Transcript 11_Muscle - bloodhounds Incorporated

MUSCLES
Muscle Tissue
 Nearly half of body's mass
 Transforms chemical energy (ATP) to directed
mechanical energy  exerts force
 Three types
 Skeletal
 Cardiac
 Smooth
 Myo, mys, and sarco - prefixes for muscle
Skeletal Muscle
Types of Muscle Tissue
 Skeletal muscles





Organs attached to bones and skin
Elongated cells called muscle fibers
Striated (striped)
Voluntary (i.e., conscious control)
Require nervous system stimulation
Cardiac Muscle
Types of Muscle Tissue
 Cardiac muscle




Only in heart; bulk of heart walls
Striated
Can contract without nervous system stimulation
Involuntary
Cardiac Muscle
Smooth Muscle
Types of Muscle Tissue
 Smooth muscle
 In walls of hollow organs, e.g., stomach, urinary bladder,
and airways
 Not striated
 Can contract without nervous system stimulation
 Involuntary
Special Characteristics of Muscle
Tissue
 Excitability (responsiveness or irritability): ability to
receive and respond to stimuli
 Contractility: ability to shorten forcibly when stimulated
 Extensibility: ability to be stretched
 Elasticity: ability to recoil to resting length
Muscle Functions
 Four important functions




Movement of bones or fluids (e.g., blood)
Maintaining posture and body position
Stabilizing joints
Heat generation (especially skeletal muscle)
 Additional functions
 Protects organs, forms valves, controls pupil size, causes
"goosebumps"
Bone
Epimysium
Epimysium
Perimysium
Tendon
Endomysium
Muscle fiber
in middle of
a fascicle
Blood vessel
Perimysium
wrapping a fascicle
Endomysium
(between individual
muscle fibers)
Muscle
fiber
Fascicle
Perimysium
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Skeletal Muscle
 Connective tissue sheaths of skeletal muscle
 Support cells; reinforce whole muscle
 External to internal
 Epimysium: dense irregular connective tissue surrounding
entire muscle; may blend with fascia
 Perimysium: fibrous connective tissue surrounding
fascicles (groups of muscle fibers)
 Endomysium: fine areolar connective tissue surrounding
each muscle fiber
Skeletal Muscle: Attachments
 Attach in at least two places
 Insertion – movable bone
 Origin – immovable (less movable) bone
Diagram of part
of a muscle
fiber showing
the myofibrils.
One myofibril
extends from the
cut end of the
fiber.
Sarcolemma
Mitochondrion
Myofibril
Dark
A band
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Light Nucleus
I band
Microscopic Anatomy of A Skeletal
Muscle Fiber
 Sarcolemma = plasma membrane
 Sarcoplasm = cytoplasm
 Glycosomes for glycogen storage, myoglobin for O2
storage
 Modified structures: myofibrils, sarcoplasmic
reticulum, and T tubules
Myofibrils
 Contain sarcomeres - contractile units
 Sarcomeres contain myofilaments
 Exhibit striations - perfectly aligned repeating series of
dark A bands and light I bands
Striations
 H zone: lighter region in midsection of dark A band
where filaments do not overlap
 M line: line of protein myomesin bisects H zone
 Z disc (line): coin-shaped sheet of proteins on midline
of light I band that anchors thin filaments and connects
myofibrils to one another
 Thick filaments: run entire length of an A band
 Thin filaments: run length of I band and partway into A
band
 Sarcomere: region between two successive Z discs
Thin (actin)
filament
Small part of one
myofibril
enlarged to show
the myofilaments
responsible for the
banding pattern.
Thick
Each sarcomere
extends from one Z (myosin)
filament
disc to the next.
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Z disc
I band
H zone
Z disc
I band
A band
Sarcomere
M line
Z disc
Enlargement of
one sarcomere
(sectioned lengthwise). Notice the
myosin heads on
the thick filaments.
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Sarcomere
M line
Z disc
Thin
(actin)
filament
Elastic
(titin)
filaments
Thick
(myosin)
filament
Longitudinal section of filaments within one
sarcomere of a myofibril
Thick filament
Thin filament
In the center of the sarcomere, the thick filaments
lack myosin heads. Myosin heads are present only
in areas of myosin-actin overlap.
Thick filament.
Thin filament
Each thick filament consists of many myosin
molecules whose heads protrude at opposite ends
of the filament.
Portion of a thick filament
Myosin head
A thin filament consists of two strands of actin
subunits twisted into a helix plus two types of
regulatory proteins (troponin and tropomyosin).
Portion of a thin filament
Tropomyosin
Troponin Actin
Actin-binding sites
Heads
ATPbinding
site Flexible hinge region
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Myosin molecule
Tail
Active sites
for myosin
attachment
Actin subunits
Actin subunits
Myofibril Banding Pattern
 Actin myofilaments = thin filaments
 Anchored to Z discs
 Myosin myofilaments = thick filaments
 Connected at M line
Myosin Thick Filament
 Myosin tails contain 2 interwoven, heavy polypeptide
chains
 Myosin heads contain 2 smaller, light polypeptide chains
that act as cross bridges during contraction
 Binding sites for actin of thin filaments
 Binding sites for ATP
 ATPase enzymes
Actin Thin Filament
 G (globular) actin bears active sites for myosin head
attachment during contraction
 Tropomyosin and troponin - regulatory proteins
bound to actin
Part of a skeletal
muscle fiber (cell)
I band
Z disc
Myofibril
Sarcolemma
A band
H zone
M
line
I band
Z disc
Sarcolemma
Triad:
• T tubule
• Terminal
cisterns of
the SR (2)
Tubules of
the SR
Myofibrils
Mitochondria
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Sarcoplasmic Reticulum (SR)
 Network of smooth endoplasmic reticulum surrounding
each myofibril
 Most run longitudinally
 Functions in regulation of intracellular Ca2+ levels
 Stores and releases Ca2+
T Tubules
 Associate with paired terminal cisterns to form triads
that encircle each sarcomere
1 Fully relaxed sarcomere of a muscle fiber
Z
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I Inc.
H
A
Z
I
2 Fully contracted sarcomere of a muscle fiber
Z
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I
Z
A
I
1 Fully relaxed sarcomere of a muscle fiber
H
A
Z
I
Z
I
2 Fully contracted sarcomere of a muscle fiber
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Z
Z
I
A
I
Sliding Filament Model of
Contraction
 In relaxed state, thin and thick filaments overlap only at
ends of A band
 Sliding filament model of contraction
 During contraction, thin filaments slide past thick
filaments  actin and myosin overlap more
 Occurs when myosin heads bind to actin  cross
bridges
Sliding Filament Model of
Contraction
 Myosin heads bind to actin; sliding begins
 Cross bridges form and break several times, ratcheting
thin filaments toward center of sarcomere
 Causes shortening of muscle fiber
 Pulls Z discs toward M line
 I bands shorten; Z discs closer; H zones disappear; A bands
move closer (length stays same)
Physiology of Skeletal Muscle
Fibers
 For skeletal muscle to contract
 Activation (at neuromuscular junction)
 Must be nervous system stimulation
 Must generate action potential in sarcolemma
 Excitation-contraction coupling
 Action potential propagated along sarcolemma
 Intracellular Ca2+ levels must rise briefly
Action potential (AP) arrives at axon
terminal at neuromuscular junction
ACh released; binds to receptors
on sarcolemma
Phase 1
Motor neuron
stimulates
muscle fiber
(see Figure 9.8).
Ion permeability of sarcolemma changes
Local change in membrane voltage
(depolarization) occurs
Local depolarization (end plate
potential) ignites AP in sarcolemma
AP travels across the entire sarcolemma
AP travels along T tubules
Phase 2:
Excitation-contraction
coupling occurs (see
Figures 9.9 and 9.11).
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SR releases Ca2+; Ca2+ binds to
troponin; myosin-binding sites
(active sites) on actin exposed
Myosin heads bind to actin;
contraction begins
The Nerve Stimulus and Events at the
Neuromuscular Junction
 Skeletal muscles stimulated by somatic motor neurons
 Axons of motor neurons travel from central nervous
system via nerves to skeletal muscle
 Each axon forms several branches as it enters muscle
 Each axon ending forms neuromuscular junction with
single muscle fiber
 Usually only one per muscle fiber
1 Action potential arrives at axon
terminal of motor neuron.
Synaptic vesicle
containing ACh
Axon terminal
of motor neuron
Synaptic
cleft
Fusing synaptic
vesiclesa
ACh
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
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1 Action potential arrives at axon
terminal of motor neuron.
2 Voltage-gated Ca2+ channels
open. Ca2+ enters the axon terminal
moving down its electochemical
gradient.
Synaptic vesicle
containing ACh
Axon terminal
of motor neuron
Synaptic
cleft
Fusing synaptic
vesiclesa
ACh
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
© 2013 Pearson Education, Inc.
1 Action potential arrives at axon
terminal of motor neuron.
2 Voltage-gated Ca2+ channels
open. Ca2+ enters the axon terminal
moving down its electochemical
gradient.
3 Ca2+ entry causes ACh (a
neurotransmitter) to be released
by exocytosis.
Synaptic vesicle
containing ACh
Axon terminal
of motor neuron
Synaptic
cleft
Fusing synaptic
vesiclesa
ACh
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
© 2013 Pearson Education, Inc.
1 Action potential arrives at axon
terminal of motor neuron.
2 Voltage-gated Ca2+ channels
open. Ca2+ enters the axon terminal
moving down its electochemical
gradient.
3 Ca2+ entry causes ACh (a
neurotransmitter) to be released
by exocytosis.
4 ACh diffuses across the synaptic
cleft and binds to its receptors on
the sarcolemma.
© 2013 Pearson Education, Inc.
Synaptic vesicle
containing ACh
Axon terminal
of motor neuron
Synaptic
cleft
Fusing synaptic
vesiclesa
ACh
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
5 ACh binding opens ion
channels in the receptors that
allow simultaneous passage of
Na+ into the muscle fiber and K+
out of the muscle fiber. More Na+
ions enter than K+ ions exit,
which produces a local change
in the membrane potential called
the end plate potential.
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Postsynaptic membrane
ion channel opens;
ions pass.
6 ACh effects are terminated by
its breakdown in the synaptic
cleft by acetylcholinesterase and
diffusion away from the junction.
ACh
Degraded ACh
Acetylcholinesterase
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Ion channel closes;
ions cannot pass.
Myelinated axon
of motor neuron
Action
potential (AP)
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
1 Action potential arrives at axon
terminal of motor neuron.
2 Voltage-gated Ca2+ channels
open. Ca2+ enters the axon terminal
moving down its electochemical
gradient.
Synaptic vesicle
containing ACh
Axon terminal
of motor neuron
Fusing synaptic
vesicles
3 Ca2+ entry causes ACh (a
neurotransmitter) to be released
by exocytosis.
ACh
4 ACh diffuses across the synaptic
cleft and binds to its receptors on
the sarcolemma.
5 ACh binding opens ion
channels in the receptors that
allow simultaneous passage of
Na+ into the muscle fiber and K+
out of the muscle fiber. More Na+
ions enter than K+ ions exit,
which produces a local change
in the membrane potential called
the end plate potential.
© 2013 Pearson
6 ACh effects are terminated by
its breakdown in the synaptic
Education,cleft
Inc.by acetylcholinesterase and
diffusion away from the junction.
Synaptic
cleft
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
Postsynaptic
membrane
ion channel opens;
ions pass.
ACh
Acetylcholinesterase
Degraded ACh
Ion channel closes;
ions cannot pass.
Neuromuscular Junction (NMJ)
 Situated midway along length of muscle fiber
 Axon terminal and muscle fiber separated by gel-filled
space called synaptic cleft
 Synaptic vesicles of axon terminal contain
neurotransmitter acetylcholine (ACh)
 Junctional folds of sarcolemma contain ACh receptors
 NMJ includes axon terminals, synaptic cleft, junctional
folds
Events at the Neuromuscular
Junction
 Nerve impulse arrives at axon terminal  ACh
released into synaptic cleft
 ACh diffuses across cleft and binds with receptors on
sarcolemma 
 Electrical events  generation of action potential
Myelinated axon
of motor neuron
Action
potential (AP)
Axon terminal of
neuromuscular
junction
Sarcolemma of
the muscle fiber
1 Action potential arrives at axon
terminal of motor neuron.
2 Voltage-gated Ca2+ channels
open. Ca2+ enters the axon terminal
moving down its electochemical
gradient.
Synaptic vesicle
containing ACh
Axon terminal
of motor neuron
Fusing synaptic
vesicles
3 Ca2+ entry causes ACh (a
neurotransmitter) to be released
by exocytosis.
ACh
4 ACh diffuses across the synaptic
cleft and binds to its receptors on
the sarcolemma.
5 ACh binding opens ion
channels in the receptors that
allow simultaneous passage of
Na+ into the muscle fiber and K+
out of the muscle fiber. More Na+
ions enter than K+ ions exit,
which produces a local change
in the membrane potential called
the end plate potential.
© 2013 Pearson
6 ACh effects are terminated by
its breakdown in the synaptic
Education,cleft
Inc.by acetylcholinesterase and
diffusion away from the junction.
Synaptic
cleft
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
Postsynaptic
membrane
ion channel opens;
ions pass.
ACh
Acetylcholinesterase
Degraded ACh
Ion channel closes;
ions cannot pass.
Destruction of Acetylcholine
 ACh effects quickly terminated by enzyme
acetylcholinesterase in synaptic cleft
 Breaks down ACh to acetic acid and choline
 Prevents continued muscle fiber contraction in absence of
additional stimulation
Generation of an Action
Potential
 Resting sarcolemma polarized
 Voltage across membrane
 Action potential caused by changes in electrical
charges
 Occurs in three steps
 End plate potential
 Depolarization
 Repolarization
Generation of an Action Potential
Across the Sarcolemma
 End plate potential (local depolarization)
 ACh binding opens chemically (ligand) gated ion
channels
 Simultaneous diffusion of Na+ (inward) and K+ (outward)
 More Na+ diffuses in, so interior of sarcolemma becomes
less negative
 Local depolarization = end plate potential
Events in Generation of an
Action Potential
 Depolarization - generation and propagation of an
action potential (AP)
 End plate potential spreads to adjacent membrane areas
 Voltage-gated Na+ channels open
 Na+ influx decreases membrane voltage toward critical
voltage called threshold
 If threshold reached, AP initiated
 Once initiated, is unstoppable  muscle fiber contraction
Events in Generation of an
Action Potential
 AP spreads across sarcolemma 
 Voltage-gated Na+ channels open in adjacent patch,
causing it to depolarize to threshold
Events in Generation of an
Action Potential
 Repolarization – restoring electrical conditions of RMP
 Na+ channels close and voltage-gated K+ channels open
 K+ efflux rapidly restores resting polarity
 Fiber cannot be stimulated - in refractory period until
repolarization complete
 Ionic conditions of resting state restored by Na+-K+ pump
ACh-containing
synaptic vesicle
Ca2+
Ca2+
Axon terminal of
neuromuscular
junction
Synaptic
cleft
Wave of
depolarization
1 An end plate potential is generated at the
neuromuscular junction (see Figure 9.8).
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Open Na+
channel
Closed K+
channel
Na+
ACh-containing
synaptic vesicle
Ca2+
Ca2+
Axon terminal of
neuromuscular
junction
Synaptic
cleft

++++++++
++++
 ++++
++++ 
K+
Action potential
2 Depolarization: Generating and propagating an action
potential (AP). The local depolarization current spreads to adjacent
areas of the sarcolemma. This opens voltage-gated sodium channels
there, so Na+ enters following its electrochemical gradient and initiates
the AP. The AP is propagated as its local depolarization wave spreads to
adjacent areas of the sarcolemma, opening voltage-gated channels there.
Again Na+ diffuses into the cell following its electrochemical gradient.
Wave of
depolarization
1 An end plate potential is generated at the
neuromuscular junction (see Figure 9.8).
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
Open Na+
channel
Closed K+
channel
Na+
ACh-containing
synaptic vesicle
Ca2+
Ca2+


++++++++
++++
++++ 
K+
Axon terminal of
neuromuscular
junction
Synaptic
cleft
 ++++
Action potential
2 Depolarization: Generating and propagating an action
potential (AP). The local depolarization current spreads to adjacent
areas of the sarcolemma. This opens voltage-gated sodium channels
there, so Na+ enters following its electrochemical gradient and initiates
the AP. The AP is propagated as its local depolarization wave spreads to
adjacent areas of the sarcolemma, opening voltage-gated channels there.
Again Na+ diffuses into the cell following its electrochemical gradient.
Wave of
depolarization
Closed Na+
channel
1 An end plate potential is generated at the
neuromuscular junction (see Figure 9.8).
Open K+
channel
Na+
++++ ++++
++++


++++ ++++++
 
K+
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3 Repolarization: Restoring the sarcolemma to its initial
polarized state (negative inside, positive outside). Repolarization
occurs as Na+ channels close (inactivate) and voltage-gated K+ channels
open. Because K+ concentration is substantially higher inside the cell
than in the extracellular fluid, K+ diffuses rapidly out of the muscle fiber.
Membrane potential (mV)
+30
0
Na+ channels
close, K+ channels
open
Depolarization
due to Na+ entry
Repolarization
due to K+ exit
Na+
channels
open
K+ channels
closed
–95
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0
5
10
Time (ms)
15
20
Excitation-Contraction (E-C)
Coupling
 Events that transmit AP along sarcolemma lead to
sliding of myofilaments
 AP brief; ends before contraction
 Causes rise in intracellular Ca2+ which  contraction
 Latent period
 Time when E-C coupling events occur
 Time between AP initiation and beginning of contraction
Events of Excitation-Contraction
(E-C) Coupling
 AP propagated along sarcomere to
T tubules
 Voltage-sensitive proteins stimulate Ca2+ release from
SR
 Ca2+ necessary for contraction
Setting the stage
The events at the neuromuscular junction (NMJ)
set the stage for E-C coupling by providing
excitation. Released acetylcholine binds to
receptor proteins on the sarcolemma and triggers
an action potential in a muscle fiber.
Axon terminal of
motor neuron at NMJ
Action potential is
generated
Synaptic
cleft
ACh
Muscle
fiber
Sarcolemma
T tubule
Terminal
cistern
of SR
Triad
One sarcomere
One myofibril
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Steps in E-C Coupling:
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cistern
of SR
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1 The action potential (AP)
propagates along the
sarcolemma and down the
T tubules.
Steps in E-C Coupling:
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cistern
of SR
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1 The action potential (AP)
propagates along the
sarcolemma and down the
T tubules.
2 Calcium ions are released.
Actin
Troponin
The aftermath
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Tropomyosin
blocking active sites
Myosin
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
Active sites exposed and
ready for myosin binding
The aftermath
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3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin. When Ca2+
binds, troponin changes
shape, exposing binding
sites for myosin (active
sites) on the thin filaments.
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
Active sites exposed and
ready for myosin binding
Myosin
cross
bridge
The aftermath
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3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin. When Ca2+
binds, troponin changes
shape, exposing binding
sites for myosin (active
sites) on the thin filaments.
4 Contraction begins:
Myosin binding to actin
forms cross bridges and
contraction (cross bridge
cycling) begins. At this
point, E-C coupling is over.
Steps in E-C Coupling:
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
1 The action potential (AP)
propagates along the
sarcolemma and down the
T tubules.
2 Calcium ions are released.
Transmission of the AP along the
T tubules of the triads causes the
voltage-sensitive tubule proteins to
change shape. This shape change
opens the Ca2+ release channels in
the terminal cisterns of the
sarcoplasmic reticulum (SR),
allowing Ca2+ to flow into the
cytosol.
Ca2+
release
channel
Terminal
cistern
of SR
Actin
Troponin
Tropomyosin
blocking active sites
Myosin
Active sites exposed and
ready for myosin binding
Myosin
cross
bridge
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3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin. When Ca2+
binds, troponin changes
shape, exposing binding
sites for myosin (active
sites) on the thin filaments.
4 Contraction begins:
Myosin binding to actin
forms cross bridges and
contraction (cross bridge
cycling) begins. At this
point, E-C coupling is over.
The aftermath
When the muscle AP ceases, the voltage-sensitive tubule proteins return to
their original shape, closing the Ca2+ release channels of the SR. Ca2+
levels in the sarcoplasm fall as Ca2+ is continually pumped back into the
SR by active transport. Without Ca2+, the blocking action of tropomyosin is
restored, myosin-actin interaction is inhibited, and relaxation occurs. Each
time an AP arrives at the neuromuscular junction, the sequence of
E-C coupling is repeated.
Steps in E-C Coupling:
Setting the stage
The events at the neuromuscular
junction (NMJ) set the stage for
E-C coupling by providing
excitation. Released acetylcholine
binds to receptor proteins on the
sarcolemma and triggers an action
potential in a muscle fiber.
Synaptic
cleft
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
1 The action potential (AP)
propagates along the
sarcolemma and down the
T tubules.
2 Calcium ions are released.
Transmission of the AP along the
T tubules of the triads causes the
voltage-sensitive tubule proteins to
change shape. This shape change
opens the Ca2+ release channels in
the terminal cisterns of the
sarcoplasmic reticulum (SR),
allowing Ca2+ to flow into the
cytosol.
Ca2+
release
channel
Terminal
cistern
of SR
Axon terminal of
motor neuron at NMJ
Action potential
is generated
ACh
Actin
Sarcolemma
Troponin
T tubule
Terminal
cistern
of SR
Muscle fiber
Tropomyosin
blocking active sites
Myosin
Triad
Active sites exposed and
ready for myosin binding
One sarcomere
One myofibril
Myosin
cross
bridge
3 Calcium binds to
troponin and removes
the blocking action of
tropomyosin. When Ca2+
binds, troponin changes
shape, exposing binding
sites for myosin (active
sites) on the thin filaments.
4 Contraction begins:
Myosin binding to actin
forms cross bridges and
contraction (cross bridge
cycling) begins. At this
point, E-C coupling is over.
The aftermath
When the muscle AP ceases, the voltage-sensitive tubule proteins return
to their original shape, closing the Ca2+ release channels of the SR. Ca2+
levels in the sarcoplasm fall as Ca2+ is continually pumped back into the
SR by active transport. Without Ca2+, the blocking action of tropomyosin
is restored, myosin-actin interaction is inhibited, and relaxation occurs.
Each time an AP arrives at the neuromuscular junction, the sequence of
E-C coupling is repeated.
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Channels Involved in Initiating Muscle
Contraction
 Nerve impulse reaches axon terminal  voltage-gated
calcium channels open 
ACh released to synaptic cleft
 ACh binds to its receptors on sarcolemma  opens
ligand-gated Na+ and K+ channels  end plate potential

 Opens voltage-gated Na+ channels  AP propagation 
 Voltage-sensitive proteins in T tubules change shape 
SR releases Ca2+ to cytosol
2+
(Ca )
Role of Calcium
Contraction
 At low intracellular Ca2+ concentration
 Tropomyosin blocks active sites on actin
 Myosin heads cannot attach to actin
 Muscle fiber relaxed
in
2+
(Ca )
Role of Calcium
Contraction
in
 At higher intracellular Ca2+ concentrations
 Ca2+ binds to troponin
 Troponin changes shape and moves tropomyosin away from
myosin-binding sites
 Myosin heads bind to actin, causing sarcomere shortening
and muscle contraction
 When nervous stimulation ceases, Ca2+ pumped back
into SR and contraction ends
Cross Bridge Cycle
 Continues as long as Ca2+ signal and adequate ATP
present
 Cross bridge formation—high-energy myosin head
attaches to thin filament
 Working (power) stroke—myosin head pivots and pulls
thin filament toward M line
Cross Bridge Cycle
 Cross bridge detachment—ATP attaches to myosin
head and cross bridge detaches
 "Cocking" of myosin head—energy from hydrolysis of
ATP cocks myosin head into high-energy state
Actin
Myosin
cross bridge
Thin filament
Thick
filament
Myosin
1 Cross bridge formation.
Energized myosin head attaches
to an actin myofilament, forming
a cross bridge.
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2 The power (working) stroke. ADP
and Pi are released and the myosin head
pivots and bends, changing to its bent
low-energy state. As a result it pulls the
actin filament toward the M line.
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3 Cross bridge detachment. After ATP
attaches to myosin, the link between myosin
and actin weakens, and the myosin head
detaches (the cross bridge “breaks”).
© 2013 Pearson Education, Inc.
ATP
hydrolysis
4 Cocking of the myosin head.
*This cycle will continue as long
as ATP is available and Ca2+ is
bound to troponin.
© 2013 Pearson Education, Inc.
As ATP is hydrolyzed to ADP and Pi,
the myosin head returns to its
prestroke high-energy, or “cocked,”
position. *
Actin
Ca2+ Thin filament
Myosin
cross bridge
Thick
filament
Myosin
1 Cross bridge formation.
Energized myosin head attaches
to an actin myofilament, forming
a cross bridge.
ATP
hydrolysis
4 Cocking of the myosin head.
As ATP is hydrolyzed to ADP and Pi,
the myosin head returns to its
prestroke high-energy, or “cocked,”
position. *
© 2013 Pearson Education, Inc.
*This cycle will continue as long
as ATP is available and Ca2+ is
bound to troponin.
2 The power (working) stroke. ADP
and Pi are released and the myosin head
pivots and bends, changing to its bent
low-energy state. As a result it pulls the
actin filament toward the M line.
In the absence
of ATP, myosin
heads will not
detach, causing
rigor mortis.
3 Cross bridge detachment. After ATP
attaches to myosin, the link between myosin
and actin weakens, and the myosin head
detaches (the cross bridge “breaks”).
Homeostatic Imbalance
 Rigor mortis
 Cross bridge detachment requires ATP
 3–4 hours after death muscles begin to stiffen with weak
rigidity at 12 hours post mortem
 Dying cells take in calcium  cross bridge formation
 No ATP generated to break cross bridges
© 2013 Pearson Education, Inc.
© 2013 Pearson Education, Inc.
© 2013 Pearson Education, Inc.
© 2013 Pearson Education, Inc.
© 2013 Pearson Education, Inc.
© 2013 Pearson Education, Inc.
© 2013 Pearson Education, Inc.