In Reply To:
In Reply To:
As I said, give me a mechanism for the leveling, and then, dropping off in cardiac output during VO2 max testing.
No, you did not. What you said was:
"The question is not whether there is a VO2 max, clearly there is. The question is why is there a VO2 max (or peak if you prefer) and why is it what it is in any particular person being tested in any particular manner? What is the specific limiting factor that determines this number, be it VO2 max or VO2 peak?"
To which I replied:
"VO2max is primarily limited by the cardiovascular system's ability to transport O2-carrying blood to the muscles."
Now if you want to change the question to "what limits the cardiovascular system's ability to transport O2-carrying blood to the muscles?", that is all well and good, but it doesn't in any way undermine my earlier answer (as Aristotle pointed out in
Posterior Analytics).
Anyway, to address your new question: the answer is still unclear, but it has been postulated that hyperthermia and tachycardia combine to reduce stroke volume.
It seems to me that "specific limiting factor" goes beyond "cardiovascular system fails". You must be hell to work for always in your professorial one-upmanship mode. You are indeed the master of obfuscation. Anyhow, I am glad to see you don't really have a mechanism to explain this finding.
Anyhow, I have two questions for you.
1. hyperthermia occurs at VO2 max? How much? How fast?
2. Wouldn't a more reasonable hypothesis, other than "hyperthermia and tachycardia" be pH changes occur in the heart interfering with optimum metabolism and reducing contractility, causing the CO to level, then fall. We know that as we approach VO2 max that more and more lactate is produced which must be buffered, primarily by the bicarbonate system? This will drop the pH systemically and optimum performance of most enzyme systems occurs only in a very narrow pH range. Makes sense to me. But, what do I know?
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Frank,
An original Ironman and the Inventor of PowerCranks