Dear Steve,
I am not sure if my last post covered all these issues - so let me try here..
YOU WROTE:
Your statement:
"Muscle glycogen depletion reduces the capacity to produce ATP and must therefore cause the muscle to run out ATP if there is no nervous control."
Does not necessarily lead to your next statement:
" ATP depletion causes the muscle to go into rigor (irreversible contraction)."
As I stated in my response, glycogen depletion certainly reduces the capacity to produce ATP at a high rate, but glygocen depletion does no necessarily result in "rigor". McArdle's patients do just fine at activities of daily living, and actually, the "second wind" phenomenon appears to alleviate the rigor or contracture if you will, to a very large extent. So, as I pointed out, glycgoen depletion simply means that rate of ATP provision is limited.
MY ANSWER:
McArdle's patients have a brain and this could protect them from developing rigor.
My point is that in the absence of any other influence or control, a muscle without ATP cannot relax and hence goes into rigor. That is a biological law. Thus if the muscle cannot produce ATP sufficiently rapidly it has to end in rigor. The idea that the muscle will simply slow down is part of the peripheral model thinking that has gone unchallenged because of the logic that "we know that is how the system works". But how does a reduced rate of ATP production causes the muscle to reduce its force production? I am not sure that anyone has ever really tried to produce an explanation for that mechanism.
YOUR WROTE:
Further, this statement:
"Since rigor has yet to be described in healthy people during exercise and since muscle ATP concentration remain within the normal range even when the muscle has (almost completely) depleted its glycogen stores, so there must be a regulation, either within the muscle or via the nervous system, to insure that ATP concentrations do not fall too low."
May or may not be true. Again, if by "rigor" you mean contracture or "cramps", then they are observed in healthy people all the time, and typically attributed to electrolyte imbalance. It is quite likely that a certain proportion of "cramps" that are observed in exercising individuals may be attributed to insufficient ATP provision for release of the cross bridges. Of course, there is no evidence of this, but there is also no evidence against it, so, in the context of this discussion, it seems to be appropriate to include.
MY ANSWER:
Muscle cramps occur with increased electrical activity whereas rigor would be electrically silent (as I confirmed by studying a dead body recently - just joking). So I think that cramps are due to a neuromuscular mechanisms whereas rigor is biochemical.
YOU WROTE:
I will agree with this part though:
" so there must be a regulation, either within the muscle or via the nervous system, to insure that ATP concentrations do not fall too low."
MY ANSWER:
Good to have some agreement!!
YOU WROTE:
Finally, the Cheetah argument again appears to be a red herring. Why not use a human example? In fact, didn't you use the Cheetah as an example of thermoregulation and the "CG"? If we put the argument in the context of physiology we are all more familiar with, the 100 m sprinter "fatigues" within a few seconds, if not immediately. Some may go into rigor, some may not, but they don't become glycogen depleted, so, why not? If the pacing strategy is intended for them to complete the bout with energy reserves, why dont' they just run twice as fast and run out of glycogen? Of course, in part it's because ATP utilization is limited by myosin ATPase, and SERCA. It's also because ATP provision is rate limited and as PC stores become depleted, ATP is provided in a much slower fashion. These factors are regulated peripherally, not centrally.
MY ANSWER:
100m sprinting pace falls off only quite late in the sprint so I am not sure that fatigue happens within the first few "seconds".
More to the point though, ATP turnover rate is not really regulated peripherally. The rate of ATP use is set by how many motor units are recruited in the exercising limbs (by the brain). Micromanagement may occur peripherally but the overall rate is set centrally.
In my view sprinting speed is likely regulated to insure that the eccentric load on the hamstring muscles does not exceed their tensile strength. It seems to me that that is the weak point of the sprinter's body.
The point about the Cheetah is simply to take the extreme case of turning on ATP production so rapidly and to show how exquisitely the rate of ATP production and use must be matched. Again I argue that the only way this can really be done is if the extent of muscle recruitment is matched to the muscle's capacity to produce ATP.
Thanks again for your great observations and questions,
Tim Noakes