Muscle Contraction. Release of the appropriate array of inhibitory and stimulatory neurotransmitters...

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.

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

Tropomyosin

Troponin

Ca2+ released from the sarcoplasmic reticulum

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

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.

Ca2+ being re-accumulated back into the sarcoplasmic reticulum

Pi

ADPATP

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.

Pi

ADP

ATP

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

ADP

ATP

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.

ADP

ATP

The myosin head continues to rotate which shortens the length of the sarcomere. You have to imagine that there are trillions of these myosin-actin interactions happening throughout the length of the muscle to generate sufficient force to actually move a limb, or a weighted limb.

ATPADP

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

ATP

Pi

ADP

Pi

ADP

Pi

ADP

ADP

ADPATP

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.

0

0.2

0.4

0.6

0.8

1

0 5 10 15 20 25

Velocity

Fo

rce

Force/velocity relationships of a fast and slow muscle

Fast twitch ~ 110 m/s

Slow twitch ~ 50 m/s

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 cross-bridge” 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