Molecular Mechanisms of Muscle Contraction

It is a "theory" but it is widely accepted. The theory was developed in the 1950s and it is called the sliding filament theory.

The basic principles of muscle contraction have been known for some time. However, the precise mechanism is still unknown or else the subject of theoretical investigation. Muscle is comprised of bundles of elongated cells called muscle fibers. At the sub-cellular level, muscle fibers contain bundles of elongated structures called myofilaments. There are two types of myofilament - actin and myosin. Two sets of actin fibers are attached to membranes and face each other in a similar way that we might observe if we placed two combs together such that their teeth faced each other. Threaded between the teeth are myosin filaments - these are not attached to the membranes at either end. The entire structure of myofilaments, including the membrane at each end (termed a z-disc), is called the sarcomere. The action of muscle contraction translates, at the sub-cellular level, to a contraction of the overall length of the sarcomere. It is generally agreed that this achieved as a result of the myosin and actin myofilaments overlapping to a greater extent.

In the Davydov model, energy released by the hydrolysis of ATP at the binding site on the myosin molecule is translated into kinetic energy. Normally, this energy would be expected to quickly dissipate. However, Davydov noted that the structure of myosin (an alpha-helix protein) was comprised of regularly spaced pairs of oxygen and carbon atoms that would give rise to a compressive force that would cancel out the dissipative tendency of the energy wave. Consequently, a highly concentrated 'lump' of energy in the form of a soliton wave would progress as a deformation of the myosin filament. This deformation would provide sufficient localized kinetic energy such that the myosin heads that protrude from the alpha-helix protein strands at their ends would slide and interlock (or 'ratchet') with the surrounding actin filaments causing the overall length of the sarcomere to decrease.

http://www.psy.cmu.edu/~davia/mbc/9start.html

What you quote came from the above. But could it be outdated research already. Davydov proposed it in 1982 when molecular scanning was not yet advanced. Now we could view the myosin in molecular details. Can't we falsify now the Davydov mechanism or confirm that elongation and conformation of the myosin heads really occur after ATP hydrolysis? Why is it hard to confirm or deny this when electron microscopes are plenty?

because electron microscopes don't show biochemical reactions taking place

Kinesis moves along microtubules by mechanical way. So it seems more likely that myosin head moves along actin using mechanical way too and no solitons involved right? Conformations of the myosin head after ATP hydrolysis is quite possible, isn't it??

I mean Kinesin...

It walks along microtubules. So if solitons are not involved, myosins don't involve solitons too.. unless it's still a mystery how kinesin walks along microtubules??

http://en.wikipedia.org/wiki/Kinesin

It's funny that you mention it because I never considered it a "theory," I thought they proved it already.

A theory is a general proposition used as principles of explanation for a class of phenomena. This is not the case with the model described here. In fact, the following sequence has been proven experimentally:

1. Acetylcholine binds to receptors on the motor end plate.
2. Chemically regulated ion channels open, causing depolarization.
3. End-plate potentials trigger action potentials.
4. Transverse tubules convey potentials into the interior of the cell.
5. Ca2+ is released from the sarcoplasmic reticulum.
6. Ca2+ ions bind to troponin-C, pulling on tropomyosin.
7. Binding sites on actin are uncovered, allowing myosin to bind and carry out power strokes.

Similarly, the following steps of smooth muscle contraction have been proven experimentally:

1. Increase in cytosolic calcium initiates contraction; calcium is released from the sarcoplasmic recticulum and also enters the extracellular fluid.
2. Calcium binds to calmodulin.
3. Calcium binding to calmodulin is the first step in a cascade that ends with contraction.
4. Phosphorylation of proteins is an essential step in smooth muscle contractions.
5. The primary control of smooth muscle contraction resides in the regulation of myosin ATPase activity.

The above are not being questioned. Davydov only dealt with how ATP hydrolysis moves the myosin head which has no detailed and proven mechanism (like how the conformation occurs). That's the reason he proposed the Soliton model. But then, kinesin biochemical profile and the movement are fully mapped already, isn't it. If Kinesin can walk like a person walking on two feet, then it's not stretch to think Myosin can do similar action with the involvement of Soliton, isn't it? What Solitons do are in the following:
 
"In the Davydov model, energy released by the hydrolysis of ATP at the binding site on the myosin molecule is translated into kinetic energy. Normally, this energy would be expected to quickly dissipate. However, Davydov noted that the structure of myosin (an alpha-helix protein) was comprised of regularly spaced pairs of oxygen and carbon atoms that would give rise to a compressive force that would cancel out the dissipative tendency of the energy wave. Consequently, a highly concentrated 'lump' of energy in the form of a soliton wave would progress as a deformation of the myosin filament. This deformation would provide sufficient localized kinetic energy such that the myosin heads that protrude from the alpha-helix protein strands at their ends would slide and interlock (or 'ratchet') with the surrounding actin filaments causing the overall length of the sarcomere to decrease."

Typo, I mean Myosin can do similar action WITHOUT the involvement of solitons, since Kinesin can literally walk on two feet along the microtubules. So their evolution should be similar

I caught that before you mentioned it lol.


Yes they are. The whole spring compression model, which is what Davydov essentially is, sounds somewhat ridiculous don't you think. I mean, due to the proteins secondary structure, this energy is absorbed to power the movement. I think its more imagination than theory.