Scand J Med Sci Sports. 2003 Dec;13(6):339-58.Neilsen, HB, Arterial desaturation during exercise in man: implication for O2 uptake and work capacity.“During maximal exercise, an extreme lactate spill-over to blood allows pH decrease to below 7.1 and according to the O2 dissociation curve this is critical for SaO2.”
I bet you’re a big hit at parties with opening lines like that…
Once again you seem to be confusing VO2max with exercise performance. The former is primarily limited by convective O2 delivery, whereas the latter is dependent upon many things (including VO2max).
Translation please for those of us who are neither physicians or scientists.
Victor
This is going to be an epic thread.
Once again you seem to be confusing VO2max with exercise performance. The former is primarily limited by convective O2 delivery, whereas the latter is dependent upon many things (including VO2max).
I am not confusing anything. VO2 max is VO2 max because it is limited by something. That is, something is preventing oxygen utillization from increasing further. You have repeatedly stated that you believe this limiter is the heart and put forth evidence that cardiac output drops as one reaches this failure point. I have repeatedly put forth I believe this cardiac failure occurs because of influences on the heart from the changes in pH, adversely influencing contractility, that come from the periphery from lactic acid production.
Does the Nielsen data better support your view or mine, and why? 
In my opinion, the drop off in cardiac output at Vo2 max is not the source of the failure but is the end result of the failure. That is what the data supports.
Does the Nielsen data better support your view or mine, and why?
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You seem to have confused VO2max and exercise performance in your choice of a title for this thread.
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The paper you cited contains no original data; it is merely a review.
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The fact that arterial desaturation can occur during high intensity exercise - something that you once vociferously disputed, IIRC - really says nothing one way or the other re. the role of convective O2 delivery vs. peripheral O2 utilization as the determinant of VO2max. It does, however, demonstrate that the lungs aren’t necessarily “overbuilt for exercise”, which is why I always write “VO2max is primarily limited by convective O2 delivery” instead of saying “VO2max is strictly limited by maximal cardiac output”.
To my knowledge there is no correlation between bloood pH and cardiomyocyte function (different for skeletal muscle).
This has been shown over and over again.
You should have come across that in med-school. back then:
http://ajplegacy.physiology.org/cgi/reprint/229/5/1305.pdf
But hey, if you have new and convincing data, please share!
And thanks for not mentioning the infamous 2 words. I am proud of you, but it must take lots of restraint!
The whole point of this thread will be to eventually show that when training on powercranks, the heart can continue maximum Cardiac Output at a more acidic PH than a non-powercrank trained heart.
This is going to be an epic thread.
Epic is right.
frank,
what was the basis for this thread? i’m looking for some background before i make an actual comment…was there a previous debate in another thread?
I also don’t understand what you’re trying to prove by posting this study? exercise is limited by a whole bunch of things. I would argue that one of the most important is blood pressure regulation…and that has very little to do with lactate.
You have done it!
You just opened the floodgates!
And I am outta here…
thank you, you just made my day.
Zach, thanks for the clarification…I’m going back to Maxwell’s equations and Schrodinger now…
I’ve read, re-read a lot of this stuff. I don’t really get it. Does it matter that much - to warrant that much discussion.
I exersize as hard and as long as i want or until i can’t do it anymore. I’ll call that Scott-max
Scott
Does the Nielsen data better support your view or mine, and why?
- You seem to have confused VO2max and exercise performance in your choice of a title for this thread.
No, I am not confusing anything. You seem to be deliberately obfuscating this simple issue. The question is what is the actual limiter for the athlete? Is it central or in the periphery?
- The paper you cited contains no original data; it is merely a review.
Well, that would make it even more powerful from my point of view.
- The fact that arterial desaturation can occur during high intensity exercise - something that you once vociferously disputed, IIRC - really says nothing one way or the other re. the role of convective O2 delivery vs. peripheral O2 utilization as the determinant of VO2max. It does, however, demonstrate that the lungs aren’t necessarily “overbuilt for exercise”, which is why I always write “VO2max is primarily limited by convective O2 delivery” instead of saying “VO2max is strictly limited by maximal cardiac output”.
I don’t believe I have ever said that arterial desaturation cannot occur during high intensity exercise. Clearly it can and one would normally expect same, at least to a small degree, because of the way that ventilation and perfusion are determined in the lungs. However, such “desaturation” is not a source of failure as such desaturation is small and has very little influence on oxygen carrying capacity or "convective O2 delivery as you prefer to call it, because of the shape of the oxyhemoglobin desaturation curve and how it varies with temperature and pH. Why on earth would you write that "VO2max is “primarily” limited by “convective O2 delivery” when there is absolutely zero evidence this is the case and the real problem is not how much oxygen is delivered but how much is extracted in the muscles. What do you mean by “primarily”. What is the evidence to support this view? Why don’t you just write that VO2 max is primarily limited by the athlete can’t push himself any harder? They are pretty much the same thing. You are seeing the end result (convective O2 delivery starts to fail) and claiming it is the source of the problem. They are not the same thing.
To my knowledge there is no correlation between bloood pH and cardiomyocyte function (different for skeletal muscle).
This has been shown over and over again.
You should have come across that in med-school. back then:
http://ajplegacy.physiology.org/...print/229/5/1305.pdf
But hey, if you have new and convincing data, please share!
And thanks for not mentioning the infamous 2 words. I am proud of you, but it must take lots of restraint!
You are kidding, of course. No tissue works very well if outside of the normal pH of 7.4. The further away, the greater the decrement in function.
frank,
what was the basis for this thread? i’m looking for some background before i make an actual comment…was there a previous debate in another thread?
I also don’t understand what you’re trying to prove by posting this study? exercise is limited by a whole bunch of things. I would argue that one of the most important is blood pressure regulation…and that has very little to do with lactate.
We have had many lengthy and heated “discussions” about this here. Do a search. I recently came across this paper over on a PowerCranks thread at rec.bicyles.racing newsgroup and thought it was relevant to the discussion, which is, as far as I am concerned, ongoing. Weigh in if you want to.
No I am not.
Last time I checked the heart was an “organ”, not “tissue” or “cells”.
And organs are generally made up of different tissues and cell types. And only a small fraction of those are “Exposed” to blood.
A little complicated, I know 
Frank, first you said:
For those of you who advocate that exercise is limited by the heart and lactate has nothing to do with it how do you explain this finding?
Then you said:
VO2 max is VO2 max because it is limited by something
I boldfaced some of those words for clarification. I agree with Dr. Coggan that you can’t seem to decide what you’re arguing about. Is it VO2 max (a measure of how much oxygen your body can suck out of the air) or athletic performance (athletic performance). They are not the same thing.