Muscle Contraction physiology

Muscle Physiology
Dr.Murad H Kazi

General Properties of Muscle
• Excitability – Able to receive and respond to external
Stimuli.
• Contractility – Muscles are able to shorten.
• Extensibility – Muscles are able to be stretched without
damage.
• Elasticity – Ability to return to its original shape after stretch.

Functions of muscle
• Motion – walking , running , Beating of heart.
• Maintenance of posture.
• Heat Production – shivering is a way to keep body
temperature constant.

Types of musclesTypes of muscles
Histologically muscles can be classified
into following three types:-
Striated Muscle:
• Skeletal muscle ( Voluntary)
• Cardiac muscle ( Involuntary)
Unstriated Muscle
• Smooth muscle ( Involuntary )

Muscular tissueMuscular tissue
• It is composed of the cells which are
specialized for shorten the length by
contraction.
• Functional and structural unit of muscle is
called muscle fiber.
• The specialized cells of muscular tissue is
regarded as MYOCYTE.

Skeletal muscleSkeletal muscle
• AKA striated muscle
• AKA voluntary muscle
• Skeletal muscle in an adult male is 42% of body
weight and in an adult female is 36% body weight.
• We can voluntarily use this muscle.
• They have transverse striation on them that’s why also
regarded as striated muscle.

• The word “Sarcolemma”“Sarcolemma” is used for the cell
membrane of myocyte.
• The word “Sarcoplasm”“Sarcoplasm” is used for the
cytoplasm of the myocyte.
• The smooth endoplasmic reticulum of muscular
cell is regarded as “Sarcoplasmic reticulum”“Sarcoplasmic reticulum”
It contains a protein called “ calsequestrin” ,
which can bind upto 40 times more Ca 2+.
• The sarcoplasm is filled with numerous
longitudinal fibrils, which is regarded as
“Myofibrils”“Myofibrils”

The sarcoplasm is filled with long cylindrical filamentous bundles
called myofibrils. The myofibrils run parallel to the long axis of the
muscle fiber.

Composition of Myofibrils
• Each myofibril contains :
(i) 1500 myosin(thick) filaments.
(ii) 3000 actin ( thin) filaments.
Actin and Myosin filaments partly interdigitate causing
alternate dark and light bands.

• Dark band is regarded as “A band” containing actin and
myosin filaments where they overlap.
• Light band is regarded as “I band” containing only actin
filament.
Dark band
Light band

In each Dark band (A band) there is a lighter zone which is regarded as “H
zone”
H zone : Light area in center of A band. Seen when muscle is stretched
beyond its resting length, due to pulling apart of actin filaments.
Dark band
Light band
Z line
H zone

Dark band
Light band
Z line
In each H zone there is a dark line in its center, which is regarded as “M line”
H zone M line

In each light band (I band) there is a dark line
which is regarded as “Z line”
Dark band
Light band
Z line
Z disc : It is a disc ( plate) of filamentous protein to which actin filaments are
attached. Z discs passes from myofibril to myofibril and attaches them together.
Sarcomere : Portion of myofibril between two successive Z discs is called
sarcomere.

• A band :A band :
dark band
• I band :I band :
light band
• Z line:Z line:
a thin dark line across the middle of I band
• H zone:H zone:
a lighter band in the centre of the A band
• M line:M line:
a thin dark line running through the centre of the H band

SarcomereSarcomere
• Part of myofibril between two consecutive
z line is regarded as sarcomere.
• It is the smallest structural and functional
unit of skeletal muscle.
• Composition: 1/2 I + A + 1/2 I

½ I½ I½ I½ I 1 A1 A++ ++
sarcomere

Two types of filaments in muscle tissueTwo types of filaments in muscle tissue
Thick filamentsThick filaments
• Composed of myosin.
• Exists in the A band
Thin filamentsThin filaments
• Composed of actin, tropomyosin, troponin
• One end is inserted into the Z line, the
other is free and extends into the A band.

Actin monomer
troponin
tropomyosin
Thin filament
Actin + Troponin + Tropomyosin = Thin filament

½ I ½ I
When muscle contracts, the
sarcomere shortens. The I band
and H Zone also shorten. But
the length of the A band remains
the same.

Arrangement of myofilaments
• I bandI band
Only thin filaments
• A bandA band
Both thick and thin filaments
• H zoneH zone
Only thick filaments
• Z lineZ line
Anchor for thin filaments
• M lineM line
Fixation of thick filaments

Sliding filament hypothesisSliding filament hypothesis
• It suggests that the thin filaments slide along the thick
filaments toward the M line.
• During the contraction, thin filaments slide more and
more into H zone.
• As a result the I bands decrease in width.
• H zone shortens or disappears.
• But the width of A bands are unchanged.

Connective tissue framework of muscleConnective tissue framework of muscle

Connective tissue framework of muscleConnective tissue framework of muscle
• EpimysiumEpimysium
• PerimysiumPerimysium
• EndomysiumEndomysium

T-tubuleT-tubule
• AKA transverse tubule
• It is a deep invagination (or inward extension)
of the sarcolemma in the form of penetrating
tubules in transverse direction to the length of
muscle fiber.
• Only found in skeletal and cardiac muscle cells.
• These invaginations allow depolarization of the
membrane to quickly penetrate to the interior of
the cell. Thus helps to conduct action potential
from sarcolemma to deep interior of muscle
fiber.

Terminal cisternaeTerminal cisternae
• Terminal cisternae are enlarged areas of
the sarcoplasmic reticulum surrounding
the transverse tubules
• These regions within the muscle cell store
calcium, increasing the capacity of the
sarcoplasmic reticulum to release calcium and
release it when an action potential courses down
the transverse tubules, eliciting muscle
contraction.

Muscle triadMuscle triad
• Only found in skeletal muscle.
• Composed of :
– T-tubuleT-tubule
– Terminal cisterna on either sideTerminal cisterna on either side

Types of skeletal muscleTypes of skeletal muscle
• Red muscle / slow twitch fibres
• White muscle / fast twitch fibres
The name has been given on the basis of
their color.

Red muscle / Slow FibersRed muscle / Slow Fibers
• AKA type I fibres.
• They look red because they have high quantity of MYOGLOBIN in
sarcoplasm.
• They are narrower and shorter because they have less myofibrils and
more sarcoplasm, so less prominent striation.
• Although they contract slowly the contraction is more sustained i.e
prolonged continued muscle contraction.
• Mitochondria is more in number.
• Increased Myosin
• Innervated by smaller nerve.
• More blood supply. Capillary bed is reacher around red fibre.
• Nuclei may not be in peripheri, it may be deeper into fibre.
• Glycogen is more.
• Sarcoplasmic reticulum is less extensive.
• They fatigue less.
• Example: Gastrocnemius

White muscle / Fast fibersWhite muscle / Fast fibers
• AKA type II fibres.
• They look white because they have low quantity of MYOGLOBIN in
sarcoplasm so more prominent striation.
• They are wider and longer because they have high amount of myofibrils and
less sarcoplasm.
• Nuclei are mostly in peripheri.
• Mitochondria is less in number.
• Glycogen is less. As they have increased glycolytic enzymes.
• Sarcoplasmic reticulum is more extensive.
• Capillary bed is not reacher around white fibre. Less blood supply.
• Although they contract fast and rapid , but the contraction is less sustained.

Features Red Fibre White fibre
• Colour Reddish Whitish
• Myoglobin Large amount Comparatively less
• Cross striation Less More
• Sarcoplasm Relatively abundant Relatively less
• Blood supply More Less
• Mode of
action
Acts slowly & capable of
sustained contraction
without fatigue
Capable of more powerful
contraction but fatigue
more rapidly

Cardiac muscleCardiac muscle
• It is involuntary.
• It is striated.
• Found in the the myocardium.
• The cells that constitute cardiac muscle are
called cardiomyocytes or myocardiocytescardiomyocytes or myocardiocytes.

Similarities between CardiacSimilarities between Cardiac
muscle and skeletal musclemuscle and skeletal muscle
• Both of them are made up of elongated fibre.
• Both of them show transverse striation.
• Connective tissue framework are same in both of
them.
• There is presence of A,I bands, H zone, M,Z lines.
• There is presence of T-tubule in both of them.

Cardiac muscle
Skeletal muscle

Differences of Cardiac muscleDifferences of Cardiac muscle
from skeletal musclefrom skeletal muscle
• They are involuntary.
• Cardiac muscle has branches.
• Only one nucleus in one cardiomyocyte.
• Nucleus is located centrally.
• There is no triad, but it has got DYAD.DYAD.
• The junction between adjoining myocyte has darkened
lines called as INTERCALATED DISK.INTERCALATED DISK.

•striated muscle
•striations less distinct.

- has two or more branches at its ends.
- one or two centrally-located nuclei.

intercalated discs.
Intercalated discsIntercalated discs

Dyad of cardiac muscleDyad of cardiac muscle
Dyad

Smooth muscleSmooth muscle
• AKA plain muscle.
• It is involuntary.
• It is non-striated muscle because it doesn’t have
transverse striation.
• But it has longitudinal striations.
• The shape is spindle like.
• Single nucleus.

Comparison of typesComparison of types

Contraction of skeletal muscleContraction of skeletal muscle

General Mechanism of Muscle ContractionGeneral Mechanism of Muscle Contraction
Steps of muscle contractionSteps of muscle contraction
1. An action potential travels along a motor nerve
to its endings on muscle fibers.
2. At each ending, the nerve secretes a small
amount of the neurotransmitter substance
acetylcholine.

3.The acetylcholine acts on a local area of the
muscle fiber membrane to open multiple
“acetylcholine gated” channels.
4. Opening of the acetylcholine-gated channels
allows large quantities of sodium ions to diffuse
to the interior of the muscle fiber membrane.
This initiates an action potential at the
membrane.

5. The action potential travels along the muscle
fiber in the same way that action potentials
travel along nerve fiber membranes.
6. The action potential depolarizes the muscle
membrane, and much of the action potential
electricity flows through the center of the
muscle fiber.
It causes the sarcoplasmic reticulum to release
large quantities of calcium ions.

7. The calcium ions initiate attractive forces between the
actin and myosin filaments, causing them to slide
alongside each other.
8. After a fraction of a second, the calcium ions are
pumped back into the sarcoplasmic reticulum by a
Ca++ pump, and they remain stored in the reticulum
until a new muscle action potential comes along.
This removal of calcium ions from the myofibrils causes
the muscle contraction to cease.

Molecular Mechanism of Muscle ContractionMolecular Mechanism of Muscle Contraction
Sliding filament hypothesisSliding filament hypothesis
• ““A” band remains the sameA” band remains the same
• ““I” band decreasesI” band decreases
• ““H” zone disappearsH” zone disappears

Thick filamentThick filament
• It is composed of myosin filament.
• Each myosin filament is composed of around
200 myosin molecule.
Myosin molecule

Myosin moleculeMyosin molecule
- Each myosin molecule is composed
of 2 heavy chains and 4 light chains.
- That is to say altogether 6 chains compose myosin
molecule.

Myosin filamentMyosin filament

Myosin filamentMyosin filament
• Body
– The tails of the myosin molecules bundled together to form
the body of the filament
• Cross bridge
– The protruding arms and heads together are called cross-
bridges.
• Hinge
– Each cross-bridge is flexible at two points called hinges—
one where the arm leaves the body of the myosin filament,
and the other where the head attaches to the arm.

Thin FilamentThin Filament
• AKA “Actin filament”
• Composed of 3 molecules.
– Actin monomer (G actin)
– Tropomyosin
– Troponin

Actin monomer
troponin
tropomyosin
Thin filament
Actin + Troponi + Tropomyosin = Thin filament

• The backbone of the actin filament is a double
stranded F-actin protein molecule.
• Each strand of the double F-actin helix is composed of
G-actin molecules.
• Attached to each one of the G-actin molecules is one
molecule of ADP.
• It is believed that these ADP molecules are the active
sites on the actin filaments with which the cross
bridges of the myosin filaments interact to cause
muscle contraction.

Tropomyosin MoleculesTropomyosin Molecules
• These molecules are wrapped spirally around
the sides of the F-actin helix.
• In the resting state, the tropomyosin molecules
lie on top of the active sites of the actin strands,
so that attraction cannot occur between the
actin and myosin filaments to cause
contraction.

TroponinTroponin
• These are complexes of three loosely bound protein subunits:
• Troponin ITroponin I
– Has a strong affinity for actin.
• Troponin TTroponin T
– Has a strong affinity for tropomyosin.
• Troponin CTroponin C
– Has a strong affinity for calcium ions.
• This complex is believed to attach the tropomyosin to the actin.
• The strong affinity of the troponin for calcium ions is believed to
initiate the contraction process.

• Actin filament without the presence of the troponin-tropomyosin
complex has a strong affinity to bind with the heads of the
myosin molecules.
• If the troponin tropomyosin complex is added to the actin
filament, the binding between myosin and actin does not take
place.
• Therefore, it is believed that the active sites on the normal actin
filament of the relaxed muscle are covered by the troponin
tropomyosin complex.
Before contraction can take place, the inhibitory effect of the
troponin-tropomyosin complex must itself be inhibited.

Inhibition of inhibitory mechanism of troponin
tropomyosin complex
• When calcium ions combine with troponin C, the
troponin complex undergoes a conformational change
and moves it deeper into the groove between the two
actin strands.
• This “uncovers” the active sites of the actin, thus
allowing these to attract the myosin cross-bridge
heads and cause contraction to proceed.

Sliding Filament mechanism of Muscle
contraction
• Action potential over muscle membrane Ca 2+
released from sarcoplasmic reticulum Active site
on actin filament uncovered Interaction between
active site (ADP) of actin and cross bridge of myosin
(they walk along) Actin filament is pulled inward
over myosin filament, i.e they slide over each other
Z discs pulled closer Sarcomere shorten
Muscle contracts.

Walk along theory of muscle
contraction
When active site of actin filament uncoveredHead of
cross bridge attaches to active site New alignment
of intermolecular forces the head tilts towards arm
(power stroke)  Actin filament move towards center
of sarcomere  Head detaches from active
siteHead bind with new active site Another power
strokeActin filaments move more towards
centerThus heads of cross bridges walk step by
step along actin filament, pulling actin filament towards
center of myosin filament Sarcomere shorten 
Muscle contracts.

The “Walk-Along” Theory of Contraction

• AKAAKA “ratchet” theory“ratchet” theory
• As soon as the cross-bridges from the myosin
filaments become attracted to the active sites
of the actin filament, in some way, causes
contraction to occur.

Greater the number of cross-bridges inGreater the number of cross-bridges in
contact with the actin filament, greater iscontact with the actin filament, greater is
the force of contraction.the force of contraction.

Sources of energy for muscle
• ATP
– Concentration of ATP in muscle fibre is
around 4 mmolar.
– Sufficient to maintain contraction only for 1-2
seconds at most.

Rigor MortisRigor Mortis
• Several hours after death, all the muscles of the body go into a
state of contracture called “rigor mortis”; that is, the muscles
contract and become rigid, even without action potentials.
• This rigidity results from loss of all the ATP, which is required to
cause separation of the crossbridges from the actin filaments
during the relaxation process.
• The muscles remain in rigor until the muscle proteins
deteriorate.
• Lasts about 15 to 25 hours.
All these events occur more rapidly at higher temperatures.

Fenn effectFenn effect
• The greater the amount of work performed
by the muscle, the greater the amount of
ATP that is cleaved to ADP, which is
called the Fenn effect.

Sources of energy for muscle
• ATP
• Phosphocreatine
• Glycolysis in cytosol
• Citric acid cycle in mitochondria

Remodeling of muscle to match function
• HYPERTROPHY – Increase in cell size
– When the total mass of a muscle increases
– This is due to increase in size of actin and myosin
– Increase in no. of muscle fiber ( hyperplasia)
• ATROPHY
– When the total mass of a muscle decreases
– When a muscle remains unused for many weeks,
the rate of decay of the contractile proteins is more
rapid than the rate of replacement.
– Muscle denervated.

Types of muscle contraction
• Isometric contraction
– When the muscle length does not change ( shorten)
during contraction, but the tension changes ; it is
called isometric contraction.
• Isotonic contraction
– When it does change (shorten) during contraction,
but the tension on the muscle remains constant
throughout the contraction; it is called isotonic
contraction.

Muscle fatigue
• Loss of capacity of muscle to respond to
stimulus is called muscle fatigue.
Causes :
(i)Prolonged and strong contractions
(ii)Glycogen depletion
(iii)Lactic acid accumulation
(iv)Decreased neuromuscular transmission.
(v)Decreased blood flow

• The process by which depolarization of the
muscle fiber initiates muscle contraction is
called Excitation –Contraction coupling.
• Tetanisation: When muscle is stimulated at
progressively greater frequency, at a certain
higher frequency successive contractions fuse
together and cannot be distinguished from one
another ; this is called tetanization

Neuromuscular JunctionNeuromuscular Junction

SynapseSynapse
• A structure that permits a neuron to pass an electrical
signal to another cell.
• Components of synapseComponents of synapse
• Pre-synaptic membrane :
– The axon ending of the neuron that secretes the
neurotransmitters.
• Synaptic cleftSynaptic cleft ::
– The space that separates the pre-synaptic terminal from the
postsynaptic cell.
Postsynaptic membrane :
– The membrane of the cell on which the neurotransmitter
acts.

Neuromuscular junctionNeuromuscular junction
• Motor nerve ending makes a junction, with the muscle
fiber called the neuromuscular junction (NMJ).
Components of NMJComponents of NMJ
• Pre-synaptic membrane :
– Membrane of motor neuron.
• Synaptic cleftSynaptic cleft ::
– The space that separates the pre-synaptic terminal from the
muscle.
• Postsynaptic membrane :

1. Presynaptic
terminal
2. Sarcolemma
3. Synaptic
vesicles
4. Acetylcholine
receptors
5. Mitchondrion

NeurotransmitterNeurotransmitter
• A chemical substance secreted by a nerve
ending into the synapse.
• Acts on receptor proteins in the post synaptic
membrane to excite / inhibit / modify its
function.
• E.g.
– Acetylcholine
– Norepinephrine
– Epinephrine
– Gamma-aminobutyric acid (GABA)

Accetylcholine
• It is the first neurotransmitter to be
identified.
• Functions both in the CNS and PNS as
neuromodulator.

Ach synthesis, storage and releaseAch synthesis, storage and release
ACh is concentrated and
stored in synaptic
vesicles.
Each vesicle stores ~
molecules.
These loaded vesicles are
released as the basic
quanta, or packets, of the
transmission process.
4
10

Destruction of Released AcetylcholineDestruction of Released Acetylcholine
• Acetyl cholinesterase breaks acetylcholine
into choline and acetate.
• Choline is taken back into the neuron.
• Some acetylcholine diffuses from the
synaptic cleft into the adjacent tissue.

• Choline is taken
by the neuron.

Release of Acetylcholine in synaptic cleftRelease of Acetylcholine in synaptic cleft
• Nerve impulse reaches NMJ
• When action potential arrives the terminal
voltage gated calcium channels opens.
• Influx of calcium ion into the axon terminal.
• This causes the release of acetylcholine from
synaptic vesicles into the synaptic cleft.

Release of Acetylcholine in synaptic cleftRelease of Acetylcholine in synaptic cleft
• Exocytosis
• The process by which vesicles attach to the
membrane and release the substance out of
the cell.

Acetylcholine ReceptorAcetylcholine Receptor
Is a protein complex made up of 5 protein
subunits.
• 2 alpha proteins
• Beta protein
• Delta protein
• Gamma protein

End Plate PotentialEnd Plate Potential
• A local positive potential change caused by the
influx of sodium ion.
• This in turn initiates an action potential along
the membrane of the muscle cell.

Fatigue of the NMJFatigue of the NMJ
• EPP created is 3 times more than what is
needed to generate the action potential along
sarcolemma.
• Stimulation 100 times/second for several
minutes.
• Number of acetylcholine vesicles decrease.
• Impulse fails to pass into the muscle fiber.
• This is called fatigue of NMJ.

Myasthenia GravisMyasthenia Gravis
• Autoimmune disease in which the person
becomes paralysed because impulses
cannot be transmitted through
neuromascular junction.
• Antibody formed against the Acetylcholine
receptors.
• Results in weakness or fatigability.

Excitation and ContractionExcitation and Contraction
of Smooth Muscleof Smooth Muscle

• Doesn’t have T-tubule.
• It doesn’t contain Troponin.
Dense bodyDense body
• Actin filaments in smooth muscle are anchored by
dense body.
• It is the similar structure to “Z-line” in skeletal muscle.

CaveolaeCaveolae
• Small invaginations of the sarcolemma of
smooth muscle cell.
• It is analog of the transverse (T) tubule system
of skeletal muscle.
• Sarcoplasmic reticulum lie near the caveolae,
which, when stimulated secretes Ca++.

• Most of the myosin filaments have “sidepolar” cross-
bridges.
• Bridges on one side hinge in one direction and those
on the other side hinge in the opposite direction.
• This allows the myosin to pull an actin filament in one
direction on one side while simultaneously pulling
another actin filament in the opposite direction on the
other side.
• It allows smooth muscle cells to contract as much as
80 per cent of their length instead of being limited to
less than 30 per cent, as occurs in skeletal muscle.

Types of Smooth MuscleTypes of Smooth Muscle
1. Multi-Unit Smooth Muscle
2. Single-Unit Smooth Muscle

Multi-Unit Smooth MuscleMulti-Unit Smooth Muscle
• Cells or groups of cells act as independent
units of smooth muscle fibers. Each unit is
covered by glycoprotein layer and
innervated by single nerve ending.
• No Gap Junction.
• Eg : Erector pili muscle of skin and iris of
eye , Ciliary muscle of eye.

Single-Unit Smooth MuscleSingle-Unit Smooth Muscle
• AKA “Visceral muscle” in which sheet or
bundles of muscle fibers are interconnected
by gap junctions that allow free flow of ions
between fibers thus forming a single
functional unit.
• Only a few muscle fibers innervated in each
group
• Impulse spreads through gap junctions
• Contracts as a single unit
• Example : Gut wall , bile duct, Ureter , Uterus

Nerve innervation of smooth muscleNerve innervation of smooth muscle
• Autonomic nerve fibers that innervate smooth muscle
generally branch.
• The axons that innervate smooth muscle fibers do not have
motor end plate as on skeletal muscle. Instead, have multiple
varicosities.
• At varicosities the Schwann cells that envelop the axons are
interrupted so that neurotransmitter can be secreted.
• In contrast to the vesicles of skeletal muscle junctions, which
always contain acetylcholine, the vesicles of the autonomic
nerve fiber endings contain acetylcholine in some fibers and
norepinephrine in others—and occasionally other substances
as well.

Excitation of Smooth muscleExcitation of Smooth muscle
Can be stimulated by multiple types of signals:
• By nervous signals
• By hormonal stimulation
• By stretch of the muscle
• In several other ways………

The AP of visceral smooth muscleThe AP of visceral smooth muscle
(1) Spike potentials
(2) Action potentials with plateaus

Spike PotentialsSpike Potentials
• Rapid depolarization &
repolarization.
• The duration of this type of
action potential is 10 to 50
milliseconds.

Action Potentials with PlateausAction Potentials with Plateaus
• Depolarization is rapid but repolarization is
delayed for several hundred to 1000
milliseconds (1 second).
• The importance of the plateau is that it can
account for the prolonged contraction.
• Such as the ureter.

Smooth muscle excitationSmooth muscle excitation
-contraction (Steps)-contraction (Steps)
1. An action potential in the ANS, motor neuron travels
through the axon and reaches the synaptic terminal.
2. The action potential causes activation of
Ca2+ channels on the presynaptic terminal inducing
influx of Ca2+ ions inside the neuron.
3. This increase in concentration of Ca2+ will cause
exocytosis of synaptic vesicle & expel of
neurotransmitter in the synaptic cleft.

Smooth muscle contraction - StepsSmooth muscle contraction - Steps
4. The Ca2+accumulated inside the smooth
muscle cell binds with calmodulin giving rise
to the Ca2+-calmodulin complex.
5. The Ca2+-calmodulin complex bind and
activates Myosin Light Chain Kinase (MLCK).
6. MLCK phosphorylates the myosin light chain
enabling the myosin crossbridge to bind to the
actin filament and allow contraction to begin.

Smooth muscle contraction - StepsSmooth muscle contraction - Steps
7. Dephosphorylation of the myosin light chain
with subsequent termination of muscle
contraction occurs through activity of another
enzyme called Myosin Light Chain
Phosphatase (MLCP).
8.Contraction occurs as long as Ca2+ is present
at high concentrations in the cytosol.

Smooth Muscle Contraction: MechanismSmooth Muscle Contraction: Mechanism

Smooth Muscle Relaxation: MechanismSmooth Muscle Relaxation: Mechanism

““Latch” MechanismLatch” Mechanism
• “Latch” literally means “to lock”.
• The mechanism by which smooth muscle can maintain
prolonged contraction for hours with little use of energy.
• Once smooth muscle has developed full contraction, the
amount of continuing excitation is reduced to far less than
the initial level, yet the muscle maintains its full force of
contraction.
• The energy consumed to maintain contraction is often
minuscule, sometimes as little as 1/300 the energy
required for comparable sustained skeletal muscle
contraction.

Mechanism of Latch PhenomenonMechanism of Latch Phenomenon
• When the MLCK & MLCP, are both strongly
activated, the cycling frequency of the myosin
heads and the velocity of contraction are great.
• When enzymes decreases, the cycling
frequency decreases, but at the same time,
myosin heads remain attached to the actin
filament for a longer and longer proportion of
the cycling period.

Muscle Contraction physiology

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