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MUSCLE PHYSIOLOGY
By Tekle H.
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CONTENTS
 Introduction
 Skeletal muscle
 Structure and organization
 Muscle fiber anatomy
 Mechanism of muscle contraction
 Neuromuscular junction
 Excitation contraction coupling
 Sliding filament mechanism
 Mechanism of muscle relaxation
 Energetics of muscle contraction
 Cardiac muscles
 Smooth muscles
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INTRODUCTION
Muscle:
 Is a fleshy, reddish colored tissue in the body
 Comprises the largest group of tissues in the body
 Muscles constitutes of 40-50% of body weight
 About 40% of the body is skeletal muscle, and
 Another 10% is smooth and cardiac muscle
 Muscle cells are specialized to generate mechanical force from chemical
energy
 This force is used to regulate the internal environment, and used for movement
of the body in reference to the external environment
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 There are three types of muscle cells and tissues
 Skeletal, cardiac, or smooth muscle cells and tissues
 The three types of muscle tissues are identified on the basis of
location, structure, contractile properties, and control
mechanisms
 Most skeletal muscles are attached to bone
 Their contraction is responsible for supporting and moving
the skeleton
 Contraction of skeletal muscle is initiated by action
potential from motor neurons of the somatic nervous
system
 That is why these are under voluntary control
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 Smooth muscle surround various hollow organs and
tubular structure
 Including the digestive tract, urinary bladder and tracts,
uterus, blood vessels, and airways
 Contraction of smooth muscle decreases either the
diameter or the length of these structures and
 Propel the luminal contents through the hollow organs, or
 Regulate internal flow by changing the tube diameter
 For example, contraction of smooth muscle cells along the
esophagus helps “squeeze” swallowed food to the stomach
 Furthermore contraction of smooth muscle stand up the
hairs of the skin and change diameter of the pupil
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 Smooth muscle contraction is involuntary
 It occurs under the control of autonomic nervous system,
hormones, autocrine or paracrine signals, and other local
chemical factors
 In some cases it occurs autonomously
 Cardiac muscle is the muscle found in the wall of the
heart
 Its contraction enables the heart to pump blood
 Like smooth muscle, this is also involuntary
 Regulated by the autonomic nervous system, hormones, and
other glandular signals
 It can undergo spontaneous contractions
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COMMON PROPERTIES OF
MUSCLES
1. Excitability- ability to respond to stimulus which could be from motor
neuron or a hormone
2. Contractility- The ability to shorten forcibly when adequately
stimulated
3. Extensibility- The ability to be stretched or extended
4. Elasticity- The ability to recoil and resume original length after being
stretched or contracted
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SKELETAL MUSCLE
Skeletal Muscles
 Are muscles that
causes the skeleton to
move at joints
 They are attached to
the skeleton by
tendons
 The tendons transmit
the muscle force to
the bone
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Skeletal muscles are
 Long cylindrical cells
 Many nuclei per cell
 Voluntary
 Rapid contractions
 Are well supplied with nerves and blood vessels
 Are striated muscle type
 Due to the distinct series of alternating light and dark
bands
 Cardiac muscles have same feature
 But, the smooth muscle lacks striation and is named after
it
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 During development, each skeletal muscle fiber is
formed by the fusion of a number myoblasts
(undifferentiated, mononucleated cells) into a single,
cylindrical, multinucleated cell
 That differentiation is completed around birth and
continue to increase in size to adulthood
 Compared to others, skeletal muscle cells are
extremely large
 Adult skeletal muscle fibers have diameters of 10-100 mm
and length of up to 20 cm
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STRUCTURE OF SKELETAL MUSCLE
EPIMYSIUM
Surrounds the entire muscle
PERIMYSIUM
Surrounds bundle of muscle
Fibers (Fascicle)
ENDOMYSIUM
Surrounds individual muscle
fibers
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MUSCLE ORGANIZATION
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NEWLY INTRODUCED
TERMINOLOGIES
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 Skeletal muscle cells are non-reproducible cells
 But have undifferentiated stem cells known as satellite cells that
can develop in to new muscle fiber
 The satellite cells are found between the cell membrane and
basement membrane
 These are quiescent under normal conditions and
 During injury they become active and differentiate into myoblasts that can
either fuse together to form new fibers or fuse with damaged muscle fibers to
repair them
 Muscle is formed from a number of muscle fibers which are
bound together by a connective tissue
 Most of the time the muscle fibers are shorter
 But in some muscles, the individual fibers could extend the entire
length of the muscle
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MUSCLE FIBER ANATOMY
 Sarcolemma - cell membrane
 Surrounds the sarcoplasm (cytoplasm of fiber)
 Contains many of the same organelles seen in other cells
 An abundance of the oxygen-binding protein myoglobin
 Myofibrils -cylindrical structures within muscle fiber
 Are bundles of protein filaments (myofilaments)
 Two types of myofilaments
1. Actin (thin) filaments
2. Myosin (thick) filaments
– Fills majority of the sarcoplasmic space
– At each end of the fiber, myofibrils are anchored to the inner
surface of the sarcolemma
 When myofibril shortens, the muscle contracts
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SARCOPLASMIC RETICULUM (SR)
 SR refers to smooth endoplasmic reticulum
 Runs longitudinally and surrounds each myofibril
 SR forms a series of sleeve like segments around each myofibril
 At it’s end there are two enlarged regions which are called terminal
cisternae (also called lateral sacs)
 The terminal cisternae are connected to each other by a series of smaller
tubular elements
 SR stores Ca2+
 When stimulated, calcium is released into sarcoplasm
 SR membrane has Ca2+
pump that function to pump Ca2+
back into
the SR after contraction
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 There is also separate tubular structure, the transverse
tubule (T-tubule), that lies between adjacent terminal
cisternae
 T-tubules and terminal cisternae surrounds the myofibrils at
the region of the sarcomeres where the A and I bands meet
 T-tubules are continuous with the sarcolemma
 Action potentials propagating along the surface membrane also travel
throughout the interior of the muscle fiber by way of the T-tubules
 The lumen of the T-tubule is continuous with the extracellular
fluid surrounding the muscle fiber
 Terminal cisternae together with T-tubules form “Triad”
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SARCOTUBULAR SYSTEM
 The T-tubule and the segments of the
sarcoplasmic reticulum surrounds the myofibrils
and these structures together are called
Sarcotubular system
 T-tubules (Transverse Tubules)
 Sarcoplasmic Reticulum Tubules
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Sarcomere - repeating functional units of a myofibril
 There around 10,000 sarcomeres per myofibril
 Each is about 2 µm long
 Extends between two successive Z lines (Z disks)
The Sarcomere contains two sets of
Myofilaments
(i) Actin filament
(ii) Myosin filament
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 It contains different bands, zones, disc, line,….
 A bands: a dark band; full length of thick (myosin)
filament
 H zone:- narrow, light band in the center of the A
band
Which is the space between the opposing ends of the
two sets of thin filaments in each sarcomere
 M line - a narrow, dark band formed by proteins that
link the central region of adjacent thick filaments
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 I bands: a light band that lies between the ends of the
A bands of two adjacent sarcomeres
 Formed by the portions of the thin filaments that do not
overlap with the thick filament
 Z disk: filamentous network of protein
 Serves as attachment for actin filaments
 The boundary between two sarcomeres
 Titin filaments
 Elastic protein extending from the Z line to the M line
(linked to both M Line proteins and the thick filaments)
 Keep thick and thin filaments in proper alignment in
the middle of each sarcomere
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THICK FILAMENT
 Around 200 myosin molecules form the thick filament
 Forms the dark band (A band) of the alternating dark and light bands
of a muscle fiber
 Located in the centre of the sarcomere and attached to the Z-
line by Titin filaments
 Myosin is contractile protein composed of two heavy polypeptide
chains and four light chains
 The polypeptides combine to form
 Two globular heads (each containing 01 folded heavy and 02 light
chains)
 Light chains help control the function of the head
 A long tail formed by the two intertwined heavy chains
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 The tail of each myosin molecule lies along the axis of the
thick filament
 The two globular heads extend out to the sides of the
filament forming cross-bridges
 This is the part that makes contact with the thin
filament and exert force during muscle contraction
 Each globular head contains two binding sites, one for
attaching to the thin filament and one for ATP
 The ATP binding site also serves as an enzyme (ATPase)
that hydrolyzes the bound ATP, producing its energy for
contraction
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THIN FILAMENT
 Composed of three proteins, Actin, Troponin and
Tropomyosin
 One end of the thin filaments is connected to the Z-line
while the other end is directed to the center
 These are about half of the diameter of the thick filaments
 An actin monomers form a polymer made up of two helical
chains (the core of a thin filament)
 Each actin molecule contains a binding site for myosin
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ACTIN:
Double-stranded helix formed from actin monomers
Having the binding site for myosin
Two types
 G Actin (Globular)
 F Actin (Filamentous)
TROPOMYOSIN:
 Two polypeptide chains coiled around each other
 Covers myosin binding sites of actin
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TROPONIN:
Globular units located at intervals along the
tropomyosin molecule
Has 3 components
 Troponin C- contain binding site for calcium
 Troponin T – binds the troponin component to
tropomyosin
 Troponin I –inhibit the interaction of myosin with actin.
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MECHANISMS OF SKELETAL MUSCLE
CONTRACTION
 Muscle contraction refers to the activation of the
force-generating sites within muscle fibers (cross-
bridges)
 But it does not mean shortening of the muscle
 Following contraction, the mechanisms that
generate force are turned off and
 Allowing relaxation of muscle fibers
 Skeletal muscles always need neuronal stimulation
to initiate an action potential
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 Motor neurons (somatic neurons) are responsible for
that stimulation
 A single motor neuron innervates many muscle fibers
 Each muscle fiber is controlled by a branch from only
one motor neuron
 A motor neuron plus the muscle fibers it innervates
is called a motor unit
 So, an action potential from the motor neuron
stimulates the muscle fibers in its motor unit
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THE NEUROMUSCULAR JUNCTION (NMJ)
 This is the area where the axon terminal of a motor
neuron and the muscle membrane meet
 The region of the muscle fiber plasma membrane
that lies directly under the axon terminal is known
as the motor end plate.
 The space in between is called synaptic cleft
 The axon terminals of a motor neuron contain vesicles
that contain the neurotransmitter acetylcholine (ACh)
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
Nerve impulse reaches
nerve terminal
 Opening of voltage gated
calcium channels
 Calcium diffuses from
the ECF into the nerve
terminal
 Release of Ach from the
synaptic vesicles into the
synaptic cleft by process
of Exocytosis
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Binding of Ach with
receptor, formation of
Ach- receptor complex
 Opening of Ligand gated
sodium channels
 Entry of sodium ions
into the ECF
 Development of end
plate potential ( EPP )
Stimulation of nearby
membrane & action
potential development
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Neuromuscular
Transmission:
Step by Step
Nerve action
potential invades
axon terminal
-
+
-
-
-
-
-
-
+
+
+
+
+
+
+
-
-
-
+ +
Depolarization
of terminal
opens Ca channels
+ +
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K+
Outside
Inside
Na+
Na+
Na+
Na+
Na+
Na+
Na+ Na+
Na+
Na+
Na+
Na+
K+ K+
K+
K+
K+
K+
K+
K+
K+
K+
K+
ACh
ACh
ACh
Ca2+
induces fusion of
vesicles with nerve
terminal membrane.
ACh is released and
diffuses across
synaptic cleft.
ACh
ACh binds to its
receptor on the
postsynaptic membrane
Binding of ACh opens
channel pore that is
permeable to Na+
and K+
.
Na+
Na+
K+
Muscle membrane
Nerve
terminal Ca2+
Ca2+
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Resting membrane potential of skeletal muscle
membrane is -90mV.
When end plate potential reaches a threshold of
30-40mV, it depolarizes the surface membrane of
the muscle and results in the generation of action
potential.
Once it reaches the muscle fibers then the muscles
give mechanical response by contraction.
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 After Ach acts on
the receptors, it is
hydrolyzed by the
enzyme cholinesterase
into Acetate and
Choline
 Choline is actively
reabsorbed into the
nerve terminal to be
used again to form Ach
 The whole process of
Ach release, action and
destruction takes
about 5 –10 ms
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Meanwhile ...
Outside
Inside
ACh
ACh unbinds from
its receptor
Muscle membrane
ACh
so the channel closes
ACh
ACh
Nerve
terminal
ACh is hydrolyzed by
AChE into Choline
and acetate
Choline
Acetate
Choline is taken up
into nerve terminal
Choline
Choline resynthesized
into ACh and repackaged
into vesicle
ACh
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EXCITATION - CONTRACTION
COUPLING
 Refers to the sequence of events by which an action
potential in the plasma membrane activates the force-
generating mechanisms
 To do so, the action potential in the membrane should
result in an increased cytosolic Ca2+
concentration
 First action potential propagates through the T tubules and
causes shape change in the dihydropyridine (DHP) receptors
 This in turn causes conformational change in ryanodine
receptors in the sarcoplasmic reticulum membrane
 Then Ca2+
channels are opened and Ca2+
will be released in to
cytosol
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 When there is adequate Ca2+
in the sarcoplasm, it will bind with
troponin C
 This relaxes its inhibitory grip and displaces tropomyosin and
exposes myosin binding sites
 Then there will be cross-bridge formation and sliding of the
filaments
 Conversely, the removal of Ca2+
from troponin reverses the
process, turning off contractile activity
 Achieved by lowering the Ca2+
concentration in the cytosol back to its
prerelease level (pumped by Ca2+
-ATPases back to sarcoplasmic
reticulum)
 So, the main source of Ca2+
in skeletal muscle contraction is the
sarcoplasmic reticulum within the muscle fiber
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SLIDING-FILAMENT MECHANISM
 Myosin head is always in activated state
 So when Ca2+
binds with troponin C, there will be
displacement of tropomyosin and exposure of myosin
binding sites
 Myosin head will bind with actin and pulls the actin
filament to the center of the sarcomere
 The filaments are sliding over each other resulting in
muscle contraction
 Therefore sliding of the thin and thick filaments is the
basis for muscle contraction
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 cross-bridges attach to thin filament pull
towards center detach attach further down
ratchet theory or walk-along theory
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 As long as myosin binding sites remain exposed, binding
of cross-bridge with actin will continue which forms cycle
called Cross-bridge cycle
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 Generally ATP has four importance in skeletal muscle
contraction
 Source of energy in Na+
/K+
ATPase
 Source of energy in Ca2+
ATPase
 Source of energy in forming energized state of myosin
 ATP binding (not hydrolysis) to myosin breaks the link
formed between actin and myosin during the cycle
 Rigor mortis – failure of the detachment of actin and
myosin after death due to the absence of energy (ATP)
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MECHANISM OF MUSCLE RELAXATION
 Increased sarcoplasmic calcium level during muscle contraction
 To decrease it and bring muscle relaxation
 Breakdown of Ach by acetyl cholinesterase
 Activation of Ca2+
ATPase
 Ca2+
pumped back into the SR
 Decreased sarcoplasmic Ca2+
level
 Detachment of Ca2+
from troponin
 Cessation of actin myosin interaction
 Muscle relaxation
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Summary of events occurring between a motor neuron
stimulation and muscle contraction
 Action potential will be initiated and propagated toward the
axon terminals
 Ca2+
channels (voltage-gated) will be opened and Ca2+
enters
axon cytosol
 Entry of Ca2+
triggers release of ACh from axon terminals
 Released ACh diffuses to motor end plate
 ACh binds to it’s receptors on motor end plate, opening
ligand gated Na+
channels
 Influx of more Na+
, depolarizing the membrane and
producing the end-plate potential (EPP)
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 EPP depolarize the adjacent plasma membrane and action
potential is generated
 The action potential propagates over the muscle fiber
surface and into T-tubules
 Action potential in T-tubules induces DHP receptors to pull
open ryanodine receptor channels
 Allowing release of Ca2+
from terminal cisternae
 Ca2+
binds to troponin, displacing tropomyosin and exposing
the myosin binding sites on actin
 Myosin cross-bridges bind to it’s binding site in actin
 ATP hydrolysis and produces an angular movement of each
cross-bridge
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 New ATP binds to myosin and breaks the linkage between
actin and myosin
 The attached ATP is hydrolyzed and newly energized myosin
cross-bridge will be formed
 Cross-bridges repeat the previous steps, producing a sliding
movement of thin and thick filaments
 Cycles of cross-bridge movement continue as long as Ca2+
and
ATP remains available
 Finally, muscle relaxation occurs when Ca2+
-ATPase is
activated and decreases cytosolic Ca2+
concentration
 Blocking action of tropomyosin restored
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 There are three sources of energy (for formation of
ATP)
1. Cleavage of phosphocreatine – can maintain muscle
contraction for only 5-8 seconds
 When phosphocreatine is cleaved, energy will be produced that
is used for the formation of ATP from ADP and phosphate ion
 Then the ATP produced will be used as source of energy for
short period
2. Glycolysis – acts a source of energy to reconstitute both
ATP and phosphocreatine
 This has two main importance
a) Can occur even in the absence of oxygen
b) The rate of ATP formation is about 2.5 times as rapid
as ATP formation by oxidative metabolism
ENERGETICS OF MUSCLE CONTRACTION
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 But too many waste product accumulation and lose of
capability to sustain maximum muscle contraction after
about 1 minute
3. Oxidative metabolism - combining oxygen with the
end products of glycolysis and with various other
cellular foodstuffs to liberate ATP.
 Majority (>95%) of all energy used by the muscles
for sustained, long-term contraction is derived
from oxidative metabolism
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Muscle contraction can
be:-
 Isometric contraction
- when the muscle does
not shorten during
contraction
 Isotonic Contraction -
muscle contraction at a
constant tension
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FIBER TYPES AND
PERFORMANCE
 Power athletes
 Sprinters
 Possess high percentage of fast fibers
 Endurance athletes
 Distance runners
 Have high percentage of slow fibers
 Others
 Weight lifters and non-athletes
 Have about 50% slow and 50% fast fibers
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THREE TYPES OF SKELETAL MUSCLE
FIBERS
(intermediate)
(slow) (fast)
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 Force Summation - adding of individual twitch
contractions which occurs in two ways
 Multiple fiber summation - increasing the number of
motor units contracting simultaneously
 Frequency summation - increasing the frequency of
contraction
 Skeletal Muscle Tone; a certain amount of
tautness at rest
 Low rate of nerve impulses coming from the spinal cord
 Muscle Fatigue; inability of the muscle fibers to
continue supplying the same work output
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MUSCLE REMODELING
 Muscles of the body are continually being remodeled
to match the required functions
 Usually diameters, lengths, strengths, and vascular
supplies are altered
 Muscle Hypertrophy
 The increase of the total mass (size) of a muscle group
 Increase in size of myofibril and enzyme system
(especially glycolytic enzymes)
 Adjustment of Muscle Length
 Hypertrophy due to increase in fiber length
 As a result of adding new sarcomeres
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 Muscle Atrophy
 Decrement of total muscle mass
 Disuse atrophy
 Dénervation induced muscle atrophy
 Atrophy due to loss of nerve supply
 Hyperplasia of Muscle Fiber
 Increase in fiber number but rare event
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PHYSIOLOGY OF CARDIAC
MUSCLE
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PHYSIOLOGIC ANATOMY OF CARDIAC MUSCLE
 Two forms of muscles fibers in the heart
 Contractile muscle fibers
 Muscle fibers found in the walls of the
heart chambers that generate force used
to pump blood
 Excitatory and conductive muscle fibers
 Specialized muscle fibers mainly involved
in either
o Automatic rhythmical electrical
discharge OR
o Conduction of the action potentials
 The muscle fibers are arranged in a latticework
fashion
o Fibers divide, rejoin, and then divide
o The muscle fibers are striated similar to that of
skeletal muscle fiber and there is almost similar
o Arrangement of actin and myosin filaments
o Sliding during contraction
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 Cardiac muscle cells form Syncytium
 Due to intercalated discs and branching, so fusion of
cytoplasm
 Intercalated disc have gap-junctions that allow rapid diffusion
of ions
 As a result ions (action potential) can move easily between two
adjacent cells
 So, when a given cell becomes excited, the action potential
rapidly spreads to all of the other muscle cells
 The heart have two syncytium
 The atrial syncytium
 The ventricular syncytium
 Fibrous connective tissue separates the atria and
ventricles preventing direct transmission of potentials
between the two syncytium
 AV bundles are the only means of potential transmission
between the two syncytium
 Any physiologic importance of this nature????
 This is important to have alternate excitation and contraction
of the atria and ventricles
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ACTION POTENTIALS IN CARDIAC
MUSCLE
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The membrane potential of ventricular
muscle fiber can reach up to +20
millivolts during depolarization
The membrane remains depolarized for
about 0.2 second (plateau), followed by
abrupt repolarization
This potential plateau is important to have
long lasting (15X that of skeletal muscle)
ventricular contraction
Two main reasons are responsible for this
plateau formation in cardiac muscle cells
1. Depolarization is happening as a result of influx
of both Na+
(fast opening and closure of ion
channels) and Ca2+
(slow opening and closure of
ion channels)
2. Decreased permeability of cardiac muscle
membrane for potassium ions (5x decreases)
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 Cardiac muscle action potential have 5 phases
 Phase 0 (depolarization) - opening of fast sodium channels
 Phase 1 (initial repolarization) - closure of fast sodium channels and opening of
potassium ions
 Phase 2 (plateau) - opening of calcium channels and closure of fast potassium
channels
 Phase 3 (rapid repolarization) - closure of calcium channels and opening of
potassium channels
 Phase 4 (regaining of resting membrane potential) averages about −90 millivolts
 The action potential conduction along cardiac muscle fibers is much slower
than nerve fibers and skeletal muscle fibers
 Cardiac muscle have refractory period which could be absolute and relative
refractory period
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EXCITATION-CONTRACTION COUPLING
 During muscle excitation, the mechanism of Ca2+
release in
skeletal muscles also applies
 But there is also additional mechanism of release
 So when there is excitation there is opening of voltage gated Ca2+
channels in the muscle membrane
 Then influx of Ca2+
in to the sarcoplasm
 That Ca2+
will stimulate the ryanodine receptors and additional
Ca2+
will be released from sarcoplasmic reticulum
 The Ca2+
diffuse into the myofibrils and initiate sliding of the
actin and myosin filaments - then muscle contraction
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 Cardiac muscle’s sarcoplasmic reticulum is less developed and it
does not store enough calcium
 Because, calcium supply in cardiac muscles is mainly dependent
from external sources
 As a result these muscles have wider T-tubules with high
mucopolysaccharides (negatively charged molecules)
 Bind more Ca2+
and let it to be ready for diffusion to sarcoplasm when
needed
 Therefore, the concentration of Ca2+
in the ECF highly determine
the strength of cardiac muscle contraction
 Finally, muscle relaxation occurs as a result of Ca2+
pumping either
to SR (Ca2+
ATPase) or to the ECF (sodium-calcium exchanger)
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SMOOTH MUSCLE
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Grouped into sheets in walls of hollow visceral organs
• Longitudinal layer – muscle fibers run parallel to organ’s long axis
• Circular layer – muscle fibers run around circumference of the
organ
Surround:
• Blood vessels
• Digestive tract
• Organs (stomach, bladder; uterus)
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Generally found in:-
 Cardiovascular system
 Respiratory system
 Digestive system
 Renal system
 Reproductive system
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General features
 Involuntary muscle – controlled by ANS, Hormones, chemicals, …
 Unstriated muscle (lack visible cross striations)- plain muscle.
 No Sarcomere
Actin and Myosin not arranged as symmetrically as in skeletal muscle, thus
NO Sarcomere and striations
 More actin than myosin, Thin filaments lack Troponin
 Smaller, spindle shaped with varying dimensions.
a) Digestive system- 30-40 µm long and 5 µm diameter.
b) Blood vessels- 15-20 µm long and 2-3 µm in diameter.
c) Uterus 300 µm long and 10 µm diameter.
 Receive dual nerve supply from two divisions of autonomic
nervous system.
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Types of smooth muscles
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Visceral or single unit smooth muscle.
Multiunit smooth muscle.
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Visceral or single unit smooth muscle.
• The fibers are arranged as large sheets
• Exhibit unstable RMP. This is responsible for their
spontaneous activity.
• Muscle fibers are connected by tight junctions and gap
junctions. Electrical activity is conducted by ionic
movements = Syncytial fashion
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 Common sites: walls of the hollow viscera- GIT, bile duct,
bronchi, uterus, ureters, urinary bladder and in some blood
vessels
 The muscles are characterized by their spontaneous activity
in certain areas due to the pacemakers
 Receives nerve supply from autonomic nervous system.
But Independent of their innervations.
Nerves only modify the activity.
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Multiunit smooth muscle.
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 Made up of individual units without interconnecting
bridges- Non Syncytial.
 Common sites: Ciliary muscles of eye, pilomotor muscles of
skin, muscles of blood vessels.
 Richly innervated and each muscle fiber has its own nerve
supply
 These muscles only contact in response to the stimulus
through their nerves.
 Muscles do not respond to stretch
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Smooth Muscle Regulation
 Innervated by autonomic nervous system
 Neurotransmitter like acetylcholine
 Hormones like epinephrine and oxytocin
 Cold, stretch stimulate contraction
 Hypoxia, hypercapnia- relaxation of smooth
muscle.
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Mechanism of smooth muscle contraction:
• Activated by opening calcium channels on the cells
surface, there is influx of extra-cellular calcium.
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Mechanism of smooth muscle relaxation:
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THANK
YOU!!!

Muscle Physiology power point presentation.pptx

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    11/29/2024 2 CONTENTS  Introduction  Skeletalmuscle  Structure and organization  Muscle fiber anatomy  Mechanism of muscle contraction  Neuromuscular junction  Excitation contraction coupling  Sliding filament mechanism  Mechanism of muscle relaxation  Energetics of muscle contraction  Cardiac muscles  Smooth muscles
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    11/29/2024 3 INTRODUCTION Muscle:  Is afleshy, reddish colored tissue in the body  Comprises the largest group of tissues in the body  Muscles constitutes of 40-50% of body weight  About 40% of the body is skeletal muscle, and  Another 10% is smooth and cardiac muscle  Muscle cells are specialized to generate mechanical force from chemical energy  This force is used to regulate the internal environment, and used for movement of the body in reference to the external environment
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    11/29/2024 4  There arethree types of muscle cells and tissues  Skeletal, cardiac, or smooth muscle cells and tissues  The three types of muscle tissues are identified on the basis of location, structure, contractile properties, and control mechanisms  Most skeletal muscles are attached to bone  Their contraction is responsible for supporting and moving the skeleton  Contraction of skeletal muscle is initiated by action potential from motor neurons of the somatic nervous system  That is why these are under voluntary control
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    11/29/2024 5  Smooth musclesurround various hollow organs and tubular structure  Including the digestive tract, urinary bladder and tracts, uterus, blood vessels, and airways  Contraction of smooth muscle decreases either the diameter or the length of these structures and  Propel the luminal contents through the hollow organs, or  Regulate internal flow by changing the tube diameter  For example, contraction of smooth muscle cells along the esophagus helps “squeeze” swallowed food to the stomach  Furthermore contraction of smooth muscle stand up the hairs of the skin and change diameter of the pupil
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    11/29/2024 6  Smooth musclecontraction is involuntary  It occurs under the control of autonomic nervous system, hormones, autocrine or paracrine signals, and other local chemical factors  In some cases it occurs autonomously  Cardiac muscle is the muscle found in the wall of the heart  Its contraction enables the heart to pump blood  Like smooth muscle, this is also involuntary  Regulated by the autonomic nervous system, hormones, and other glandular signals  It can undergo spontaneous contractions
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    8 COMMON PROPERTIES OF MUSCLES 1.Excitability- ability to respond to stimulus which could be from motor neuron or a hormone 2. Contractility- The ability to shorten forcibly when adequately stimulated 3. Extensibility- The ability to be stretched or extended 4. Elasticity- The ability to recoil and resume original length after being stretched or contracted 11/29/2024
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    11/29/2024 9 SKELETAL MUSCLE Skeletal Muscles Are muscles that causes the skeleton to move at joints  They are attached to the skeleton by tendons  The tendons transmit the muscle force to the bone
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    10 Skeletal muscles are Long cylindrical cells  Many nuclei per cell  Voluntary  Rapid contractions  Are well supplied with nerves and blood vessels  Are striated muscle type  Due to the distinct series of alternating light and dark bands  Cardiac muscles have same feature  But, the smooth muscle lacks striation and is named after it 11/29/2024
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    11/29/2024 11  During development,each skeletal muscle fiber is formed by the fusion of a number myoblasts (undifferentiated, mononucleated cells) into a single, cylindrical, multinucleated cell  That differentiation is completed around birth and continue to increase in size to adulthood  Compared to others, skeletal muscle cells are extremely large  Adult skeletal muscle fibers have diameters of 10-100 mm and length of up to 20 cm
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    11/29/2024 12 STRUCTURE OF SKELETALMUSCLE EPIMYSIUM Surrounds the entire muscle PERIMYSIUM Surrounds bundle of muscle Fibers (Fascicle) ENDOMYSIUM Surrounds individual muscle fibers
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    11/29/2024 15  Skeletal musclecells are non-reproducible cells  But have undifferentiated stem cells known as satellite cells that can develop in to new muscle fiber  The satellite cells are found between the cell membrane and basement membrane  These are quiescent under normal conditions and  During injury they become active and differentiate into myoblasts that can either fuse together to form new fibers or fuse with damaged muscle fibers to repair them  Muscle is formed from a number of muscle fibers which are bound together by a connective tissue  Most of the time the muscle fibers are shorter  But in some muscles, the individual fibers could extend the entire length of the muscle
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    11/29/2024 16 MUSCLE FIBER ANATOMY Sarcolemma - cell membrane  Surrounds the sarcoplasm (cytoplasm of fiber)  Contains many of the same organelles seen in other cells  An abundance of the oxygen-binding protein myoglobin  Myofibrils -cylindrical structures within muscle fiber  Are bundles of protein filaments (myofilaments)  Two types of myofilaments 1. Actin (thin) filaments 2. Myosin (thick) filaments – Fills majority of the sarcoplasmic space – At each end of the fiber, myofibrils are anchored to the inner surface of the sarcolemma  When myofibril shortens, the muscle contracts
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    11/29/2024 18 SARCOPLASMIC RETICULUM (SR) SR refers to smooth endoplasmic reticulum  Runs longitudinally and surrounds each myofibril  SR forms a series of sleeve like segments around each myofibril  At it’s end there are two enlarged regions which are called terminal cisternae (also called lateral sacs)  The terminal cisternae are connected to each other by a series of smaller tubular elements  SR stores Ca2+  When stimulated, calcium is released into sarcoplasm  SR membrane has Ca2+ pump that function to pump Ca2+ back into the SR after contraction
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    20  There isalso separate tubular structure, the transverse tubule (T-tubule), that lies between adjacent terminal cisternae  T-tubules and terminal cisternae surrounds the myofibrils at the region of the sarcomeres where the A and I bands meet  T-tubules are continuous with the sarcolemma  Action potentials propagating along the surface membrane also travel throughout the interior of the muscle fiber by way of the T-tubules  The lumen of the T-tubule is continuous with the extracellular fluid surrounding the muscle fiber  Terminal cisternae together with T-tubules form “Triad” 11/29/2024
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    22 SARCOTUBULAR SYSTEM  TheT-tubule and the segments of the sarcoplasmic reticulum surrounds the myofibrils and these structures together are called Sarcotubular system  T-tubules (Transverse Tubules)  Sarcoplasmic Reticulum Tubules 11/29/2024
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    11/29/2024 24 Sarcomere - repeatingfunctional units of a myofibril  There around 10,000 sarcomeres per myofibril  Each is about 2 µm long  Extends between two successive Z lines (Z disks) The Sarcomere contains two sets of Myofilaments (i) Actin filament (ii) Myosin filament
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    26  It containsdifferent bands, zones, disc, line,….  A bands: a dark band; full length of thick (myosin) filament  H zone:- narrow, light band in the center of the A band Which is the space between the opposing ends of the two sets of thin filaments in each sarcomere  M line - a narrow, dark band formed by proteins that link the central region of adjacent thick filaments 11/29/2024
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    11/29/2024 28  I bands:a light band that lies between the ends of the A bands of two adjacent sarcomeres  Formed by the portions of the thin filaments that do not overlap with the thick filament  Z disk: filamentous network of protein  Serves as attachment for actin filaments  The boundary between two sarcomeres  Titin filaments  Elastic protein extending from the Z line to the M line (linked to both M Line proteins and the thick filaments)  Keep thick and thin filaments in proper alignment in the middle of each sarcomere
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    11/29/2024 31 THICK FILAMENT  Around200 myosin molecules form the thick filament  Forms the dark band (A band) of the alternating dark and light bands of a muscle fiber  Located in the centre of the sarcomere and attached to the Z- line by Titin filaments  Myosin is contractile protein composed of two heavy polypeptide chains and four light chains  The polypeptides combine to form  Two globular heads (each containing 01 folded heavy and 02 light chains)  Light chains help control the function of the head  A long tail formed by the two intertwined heavy chains
  • 32.
    11/29/2024 32  The tailof each myosin molecule lies along the axis of the thick filament  The two globular heads extend out to the sides of the filament forming cross-bridges  This is the part that makes contact with the thin filament and exert force during muscle contraction  Each globular head contains two binding sites, one for attaching to the thin filament and one for ATP  The ATP binding site also serves as an enzyme (ATPase) that hydrolyzes the bound ATP, producing its energy for contraction
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    11/29/2024 34 THIN FILAMENT  Composedof three proteins, Actin, Troponin and Tropomyosin  One end of the thin filaments is connected to the Z-line while the other end is directed to the center  These are about half of the diameter of the thick filaments  An actin monomers form a polymer made up of two helical chains (the core of a thin filament)  Each actin molecule contains a binding site for myosin
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    11/29/2024 35 ACTIN: Double-stranded helix formedfrom actin monomers Having the binding site for myosin Two types  G Actin (Globular)  F Actin (Filamentous) TROPOMYOSIN:  Two polypeptide chains coiled around each other  Covers myosin binding sites of actin
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    11/29/2024 36 TROPONIN: Globular units locatedat intervals along the tropomyosin molecule Has 3 components  Troponin C- contain binding site for calcium  Troponin T – binds the troponin component to tropomyosin  Troponin I –inhibit the interaction of myosin with actin.
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    11/29/2024 38 MECHANISMS OF SKELETALMUSCLE CONTRACTION  Muscle contraction refers to the activation of the force-generating sites within muscle fibers (cross- bridges)  But it does not mean shortening of the muscle  Following contraction, the mechanisms that generate force are turned off and  Allowing relaxation of muscle fibers  Skeletal muscles always need neuronal stimulation to initiate an action potential
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    11/29/2024 39  Motor neurons(somatic neurons) are responsible for that stimulation  A single motor neuron innervates many muscle fibers  Each muscle fiber is controlled by a branch from only one motor neuron  A motor neuron plus the muscle fibers it innervates is called a motor unit  So, an action potential from the motor neuron stimulates the muscle fibers in its motor unit
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    11/29/2024 40 THE NEUROMUSCULAR JUNCTION(NMJ)  This is the area where the axon terminal of a motor neuron and the muscle membrane meet  The region of the muscle fiber plasma membrane that lies directly under the axon terminal is known as the motor end plate.  The space in between is called synaptic cleft  The axon terminals of a motor neuron contain vesicles that contain the neurotransmitter acetylcholine (ACh)
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    11/29/2024 42  Nerve impulse reaches nerveterminal  Opening of voltage gated calcium channels  Calcium diffuses from the ECF into the nerve terminal  Release of Ach from the synaptic vesicles into the synaptic cleft by process of Exocytosis
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    11/29/2024 43 Binding of Achwith receptor, formation of Ach- receptor complex  Opening of Ligand gated sodium channels  Entry of sodium ions into the ECF  Development of end plate potential ( EPP ) Stimulation of nearby membrane & action potential development
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    11/29/2024 44 Neuromuscular Transmission: Step by Step Nerveaction potential invades axon terminal - + - - - - - - + + + + + + + - - - + + Depolarization of terminal opens Ca channels + +
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    11/29/2024 45 K+ Outside Inside Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ K+ K+ K+ K+ K+ K+ K+ K+ K+ K+ K+ ACh ACh ACh Ca2+ inducesfusion of vesicles with nerve terminal membrane. ACh is released and diffuses across synaptic cleft. ACh ACh binds to its receptor on the postsynaptic membrane Binding of ACh opens channel pore that is permeable to Na+ and K+ . Na+ Na+ K+ Muscle membrane Nerve terminal Ca2+ Ca2+
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    11/29/2024 46 Resting membrane potentialof skeletal muscle membrane is -90mV. When end plate potential reaches a threshold of 30-40mV, it depolarizes the surface membrane of the muscle and results in the generation of action potential. Once it reaches the muscle fibers then the muscles give mechanical response by contraction.
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    11/29/2024 47  After Achacts on the receptors, it is hydrolyzed by the enzyme cholinesterase into Acetate and Choline  Choline is actively reabsorbed into the nerve terminal to be used again to form Ach  The whole process of Ach release, action and destruction takes about 5 –10 ms
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    11/29/2024 48 Meanwhile ... Outside Inside ACh ACh unbindsfrom its receptor Muscle membrane ACh so the channel closes ACh ACh Nerve terminal ACh is hydrolyzed by AChE into Choline and acetate Choline Acetate Choline is taken up into nerve terminal Choline Choline resynthesized into ACh and repackaged into vesicle ACh
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    11/29/2024 49 EXCITATION - CONTRACTION COUPLING Refers to the sequence of events by which an action potential in the plasma membrane activates the force- generating mechanisms  To do so, the action potential in the membrane should result in an increased cytosolic Ca2+ concentration  First action potential propagates through the T tubules and causes shape change in the dihydropyridine (DHP) receptors  This in turn causes conformational change in ryanodine receptors in the sarcoplasmic reticulum membrane  Then Ca2+ channels are opened and Ca2+ will be released in to cytosol
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    11/29/2024 50  When thereis adequate Ca2+ in the sarcoplasm, it will bind with troponin C  This relaxes its inhibitory grip and displaces tropomyosin and exposes myosin binding sites  Then there will be cross-bridge formation and sliding of the filaments  Conversely, the removal of Ca2+ from troponin reverses the process, turning off contractile activity  Achieved by lowering the Ca2+ concentration in the cytosol back to its prerelease level (pumped by Ca2+ -ATPases back to sarcoplasmic reticulum)  So, the main source of Ca2+ in skeletal muscle contraction is the sarcoplasmic reticulum within the muscle fiber
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    11/29/2024 52 SLIDING-FILAMENT MECHANISM  Myosinhead is always in activated state  So when Ca2+ binds with troponin C, there will be displacement of tropomyosin and exposure of myosin binding sites  Myosin head will bind with actin and pulls the actin filament to the center of the sarcomere  The filaments are sliding over each other resulting in muscle contraction  Therefore sliding of the thin and thick filaments is the basis for muscle contraction
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    11/29/2024 56  cross-bridgesattach to thin filament pull towards center detach attach further down ratchet theory or walk-along theory
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    11/29/2024 57  As longas myosin binding sites remain exposed, binding of cross-bridge with actin will continue which forms cycle called Cross-bridge cycle
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    11/29/2024 58  Generally ATPhas four importance in skeletal muscle contraction  Source of energy in Na+ /K+ ATPase  Source of energy in Ca2+ ATPase  Source of energy in forming energized state of myosin  ATP binding (not hydrolysis) to myosin breaks the link formed between actin and myosin during the cycle  Rigor mortis – failure of the detachment of actin and myosin after death due to the absence of energy (ATP)
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    11/29/2024 60 MECHANISM OF MUSCLERELAXATION  Increased sarcoplasmic calcium level during muscle contraction  To decrease it and bring muscle relaxation  Breakdown of Ach by acetyl cholinesterase  Activation of Ca2+ ATPase  Ca2+ pumped back into the SR  Decreased sarcoplasmic Ca2+ level  Detachment of Ca2+ from troponin  Cessation of actin myosin interaction  Muscle relaxation
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    11/29/2024 62 Summary of eventsoccurring between a motor neuron stimulation and muscle contraction  Action potential will be initiated and propagated toward the axon terminals  Ca2+ channels (voltage-gated) will be opened and Ca2+ enters axon cytosol  Entry of Ca2+ triggers release of ACh from axon terminals  Released ACh diffuses to motor end plate  ACh binds to it’s receptors on motor end plate, opening ligand gated Na+ channels  Influx of more Na+ , depolarizing the membrane and producing the end-plate potential (EPP)
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    11/29/2024 63  EPP depolarizethe adjacent plasma membrane and action potential is generated  The action potential propagates over the muscle fiber surface and into T-tubules  Action potential in T-tubules induces DHP receptors to pull open ryanodine receptor channels  Allowing release of Ca2+ from terminal cisternae  Ca2+ binds to troponin, displacing tropomyosin and exposing the myosin binding sites on actin  Myosin cross-bridges bind to it’s binding site in actin  ATP hydrolysis and produces an angular movement of each cross-bridge
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    11/29/2024 64  New ATPbinds to myosin and breaks the linkage between actin and myosin  The attached ATP is hydrolyzed and newly energized myosin cross-bridge will be formed  Cross-bridges repeat the previous steps, producing a sliding movement of thin and thick filaments  Cycles of cross-bridge movement continue as long as Ca2+ and ATP remains available  Finally, muscle relaxation occurs when Ca2+ -ATPase is activated and decreases cytosolic Ca2+ concentration  Blocking action of tropomyosin restored
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    11/29/2024 67  There arethree sources of energy (for formation of ATP) 1. Cleavage of phosphocreatine – can maintain muscle contraction for only 5-8 seconds  When phosphocreatine is cleaved, energy will be produced that is used for the formation of ATP from ADP and phosphate ion  Then the ATP produced will be used as source of energy for short period 2. Glycolysis – acts a source of energy to reconstitute both ATP and phosphocreatine  This has two main importance a) Can occur even in the absence of oxygen b) The rate of ATP formation is about 2.5 times as rapid as ATP formation by oxidative metabolism ENERGETICS OF MUSCLE CONTRACTION
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    11/29/2024 68  But toomany waste product accumulation and lose of capability to sustain maximum muscle contraction after about 1 minute 3. Oxidative metabolism - combining oxygen with the end products of glycolysis and with various other cellular foodstuffs to liberate ATP.  Majority (>95%) of all energy used by the muscles for sustained, long-term contraction is derived from oxidative metabolism
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    11/29/2024 69 Muscle contraction can be:- Isometric contraction - when the muscle does not shorten during contraction  Isotonic Contraction - muscle contraction at a constant tension
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    11/29/2024 74 FIBER TYPES AND PERFORMANCE Power athletes  Sprinters  Possess high percentage of fast fibers  Endurance athletes  Distance runners  Have high percentage of slow fibers  Others  Weight lifters and non-athletes  Have about 50% slow and 50% fast fibers
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    11/29/2024 75 THREE TYPES OFSKELETAL MUSCLE FIBERS (intermediate) (slow) (fast)
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    11/29/2024 76  Force Summation- adding of individual twitch contractions which occurs in two ways  Multiple fiber summation - increasing the number of motor units contracting simultaneously  Frequency summation - increasing the frequency of contraction  Skeletal Muscle Tone; a certain amount of tautness at rest  Low rate of nerve impulses coming from the spinal cord  Muscle Fatigue; inability of the muscle fibers to continue supplying the same work output
  • 77.
    11/29/2024 77 MUSCLE REMODELING  Musclesof the body are continually being remodeled to match the required functions  Usually diameters, lengths, strengths, and vascular supplies are altered  Muscle Hypertrophy  The increase of the total mass (size) of a muscle group  Increase in size of myofibril and enzyme system (especially glycolytic enzymes)  Adjustment of Muscle Length  Hypertrophy due to increase in fiber length  As a result of adding new sarcomeres
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    11/29/2024 78  Muscle Atrophy Decrement of total muscle mass  Disuse atrophy  Dénervation induced muscle atrophy  Atrophy due to loss of nerve supply  Hyperplasia of Muscle Fiber  Increase in fiber number but rare event
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    80 PHYSIOLOGIC ANATOMY OFCARDIAC MUSCLE  Two forms of muscles fibers in the heart  Contractile muscle fibers  Muscle fibers found in the walls of the heart chambers that generate force used to pump blood  Excitatory and conductive muscle fibers  Specialized muscle fibers mainly involved in either o Automatic rhythmical electrical discharge OR o Conduction of the action potentials  The muscle fibers are arranged in a latticework fashion o Fibers divide, rejoin, and then divide o The muscle fibers are striated similar to that of skeletal muscle fiber and there is almost similar o Arrangement of actin and myosin filaments o Sliding during contraction 11/29/2024
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    81  Cardiac musclecells form Syncytium  Due to intercalated discs and branching, so fusion of cytoplasm  Intercalated disc have gap-junctions that allow rapid diffusion of ions  As a result ions (action potential) can move easily between two adjacent cells  So, when a given cell becomes excited, the action potential rapidly spreads to all of the other muscle cells  The heart have two syncytium  The atrial syncytium  The ventricular syncytium  Fibrous connective tissue separates the atria and ventricles preventing direct transmission of potentials between the two syncytium  AV bundles are the only means of potential transmission between the two syncytium  Any physiologic importance of this nature????  This is important to have alternate excitation and contraction of the atria and ventricles 11/29/2024
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    82 ACTION POTENTIALS INCARDIAC MUSCLE 11/29/2024 The membrane potential of ventricular muscle fiber can reach up to +20 millivolts during depolarization The membrane remains depolarized for about 0.2 second (plateau), followed by abrupt repolarization This potential plateau is important to have long lasting (15X that of skeletal muscle) ventricular contraction Two main reasons are responsible for this plateau formation in cardiac muscle cells 1. Depolarization is happening as a result of influx of both Na+ (fast opening and closure of ion channels) and Ca2+ (slow opening and closure of ion channels) 2. Decreased permeability of cardiac muscle membrane for potassium ions (5x decreases)
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    83  Cardiac muscleaction potential have 5 phases  Phase 0 (depolarization) - opening of fast sodium channels  Phase 1 (initial repolarization) - closure of fast sodium channels and opening of potassium ions  Phase 2 (plateau) - opening of calcium channels and closure of fast potassium channels  Phase 3 (rapid repolarization) - closure of calcium channels and opening of potassium channels  Phase 4 (regaining of resting membrane potential) averages about −90 millivolts  The action potential conduction along cardiac muscle fibers is much slower than nerve fibers and skeletal muscle fibers  Cardiac muscle have refractory period which could be absolute and relative refractory period 11/29/2024
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    84 EXCITATION-CONTRACTION COUPLING  Duringmuscle excitation, the mechanism of Ca2+ release in skeletal muscles also applies  But there is also additional mechanism of release  So when there is excitation there is opening of voltage gated Ca2+ channels in the muscle membrane  Then influx of Ca2+ in to the sarcoplasm  That Ca2+ will stimulate the ryanodine receptors and additional Ca2+ will be released from sarcoplasmic reticulum  The Ca2+ diffuse into the myofibrils and initiate sliding of the actin and myosin filaments - then muscle contraction 11/29/2024
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    85  Cardiac muscle’ssarcoplasmic reticulum is less developed and it does not store enough calcium  Because, calcium supply in cardiac muscles is mainly dependent from external sources  As a result these muscles have wider T-tubules with high mucopolysaccharides (negatively charged molecules)  Bind more Ca2+ and let it to be ready for diffusion to sarcoplasm when needed  Therefore, the concentration of Ca2+ in the ECF highly determine the strength of cardiac muscle contraction  Finally, muscle relaxation occurs as a result of Ca2+ pumping either to SR (Ca2+ ATPase) or to the ECF (sodium-calcium exchanger) 11/29/2024
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    11/29/2024 88 Grouped into sheetsin walls of hollow visceral organs • Longitudinal layer – muscle fibers run parallel to organ’s long axis • Circular layer – muscle fibers run around circumference of the organ Surround: • Blood vessels • Digestive tract • Organs (stomach, bladder; uterus)
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    11/29/2024 89 Generally found in:- Cardiovascular system  Respiratory system  Digestive system  Renal system  Reproductive system
  • 90.
    11/29/2024 90 General features  Involuntarymuscle – controlled by ANS, Hormones, chemicals, …  Unstriated muscle (lack visible cross striations)- plain muscle.  No Sarcomere Actin and Myosin not arranged as symmetrically as in skeletal muscle, thus NO Sarcomere and striations  More actin than myosin, Thin filaments lack Troponin  Smaller, spindle shaped with varying dimensions. a) Digestive system- 30-40 µm long and 5 µm diameter. b) Blood vessels- 15-20 µm long and 2-3 µm in diameter. c) Uterus 300 µm long and 10 µm diameter.  Receive dual nerve supply from two divisions of autonomic nervous system.
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  • 92.
  • 93.
    11/29/2024 93 Visceral or singleunit smooth muscle. Multiunit smooth muscle.
  • 94.
    11/29/2024 94 Visceral or singleunit smooth muscle. • The fibers are arranged as large sheets • Exhibit unstable RMP. This is responsible for their spontaneous activity. • Muscle fibers are connected by tight junctions and gap junctions. Electrical activity is conducted by ionic movements = Syncytial fashion
  • 95.
  • 96.
    11/29/2024 96  Common sites:walls of the hollow viscera- GIT, bile duct, bronchi, uterus, ureters, urinary bladder and in some blood vessels  The muscles are characterized by their spontaneous activity in certain areas due to the pacemakers  Receives nerve supply from autonomic nervous system. But Independent of their innervations. Nerves only modify the activity.
  • 97.
  • 98.
    11/29/2024 98  Made upof individual units without interconnecting bridges- Non Syncytial.  Common sites: Ciliary muscles of eye, pilomotor muscles of skin, muscles of blood vessels.  Richly innervated and each muscle fiber has its own nerve supply  These muscles only contact in response to the stimulus through their nerves.  Muscles do not respond to stretch
  • 99.
  • 100.
    11/29/2024 100 Smooth Muscle Regulation Innervated by autonomic nervous system  Neurotransmitter like acetylcholine  Hormones like epinephrine and oxytocin  Cold, stretch stimulate contraction  Hypoxia, hypercapnia- relaxation of smooth muscle.
  • 101.
    11/29/2024 101 Mechanism of smoothmuscle contraction: • Activated by opening calcium channels on the cells surface, there is influx of extra-cellular calcium.
  • 102.
  • 103.
  • 104.
  • 105.
  • 106.
  • 107.
  • 108.
  • 109.