Transcript muscle fiber

“How Do Muscles Contract?”
This theory states that during contraction, the
thin filaments slide pass the thick filaments so
that they over lap by a greater degree.
The result is that the I bands shorten and the
distance between the Z discs decrease.
The H band disappears and the A bands
remain the same length.
Z
Z
H
A
I
1 Fully relaxed sarcomere of a muscle fiber
Z
I
I
Z
A
I
2 Fully contracted sarcomere of a muscle fiber
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For a muscle to contract, three events need to
occur:
a) The muscle needs to be stimulated by a
nerve ending.
This leads to a change in the membrane
potential.
The site of this is called the neuromuscular
junction.
For a muscle to contract, three events need to
occur:
b) An electrical current (action potential) then
needs to be generated along the sarcolemma.
For a muscle to contract, three events need to
occur:
c) The electrical current results in the final
trigger which is a short lived rise in
intracellular calcium ions which results in the
in the contraction.
The nerve cells that activate skeletal muscle
fibers at the neuromuscular junction called
somatic (body) motor (think muscles)
neurons.
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The motor neurons reside in the spinal column
and brain, they have long cyctoplasmic
extensions called axons.
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The motor neurons reside in the spinal column
and brain, they have long cytoplasmic
extensions called axons.
These enter the muscle and divide extensively
so that each muscle fiber (cell) has its own
axon terminal which forms a neuromuscular
junction.
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Spinal cord
Motor Motor
unit 1 unit 2
Axon terminals at
Branching axon
neuromuscular junctions to motor unit
Nerve
Motor neuron
cell body
Motor neuron
axon
Muscle
Muscle
fibers
(a) Axons of motor neurons extend from the spinal cord to the muscle.
There each axon divides into a number of axon terminals that form
neuromuscular junctions with muscle fibers scattered throughout
the muscle.
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(b) Branching axon
terminals form
neuromuscular
junctions, one per
muscle fiber (photomicrograph 330x).
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The axon does NOT come into direct contact
with the sacrolemma of the muscle fiber. T
There is a 1 to 2 nm cleft between them called
the synaptic cleft. This cleft is not empty but is
filled with a gel like extracellular matrix.
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The nerve impulse is transmitted across this
cleft by the release of a neurotransmitter.
This crosses the space and attaches to specific
membrane receptors on the sacrolemma.
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The typical neurotransmitter found at these
synaptic junctions is acetylcholine.
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This molecule resides is vesicles in the axon
and is released upon depolarization of the axon
terminal.
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These diffuse across the cleft and attach to
receptors which then stimulate the
depolarization of the muscle fiber.
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Recall that all cells are polar, they are positively
charged on the outside and negatively charged
on the inside.
Sodium ions, Na+ are in high concentration on
the outside and potassium ions, K+, are in high
concentration on the inside.
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Acetylcholine binds to its receptor on the
sarcolemma and a gated ion channel is opened.
This causes sodium ions to diffuse into the
muscle fiber and potassium ions to diffuse out.
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This is an autoimmune disease that specifically
attacks the acetylcholine receptor.
Symptoms include:
 Weakness starting with the eye lids (ptosis)
 Progressing to a general weakness
 Ends with difficulty swallowing and SOB
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Curare competitively binds to the acetyl
choline receptor but does not lead to
depolarization.
Death from asphyxiation quickly follows
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1 Action potential
arrives at axon terminal
of motor neuron.
2 Voltage-gated Ca2+
channels open and
Ca2+ enters the axon
terminal.
3 Ca2+ entry
causes some
synaptic vesicles
to release their
contents
(acetylcholine)
by exocytosis.
4 Acetylcholine, a
neurotransmitter, diffuses
across the synaptic cleft
and binds to receptors in
the sarcolemma.
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Ca2+
Ca2+
Axon terminal
of motor neuron
Synaptic vesicle
containing ACh
Mitochondrion
Synaptic cleft
Fusing
synaptic
vesicles
ACh
Junctional
folds of
sarcolemma
Sarcoplasm of muscle fiber
5 ACh binding opens ion channels that allow
simultaneous passage of Na+ into the muscle
fiber and K+ out of the muscle fiber.
Na+
K+
Postsynaptic membrane ion channel
opens; ions pass.
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The initial depolarization at the neuromuscular
junction ignites an action potential that spreads
out in all directions across the sarcolemma.
The depolarization opens voltage- gated
sodium channels.
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As the polarization moves down the
sarcolemma, other voltage gated channels are
opened and the process continues.
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Axon terminal
Open Na+
Channel
Na+
Synaptic
cleft
Closed K+
Channel
ACh–
ACh
Na+ K+
K+
Na+ K+
Generation and propagation of
the action potential (AP)
2
Closed Na+ Open K+
Channel
Channel
+
Na
Local depolarization:
generation of the end
plate potential on the
sarcolemma
1
Sarcoplasm of muscle fiber
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3
K+
Repolarization
This process restores the resting potential.
The sodium channels initially opened by the
depolarization close and at the same time a
potassium channel opens, letting potassium to
diffuse out of the cell, restoring the negative
voltage inside the muscle fiber.
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Depolarization
due to Na+ entry
Na+ channels
close, K+ channels
open
Repolarization
due to K+ exit
Na+
channels
open
Threshold
K+ channels
close
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Before the muscle fiber contracts, there has to
be an excitation coupling.
This is the sequence of steps where the action
potential along the sarcolemma leads to
changes in the levels of calcium ions which
results in the mechanical contraction.
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These are two sets of intracellular tubules that
participate in the regulation of muscle
contraction and excitation coupling.
These are found at each A and I band junction.
A T-tubule (or transverse tubule), is a deep
invagination of the plasma membrane
(sarcolemma).
These invaginations allow depolarization of the
membrane quickly to the interior of the cell.
This is a modified smooth endoplasmic
reticulum. Its tubules run longitudinally
surround each myofibril.
They communicate with each other in the H
zone.
They function to store calcium ions.
Setting the stage
Axon terminal
of motor neuron
Synaptic cleft
ACh
Terminal cisterna of SR
Muscle fiber Ca2+
Action potential
is generated
Sarcolemma
Triad
One sarcomere
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1 Action potential is
Steps in
E-C Coupling:
propagated along the
sarcolemma and down
the T tubules.
Voltage-sensitive
tubule protein
Sarcolemma
T tubule
Ca2+
release
channel
Terminal
cisterna
of SR
Ca2+
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2 Calcium
ions are
released.
Myosin makes up the thick filament. This is a
complex molecule that consists of two heavy
and four light polypeptides.
These form a molecule with a rod like tail with
two flexible globular “heads”.
Thick 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
Actin-binding sites
Heads
ATPbinding
site
Flexible hinge region
Myosin molecule
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Tail
Actin makes up the bulk of the thin filament.
This molecule has ”kidney shaped”
polypeptide subunits called globular actin or G
actin which combine with the myosin head
during the contracting process.

Troponin is a globular three polypeptide
complex. It has several regulatory roles with
actin.
TnI binds to actin
 TnT binds to Tropomyosin and helps to position it on
actin
 TnC binds calcium ions.

Tropomyosin a rod shaped protein which
helps to stabilize the actin molecule. In a
relaxed muscle fiber, they block myosin
blinding sites on the actin molecule.
Thin filament
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
Active sites
for myosin
attachment
Actin subunits
Actin subunits
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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.
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Thin filament (actin)
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Myosin heads
Thick filament (myosin)
Titin is the primary protein found in the elastic
filament.
This protein extends from the Z disc to the
thick filament.
It helps the muscle spring back to its original
shape after stretching.
The cross bridge formation is the attachment of
the myosin heads to the actin.
This process requires calcium ions.
Calcium is the key ion in the contraction
process.
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The muscle is relaxes when there are low levels
of intracellular calcium ions.
The myosin binding sites on the actin molecule
are blocked by Tropomyosin proteins.
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As intracellular calcium levels rise, the ions
bind to regulatory sites on the protein
troponin.
This results in a change in troponin’s shape
causing it to move the Tropomyosin off the
myosin binding sites.
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1. Myosin heads bind to the passive actin
filaments at the myosin binding sites.
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1. Myosin heads bind to the passive actin
filaments at the myosin binding sites.
2. Upon strong binding, myosin and actin
undergo an isomerization (myosin rotates
at the myosin-actin interface) extending
an extensible region in the neck of the
myosin head.
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Thin filament
Actin
Myosin
head
Ca2+
ADP
Pi
Thick filament
Myosin
1 Cross bridge formation.
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ADP
Pi
2 The power (working) stroke.
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3. Shortening occurs when the extensible region
pulls the filaments across each other (like the
shortening of a spring). Myosin remains
attached to the actin.
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3. Shortening occurs when the extensible region
pulls the filaments across each other (like the
shortening of a spring). Myosin remains
attached to the actin.
4. The binding of ATP allows myosin to detach
from actin. While detached, ATP hydrolysis
occurs "recharging" the myosin head. If the
actin binding sites are still available, myosin
can bind actin again.
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ATP
3 Cross bridge detachment.
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ADP
PI
ATP
hydrolysis
4 Cocking of myosin head.
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Action potential (AP) arrives at axon
terminal at neuromuscular junction
ACh released; binds to receptors
on sarcolemma
Phase 1
Muscle fiber is
stimulated by motor
neuron (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
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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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Illustrates the cross
bridging requires ATP.
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Illustrates the cross
bridging requires ATP.
Most muscles stiffen 3
to 4 hours after death.
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Illustrates the cross
bridging requires ATP.
Most muscles stiffen 3
to 4 hours after death.
Calcium leaks into the
cells, causing cross
bridging.
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Illustrates the cross bridging
requires ATP.
Most muscles stiffen 3 to 4
hours after death.
Calcium leaks into the cells,
causing cross bridging.
ATP is no longer being
produced, leaving the
muscles stiff.
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Rigor mortis disappears
after the muscle
proteins begin to break
down.
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