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Muscle Contraction
Release of the appropriate array of inhibitory and
stimulatory neurotransmitters in the brain will activate the
appropriate motor nerves in the appropriate order to
accomplish a movement task. This, of course, demands
muscle contraction.
At the local muscle level; release of the
neurotransmitter acetylcholine at the
neuromuscular junction will depolarize the
muscle cell membrane at that spot – initiating
a series of action potentials throughout the
muscle cell and ultimately resulting in muscle
contraction.
The amount of
neurotransmitter
released depends
on the degree of
neural activation
as well as the type
of nerve activated
Small diameter “lightly” myelinated nerves are very easy to
activate with the resulting action potentials propagated at a
slower rate, a lower maximum frequency, and with a lower
maximum amplitude compared to the larger, more heavily
myelinated neurons.
Obviously, with maximal neural activation, the larger
neurons will release a lot more neurotransmitters at a higher
frequency resulting in much greater depolarization of the
post-synaptic membrane. (With obvious consequences for
action potentials in the post-synaptic membrane.)
Motor unit
Copyright: Pearson Education, Inc., publishing as Benjamin Cummings, 2004
Acetylcholine released by motor nerve activates Ach-gated sodium channels to create
an EPSP in the sarcolemma; resulting in action potentials being propagated
throughout the sarcolemmal membrane, through the t-tubule system, and along the
sarcoplasmic reticulum. V.G.-calcium channels in the SR are activated by the action
potentials to “flood” the cell with calcium.
Copyright: Pearson Education, Inc., publishing as Benjamin Cummings, 2004
The real action of
muscle contraction
occurs at the level of
the sarcomere; the
interaction of
myosin proteins and
actin proteins. The
myosin protein
simply “walks”
along the actin
filament pulling the
ends of the
sarcomere together;
resulting in a shorter
myofibril and a
shorter muscle.
The sarcoplasmic reticulum
surrounding the sarcomeres
stores calcium. Calcium, of
course, is the signal used to
initiate the events of ontraction.
Ca2+ released from
the sarcoplasmic
reticulum
Troponin
Tropomyosin
The myosin head is prevented from binding to the
actin by the presence of tropomyosin. Only when
calcium binds to the troponin (c) will the inhibiting
protein be moved out of the way
4 Ca2+ molecules bind to the troponin c, changing the
distribution of charges in this protein which causes the
tropomyosin to move and expose myosin binding sites on
the actin filament. The myosin can then bind to the actin
and do the contraction-thing
Ca2+ being reaccumulated back
into the sarcoplasmic
reticulum
For the muscle to relax the calcium has to be removed and
pumped back into the sarcoplasmic reticulum by calcium
pumps. At very high calcium concentrations (very hard
contractions) some of the calcium will be sequestered by the
mitochondria.
ATP
Only through the hydrolysis of ATP can the
contraction-thing happen. The myosin head contains
the enzyme myosin ATP’ase which splits ATP to ADP
and Pi.
ATP
Pi
ADP
The hydrolysis of ATP changes the distribution of charges
in the myosin head which changes the shape of the protein
to make it “bind” to actin. Not much can happen yet
because another change in shape has to occur.
Pi
ATP
ADP
The change resulting in cross-bridge formation (binding)
alters the ability for phosphate to stay bound to the myosin so
it is released, resulting in another change is shape of the
myosin head. The protein rotates and develops a “large”
force, resulting in the myosin pulling hard on the actin
filament.
ATP
ADP
The myosin head continues to rotate which shortens the length of the
sarcomere. You have to imagine that there are trillions of these myosinactin interactions happening throughout the length of the muscle to
generate sufficient force to actually move a limb, or a weighted limb.
ATP
ADP
When the myosin protein rotates fully the binding site
for ADP in the myosin ATP’ase has changed shape so
it can no longer bind ADP and ADP falls out. The
actin-myosin bond can only be broken when another
ATP molecule binds into the ATP-binding site of the
enzyme – starting the contraction-cycle over again.
ATP
Pi
ADP
Pi
ADP
ADP
ATP
ADP
And so on …… as long as there is ATP available
As the sarcomeres shorten force is developed, with the speed of
shortening dependent on the speed at which the myosin ATP’ase
enzyme can work.
1
Force/velocity relationships of
a fast and slow muscle
Force
0.8
0.6
0.4
0.2
Fast twitch ~ 110 m/s
0
0
5
10
15
20
25
Slow twitch ~ 50 m/s
Velocity
Remember:
Small/slow nerves –
small/slow muscle cells
Large/fast nerves –
Large/fast muscle cells
Fast contraction is due predominantly to the myosin ATP-ase
enzyme. There are two forms; the fast one and the slow one.
The fast one makes the ADP fall off the myosin head faster than
the slow one
This results in a faster capacity to recycle the “form a crossbridge” then “break a cross-bridge” and then “form another”
during a contraction cycle and produces a faster speed of
shortening.
Notice that the slow speed of shortening (50 m/s) for slow twitch
muscle cells is still a lot faster than we can actually move our
limb when running or moving an object.
Another basic difference between the fast and slow muscle cells
is in the number of mitochondria. Slow muscles have a lot
more mitochondria than fast muscles. This means they have a
much greater capacity to make ATP through oxidative
mechanisms.
Fast muscle cells, on the other hand have a much greater
capacity to make ATP through glycolysis.
Maintaining muscle contractions depends on regenerating ATP
as it is being used up.
(Details of metabolic production of ATP will follow.)
*Binding of ATP to a protein significantly changes the distribution of charges in
the protein and leads to a change in shape - resulting in some type of movement
(conversion of one form of chemical energy into another form of chemical
energy plus kinetic energy); hydrolysis of ATP to ADP + phosphate also allows
for a redistribution of charges and another change in shape – resulting in
movement; most often the only form of energy “released” during chemical
reactions is heat