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What
is Skeletal Muscle?
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Fig 1: Photo
and information resource:
U.
California, San Diego Muscle Physiology Lab
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Skeletal
muscle is usually attached to two bones, and thus a muscle contraction
will move one bone relative to the other bone. Skeletal muscle is also
called voluntary muscle because the brain has conscious control over its activity as opposed to cardiac and smooth muscle which are considered involunatry muscle because they can not be willed to contract. Skeletal muscle is also used to control sphincters in the urinary and digestive tracts which allows for voluntary control of urine and feces release.
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Skeletal muscles
are made of groups of muscle cells called muscle
fibers. Within muscle cells are
smaller non- membrane bound organelles containing the contractile machinery called myofibrils.
Within myofibrils is the contraction mechanism made from thick and thin
myofilaments.
Thick
myofilaments
are made of the protein myosin, and have cross bridges that connect to the the thin
myofilaments which are made of the protein actin.
Muscle movement
occurs
when myosin cross bridges
attach to actin myofilaments and move the actin. This action pulls opposite ends of myofibrils together which ultimately
pulls opposite ends of the muscle cell together called shortening. When mulitple muscle
cells shorten, the entire muscle shortens. |
|<-------Sarcomere------->|
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Fig 2. The contraction unit of muscle is called a sarcomere.
Thick and thin myofilaments interact to bring opposite ends of the
sarcomere (denoted as Z lines) together. Adjacent sarcomeres undergo
the same contraction process simultaneously which shortens the entire
muscle cell.
Image Ref: |
The
contractile
process is dependent upon ATP
as a source of energy for 1) cross bridge
movement, 2) crossbridge release, and 3) the pumping of calcium,
potassium and sodium ions against their concentration gradients via
the
process
known as active transport.
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The
trigger
that starts the process of skeletal muscle contraction is the arrival
of
an action potential at the synaptic terminal of a motor neuron. A motor neuron brings commands from the Central Nervous System to muscle cells. The interface between the neuron and the muscle cell is called the neuromuscular junction.
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Fig
3. At the neuromuscular junction between a motor neuron of the somatic
nervous system and a skeletal muscle cell, a chemical known as a
neurotransmitter is released when electrical events known as action
potentials arrive in the motor neuron. The arrival of the
neurotransmitter on the surface of the muscle cells creates a second
action potential which triggers the contraction mechanism.
Therefore neuromuscular communication is an electrochemical event.
Click on this image for greater detail. Image Ref:
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The end of the motor neuron is called the synaptic terminal
(as seen in Figure 4 or presynaptic terminal in Fig 3 expanded).
The end membrane of the motor neuron, the membrane of the muscle cell,
and the space between them is called the synapse. Therefore the presynaptic membrane belongs to the motor nueron. The space between cells is called the synaptic cleft and the muscle cell membrane is called the postsynaptic membrane.
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Fig
4. The trigger for release of acetylcholine into the synaptic cleft in
a neuromuscular junction is the arrival of an action potential in the
motor neuron. Click on this image for greater
detail.
Image Ref:
To see how the ACh receptor works, click on NICOTINIC RECEPTOR. (ref)
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Voltage
gated calcium channels (not shown in figure 4) in the presynaptic membrane open once the action
potential has arrived (See event 1 in figure 4). The neurotransmitter acetylcholine (ACh) is stored within synaptic vesicles
ahead of time. The influx of calcium ions into the cytoplasm of
the axon terminal induces the release from the presynaptic membrane, of
ACh via the process of exocytosis of the synaptic vesicles (See events 2 and 3 in figure 4). Motor
neurons activate muscle cells after the acetylcholine diffuses across
the synaptic cleft and binds with a postsynaptic acetylcholine receptor (See event 4 in figure 4). If you click on Figure 4, the entire image shows the receptor mechanism. The receptor is called a ligand-gated ion channel transmembrane protein
because without the ligand (the neurotransmitter) attached, the protein
channel (the gate) is closed and sodium ions are locked out from
diffusing inward. Once the neurotransmitter attaches (ligates),
the ion channel gate opens up and positively charged sodium ions
diffuse inward which is a case of facilitated diffusion.
Increasing positive charges on the inside of the muscle cell creates
another action potential in the muscle cell membrane (also known as the
sarcolemma). On
muscle cells, the ACh receptors (AChR) are highly concentrated at
post-synaptic site, and
sparse or absent elsewhere. for isntance there are around 20,000 AChRs
per square micron on
muscle at neuromuscular junction synapse, while away from synapse,
receptors are present
at density of 20 per square micron or less. In case you are
looking for more information, the type of AChR found in skeletal muscle
is also called a nicotinic ACh receptor (nAChR) because the molecule nicotine stimulates the receptor as well.
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Once again,
another trigger mechanism is dependent upon calcium ions inside muscle
cells (muscle fibers). Activation of the acetylcholine receptor
induces the spread of a second action potential across the surface of
the muscle cell and into the cell via indentations called transverse
tubules or T tubules. |
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Fig
5. The trigger for the inhibition of the inhibition of muscle
contraction is the release of calcium ions into the cytoplasm of muscle
fibers (cells). Click on this image for greater
detail.
Image Ref:
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Action
potential arrival deep inside the transverse tubules initiates the
opening of another set of voltage gated calcium channels (not shown in figure 5) in the
membranes of the cytoplasmic organelle called sarcoplasmic reticulum. Sarcoplasmic reticula are basically bags of calcium ions sequestered by a calcium ion active transport pump
that pulls most of the calcium out of the muscle cell cytoplasm when at
rest. However, if an action potential arrives, the voltage gated
calcium channels open, and the calcium ions pour out into the cytoplasm
down their concentration gradient.
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The increase in calcium ions cause the muscle contraction inhibitor protein troponin
to remove its inhibition which thereby induces startup of muscle
contraction activity between thick and thin filaments. Contraction
continues as long as ATP is available and the calcium ion concentration
is elevated. |
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Fig 6. When calcium ions bind to troponin, troponin acts to move another protein, tropomyosin
so that actin's binding sites for myosin crossbridges are open. Once
these cross bridge binding sites are open, myosin cross bridges connect
and begin the contraction event. Click on this image for greater
detail.
Image Ref: |
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To
stop contraction, the arrival of action potentials in the motor neuron
must stop, which stops the release of acetylcholine. The remaining
acetylcholine in the synaptic cleft and those disconnect from the
acetylcholine receptors are broken into acetate and choline molecules
by the enzyme acetylcholine esterase. |
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Fig
7. Acetylcholine is synthesized from acetylCoenzyme A and choline in
the cytoplasm of motor neuron synaptic endings. It is then stored
in synaptic vesicles until released into the synaptic cleft. ACh
is broken down by the enzyme ACh Esterase (AChE) which resides within the
synaptic cleft. It breaks ACh back into acetate and
choline. Choline is pumped back into the synaptic ending for use
again. Acetate is not taken back up again, so new acetylCoAs must be
synthesized via the breakdown of glucose via glycolysis and pyruvate
processing. Click on this image for greater
detail. Image Ref: |
Once this happens, action potentials in the muscle cell transverse
tubules stop, which causes the calcium channels in the sarcoplasmic
reticulum to close. This allows the calcium pumps to remove the
calcium ions from the cytoplasm back into the sarcoplasmic
reticula. Lowering of the calcium ion concentration in the
cytoplasm allows the inhibitor troponin / tropomyosin to cover up the
binding sites for the myosin cross bridge heads on the thin filaments.
If ATP is available, the cross bridges disconnect and the muscle
relaxes.
For a nice visual summary: MUSCLE CONTRACTION (ref)
If the reason for the cessation of action potentials is death, then ATP
will not be available also, and the cross bridges will remain connected
to the thin filaments, leaving the muscle cells and thereby the muscle
stiff. This is called rigor mortis.
Rigor mortis can be used to help estimate time of death. The onset of
rigor mortis may range from 10 minutes to several hours, depending on
factors including temperature (rapid cooling of a body can inhibit
rigor mortis, but it occurs upon thawing). Maximum stiffness is reached
around 12-24 hours post mortem. Depending on temperature and other
conditions, rigor mortis lasts approximately 72 hours. Rigor mortis
disappears due to the general breakdown of cells from the leakage of
lysosomal enzymes into the cytoplasm. (ref)
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