Sorry, I was trying to be brief and left a little bit out. Let me be precise.
Vo2 max occurs somewhere around the point of maximal cardiac output, and certainly BEFORE the point that cardiac output begins to fall because the rate has gone too high. What happens before it starts to fall is that it LEVELS OFF. There is no reserve to be had, because the output is not changing appreciably one way or the other within those few beats per minute, at least not in any meaningful way we can measure.
I am giving you a mechanism. I am saying that HR increases to the point that the ventricles have balanced filling perfectly with rate, as much as is possible and as much as we can tell with our technology. This is V02 max. As the heart futily tries to provide more blood, rate increases and the ventricles no longer fill completely. Thus CO cannot increase any more. The failure of the muscle is secondary to the primary problem of the heart to provide any additional oxygenated blood. Which part of this don't you get? That sounds like a problem with the heart to me, doesn't it to you?
But really, Frank, it isn't up to me to prove my position with mechanisms. I am merely stating what is obvious from the texts. You are the one proposing mechanims that differ from the established literature. It is up to YOU to provide us with data or literature to back up your points. So far, you have not provided a mechanism that has any backing other than your say-so, and your knowledge of anesthesia that you brought up earlier. I have provided citations to support my case. Don't beat around the bush. The reason you are is that you cannot provide any citations to back up yours. I have tried to find some to back up your mechanism, but I can't. That makes it your opinion, which you are entitled to but which is not defensible via literature. Period.
Now I really AM through with this.
Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!
Vo2 max occurs somewhere around the point of maximal cardiac output, and certainly BEFORE the point that cardiac output begins to fall because the rate has gone too high. What happens before it starts to fall is that it LEVELS OFF. There is no reserve to be had, because the output is not changing appreciably one way or the other within those few beats per minute, at least not in any meaningful way we can measure.
I am giving you a mechanism. I am saying that HR increases to the point that the ventricles have balanced filling perfectly with rate, as much as is possible and as much as we can tell with our technology. This is V02 max. As the heart futily tries to provide more blood, rate increases and the ventricles no longer fill completely. Thus CO cannot increase any more. The failure of the muscle is secondary to the primary problem of the heart to provide any additional oxygenated blood. Which part of this don't you get? That sounds like a problem with the heart to me, doesn't it to you?
But really, Frank, it isn't up to me to prove my position with mechanisms. I am merely stating what is obvious from the texts. You are the one proposing mechanims that differ from the established literature. It is up to YOU to provide us with data or literature to back up your points. So far, you have not provided a mechanism that has any backing other than your say-so, and your knowledge of anesthesia that you brought up earlier. I have provided citations to support my case. Don't beat around the bush. The reason you are is that you cannot provide any citations to back up yours. I have tried to find some to back up your mechanism, but I can't. That makes it your opinion, which you are entitled to but which is not defensible via literature. Period.
Now I really AM through with this.
Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!