reticulum to the sarcoplasm.
 Adjacent to opposite sides of each T tubules are
expanded terminal cisternae that serves are reservoirs
of calcium
 It is known as the TRIAD. It consists of a T tubule and
two small sarcoplasmic reticulum.
o Where depolarization of sarcolemma-derived T-
tubules is transmitted to the sarcoplasmic
reticulum membrane.
 From axon terminal, synaptic vesicles will release
o Thi activates the depolarization-sensitive
acetylcholine.
transmembrane channels called voltage-sensor
 Acetylcholine will bind in the receptors found in the
proteins. Changes in this proteins affect gated
sarcolemma that cause nerve impulse to spread in the
calcium-released channels located in the
sarcolemma and along T tubules
adjacent plasma membrane.
 Spread of nerve impulse cause release of nerve
 An axon is connected to the sarcolemma that
impulse in the sarcoplasmic reticulum and
transmits the nerve impulses.
sarcoplasm.
 This diagram illustrates the organization of the
 Muscle cell contraction cycle is initiated.
sarcoplasmic reticulum and its relationship to the
myofibrils.
EVENTS OF MUSCLE CONTRACTION
 Neither the thick nor the thin filaments change their
length during contraction.
 Contraction is the result of an increase in the amount
of overlap between the filaments caused by the
sliding of thin and thick filaments past one another.
 Each contraction cycle consists of five stages:
o attachment
o release
o bending
o force generation
o reattachment

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 Stage 1: Attachment- the myosin head is tightly bound o The head advances about 5nm away from the
to the actin molecule of the thin filament. ATP is thin filament and moving towards the A bond
absent.
 Stage 4: Force generation- the myosin head releases
inorganic phosphate and the power stroke occurs. The
myosin head binds weakly to its new binding site on
the neighboring act in molecule of the thin filament,
causing release of the inorganic phosphate. This
release has two effects:
o First, the binding affinity between the myosin
head and its new attachment site increases.
o Second, the myosin head generates a force as
it returns to its original unbent position. Thus, as
o The appearance of the myosin head and that of
the myosin head straightens, it forces
the thin filament is called the rigor configuration
movement of the thin filament along the thick
o In this stage, the muscle is still in its relaxed state
filament. This is the power stroke" of the cycle.
CLINICAL CORRELATION During this stage, ADP is lost from the myosin
 The absent of ATP in the initial stage of contraction head
cycle results to stable actin-myosin complex. This
arrangement in the initial cycle is known as the rigor
configuration. The muscular extreme stiffening and
rigidity that begins at the moment of death is caused
by lack of ATP and is known as rigor m ortis. In an
actively contracting muscle, this step ends with the
binding of ATP to the myosin head.

 Stage 2: Release- myosin head is uncoupled from the

thin filament. In this stage of the contraction cycle, ATP
binds to the myosin head and induces conformational
changes of the actin-binding site. This change
reduces the affinity of the myosin head for the actin
molecule of the thin filament, causing the myosin  Stage 5: Reattachment- the myosin head binds tightly
head to uncouple from the thin filament. to a new actin molecule. The myosin head is again
tightly bound to a new actin molecule of the thin
filament (rigor configuration), and the cycle can
repeat. Although an individual myosin head may
detach from the thin filament during the cycle, other
myosin heads in the same thick filament will attach to
actin molecules, thereby resulting in movement.
Because the myosin heads are arranged as mirror
images on either side of the H band (antiparallel
arrangement), this action pulls the thin filaments into
the A band, thus shortening the sarcomere.
 Stage 3: Bending- the myosin head, as a result of
hydrolysis of ATP, advances a short distance in relation
to the thin filament. The ATP-binding site on the myosin
head undergoes further conformational changes,
causing the myosin head to bend. This movement is
initiated by the breakdown of ATP into adenosine
diphosphate (ADP) and inorganic phosphate; both
products, however, remain bound to the myosin
head. In this stage of the cycle, the lincar
displacement of the myosin head relative to the thin
filament is approximately 5 nm.

SLIDING FILAMENTS AND SARCOMERE SHORTENING

IN CONTRACTION
 During contraction, the I band decreases in size as thin
filaments penetrate the A band. The sarcomere, and
therefore the entire cell (fiber), is shortened
considerably as the H band - the portion of the A band
containing only thick filaments decreases in width as

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thin filaments overlap the thick filaments entirely (see are anchored to the Z lines, the sarcomere shortens
figures below). from both sides when actin filaments slide along the
myosin filaments.
 Although the action between the filaments is
described as sliding, the myosin filament actually pulls
the actin along its length. The cross bridges of the
myosin filament attached to the actin filaments and
exert force on them to move. This action is known as
the sliding filament mechanism of muscle contraction.
In this model the sarcomeres shorten without the stick
or thin filaments changing in length. A contraction
begins when a bound ATP is hydrolyzed to ADP and
inorganic phosphate. This causes the myosin head to
extend and can attach to a binding site on actin,
forming a cross bridge.
 An action called the power stroke is triggered allowing
myosin to pull the actin filament toward the M line
thereby shortening the sarcomere. ADP and inorganic
phosphate are released during the power stroke. The
myosin remains attached to actin until a new
molecule of ATP binds, freeing the myosin to either go
through another cycle of binding and more
contraction, or remain unattached to allow the
muscle to relax.
 Muscle contractions are controlled by the actions of
calcium, the thin actin filaments are associated with
regulatory proteins called troponin and tropomyosin.
 When a muscle is relaxed tropomyosin blocks the cross
bridge binding sites on actin. When calcium ion levels
are high enough and ATP is present, calcium ions bind
to the troponin which displaces tropomyosin, exposing
the myosin binding sites on actin. This allows myosin to
attach to a binding site on actin forming a cross
bridge.
 Calcium ions are stored in the sarcoplasmic reticulum
and are released in response to signals from the
nervous system to contract.
 Neurotransmitter molecules are released from a
neuron and bind to receptors which depolarizes the
membrane of the muscle fiber.
 The electrical impulse travels down the T tubules and
opens calcium stores.
Video link: https://www.youtube.com/watch?v=S5uFaqpEPMI  Calcium ions flow to the myofibrils where they trigger
a muscle contraction. As the actin and myosin slide
Video content: along each other the entire sarcomere shortens as the
 Skeletal muscle works under voluntary control. Skeletal Z lines draw closer to the M line.
muscles are composed of bundles of muscle fibers.  As the sarcomeres in myofibrils contract, the entire
 Muscle fibers are long cylindrical cells containing muscle fiber will shorten. When muscle fibers contract
several nuclei. Muscles will contract or relax when they in unison a muscle can produce enough force to
receive signals from the nervous system. move the body.
 A neuromuscular junction is the site of the signal
exchange. This is where the synaptic bulb of an axon
MOTOR INNERVATION
terminal and muscle fiber connect.
 Myelinated motor nerves branch out within the
 Muscle fibers are composed of many myofibrils. A
perimysium connective tissue, where each nerve gives
myofibril contains contractile units called sarcomeres.
rise to several terminal twigs. At the site of innervation,
Sarcomeres run adjacent to one another down the
the axon loses its myelin sheath and forms a dilated
length of the myofibril. Each sarcomere consists of
termination situated within a trough on the muscle cell
alternating thick and thin protein filaments giving
surface. This structure is called the motor end-plate, or
skeletal muscle its striated appearance.
the neuromuscular junction (see figure below).
 The muscle contract when these filaments slide past
each other. The thick filaments are myosin, which are
anchored at the center of the sarcomere called the
M line. The thin filaments are composed of the protein
actin which are anchored to the Z lines on the outer
edges of the sarcomere. Because the actin filaments

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avoid prolonged contact of the transmitter with its

receptors.
o 3: Voltage-gated Na' channels open, and Na
enters the cell.
o 4: General depolarization spreads over the
plasma membrane of the muscle cell and
continues via membranes of the T tubules.
o 5: Voltage sensor proteins in the plasma
membrane of T tubules change their
conformation.
o 6: At the muscle cell triads, the T tubules are in
close contact with the lateral enlargements of the
sarcoplasmic reticulum, where gated Ca2+
release channels are activated by
 At this site, the axon is covered only by a thin conformational changes of voltage-sensor
cytoplasmic extension from a Schwann cell. Within the proteins.
axon terminal are numerous mitochondria and o 7: Ca2+ is rapidly released from the sarcoplasmic
synaptic vesicles, the latter containing the reticulum into the sarcoplasm.
neurotransmitter acetylcholine. Between the axon o 8: Ca2+ binds to the TnC portion of the troponin
and the muscle is a space, the synaptic cleft, in which complex,
lies an amorphous basal lamina matrix from the o 9: The contraction cycle is initiated, and Ca2+ is
muscle fiber. The sarcolemma is forced into several returned to the terminal cisternae of the
deep junctional folds at the junction, which allow for sarcoplasmic reticulum.
greater surface area. Several nuclei and various
mitochondria, ribosomes, and glycogen granules are
located in the sarcoplasm under the folds.

 Diagram indicating key features of a typical

neuromuscular junction: synaptic vesicles of CLINICAL CORRELATION
acetylcholine (ACh), a synaptic cleft, and a  Myasthenia gravis is an autoimmune disorder
postsynaptic membrane. This membrane, the characterized by progressive muscular weakness
roolemma, is highly folded to increase the number of resulting from an error in the transmission of nerve
Ach receptors at the NMJ. Receptor binding initiates impulses to muscles caused by a reduction in the
muscle fiber depolarization, which is carried to the number of functionally active acetylcholine receptors
deeper myofibrils by the T tubules. in the sarcolemma of the myoneural junction. This
 The events leading to contraction of skeletal muscle reduction is caused by circulating antibodies that bind
can be summarized as a series of steps. to the acetylcholine receptors in the junctional folds
o 1: The contraction of a skeletal muscle fiber is and inhibit normal nerve-muscle communication. As
initiated when a nerve impulse traveling along the the body attempts to correct the condition,
axon of a motor neuron arrives at the membrane segments with affected receptors are
neuromuscular junction. internalized, digested by lysosomes, and replaced by
o 2: The nerve impulse prompts the release of newly formed receptors. These receptors, however,
acetylcholine into the synaptic cleft that binds are again made unresponsive to acetylcholine by
into ACHgated Na' channels causing local similar antibodies, and the disease follows its
depolarization of sarcolemma. Excess progressive course.
acetylcholine is hydrolyzed by the enzyme  There's no cure for myasthenia gravis, but treatment
cholinesterase bound to the synaptic cleft basal can help relieve signs and symptoms, such as
lamina. Acetylcholine breakdown is necessary to weakness of arm or leg muscles, double vision,

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drooping eyelids, and difficulties with speech, about the extent to which a muscle is stretched which
chewing, swallowing and breathing in turn modulates the activity of the gamma (y) motor
 Though this disease can affect people of any age, it's (efferent) nerve fibers innervating the specific muscle.
more common in women younger than 40 and in men SCHEMATIC DIAGRAM OF MUSCLE SPINDLE:
older than 60.
 A single nerve fiber (axon) can innervate one muscle
fiber, or it may branch and be responsible for
innervating 160 or more muscle fibers. In the case of
multiple innervation, a single nerve fiber and all the
muscle fibers it innervates are called a motor unit.
Individual striated muscle fibers do not show graded
contraction they contract either all the way or not at
all. To vary the force of contraction, the fibers within a
muscle bundle do not all contract at the same time.
Since muscles are composed of many motor units, the
firing of a single motor axon will generate tension
proportional to the number of muscle fibers
innervated by that axon. Thus, the number of motor
units and the variable size of each unit can control the Different types of fiber in spindle fiber:
intensity of a muscle contraction. The ability of a
muscle to perform delicate movements depends on  Nuclear bag fiber
the size of its motor units. For example, because of the o Contains an aggregation of nuclei in an
fine control required by eye muscles, each neuron expanded midregion.
innervates three muscle fibers. In larger muscles o Bulging center for many nuclei are concentrated
exhibiting coarser movements, such as those of the in that are
limb, a single, profusely branched axon innervates a  Nuclear chain fiber
motor unit that consists of more than 100 individual o Has many nuclei arranged in chain manner.
muscle fibers. The number of fibers innervated by a
motor unit is called its innervation ratio. Additional content from module:
o Each spindle contains approximately two-two four
CLINICAL CORRELATION nuclear bag fibers and six-eight nuclear chain
 If the nerve supply to a muscle is disrupted, the muscle fibers
cell undergoes regressive changes known as tissue o In the nuclear bag fibers, the muscle fiber nuclei
atrophy. The most conspicuous indication of this a are clumped in the expanded central portion of
trophy is thinning of the muscle and its cells. If the fiber, hence name bag.
innervation is re-established surgically or by the slower o In contrast, the nuclei concentrated in the central
process of natural regeneration of the nerve, the portion of the nuclear chain fibers are arranged in
muscle can regain normal shape and strength. chain.
 o Both afferent Ia (sensory and efferent (motor)
SENSORY INNERVATION nerve fibers supply muscle spindle cells,
 Proprioreceptors are encapsulated sensory receptors, o The afferent nerve fibers respond to excessive
examples are that of muscles and tendons. Such stretching of the muscle, which in turn inhibits
receptors are part of the sensory somatic system somatic motor stimulation of the muscle.
providing information on the degree of stretching and o The efferent nerve fibers regulate the sensitivity of
tension in a muscle. Proprioreceptors inform the the afferent endings in the muscle spindle
central nerve system about the body's position and
movement in space.
 The muscle spindle is a specialized stretch receptor in
muscle; it consists of two types of modified muscle
fibers
O Spindle cells
O Neuron terminals
O This muscle spindle lets our brain determine how
much the muscle is stretched, and is also helpful in
maintaining the balance of our body thru the brain
by transmitting impulses (ex. when we’re
performing yoga or any aerobic exercises)
 Both types of modified muscle fibers are surrounded Video content:
by an internal capsule. A fluid-filled space separates  motor fibers proprioception is imperative in
the internal capsule from an outer extemal capsule. the body's ability to retain balance and
Type of spindle cells includes: nuclear bag fiber and posture without conscious effort.
nuclear chain fiber  In order for the human body to orient itself in
 the muscle spindle transmits information via sensory space special sensory receptors called
(afferent, ia) nerve fibers to the central nervous system muscle spindles are embedded in the belly of

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skeletal muscle; these receptors detect component of the intercalated disc and is
changes in length. responsible for its staining in routine H&E
 typical muscle spindles consist of three types preparations. It holds the cardiac muscle cells
of intrafusal muscle fibers surrounded by a at their ends to form the functional cardiac
connective tissue sheath muscle fiber. The fascia adherens also acts as
the site where the thin filaments in the terminal
o one dynamic sarcomere attach onto the plasma
nuclear bag fiber membrane. In this way, the fascia adherens is
o one static nuclear functionally similar to the epithelial zonula
bag fiber adherens, where actin filaments of the
o around five terminal web are also anchored.
nuclear chain  Maculae adherentes (desmosomes) - bind
fibers the individual muscle cells to one another.
 as action potentials reach the muscle via Maculae adherentes help keep the cells from
alpha motor neurons, the surrounding pulling apart under the strain of frequent
extrafusal fibers contract or relax stretching repeated contractions. They support the
the muscle spindle along with them fascia adherentes and are located in the
 Sensory information on the velocity of this intercalated discs' transverse and lateral
stretch and muscle length is transmitted via components.
afferent sensory neurons.  Gap junctions (communicating junctions) -
 These signals are transmitted to the central constitute the major structural element of the
nervous system and modulated by efferent lateral component of the intercalated disc.
gamma motor neurons that regulate the Gap junctions provide ionic cohesion
contraction of the muscle spindle fibers. between neighboring cardiac muscle cells,
 the co-activation of muscle fibers allows the allowing for the movement of informational
body to sense and maintain its position in macromolecules from cell to cell. This
space without it balance becomes a near exchange helps the cardiac muscle fibers to
impossible task. serve as a syncytium while maintaining the
integrity and individuality of the cells. The
CARDIAC MUSCLE location of the gap junctions on the
intercalated disc's lateral surfaces protects
 cardiac muscle has the same types and arrangement them from the forces produced during the
of contractile filaments as skeletal muscle- exhibit contraction process.
cross-striations
 exhibit densely staining cross-bands, termed  cardiac muscle fibers consist of multiple/branched
intercalated discs, that cross the fibers in a linear end-to-end organized cylindrical cells
fashion.  cardiac muscle cell has either one or two centrally
Intercalated discs – unique characteristics located pale-staining nuclei
Cardiac muscle cells are  Fatty acids - major fuel of the heart and are stored as
connected cell to cell end okay that is via triglycerides in numerous lipid droplets
the intercalated discs o Glycogen particles
From module: About intercalated discs: o Lipofuscin pigment- often found near the nuclei
o It represents the place of attachment between (in the heart)
the cells of the cardiac muscle  Cardiac muscles are exclusively in the heart and form
o In the light microscope, the disc appears as a the bulk of cardiac mass.
densely staining linear structure that is oriented DIAGRAM OF CARDIAC MUSCLE
transversely to the muscle fiber.
o When the site of the intercalated disc is examined
with the TEM, the densely staining structure seen in
the light microscope can be attributed to the
presence of a transverse component that crosses
the fibers at a right angle to the myofibrils. The
transverse component is analogous to the risers of
the stairway.
o A lateral component (not visible in the light
microscope) occupies a series of surfaces
perpendicular to the transverse component and
lies parallel to the myofibrils. The lateral
component is analogous to the steps of the
stairway. Both components of the intercalated Notes:
disc contain specialized cell-to-cell junctions o Cardiac muscle contains only one Transverse
between adjoining cardiac muscle cells: tubule per sarcomere (found in z-line)
 Fascia adherens (adhering junction) - is the o nucleus are centrally located
major constituent of the transverse

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o Has different cell to cell junction like desmosomes,

gap junctions… Compare and contrast skeletal muscle and cardiac
o has also large mitochondria for it needs abundant muscle:
amount of energy to pump blood.  Like skeletal muscle, transverse tubule well as the
sarcoplasmic reticulum of cardiac muscle also is
From module: Diagram of cardiac muscle cells responsible in the initiation of contraction.
indicates characteristic features of this muscle  In skeletal T tubules forms triad (since terminal
type. The fibers consist of separate cells with cisternae appear like tubes because they form flunks
interdigitating processes where they are held surrounding the tubule while it is diad in cardiac
together. These regions of contact are called the muscle (since it lacks terminal cisternae)
intercalated discs, which cross an entire fiber  In the skeletal muscle per sarcomere contains two T
between two cells. The transverse regions of the tubules and are found in A-I junction while in cardiac
steplike intercalated disc have abundant muscle per sarcomere contains one T tubules and are
desmosomes and other adherent junctions which found in Z-line.
hold the cells firmly together. Longitudinal regions  T-tubules of cardiac muscle are bigger/larger that T
of these discs contain abundant gap junctions, tubule of skeletal muscle.
which form "electrical synapses" allowing
contraction signals to pass from cell to cell as a
single wave. Cardiac muscle cells have central
nuclei and myofibrils that are less dense and
organized than those of skeletal muscle. Also the
cells are often branched, allowing the muscle
fibers to interweave in a more complicated
arrangement within fascicles that produces an
efficient contraction mechanism for emptying the
heart.

 The structure and function of the contractile proteins

in cardiac cells are essentially the same as in skeletal
muscle.
 The tubules are more numerous and larger in cardiac
muscle than in skeletal muscle and the sarcoplasmic CARDIAC MUSCLE ULTRASTRUCTURE
reticulum is less well developed
 Mitochondria occupies 40% of the cytoplasmic
volume
o reflecting the need for continuous aerobic
metabolism
o Type 1 muscle fiber - utilize aerobic metabolism or
your aerobic respiration or oxidative
phosphorylation.

DIAGRAM OF THE ORGANIZATION OF CARDIAC

MUSCLE FIBER.
The T tubules of cardiac muscle are much larger than the
T tubules of skeletal muscle and carry an investment of
external lamina material into the cell. They also differ in
that they are located at the level of the Z disc. The portion
of the sarcoplasmic reticulum adjacent to the T tubule is
not in the form of an expanded cisterna but rather is
organized as an anastomosing network.

(a): TEM of cardiac muscle shows an abundance of

mitochondria (M) and rather sparse sarcoplasmic
reticulum (SR) in the areas between myofibrils. T
tubules are less well- organized and are usually
associated with one expanded terminal cisterna
of SR, forming dyads (D) rather than the triads of
skeletal muscle.Functionally these structures are
similar in these two muscle types. X30,000

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 No cross-striations because of the arrangement of

thick and thin filaments (unique)

THICK AND THIN FILAMENTS

 bundles of thin and thick myofilaments in smooth
muscle cells crisscross obliquely through the
membranelattice network
 myosin (thick filaments) proteins are bundled
differently and the cross-bridges interact with fewer F-
actin filaments
 Thin filaments of smooth muscle cells lack troponin
complexes and instead utilize s- a calcium-binding
protein that is also involved in the contraction of non-
muscle cell
 myosin light chain kinase (MLCK), the enzyme that
phosphorylates myosin, which is required for myosin's
interaction with F-actin – hormones and other factors
(b): Muscle cell from the cardiac atrium shows the affect the activity of MLCK
presence of membrane-bound granules
aggregated at the nuclear poles. These granules INTERMEDIATE FILAMENT
are most abundant in muscle cells of the right  Desmin- major intermediate filament protein in all
atrium (~600 per cell), but smaller quantities are smooth muscles
also found in the left atrium and the ventricles. The  Vimentin- additional component in vascular smooth
atrial granules contain the precursor of a muscle.
polypeptide hormone, atrial natriuretic factor  Both intermediate filaments and F-actin filaments
(ANF). ANF targets cells of the kidneys to bring insert into dense bodies
about sodium and water loss (natriuresis and  Dense bodies contain –actinin
diuresis). This hormone thus opposes the actions of o functionally similar to the Z discs of striated and
aldosterone and antidiuretic hormone, whose cardiac muscles
effects on kidneys result in sodium and water
conservation. X10,000. x, DENSE BODIES AND MYOFILAMENTS

INJURY AND REPAIR

 A localized injury to cardiac muscle tissue that results
in the death of cells is repaired by replacement with
fibrous connective tissue.
o Scarring is the result of fibrous connective tissue
 Cardiac function is lost at the site of injury
o Also, it can’t be regenerated
 Example: Myocardial Infarction where TnI is used as a
marker for diagnosis
o Localized heart injury
o Dead muscles in the site of injury that is replaced
by the fibrous connective tissue
o Most excellent marker of myocardial infarction
is the measurement of TnI or troponin I levels
o Troponin T and Troponin I are usually released in
the bloodstream after 2-3 hours of a myocardial
CONTRACTION OF SMOOTH MUSCLES
infarction
 Events that lead to elevation of intracellular Ca2+
o TnI remains elevated for about 2 weeks hence it
concentration, which is directly responsible for muscle
is the excellent marker for myocardial infarction
contraction
 Recent studies of hearts removed from individuals who
o Electrical depolarizations - release of
had received transplants reveal nuclei undergoing
acetylcholine and norepinephrine
mitosis.
neurotransmitters
o Electrical depolarizations - release of
SMOOTH MUSCLE acetylcholine and norepinephrine
 Cells or fibers of smooth muscle are long, tapering neurotransmitters
structures with elongated nuclei centrally located at o Mechanical impulses- such as passive vascular
the cell's widest part smooth muscle stretching
 Involuntary control  Events that lead to elevation of intracellular Ca2+
 Concentrated near the nucleus are mitochondria, concentration, which is directly responsible for muscle
polyribosomes, cisternae of rough ER, and the Golgi contraction
apparatus

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 Different factors that are responsible in the initiation of

In smooth muscle cell contraction these are the
muscle cell contraction:
factors that initiate the contraction cycle:
o Electrical depolarizations – can occur, such as
- Electrical depolarization
those during neural stimulation of smooth muscle.
- Chemical stimuli
The release of acetylcholine and norepinephrine
- Mechanical impulses
neurotransmitters from their synaptic nerve
endings activates receptors found in the
membrane of the neuronal plasma membrane, - Anong difference nito maalala niyo dun sa
which changes the membrane potential. This skeletal muscle what initiates now muscle cell
causes opening of voltage-sensitive Ca2+ contraction, is the release of the calcium as a
channels result of the spread of nerve impulse from the axon
terminal papunta dun sa sarcolemma ninyo and
along the T-tubule. Un ung nag I initiate ng
contraction dun sa ating skeletal muscle and the
cardiac.
- Pero sa smooth muscle there are other factors like
electrical depolarization, chemical stimuli and
mechanical impulse. Ito lang ung mga nag
iinitiate.
- And the contraction cycle mismo is the same with
your skeletal muscle.
Take Note:
- Ano pang tatandaan natin dun sa contraction
nung smooth muscle maalala ninyo sa skeletal
muscle natin nagkakaroon tayo ng muscle
contraction kapag nag bind si calcium kay
Troponin C, un ung nag iinitiate sa contraction
– Release of acetylcholine and norepinephrine natin. Pero dun sa smooth muscle nagkakaroon
neurotransmitters are responsible in the tayo initiation.
activation of receptors in the neuronal - After this electrical depolarization, chemical
membrane that will activate the voltage stimuli and mechanical impulse. Nagkakaroon
sensitive calcium channels. tayo ng phosphorylation ng myosin light-chain
o Chemical stimuli by angiotensin II, vasopressin or kinase. And that is because of the binding of your
thromboxane A2 calmodulin to calcium. Yan ay kay smooth
– Examples of substances like your angiotensin II, muscle.
vasopressin or your (ADH) or Antidiuretic - Pag kay cardiac muscle at skeletal through the
Hormone and thromboxane A2. binding of calcium and Troponin C.
– Such as those triggered by angiotensin II, - Bakit naiiba si smooth muscle kasi wala siyang
vasopressin or thromboxane A2 act on specific troponin complex at ang meron sa kanya ay ung
cell membrane receptors resulting in muscle calmodulin which is a calcium binding protein.
contraction. These compounds use second-
 There are just the events that lead to
messenger pathways that do not need action
intracellular calcium concentration elevation.
potential generation and depolarization of cells
 Contraction cycle is the same with skeletal
to trigger contraction. Inositol 1,4,5-triphosphate
muscle and cardiac. The only difference is the
(IP3), G-protein-coupled, and nitict oxide (NO)-
initiation
cGMP pathways are the most common second-
messenger pathways utilized by smooth muscle.
o Mechanical impulses- such as passive vascular
smooth muscle stretching, activate DIFFERENT TYPES:
mechanosensitive ion channels, resulting to  Multiunit smooth muscle- each cell is innervated and
initiation of spontaneous muscle contraction can contract independently
(myogenic reflex). o Each cell is innervated means the cells can
– When we say mechanical impulse referring to contract independently from each other.
the activation of mechanosensitive ion  Unitary smooth muscle- only a few cells are innervated
channels. but all cells are interconnected by gap junctions
– The activation of this mechanosensitive ion o Their contractions are unitary
channels result to the initiation of spontaneous  Gap junctions cause the contraction stimulation to
contraction or tinatawag nating Myogenic spread across adjacent cells as a synchronized wave.
reflex.  Smooth muscle, like that in skeletal muscle, lacks
neuromuscular junctions. Alternatively, axonal
swellings of synaptic vesicles simply lie in near contact
with the sarcolemma, with the junctions possessing
little to no specialized structure.

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 Since smooth muscle are typically spontaneously What is the difference of the smooth muscle from skeletal
active without nervous stimulus, its nerve supply is and cardiac muscle in their regeneration abilities?
mainly used to alter activity rather than initiate it.  Skeletal muscles are capable of regeneration but
Smooth muscle receives both the adrenergic and their ability to regenerate are limited and the
cholinergic nerve endings that acts antagonistically, regeneration is through the satellite cell. When there
stimulating and inhibiting its activity. The cholinergic is an injury in the skeletal muscle the satellite cell
endings activate in some organs, and the adrenergic undergo proliferation and then differentiation and
neurons depress; the reverse happens in others. eventually form myotubes and this myotubes will
sequentially fused together and then form new
muscle fibers to replace those injured muscle fibers sa
skeletal muscle.
 While in the heart in normal conditions they are not
capable in regenerating after injury. Example is
during myocardial infarction.
 There are researches that are being conducted to
In addition to the contractile action, smooth muscle determine the ability of the muscle cells or cardiac
cells often synthesize components of the extracellular muscle cells to regenerate and how will they
matrix (ECM), usually synthesized by fibroblasts, such enhanced it or how they will use technologies in
as collagen, elastin, and proteoglycans. medicine that will later show advancement in the
TANDAAN KAY SMOOTH MUSCLE: repair as well as the renewal of the cardiac muscle.
o Si smooth muscle ang nag co cause ng  To all the type of muscle tissue that we have smooth
synchronized wave of contraction niya is si gap muscle has the huge ability to regenerate. Smooth
junction muscle is capable of regenerating after an injury.
o Difference between skeletal muscle and smooth  The skeletal muscle the regeneration capacity is
muscle. Remember in skeletal muscle has no cell limited and the cardiac muscle in normal conditions
to cell junction and the cells are elongated cells they are not capable of regenerating themselves
single. Bawat cell fiber or Muscle cells are after injury.
separate or single. While in cardiac branched siya.  In adventitia of the blood vessels, new smooth
So ung cell to cell communication or cell to cell muscles have been found to differentiate from
junction is via desmosomes and gap junction and undifferentiated mesenchymal stem cells. Smooth
of course your faciae adherentes. muscle progenitor cells differentiation is regulated by
o And for smooth muscle Gap junction lang ang a combination of intracellular and environmental
meron sa kanya factors, and developing muscles displays a wide
range of different phenotypes at various stages of
RENEWAL, REPAIR, AND DIFFERENTIATION their development. To date, no transcription factors
that are typical of smooth muscle cell lineage have
 The smooth muscles are composed of simpler, been identified.
mononucleated cells that are capable of dividing to  Smooth muscle cells have also been shown to
maintain or increase their number. develop from the division and differentiation of
o It means they are very active in mitosis. endothelial cells and pericytes during the repair
o Example of this cells are endothelial cells of the process after vascular injury. Vascular pericytes are
blood vessels as well as the pericytes that is also located within the basal lamina of the capillaries and
found in the blood vessels. postcapillary venules. They function as multipotential
o So ibig sabihin kapag nagkaroon tayo ng injury for menechymal progenitor cells. Its cytoplasmic
example sa blood vessel diba after sometime nag composition is hard to differentiate from that of the
he heal yan kasi very sa regeneration itong mga endothelial cell in capillaries.
cells natin sa smooth muscle tissue.
 By undergoing mitosis, viable smooth muscle cells may
REGENERATION OF MUSCLE TISSUE
respond to injury and remove the damage tissue
 Skeletal muscle- tissue can undergo limited
 In addition, smooth muscle contains regularly
regeneration
replicating populations of cells. During the usual
o Responsible for the regeneration is the myoblast
menstrual cycle and throughout birth, smooth muscle
that undergo proliferation and differentiation
in the uterus proliferates; these processes are
fused together to form muscle fibers
regulated under hormonal control.
o source of regenerating cells is the sparse
 The smooth muscle cells of the blood vessels also
population of mesenchymal satellite cells that lies
divide regularly in the adult, presumably to replace
within the external lamina of each mature muscle
damaged or senile cells; the smooth muscle of the
fiber
muscularis externa of the stomach and colon regularly
o Satellite cells become activated, proliferating and
replicates and may even slowly thicken throughout
fusing to form new skeletal muscle fibers after
lifespan.
injury
 Smooth muscle cells have also been shown to
 Cardiac muscle- no regenerative capacity beyond
develop from the division and differentiation of
early childhood
endothelial cells and pericytes during the repair
 Cardiac muscle when damage is not capable of
process after vascular injury
generating but some researches says that they are
REMEMBER:

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capable and also some research say may limited

capacity ang ating cardiac muscle. But in normal Cagayan State University PowerPoint presentation
condition they are not capable of regeneration.
o defects or damage in heart muscle are generally
replaced by fibroblast proliferation and growth of
connective tissue, forming myocardial scars
 Smooth muscle- capable of a more active
regenerative response.
o This can be observe in the blood vessel where we
can find the contractile pericytes
o viable smooth muscle cells undergo mitosis and
replace the damaged tissue after injury
o contractile pericytes- participate in the repair of
vascular smooth muscle
o if there is an injury in the blood vessel it can easily
heal because of the active regenerative capacity
of our smooth muscle

REFERENCES

Notes from the discussion by Prof. Ethel Mangada, RMT

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