SKELETAL MUSCLES

Muscular tissues contribute to homeostasis by producing body movements,

moving substances through the body & producing heat to maintain normal body
temperature.
 The three types of muscular tissue are : Skeletal, Cardiac & Smooth

Functions of Muscular Tissue

 Producing Body Movements

Skeletal muscles along with bones and joints are responsible for producing whole
body movements like running or localized movements like holding a pen.
 Maintenance of body posture
Skeletal muscle contractions stabilize joints and help maintain body posture,
such as standing or sitting.
 Storing and Moving Substances Within the Body
 Skeletal muscle contractions promote flow of lymph and venous return to heart.
 Cardiac muscle contractions of the heart pump blood through the blood vessels
of the body
 Smooth muscle contractions move food and substances such as bile and enzymes
through the gastrointestinal tract, push gametes (sperm and oocytes) through the
passageways of reproductive systems, and propel urine through urinary system.
 Temporary storage of food in the stomach or urine in the urinary bladder is
possible via smooth muscle sphincters.
 Generating heat
As muscular tissue contracts, it produces heat by a process known as
thermogenesis. This heat is used to maintain normal body temperature.
Involuntary contractions of skeletal muscles – shivering - can increase the rate of
heat production.

PROPERTIES OF MUSCULAR TISSUE

1. Excitability
Ability to respond to stimuli by producing action potentials. Action potentials
generated in muscles are called muscle action potentials. Both electrical signals
and chemical stimuli trigger muscle action potentials.

2. Contractility
It is the ability of muscular tissue to contract forcefully when stimulated by an
action potential. When a skeletal muscle contracts, it generates tension (force of
contraction) while pulling on its attachment points. If the tension generated is
great enough to overcome the resistance of the object to be moved, the muscle
shortens and movement occurs.
3. Extensibility
It is the ability of muscular tissue to stretch, within limits, without being
damaged. The connective tissue within the muscle limits the range of extensibility
and keeps it within the contractile range of the muscle cells.

4. Elasticity
It is the ability of muscular tissue to return to its original length and shape after
contraction or extension.

5. Refractory Period
A brief period of time during which the previously excited muscle fibre fails to
respond to the normal stimuli is termed as refractory period. It is very short about
2msec in mammals.

6. Tonicity
Muscle tone is defined as a reflex sustained & partial contraction of the muscle
that facilitates the maintenance of posture without causing muscle fatigue. A
muscle without a tone does not undergo fatigue because during tone production,
muscle fibers excite as batches - when one batch contracts, the other relaxes.

7. Conductivity
After the stimulation of muscle, a wave of contraction begins to flow from the point
of application of stimulus in both the direction along the complete muscle.

ANATOMY OF SKELETAL TISSUE

 Each skeletal muscle is composed of numerous muscle fibers or muscle cell.

 Skeletal muscle also contains connective tissues surrounding muscle fibers –
serves to protect, support and strengthen the skeletal muscle tissue.

CONNECTIVE TISSUE

The 3 layers of connective tissue are:

a) Epimysium: outermost dense & irregular C.T which covers the entire muscle.
b) Perimysium: The complete muscle is divided into numerous small bundles
(groups of 10-100 muscle fibers) called fascicles. Perimysium is a dense, irregular
C.T that surrounds or bounds each & every fascicle.
c) Endomysium: It is the thin, fine & delicate areolar C.T that covers each & every
muscle fibre & separates them from each other.

Tendon: all the three connective tissue sheaths i.e, epimysium, perimysium, &
endomysium run continously along the length of the muscle & merge at both the
ends of the muscle to form highly organized cord or rope like structure referred
as tendon. Tendon attach muscles to bones.
Blood & Nerve supply
 Each muscle is supplied with somatic motor neurons which helps the muscles to
contract.
 Along with each nerve, one artery and one or more veins penetrate into the
muscles. Arteries supply nutrients & oxygen required for the functioning of
muscle whereas veins help in the removal of waste material & heat produced
during muscle contraction.

MUSCLE FIBRE

 It is the structural & functional unit of the skeletal muscle. These muscle fibres
are long, elongated cylindrical structures with many nuclei.
 Muscle fibres lie parallel to one another with distinctive band-like appearance
having alternate dark & light striations.
 They are very long cells with length ranging from 10-30 cm & width ranging from
10-100 μm.

Components of Muscle Fibres

 Sarcolemma: the plasma membrane of a muscle cell. It is made up of lipid bilayer

sandwiched between the two protein layers.
 Transverse Tubule (T tubules): tiny invaginations from the surface of the
sarcolemma which emerge & move towards the centre of each muscle fibre. T-
tubules open to the outside of the fibre & are filled with interstitial fluid. Action
potential is tranferred along the sarcolemma to these T-tubules & spreads
throughot the muscle fibre.
 Sarcoplasm: the cytoplasm of muscle cells. It consist of :- (a) Mitochondria-
required for producing ATP. (b)Glycosomes-store glycogen for producing ATP.
(c)Myoglobin - oxygen binding, red coloured protein with function similar to Hb.
 Myofibrils: small elongated thread like structures which run parallel to the length
of the muscle fibre. About 100-1000s of myofibrils are present in a single muscle
fibre. Actually, myofibrils are bundles of myofilaments which are the contractile
 organelles or elements of the skeletal muscles. Responsible for the striated
appearance of the skeletal muscles.
 Each myofibril is encircled by membraneous fluid filled sacs called sarcoplasmic
reticulum (SR). SR stores Ca2+ & releases it to enhance the contraction of muscle.
 Sarcomere: basic functional unit of myofibrils. It is made up of thick & thin
myofilaments which are responsible for the straitions seen in the skeletal muscle.
 The central thick filaments are made up of a protein called myosin & they
form the dark band.
 Thin filaments which are made up of protein actin form the light band.

 Part of thin filaments overlap with thick filaments forming different bands.
 A band: Darker middle part of the sarcomere, dark band formed by overlapping
of thin filaments over thick filaments. It extends the entire entire length of the
thick filaments.
 I band: It is a light band formed only by thin filaments.
 H Zone: found in the middle of each A band, that contains only thick filaments.
 Z disc: it is a narrow region that passes through the centre of each I band. it
separates one sarcomere from the other.
 M line: It is a narrow region present in the centre of the H zone that contains
proteins that hold the thick filaments together at the centre of the sarcomere.
 Composition of Myofibrils
Myofibrils are made up of 3 types of proteins:
 Contractile proteins : Actin & Myosin
 Regulatory proteins: Tropomyosin & Troponin
 Structural proteins:- Titin, Myomesin, Nebulin & Dystrophin

(a) Contractile proteins: responsible for the generation of force for contraction.
 Actin (Component of thin flament) - The main component of the thin filament
is the protein actin. Individual actin molecules join to form an actin filament that
is twisted into a helix. On each actin molecule is a myosin-binding site, where a
myosin head can attach during muscle contraction.
 Myosin (component of thick filament) - consist of a tail & 2 myosin heads which
bind to the myosin binding sites on actin molecules of thin filament during muscle
contraction. Each myosin head has two binding sites: (1) an actin-binding site
and (2) an ATP-binding site. The ATP-binding site also functions as an ATPase—
an enzyme that hydrolyzes ATP to generate energy for muscle contraction.

(b) Regulatory proteins (Tropomysin & Troponin): control actin –myosin interaction
or on-off function of contraction.
 In a relaxed muscle, tropomyosin occupy the myosin binding sites present on
actin whereas troponin functions to hold the tropomyosin strands properly.
 When Ca2+ bind to troponin, it changes shape, this conformational change moves
tropomyosin away from myosin binding sites on actin molecules & muscle
contraction begins as myosin bind to actin.
(c) Structural proteins: help in maintaining accurate alignment, stability,
extensibility & elasticity of myofibrils.
 Titin:- it prevents sarcomeres from being pulled apart. connects the Z disc to
M line of sarcomere.
 Myomesin:- binds to titin & helps in holding successive thick filaments
together.
 Nebulin:- assists in the binding of thin filaments with Z line .
 Dystrophin:- it is a cytoskeleton protein that binds thin filaments of
sarcomere to sarcolemma via integral membrane proteins.

PHYSIOLOGY OF MUSCLE CONTRACTION

 Physiology of contraction of skeletal muscle is explained by Sliding filament

theory.
 According to this theory, contraction is due to the sliding of thin filaments over
the thick ones such that actin & myosin filaments overlap to greater extent,
meeting at the centre of sarcomere  shortening of sarcomere shortening of
whole muscle fibre.
 For a contraction to begin, it mainly needs to be stimulated by a nerve ending or
axon that transmits action potential or electrical impulse. This impulse results in
increased intracellular levels of Ca2+ ions which finally induces contraction.
 The events that cause muscle contraction are as follows:
 CONTRACTION CYCLE

 It begins with the release of Ca2+ ions from the Sarcoplasmic reticulum into the
cytosol.
 Ca2+ bind to troponin & result in the removal of tropomyosin from the myosin-
binding sites present on actin.
 Once the binding sites become free, the repeating sequence of events that cause
muscle contraction begins:
a) Hydrolysis of ATP: Myosin head consists of ATP binding site & ATPase. The
enzyme ATPase brings about hydrolysis of ATP to ADP & a Phosphate group (both
attach to myosin head). The energy obtained from ATP hydrolysis is stored in
myosin head thereby reorients and activates the myosin head.
b) Attachment of myosin to actin to form Cross-bridges: Activated myosin heads
bind to myosin-binding site actin & release the phosphate group.  thus form
cross-bridges.
c) Power Stroke:
 After the cross-bridges form, the myosin head pivots  causing the cross-bridge
to rotate inwards towards the sarcomere  producing a force which results in
the sliding of thin filament over thick filaments towards the M-line & this in turn
results in the shortening of sarcomere. This process is known as power stroke.
During power stroke, ADP is released from myosin head.
 If enough nerve fibres are stimulated, it results in shortening (contraction) of the
entire muscle.
d) Detachment of myosin from actin: At the end of powerstroke, the crossbridge
remains firmly attached to actin until it binds another molecule of ATP. As ATP
binds to the ATP- binding site on the myosin head, the myosin head detaches
from actin.

 This contraction cycle continues as long as ATP & Ca2+ ions are available & the
newly bound ATP is hydrolyzed.
 The cross-bridges keep rotating back and forth with each power stroke, pulling
thin filaments towards M-line.
 At a time, few myosin heads attach to actin while few detach & get ready to bind
again.
 Contraction cycle

EXCITATION – CONTRACTION COUPLING

 Excitation-contraction coupling is defined as the series of events that result

in the propagation of action potential along the length of sarcolemma &
consequent sliding of thick & thin myofilaments.
 Action potential stops well before the signs of contraction appear.
 Excitation –contraction coupling occurs in the latent period present between the
initiation of action potential & shortening of muscle fibres. It takes place in the
following order:
 Muscle action potential propagates along the sarcolemma to the transverse T-
tubules.
 Propagation of action potential to the T-tubules causes the Ca2+ release channels
on SR to open  the release of Ca2+ ions from the SR into sarcoplasm around the
 thick & thin filaments. As a result, the levels of Ca2+ ions in the sarcoplasm
increase by tenfold or even more.
 This released Ca2+ binds to troponin  troponin undergoes a conformational
change  The altered troponin moves tropomyosin away from the myosin binding
site present on actin & thus sets the binding site free for the myosin heads to bind
& form cross bridges  leads to muscle contraction.
 After the last action potential has propagated throughout the T tubules, the Ca2+
release channels close. As the Ca2+/ATPase pumps move Ca2+ back into the SR,
the Ca2+ level in the sarcoplasm rapidly decreases  Ca2+ is released from
troponin  tropomyosin covers the myosin-binding sites on actin  the muscle
fiber relaxes.

NEUROMUSCLAR JUNCTION & GENERATION OF ACTION POTENTIAL

 Somatic motor neurons are responsible for stimulating the skeletal muscle. A
single motor neuron supplies to various muscle fibres.
 Synapse formed between a motor neuron axon & a muscle fibre is called a
neuromuscular junction (NMJ).
 Each somatic motor nerve cell consists of an axon that runs from brain or spinal
cord to a bundle of skeletal muscle fibres. The region of muscle facing the synaptic
end bulbs of axon is called motor end plates.
 ACh (Acetyl choline) is the neurotransmitter which helps in transmitting action
potential from one cell to another.

A nerve impulse (nerve action potential) elicits a muscle action potential in

the following way:

a) Release of ACh: arrival of nerve impulse at the synaptic end bulbs stimulate
opening of voltage-gated Ca2+ channels  Ca2+ influx  stimulates exocytosis of
synaptic vesicles  releasing Ach into synaptic cleft  ACh then diffuses across
the synaptic cleft between the motor neuron and the motor end plate.
b) Activation of ACh receptors: Binding of two molecules of ACh to the receptor on
the motor end plate, opens an ion channel in the ACh receptor. As a result, most
ions especially Na+ ions can flow across the membrane.
c) Production of muscle action potential: Influx of Na+ ion causes slight alteration
in the membrane potential. The inner side of the membrane becomes more
positively charged (depolarization)  triggers a muscle action potential  which
propagates along sarcolemma into T tubules  cause sarcoplasmic reticulum to
release Ca2+ into sarcoplasm  muscle fibre contract.
d) Termination of ACh activity: effect of ACh is stopped by hydrolysis of ACh by
the enzyme Acetylcholinesterase (AChE). AChE breaks down ACh into acetyl
and choline, products that cannot activate the ACh receptor.
 DISORDERS

 Myasthenia Gravis:- It is an autoimmune disease that causes chronic,

progressive damage of the neuromuscular junction. The immune system produces
antibodies, which binds to Ach receptors & decreasing the number of functional
ach receptor at motor end plates of skeletal muscles.
 Muscular dystrophy:- refers to a group of inherited muscle desroying diseases
that cause progressive degeneration of skeletal fibres.
 Fibromyalgia:- is a painful nonarticular rheumatic disorder that usually appears
between the ages of 25 & 50. The disorder affects the fibrous C.T components of
muscles, tendons & ligaments.