Transcript 10 Muscle - bloodhounds Incorporated

Physiology
Skeletal Muscle Contraction
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: Attachments

Attach in at least two places
◦ Insertion – movable bone
◦ Origin – immovable (less movable) bone

Attachments direct or indirect
◦ Direct—epimysium fused to periosteum of
bone or perichondrium of cartilage
◦ Indirect—connective tissue wrappings
extend beyond muscle as ropelike tendon or
sheetlike aponeurosis
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Microscopic Anatomy of A Skeletal Muscle Fiber

Long, cylindrical cell
◦ 10 to 100 µm in diameter; up to 30 cm long
Multiple peripheral nuclei
 Sarcolemma = plasma membrane
 Sarcoplasm = cytoplasm

◦ Glycosomes for glycogen storage,
myoglobin for O2 storage

Modified structures: myofibrils,
sarcoplasmic reticulum, and T
tubules
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Myofibrils
Densely packed, rodlike elements
 ~80% of cell volume
 Contain sarcomeres - contractile units

◦ Sarcomeres contain myofilaments

Exhibit striations - perfectly aligned
repeating series of dark A bands and light
I bands
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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
Light Nucleus
I band
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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
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Sarcomere: region between
two successive Z
Connective Tissue

Endomysium
◦ Surrounds each muscle fiber (cell)
◦ Attaches to Z-lines in each sarcomere

Perimysium
◦ Surrounds bundles (fascicles) of muscle fibers
◦ Attaches to endomysium

Epimysium
◦ Attaches to the Perimysium
◦ Continuous with tendon
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.
Z disc
I band
H zone
Z disc
I band
A band
Sarcomere
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M line
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.
Z disc
I band
H zone
Z disc
I band
A band
Sarcomere
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M line
Sarcomere
Repeating Patterns within the myofibrils
 Myofibrils

◦ Proteins within the myofibers
◦ Myosin
◦ Actin
Muscle Anatomy

Sarcolemma
◦ Muscle fiber cell membrane

Myofibrils
◦ Highly organized bundles of contractile and
elastic proteins
◦ Carries out the work of contraction
Myofibrils = Contractile Organelles of Myofiber
Contain 6 types of protein:






Actin
Myosin
Tropomyosin
Troponin
Titin
Nebulin
Contractile
Regulatory
Accessory
Titin and Nebulin

Titin: biggest protein known (25,000 aa);
elastic!



Stabilizes position of contractile filaments
Return to relaxed location
Nebulin: inelastic
giant protein

Alignment of A & M
Structure of Myofibril

Elastic filament
◦ Composed of protein titin
◦ Holds thick filaments in place; helps recoil
after stretch; resists excessive stretching

Dystrophin
◦ Links thin filaments to proteins of sarcolemma

Nebulin, myomesin, C proteins bind
filaments or sarcomeres together;
maintain alignment
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Changes in a Sarcomere during Contraction
Myosin
Myo- muscle
 Motor protein of the myofibril
 Thick filament
 Attaches to the M-line

◦ Heads point towards Z-lines
Myosin heads are clustered at the ends of
the filament
 Myosin tails are bundled together

Role of calcium
Tropomyosin
Troponin complex
•Troponin and Tropomyosin bind to actin
block the actin – myosin binding sites
•Troponin is a calcium binding protein
Actin

Thin Filament
◦ Attached to Z-lines

Globular protein
◦
◦
◦
◦
G-Actin
Has binding site for myosin head
Forms a Cross-Bridge when myosin binds to G-actin
Five Actin proteins surround the myosin in 3-D pattern
Actin

Tropomyosin
◦ Protein that covers over the myosin binding
site on G-Actin
 Myosin head can’t bind to G-Actin, muscle relaxes
◦ If the binding site on G-Actin is uncovered by
removing Tropomyosin then myosin and actin
bind, muscle contracts
Actin

Troponin C
◦ Protein attached to Tropomyosin
◦ When Troponin C changes shape it pulls on Tropomyosin
 Calcium binding to Troponin C causes this protein to
change shape
◦ Tropomyosin moves and uncovers the binding site on GActin, so Actin and Myosin can bind
 Contraction
Regulation of Contraction by Troponin and
Tropomyosin

Tropomyosin blocks myosin binding site (weak
binding possible but no powerstroke)

Troponin controls position of tropomyosin and has
Ca2+ binding site

Ca2+ present: binding of A & M

Ca2+ absent: relaxation
Sarcoplasmic Reticulum (SR)

Network of smooth endoplasmic
reticulum surrounding each myofibril
◦ Most run longitudinally
Pairs of terminal cisternae form
perpendicular cross channels
 Functions in regulation of intracellular
Ca2+ levels

◦ Stores and releases Ca2+
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T Tubules
Continuations of sarcolemma
 Lumen continuous with extracellular
space
 Increase muscle fiber's surface area
 Penetrate cell's interior at each A band–I
band junction
 Associate with paired terminal cisterns to
form triads that encircle each sarcomere

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Muscle Anatomy

Sarcoplasmic Reticulum
◦ Modified endoplasmic reticulum
◦ Wraps around each myofibril like a piece of lace
◦ Stores Calcium

Terminal Cisternae
◦ Longitudinal tubules

Transverse tubules (T-tubules)
◦ Triad-two flanking terminal cisternae and one t-tubule
◦ T-tubules are continuous with cell membrane

When Troponin binds calcium it moves
Tropomyosin away from the actin-myosin
binding site
Ca
Ca
Where does Calcium come from?




Intracellular storage called Sarcoplasmic
Reticulum
Surround each myofibril of the whole muscle
Contains high concentration of calcium
Transverse Tubules connects plasma membrane
to deep inside muscle
T-Tubules

Rapidly moves action potentials that
originate at the neuromuscular junction
on the cell surface
Motor nerve
Membrane depolarization or APs
carried deep into the muscle by Ttubules
T-tubule
+
Neurotransmitter
receptors
SR
SR
Ryanodine Receptor
T-tubule My
SR
myoplasm
Dihydropyridine
receptor
Ca++
Ca++
Ca++
SR
Ca++
pump
Myoplasm
(intracellular)
_
+
_
+_ +
_+
_
_ + +
_ + _
+
_
_ + _+ _+ +
T-tubule
(extracellular)
Actin filament
Binding sites
Strong
binding
Weak
binding
Myosin head group
S2 link
Stretching of the link generates tension
Myosin filament
Why do thin filaments move?
Net force
Net force
Equal and opposite force
on thick filament
Sliding Filament Theory
When myosin binds to the binding site on
G-actin muscular contraction occurs.
 The more myosin that bind to G-actin the
greater the force of contraction
 Calcium must be present

Slide 1
1 Fully relaxed sarcomere of a muscle fiber
H
A
Z
I
Z
I
2 Fully contracted sarcomere of a muscle fiber
Z
I
Z
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IInc.
A
Slide 2
1 Fully relaxed sarcomere of a muscle fiber
Z
I
H
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A Education,
Inc.
Z
I
Slide 3
2 Fully contracted sarcomere of a muscle fiber
Z
I
Z
A
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Inc.
I
Slide 4
1 Fully relaxed sarcomere of a muscle fiber
H
A
Z
I
Z
I
2 Fully contracted sarcomere of a muscle fiber
Z
I
Z
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A
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).
SR releases Ca2+; Ca2+ binds to
troponin; myosin-binding sites
(active sites) on actin exposed
Myosin heads bind to actin;
contraction begins
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Inc.
Slide 1
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+
© 2013
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
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Education,
than in the extracellular
fluid, K+ diffuses rapidly out of the muscle fiber.
Inc.
Slide 2
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).
© 2013 Pearson Education,
Inc.
Slide 3
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
1 An end plate potential is generated at the
neuromuscular junction (see Figure 9.8).
© 2013 Pearson Education,
Inc.
Slide 4
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+
© 2013
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
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Education,
than in the extracellular
fluid, K+ diffuses rapidly out of the muscle fiber.
Inc.
Sliding Filament Theory
Cross Bridge
◦ Myosin in the High Energy Configuration binds to G-Actin
◦ ADP + Pi are bonded to the myosin head when the cross bridge
forms
 Power Stroke
◦ When the myosin and actin bind the myosin head changes shape
◦ Myosin pulls the actin and pulls on the Z-line
◦ Sarcomere shortens
◦ ADP+Pi no longer binds to myosin head

Sliding Filament Theory

ATP binds to the myosin head
◦ Myosin changes to its Low Energy
Confirmation
◦ In the Low Energy Confirmation Myosin
breaks its bonds with Actin
 Rigor Mortis
 Lack of ATP
 Build up of Lactic Acid
Sliding Filament Theory

ATPase
◦ ATP is hydrolyzed to ADP + Pi
◦ ATPase is on the myosin head
◦ Myosin changes shape back to its High Energy
Confirmation
Sliding Filament Theory

Some Myosin heads detach from Actin
while other heads continue to keep their
attachments
◦ No slipping of the Z-lines
◦ Contraction is held in place
What if we don’t have this?
ATP
X
Actin + myosin  Actomyosin complex
Rigor mortis
Events at Neuromuscular Junction

Converts a chemical signal from a somatic
motor neuron into an electrical signal in
the muscle fiber
Events at Neuromuscular Junction




Acetylcholine (Ach) is released from the somatic
motor neuron
Ach initiates an action potential in the muscle fiber
The muscle action potential triggers calcium release
from the sarcoplasmic reticulum
Calcium combines with troponin C and initiates
contractions
Slide 1
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.
6 ACh effects are terminated by
its breakdown in the synaptic
© 2013
cleft 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
Degraded ACh
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Ion channel closes;
ions cannot pass.
Slide 2
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
© 2013 Pearson Education,
Inc.
Slide 3
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.
Slide 4
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.
Slide 5
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
4 ACh diffuses across the synaptic
cleft and binds to its receptors on
the sarcolemma.
Junctional
folds of
sarcolemma
Sarcoplasm of
muscle fiber
© 2013 Pearson Education,
Inc.
Slide 6
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.
Postsynaptic membrane
ion channel opens;
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ions pass.
Inc.
Slide 7
6 ACh effects are terminated by
its breakdown in the synaptic
cleft by acetylcholinesterase and
diffusion away from the junction.
ACh
Degraded ACh
Acetylcholinesterase
Ion channel closes;
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ions
cannot pass.
Inc.
Slide 8
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.
6 ACh effects are terminated by
its breakdown in the synaptic
© 2013
cleft 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
Degraded ACh
AcetylchoPearson
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Inc.
Ion channel closes;
ions cannot pass.
Events at Neuromuscular Junction
Ach binds to cholinergic receptors on the
motor end plate
 Na+ channels open

◦ Na+ influx exceeds K+ efflux across the
membrane

End-Plate Potential (EPP)
◦ EPP reaches threshold and initiates a muscle
action potential
Events at Neuromuscular Junction

Action Potentials move down the
membrane
◦ K+ builds up in the t-tubules
◦ Depolarization occurs
 Calcium gates on the SR opens
 Calcium diffuses into the cytoplasm of the cell
Excitation-Contraction Coupling

The process where muscle action
potentials initiate calcium signals that in
turn activates a contraction-relaxation
cycle
Initiation of Contraction
Excitation-Contraction Coupling explains how you get from
AP in axon to contraction in sarcomere
ACh released from somatic motor neuron at the Motor End
Plate
AP in sarcolemma and T-Tubules
Ca2+ release from sarcoplasmic reticulum
Ca2+ binds to troponin
Slide 1
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. *
*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
© 2013
Pearson
Education,
and actin
weakens,
and the
myosin head
detaches (the cross bridge “breaks”).
Inc.
Slide 2
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.
© 2013 Pearson Education,
Inc.
Slide 3
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.
© 2013 Pearson Education,
Inc.
Slide 4
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.
Slide 5
ATP
hydrolysis
4 Cocking of the myosin head.
*This cycle will continue as long
as ATP is available and Ca2+ is
bound to troponin.
As ATP is hydrolyzed to ADP and Pi,
the myosin head returns to its
prestroke high-energy, or “cocked,”
position. *
© 2013 Pearson Education,
Inc.
Slide 6
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. *
*This cycle will continue as long
as ATP is available and Ca2+ is
bound to troponin.
© 2013
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
Pearson
andEducation,
actin weakens, and the myosin head
detaches (the
cross bridge “breaks”).
Inc.
Details of E/C
Coupling
Nicotinic cholinergic receptors on motor end plate
= Na+ /K+ channels
 Net Na entry creates EPSP
 AP to T-tubules
 DHP (dihydropyridine) receptors in T-tubules
+
sense depolarization
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
© 2013 Pearson Education,
Inc.
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
© 2013 Pearson Education,
Inc.
Nicotinic Cholinergic Receptors
DHP (dihydropyridine) receptors open Ca2+ channels in t-tubules
Intracytosolic [Ca2+] 
Contraction
Ca2+ re-uptake into SR
Relaxation
Excitation-Contraction Coupling

High cytosolic Calcium levels binds to Troponin C
◦ Tropomyosin moves to the “on” position and contraction
occurs


Calcium-ATPase pumps Calcium back into the SR
The more myosin heads that binds to actin to
stronger the force of contraction
Summary of events
1.
2.
3.
4.
Synaptic Depolarization of the plasma
membrane is carried into the muscle by TTubules
Conformational change of dihydropyridine
receptor directly opens the ryanodine
receptor calcium channel
Calcium flows into myoplasm where it binds
troponin
Calcium pumped back into SR
Neuromuscular Junction
The more terminal boutons to attach to
myofibers the greater the control of the
muscle.
 Recruitment

◦ The greater the number of terminal boutons
attached to myofibers there is more fine
control of the muscle
Excitation-Contraction Coupling

Twitch
◦ A single contraction-relaxation cycle in a
skeletal muscle fiber
◦ A single action potential in a muscle fiber

Latent Period
◦ Between the muscle action potential
◦ Time required for excitation-contraction
coupling to take place
Is There Truth In Advertising?
Is the banana company telling the truth
when they claim that bananas being high
in Potassium actually prevents or relieves
muscle cramps?
 If so, how does this increase in Potassium
relieve muscle cramps?
 If not, why not and how do we actually
relieve muscle cramps?

What produces a muscle cramp?
 How is Potassium related to muscle
cramps?

◦ Look up Hypokalemia and Hyperkalemia
Muscle Contraction and ATP Supply

Phosphocreatine
◦ Backup energy source
◦ Quick energy used up in approx. 15 minutes
Causes of Fatigue

Central Fatigue
◦ Subjective feelings of tiredness
◦ Arises in the CNS
◦ Psychological fatigue precedes physiological
fatigue in the muscles
 Subjective feelings of tiredness
 Low pH may cause fatigue
Oxidative only
Oxidative or
glycolytic
Muscle Fiber Classification
Muscle Adaptation to Exercise
Endurance training:
 More & bigger
mitochondria

More enzymes for
aerobic respiration
Resistance training:
 More actin & myosin
proteins & more
sarcomeres


More myofibrils
More myoglobin
muscle hypertrophy
no hypertrophy
Causes of Fatigue

Peripheral Fatigue
◦ Arises between the neuromuscular junction
and the contractile elements of the muscle
◦ Ach depletion, neuromuscular junction
receptor loss
 Myasthenia Gravis
Skeletal Muscle Types

Fast-twitch muscle fibers (type II)
◦ White Fibers
 Low Myoglobin
◦ Develops tension two to three times faster
than slow-twitch fibers
◦ Splits ATP more rapidly to complete
contraction faster
◦ Fatigues quickly
Skeletal Muscle Types

Slow-twitch Muscle Fibers (Type I)
◦ Red
◦ High Myoglobin levels
◦ Slow to Fatigue
Contractions

Isometric Contractions
◦ Creates force without movement

Isotonic Contractions
◦ Moves loads
During skeletal muscle contraction the binding of the
myosin head to G-actin occurs at which step?
A.
B.
C.
D.
Cross bridge
Power stroke
Working stroke
Force stroke
During the cross bridge the myosin head is
in the ____ configuration.
A.
B.
C.
D.
Low energy
High energy
Medium energy
Power energy
Name the connective tissue layer that
surrounds a fascicle in skeletal muscle.
A.
B.
C.
D.
E.
Endomysium
Epimysium
Perimyseum
Tendon
Epicardium
Name the functional unit of skeletal
muscle.
A.
B.
C.
D.
Sarcolemma
Saroplasmic Reticulum
Sarcomere
Myosin
The thick filament is also referred to as
A.
B.
C.
D.
E.
Actin
Myosin
Tropomyosin
Troponin C
G Actin
Which protein in G-Actin is responsible
for blocking the bind site of myosin?
A.
B.
C.
D.
Tropomyosin
Troponin C
Sarcoplasmic Reticulum
Sarcolemma
During skeletal muscle contraction
Calcium is stored in the
A.
B.
C.
D.
E.
Sarcolemma
Sarcomere
Sarcoplasmic Reticulum
Golgi Apparatus
Transverse Tubules
The build-up of potassium in the _______
causes the resting membrane potential of
skeletal muscle to depolarize.
A.
B.
C.
D.
Sarcolemma
Sarcoplasmic reticulum
Transverse tubule
Tropomyosin
Which enzyme is located on the myosin
head?
A.
B.
C.
D.
E.
ATP synthase
ATP ase
ATP reductase
Phophodiesterase
Oxidase
During cross bridge formation myosin
will bind to ________.
A.
B.
C.
D.
Troponin C
Tropomyosin
G-Actin
Myosin
The phenomenon of rigor mortis is a
direct result of
A. The breaking of myosin bonds by ATP
B. The breaking of actin bonds by ATP
C. The inability of the myosin cross bridges to
combine with single amino acids
D. The loss of ATP in dead muscle cells