The physiology thread

[FrankDay]

Frank,

If cardiac output does drop at VO2max, it seems there must be something that triggers the drop. If it is your 'peripheral limiter theory', then that would imply that the overall blood 'content' (O2, CO, etc.) and its 'flow amount' is at a level such that improved 'content' or 'flow' would not be of benefit to increase O2 usage.

I also read briefly about the 'Hill governor therory' which pre-dates Noakes, but I really don't know much about physiology involved with either.

Jay Kosta
Endwell NY USA

It is my contention that the total body change in pH that occurs as a result of the anaerobic metabolism in the skeletal muscles affects the mitochondrial/contractile enzyme efficiency in the cardiac muscle, resulting in reduced contractility and, of course, reduced cardiac output at VO2max. Of course, as soon as the effort stops the pH is rapidly restored and contractility will be close to near normal within a minute or so after stopping.

No one can deny that a fairly large mass of skeletal muscle is anaerobic at VO2max. The only area up for discussion is what are the effects of this metabolism on the ability to exercise and deliver oxygen to the tissues. Is it what stops the athlete from going further or is there another mechanism involved?

 

[Krebs cycle]

Perhaps I can get everyone to look at this problem in a different way.

Let's take a sedentary college student and test his VO2max and then start him on a triathlon training program (where he both runs and cycles). His first test may result in a VO2max of 35 ml/kg then he starts training.

6 months later he is tested again. Now he tests at 40 ml/kg. 6 months later he tests at 45 ml/kg when cycling and 47ml/kg when tested running.

Now, in each of these tests he ran up against a "supply" limit but with training whatever that limit was changed.

We know the number of lung alveoli didn't increase. His red cells didn't change. His His oxyhemoglobin dissociation curve didn't change. His weight didn't change.Hb/Hct didn't change, etc. The only two things that we can determine changed between each of these tests is his cardiac output increased and his muscle capillary density changed (at least in the muscles being exercised). This would suggest that the limiter for the VO2max test has to be either the heart or the capillary density. Which is it? Well, if he tests differently depending upon whether he is cycling or running (with a different cardiac output for each test) we can eliminate the heart as the limiter. And, can we come up with a heart mechanism that explains why cardiac output is observed to drop after reaching a max at VO2max? I cannot. This only leaves the capillary density and the diffusion from the capillary to the mitochondria as the limiting element in the cascade that forces the athlete to stop at VO2max.

Come on Dr Frank, you're completely ignoring everything that I've posted and are yet again failing to cover the literature from 20yrs ago. How do you ever expect to be able to make a complete physiological mechanistic picture if you are missing so many of the pieces?

His red cells didn't change?

Review from 1991.....

Med Sci Sports Exerc. 1991 Dec;23(12):1338-48.
Blood volume: its adaptation to endurance training.
Convertino VA.

Abstract
Expansion of blood volume (hypervolemia) has been well documented in both cross-sectional and longitudinal studies as a consequence of endurance exercise training. Plasma volume expansion can account for nearly all of the exercise-induced hypervolemia up to 2-4 wk; after this time expansion may be distributed equally between plasma and red cell volumes. The exercise stimulus for hypervolemia has both thermal and nonthermal components that increase total circulating plasma levels of electrolytes and proteins. Although protein and fluid shifts from the extravascular to intravascular space may provide a mechanism for rapid hypervolemia immediately after exercise, evidence supports the notion that chronic hypervolemia associated with exercise training represents a net expansion of total body water and solutes. This net increase of body fluids with exercise training is associated with increased water intake and decreased urine volume output. The mechanism of reduced urine output appears to be increased renal tubular reabsorption of sodium through a more sensitive aldosterone action in man. Exercise training-induced hypervolemia appears to be universal among most animal species, although the mechanisms may be quite different. The hypervolemia may provide advantages of greater body fluid for heat dissipation and thermoregulatory stability as well as larger vascular volume and filling pressure for greater cardiac stroke volume and lower heart rates during exercise.

 

[Krebs cycle]

And, can we come up with a heart mechanism that explains why cardiac output is observed to drop after reaching a max at VO2max?

A link to some real data might be nice so I can figure out what you're talking about here.


edit: whilst looking for evidence to support this claim I did find the following...

Eur J Appl Physiol. 2013 Feb]http://www.ncbi.nlm.nih.gov/pubmed/22752344[/url]

In the above study they manipulate the workload so that the subject stays at VO2max for as long as possible (ie: they decrease it far enough to delay fatigue but keep it high enough to maintain VO2max). But cardiac output does not go down. In fact it does the opposite, the longer the person stays at VO2max both SV and HR gradually increase.

 

[elapid]

@ Krebs cycle - Frank is a glorified troll. He is not here to listen, learn and engage in meaningful debate; he is here to tell you his point of view and defend that view regardless of your evidence and rationality. No point engaging him in his so-called discussions, that's just feeding the troll.

 

[JayKosta]

...
edit: whilst looking for evidence to support this claim I did find the following...

Eur J Appl Physiol. 2013 Feb;113(2):385-94. doi: 10.1007/s00421-012-2424-7. Epub 2012 Jul 3.
The sustainability of VO2max: effect of decreasing the workload.
Billat V, Petot H, Karp JR, Sarre G, Morton RH, Mille-Hamard L.
http://www.ncbi.nlm.nih.gov/pubmed/22752344
...

-
A pdf of the entire article is here -
http://www.billat.net/attachments/article/603/The sustainability of VO2max effect of.pdf

Jay Kosta
Endwell NY USA

 

[FrankDay]

A link to some real data might be nice so I can figure out what you're talking about here.


edit: whilst looking for evidence to support this claim I did find the following...

Eur J Appl Physiol. 2013 Feb;113(2):385-94. doi: 10.1007/s00421-012-2424-7. Epub 2012 Jul 3.
The sustainability of VO2max: effect of decreasing the workload.
Billat V, Petot H, Karp JR, Sarre G, Morton RH, Mille-Hamard L.
http://www.ncbi.nlm.nih.gov/pubmed/22752344

In the above study they manipulate the workload so that the subject stays at VO2max for as long as possible (ie: they decrease it far enough to delay fatigue but keep it high enough to maintain VO2max). But cardiac output does not go down. In fact it does the opposite, the longer the person stays at VO2max both SV and HR gradually increase.

While I have not performed any of these experiments myself I have relied upon the assertions of Dr. Andrew Coggan, a well respected exercise physiologist, that CO drops at VO2max in previous "discussions" on this subject as his evidence that the heart is the limiter at VO2max. (note in the link he backs off on the assertion that it is the heart and prefers to say "cardiovascular system" then gives a mechanism solely related to the heart.) In addition, I was able to find this link in support of this assertion. Check out the 3rd slide.

Anyhow, I think the best way to discuss this point is to discuss exactly what allows the change the VO2max limit in any particular person with training or when stopping training. Obviously, in each instance there is a limit and that limiting factor, whatever it is, must have changed and we would expect that change to be the same for everyone. As I said before the only things that I see that reliably change that can explain these changes in VO2max with training or not training (or the kind of training) is cardiac output and muscle capillary density. One of those two must be the limiting factor unless you have another suggestion. If we acknowledge that then we can examine which of those factors makes the most sense. My analysis suggests to me that capillary density in the exercised muscle (along with the exercised muscle mass) is, generally, the limiting factor to any given VO2max test.

Edit: here is another "paper" that seems to be asking the right questions although i don't agree completely with all of their answers. http://quizlet.com/17050564/print/

 

[Krebs cycle]

@ Krebs cycle - Frank is a glorified troll. He is not here to listen, learn and engage in meaningful debate; he is here to tell you his point of view and defend that view regardless of your evidence and rationality. No point engaging him in his so-called discussions, that's just feeding the troll.

Someone said he was a cardiologist? I was under the assumption it would be possible to have a rational discussion about physiology with him!

Maybe not??

 

[Krebs cycle]

-
A pdf of the entire article is here -
http://www.billat.net/attachments/article/603/The sustainability of VO2max effect of.pdf

Jay Kosta
Endwell NY USA

Are you a coach Jay? There are some interesting training ideas that I think can be taken from Billat's most recent studies.

The idea that you can maintain VO2max for 12min seems unreal but it is mainly predicated on years and years of data from constant load time to exhaustion tests which have indicated around 5min is normal and up to 7 or 8 mins in a super highly trained individual.

I wonder whether doing this sort of interval ie: get up to VO2max, then lower the workload slightly and hold on longer, can result in a better stimulus than doing the slightly higher intensity but shorter VO2max interval. A recent paper by Stephen Seiler (http://www.ncbi.nlm.nih.gov/pubmed/21812820) suggests it is indeed possible.

 

[FrankDay]

Someone said he was a cardiologist? I was under the assumption it would be possible to have a rational discussion about physiology with him!

Maybe not??

Nope, trained as an anesthesiologist - IMHO the medical specialty that focuses most on the physiology of getting oxygen to the tissues. What is your training? And, it is possible to have a rational discussion with me if you would focus on the question at hand: What mechanism specifically limits the athlete from going beyond VO2max. I know lots of things can affect VO2max. But, in any individual, "everything" is fixed at the point in time of the test. In each of these instances, what is the limiting factor? What is your evidence to support your answer?

Or, if you want to discuss something else, define it and let's discuss it.

 

[Krebs cycle]

Nope, trained as an anesthesiologist - IMHO the medical specialty that focuses most on the physiology of getting oxygen to the tissues. What is your training? And, it is possible to have a rational discussion with me if you would focus on the question at hand: What mechanism specifically limits the athlete from going beyond VO2max. I know lots of things can affect VO2max. But, in any individual, "everything" is fixed at the point in time of the test. In each of these instances, what is the limiting factor? What is your evidence to support your answer?

Or, if you want to discuss something else, define it and let's discuss it.

I did a PhD on hypoxia acclimatization in endurance trained athletes, IMHO a topic which is much more focussed on examining how oxygen is delivered and used by muscle during maximal intensity exercise as opposed to say, a person lying unconscious on an operating table.

I don't expect anyone to take my word, so I post links to the science to support everything I say. I've posted links to many studies and review articles which answer the question at hand in great detail, ie: no single factor on its own limits whole body VO2max (at sea level), various factors can interact with each other and each of them contributes to the limitation by varying degrees. You've repeatedly ignored that evidence and stuck to the same 20-30yr old story (which has been disproven many times over in the scientific literature), but you don't link to any evidence whatsoever to support your theory, which I repeat, has already been robustly disproven over 15yrs ago.

That is what I call not having a rational discussion.

It beggars belief that someone with your level of training would point blank ignore the worldwide general scientific consensus on a topic in physiology. I hate to think what would happen in the event that you disagreed with a large body of evidence, say for example, that demonstrated your preferred method in anaesthesiology was extremely dangerous for a patient with some particular condition, and then a person with that condition ends up under your responsibility.

 

[FrankDay]

I did a PhD on hypoxia acclimatization in endurance trained athletes, IMHO a topic which is much more focussed on examining how oxygen is delivered and used by muscle during maximal intensity exercise as opposed to say, a person lying unconscious on an operating table.

I don't expect anyone to take my word, so I post links to the science to support everything I say. I've posted links to many studies and review articles which answer the question at hand in great detail, ie: no single factor on its own limits whole body VO2max (at sea level), various factors can interact with each other and each of them contributes to the limitation by varying degrees. You've repeatedly ignored that evidence and stuck to the same 20-30yr old story (which has been disproven many times over in the scientific literature), but you don't link to any evidence whatsoever to support your theory, which I repeat, has already been robustly disproven over 15yrs ago.

That is what I call not having a rational discussion.

It beggars belief that someone with your level of training would point blank ignore the worldwide general scientific consensus on a topic in physiology. I hate to think what would happen in the event that you disagreed with a large body of evidence, say for example, that demonstrated your preferred method in anaesthesiology was extremely dangerous for a patient with some particular condition, and then a person with that condition ends up under your responsibility.

You have given links to a bunch of studies but as of yet not taken a stand as to what is the limiting step in the oxygen delivery cascade and what the evidence is that supports that specific stand. What is it that makes the athlete say "I cannot go on" at the end of a VO2max test?

Now, I will give you that at 14000 feet in the face of pulmonary edema the limiter might be oxygen diffusion across the lungs (or cerebral edema) but that is not the situation we are "discussing".

That is what the discussion has been.

And, I think you underestimate the situations anesthesiologists are trained to deal with. It is a tad more complicated than "a person lying unconscious on an operating table". In the old days the question before a surgery was "is the patient healthy enough to survive the anesthetic/surgery?" That question is never asked anymore, everyone who needs an operation is taken to the OR without regard to their curren health and almost all of them survive due to the efforts of the anesthesiologist. Anyhow, if you happen to know an anesthesiologist I might suggest you ask him/her what their training is like regarding cardiovascular/cardiopulmonary physiology and why. PhD or not, I would submit your physiological training and experience is quite limited compared to the average anesthesiologist. What experience do you have working with acid base imbalances? What experience do you have working with various forms of shock (cardiogenic, septic, etc.)? Any experience with high frequency ventilation or oscillation as a method of ventilation? How about working with ventilation perfusion defects or right to left shunts? Or, left to right shunts? Or, severe hypovolemia or anemia. All of the above (and more) affect oxygen delivery to the tissues in different ways that anesthesiologists need to understand and be prepared to deal with effectively. It is this understanding, I believe, that makes it possible for me to see this problem in more of a nuanced "big picture" kind of way than someone with more limited experience. Why don't you give me a chance to explain my position?

 

[Krebs cycle]

You have given links to
And, I think you underestimate the situations anesthesiologists are trained to deal with. It is a tad more complicated than "a person lying unconscious on an operating table". In the old days the question before a surgery was "is the patient healthy enough to survive the anesthetic/surgery?" That question is never asked anymore, everyone who needs an operation is taken to the OR without regard to their curren health and almost all of them survive due to the efforts of the anesthesiologist. Anyhow, if you happen to know an anesthesiologist I might suggest you ask him/her what their training is like regarding cardiovascular/cardiopulmonary physiology and why. PhD or not, I would submit your physiological training and experience is quite limited compared to the average anesthesiologist. What experience do you have working with acid base imbalances? What experience do you have working with various forms of shock (cardiogenic, septic, etc.)? Any experience with high frequency ventilation or oscillation as a method of ventilation? How about working with ventilation perfusion defects or right to left shunts? Or, left to right shunts? Or, severe hypovolemia or anemia. All of the above (and more) affect oxygen delivery to the tissues in different ways that anesthesiologists need to understand and be prepared to deal with effectively. It is this understanding, I believe, that makes it possible for me to see this problem in more of a nuanced "big picture" kind of way than someone with more limited experience. Why don't you give me a chance to explain my position?

We are talking about the limits to VO2max. How many VO2max tests have you conducted on healthy or well trained individuals?

 

[Krebs cycle]

Why don't you give me a chance to explain my position?

You have explained your position. It's wrong. End of story.

 

[JayKosta]

Are you a coach Jay? There are some interesting training ideas that I think can be taken from Billat's most recent studies.

The idea that you can maintain VO2max for 12min seems unreal but it is mainly predicated on years and years of data from constant load time to exhaustion tests which have indicated around 5min is normal and up to 7 or 8 mins in a super highly trained individual.

I wonder whether doing this sort of interval ie: get up to VO2max, then lower the workload slightly and hold on longer, can result in a better stimulus than doing the slightly higher intensity but shorter VO2max interval. A recent paper by Stephen Seiler (http://www.ncbi.nlm.nih.gov/pubmed/21812820) suggests it is indeed possible.

-
Thank you for the references to the Stephen Seiler article, and also the mention of the various Billat articles at -
http://www.billat.net/index.php/en/research.html

I not a coach or trainer; at age 64, I cycle for exercise and recreation.
I'm interested in topics of physiology, training, and recovery that I can apply to myself. And am also interested in how they can be of use for other cyclsits of different ages and fitness. An additional concern for me is to avoid injury and/or the need for 'extended recovery' that is caused by excessive intensity, duration, enthusiasm, etc.
I'm looking for the 'Goldilocks point' of:
Not too little
Not too much
But, JUST RIGHT

Jay Kosta
Endwell NY USA

 

[FrankDay]

You have explained your position. It's wrong. End of story.

No, it is not the end of the story until you tell me why and what is the weakest link in that oxygen supply cascade.

Edit: it is a shame that you have taken the A. Coggan approach to internet "discussion." That is to simply declare the opposition wrong without saying why or what the correct answer really is. It is an alternative way to present and "ad hominem" attack and ad hominem attacks always expose an underlying weakness in the attackers point of view because they are almost certainly irrelevant. So, I, again, ask you to assert your case in a positive fashion.

 

[Krebs cycle]

No, it is not the end of the story until you tell me why and what is the weakest link in that oxygen supply cascade.

Edit: it is a shame that you have taken the A. Coggan approach to internet "discussion." That is to simply declare the opposition wrong without saying why or what the correct answer really is. It is an alternative way to present and "ad hominem" attack and ad hominem attacks always expose an underlying weakness in the attackers point of view because they are almost certainly irrelevant. So, I, again, ask you to assert your case in a positive fashion.

No what is a shame is that someone with so much knowledge and training as yourself chooses to completely ignore a vast body of scientific research spanning 20yrs and sticks his head in the sand and starts acting as if he knows better than dozens upon dozens of world renowned experts in the field. I am evidence based. I have posted links, not just to a few studies, but to a large body of science. You have ignored that science at every opportunity and you have posted links to absolutely nothing.

It is end of story until you man up and start posting links to evidence. I challenge you to post a link to ONE SINGLE REVIEW article published in the last 10yrs which concludes that peripheral diffusion is the specific limiter to whole body VO2max at sea level. If this is true, you must show evidence that increasing convective oxygen supply has no effect on VO2max since peripheral diffusion limits any further increase in VO2max despite the increased oxygen supply.

 

[FrankDay]

No what is a shame is that someone with so much knowledge and training as yourself chooses to completely ignore a vast body of scientific research spanning 20yrs and sticks his head in the sand and starts acting as if he knows better than dozens upon dozens of world renowned experts in the field. I am evidence based. I have posted links, not just to a few studies, but to a large body of science. You have ignored that science at every opportunity and you have posted links to absolutely nothing.

It is end of story until you man up and start posting links to evidence. I challenge you to post a link to ONE SINGLE REVIEW article published in the last 10yrs which concludes that peripheral diffusion is the specific limiter to whole body VO2max at sea level. If this is true, you must show evidence that increasing convective oxygen supply has no effect on VO2max since peripheral diffusion limits any further increase in VO2max despite the increased oxygen supply.

Hey, you know the tough thing about science is not in the data collection but in the interpretation of the data. Anyhow, I am arguing a very specific, very narrow point, and the EVIDENCE is quite compelling. Of course, there is no review article that has concluded that because none of the exercise physiologists even consider acid base issues as being an issue and so they cannot see the forest for the trees. However, anesthesiologists run across this issue all the time and the various conditions that can cause this potential problem are well known to the medical community. The problem is it isn't really of any great clinical concern because it is self imposed, self limiting, and self correcting and very transient, when the cause is due to exercise occurring at or near the VO2 max level. Just because your training (and the training of your cohorts) does not allow you to understand or to consider this possibility does not make my understanding of the physiology wrong. Anyhow, I have put a couple of links to some articles that address these issues in general. When reading them remember that we are talking about a condition when the athlete is beyond the anaerobic threshold and a reasonably large mass of muscle is exercising anaerobically and making lactic acid.

http://www.merckmanuals.com/home/hormonal_and_metabolic_disorders/acid-base_balance/acidosis.html

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

Acidosis and contractility of heart muscle.

Effects of changes of pH on the contractile function of cardiac muscle
From the above paper: "It has been known for over 100 years that acidosis decreases the contractility of cardiac muscle." - except for, perhaps, by the exercise physiologists.

So, I ask you again, tell me again why you think I am wrong and what you think is the limiting factor in the oxygen delivery cascade that accounts for what is observed at VO2max (like the drop in cardiac output) and accounts for the ability to change VO2max through simple training.

 

[JayKosta]

Is identifying the specific limiter (or mechanism) important for training typical healthy athletes?

Would there be differences in the training methods for health athletes depending on the 'limiter'?
- or said another way -
Are there certain training methods that are more beneficial depending on what the limiter happens to be?

I can see how having a better understanding of this could be important in a clinical setting, and when treating a person who has health-related O2-uptake problems.

Jay Kosta
Endwell NY USA

 

[FrankDay]

Is identifying the specific limiter (or mechanism) important for training typical healthy athletes?

Probably not. However, being able to explain the mechanism might turn out to be useful if it is something that can be corrected. It is more than likely just an intellectual curiosity.

Would there be differences in the training methods for health athletes depending on the 'limiter'?
- or said another way -
Are there certain training methods that are more beneficial depending on what the limiter happens to be?

Perhaps I guess if the limiter varied under different conditions. I don't see that happening. All I see is training methods varying depending upon how important anerobic metabolism is (sprinters vs marathoners)

I can see how having a better understanding of this could be important in a clinical setting, and when treating a person who has health-related O2-uptake problems.

Jay Kosta
Endwell NY USA

One of the problems with "research" is one never really knows the significance of something until one has explored it and understands it completely. Awhile back there was a supplement that was designed to counteract acidosis and improve capability. I thought it was a big waste of time because the amount of buffer that could be ingested was so tiny as to be irrelevant. But, it was an attempt to address the issue I am discussing.

Let me give an example of a possibility. Let's take a 100 m sprinter. In general, the best sprinters are the ones who slow the least in the last 40 m. Maybe it might be possible to take enough bicarb of soda to get ones pH on the alkaline side of normal such as to delay the failure slightly seen due to acidosis (assuming that is the cause of the failure). Then, the question would be whether such a manipulation was legal.

 

[JayKosta]

In the Wikipedia article about "Acidosis", it was stated that -

"Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid."

Do you know of any comparisons about different 'styles' of breathing by athletes for maximum performance in endurance events?

I'm thinking of 4 'styles' that could be compared -
a) concentrate on large inhalation (to fill the lungs), without emphasis on exhalation.
b) concenrate on large exhalation (to empty the lungs) without emphasis on inhalation.
c) concentrate on BOTH large inhale and exhale.
d) breathe without conscious emphasis on inhale or exhale (control group)

Jay Kosta
Endwell NY USA

 

[FrankDay]

In the Wikipedia article about "Acidosis", it was stated that -

"Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid."

Do you know of any comparisons about different 'styles' of breathing by athletes for maximum performance in endurance events?

I'm thinking of 4 'styles' that could be compared -
a) concentrate on large inhalation (to fill the lungs), without emphasis on exhalation.
b) concenrate on large exhalation (to empty the lungs) without emphasis on inhalation.
c) concentrate on BOTH large inhale and exhale.
d) breathe without conscious emphasis on inhale or exhale (control group)

Jay Kosta
Endwell NY USA

There is no advantage to any different style of breathing that an athlete can do (there are some advantages to some special ventilatory methods available in the OR/ICU when necessary but these are rarely used and not generally available) that I can conceive. The problem is that the ability to compensate for acidosis is limited by the alveolar minute ventilation. Minute ventilation is limited by the development of turbulent flow in the trachea. When turbulent flow develops it is really not possible to increase ventilation (regardless of how much pressure the diaphragm can produce) except though extraordinary efforts such as substituting helium for nitrogen in the inspired air.

Most of the time the oxygen consumption and the CO2 production is pretty well balanced and ventilation is adequate to keep the tissues oxygenated and to get rid of all of the CO2. However, when there is anaerobic metabolism the production of CO2 becomes much larger than the consumption of oxygen. (For each ATP produced anaerobically there are 20 more CO2 - as I remember- than for each ATP produced aerobically.) Therefore, because of this turbulent flow issue, it is not possible to increase the minute ventilation enough to get rid of the CO2 load when there is substantial anaerobic metabolism and CO2 will accumulate and pH will change to be come more acid. It is fairly simple to understand and follow if one tries. The only question, IMO, is whether this is the element of the cascade that stops the athlete or is there something I am missing?

 

[Krebs cycle]

-
Thank you for the references to the Stephen Seiler article, and also the mention of the various Billat articles at -
http://www.billat.net/index.php/en/research.html

I not a coach or trainer; at age 64, I cycle for exercise and recreation.
I'm interested in topics of physiology, training, and recovery that I can apply to myself. And am also interested in how they can be of use for other cyclsits of different ages and fitness. An additional concern for me is to avoid injury and/or the need for 'extended recovery' that is caused by excessive intensity, duration, enthusiasm, etc.
I'm looking for the 'Goldilocks point' of:
Not too little
Not too much
But, JUST RIGHT

Jay Kosta
Endwell NY USA

One of the things I love about cycling is the age range that it encompasses. I did a road race on the weekend and in the same bunch there was a 15yr old, a 55yr old and a spread of ages everywhere in between!

Here is a link to a fulltext article that you will be interested in....

J Physiol. 2008 Jan 1;586(1):55-63. Epub 2007 Aug 23.
Endurance exercise performance in Masters athletes: age-associated changes and underlying physiological mechanisms.
Tanaka H, Seals DR.

http://www.ncbi.nlm.nih.gov/pubmed/17717011

 

[Krebs cycle]

T
However, when there is anaerobic metabolism the production of CO2 becomes much larger than the consumption of oxygen. (For each ATP produced anaerobically there are 20 more CO2 - as I remember- than for each ATP produced aerobically.) Therefore, because of this turbulent flow issue, it is not possible to increase the minute ventilation enough to get rid of the CO2 load when there is substantial anaerobic metabolism and CO2 will accumulate and pH will change to be come more acid. It is fairly simple to understand and follow if one tries.

Fairly simple to understand but your version here is (almost) entirely incorrect.

CO2 production DOES NOT occur during anaerobic metabolism and there is no fixed stoichoimetric relationship between metabolic CO2 production and anaerobic ATP synthesis as you described above (ie: 20:1).

Human physiology 101:
CO2 production occurs during aerobic metabolism in two places 1. Pyruvate -> acetyl-CoA and 2. in the Kreb's cycle.

The "extra" CO2 produced during high intensity exercise is a result of metabolic acidosis and subsequent bicarbonate buffering. This extra CO2 is actually "produced" in the lungs during gas exchange as a result of carbonic anhydrase activity.

CO2 does not accumulate in the blood as a result of inadequate ventilation. In fact, in normal healthy individuals PaCO2 actually begins to decrease above the lactate threshold as a result of exercise hyperventilation. This is textbook exercise physiology and you are getting it badly wrong.

The only thing that you got right in your above post is that acidosis does indeed occur during high intensity exercise. The how and why is wrong.


Yes, metabolic acidosis occurs during high intensity exercise.

Yes, acidosis likely plays a role in contributing to muscle fatigue.

Does muscle fatigue cause VO2 to stop increasing during high intensity exercise? Definitely not! This would imply that muscle fatigue always occurs at VO2max. If you had ever conducted a VO2max test in your entire life you would know this is simply not true.

And really, the stuff about exercise physiologists "not seeing the forest for the trees" is completely absurd. Metabolic acidosis and the mechanisms underlying the lactate threshold and muscle fatigue are central topics in exercise physiology. In fact your overemphasis on the role of acidosis in muscle fatigue is also very out of date. It is well recognised now that it just one of a number of metabolic factors that can influence muscle contractile function either directly or indirectly.

Skeletal Muscle Fatigue: Cellular Mechanisms
D. G. Allen, G. D. Lamb, and H. Westerblad

The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals.

http://physrev.physiology.org/content/88/1/287.abstract

 

[Alex Simmons/RST]

No, it is not the end of the story until you tell me why and what is the weakest link in that oxygen supply cascade.

Edit: it is a shame that you have taken the A. Coggan approach to internet "discussion." That is to simply declare the opposition wrong without saying why or what the correct answer really is. It is an alternative way to present and "ad hominem" attack and ad hominem attacks always expose an underlying weakness in the attackers point of view because they are almost certainly irrelevant. So, I, again, ask you to assert your case in a positive fashion.

That was not an ad hominem.

It may be that the statement is an error of fact (or it might not), but that in itself is not a logical fallacy (which is an error of reasoning).

As for asserting for an argument to be presented in a "positive fashion", that is not a requirement for a logically consistent argument, only for an argument to adhere to standards of conversational courtesy.

IOW, the truth isn't changed just because we say it nicely.


Anyway, as you were....

 

[Tapeworm]

I'm just going to leave this here.

http://rpws1.ad.onyxlight.net/edocs/2.3_Exercise_Lactate_and_Anaerobic_Threshold.pdf

Happy reading Frank.