The physiology thread

[FrankDay]

Cool thread.... stuff I love!! Without reading the whole thread right now, I'll just point out that maybe # 2 is being too limited?

A more contemporary view of the potential limits to VO2max would be as follows....

1. Noakes' central governor theory
2. Oxygen transport and supply
3. Oxygen extraction and utilisation

I appreciate your attempt to broaden the issue somewhat but I framed it as I did based upon many previous discussions (with Dr. Coggan and some Noakes followers) regarding the one specific limiter and the mechanism of that limitation. Such discussions are almost impossible with advocates of #1 since it is a "black box" theory with no known or, even, hypothsized mechanism. #2 supporters (Dr. Coggan), have always maintained that the heart is the specific limiter because cardiac output stops increasing and then begins to drop at VO2max. I use that same data as evidenc that the limiter is #3. The devil is in the details

IMO the evidence overwhelmingly supports number 2 as the dominant factor (which of course in reality is a combination of several things) limiting VO2max over the other two.

I disagree, more below

The general themes that support this conclusion are as follows....

1. Breathing hypoxic gas mixtures decreases VO2max in whole body exercise whereas breathing hyperoxic gas mixtures increases it.

This finding can support both #2 and #3, depending upon the details

2. Acutely increasing O2 carrying capacity by transfusion or artificial O2 carriers increases VO2max.

This finding can support both #2 and #3, depending upon the details

3. The vast array of studies using the single knee extensor model (Peter Wagner's lab) clearly show that muscle VO2 is higher at maximal exercise intensity than it is at VO2max in whole body exercise ie: peripheral O2 extraction and utilisation is higher when the available cardiac output can be redistributed to the smaller working muscle mass.

This finding can support both #2 and #3, depending upon the details

4. The classic study by Jim Stray-Gundersen which shows that pericardiectomy in dogs increases VO2max.

While seeming to support #2 I would want more details. Were the dogs aerobically trained? The pericardium adapts to exercise just as do all the other tissues, allowing larger stroke volumes in the aerobically trained. Such a dog finding may not apply to the athlete. What has happened to humans who have had this operation? (surely it has been done in athletes.) The devil is in the details.

5. Superimposing arm exercise and leg exercise isn't additive ie: if the legs are exercising at a work rate which demands 70% of whole body VO2max and then you superimpose arm exercise that on its own, demands 40% VO2max, you don't get 110% of VO2max (which would be a higher VO2max of course). There will be a decrease in blood supply to one or both of those working muscle groups. Same phenomenon is demonstrated if you add resisted breathing to cycling exercise at or near VO2max. The elevated work of breathing creates a metabolic reflex which increases MSNA and vasoconstriction in the exercising legs. Available CO is redistibuted to the respiratory muscles. Whole body VO2 stays the same but cycling performance goes down (since leg O2 supply goes down).

This finding can support both #2 and #3, depending upon the details. For instance, what was the training condition of the two extremities. In view of this finding how does one explain the fact that athletes who use both their upper and lower extremities aerobically tend to hav higher VO2max than those who don't? rowers/xc skiers > runners > cyclists > chess players. The training condition of the muscles being tested can make a huge difference.

There are a number of factors obviously which contribute to the limitation of O2 supply which you've discussed above eg: blood volume, maximal cardiac output, [Hb], pulmonary diffusing capacity. But the main point is that I think discussing the pumping capacity of the heart on its own doesn't fully represent the "supply side" argument.

The problem comes from determining what the limiter is in the healthy athlete. Where does the "supply side" break down specifically? How do you explain the drop in cardiac output at VO2max?

Do you agree that VO2max is an artificial number that will vary somewhat based upon the protocol used. How fast is the effort ramped up? Why can't 100 m runners maintain that effort for 200 meters? 200m runners for 400m? 400m for 800m, etc? What allows them to quickly recover from these efforts at the edge of failure to essentially repeat them in just a few minutes.

What is happening in the periphery as one passes threshold on the way towards VO2max? How do these "changes" affect total body (heart) pCO2, HCO3, and pH? What happens to muscle function as pH changes? Can such muscle function changes due to pH changes explain the drop in CO seen at VO2max?

To me, the evidence is overwhelming. The specific limiter to aerobic athletic performance and VO2max occurs in the periphery, the skeletal muscles, #3 on the list. Once the athlete has passed threshold he is on the slippery slope towards failure. The only question is how long can he hold out. This is the basis of the VO2max test but what is measured will vary based upon how fast the effort is raised. 1 min intervals, 2 minute intervals, 5 minute intervals. The result will vary. How is that explained?

I look forward to your thoughts.

 

[Krebs cycle]

I appreciate your attempt to broaden the issue somewhat but I framed it as I did based upon many previous discussions (with Dr. Coggan and some Noakes followers) regarding the one specific limiter and the mechanism of that limitation.

#2 supporters (Dr. Coggan), have always maintained that the heart is the specific limiter

Where does the "supply side" break down specifically? How do you explain the drop in cardiac output at VO2max?

To me, the evidence is overwhelming. The specific limiter to aerobic athletic performance and VO2max occurs in the periphery, the skeletal muscles, #3 on the list.

I look forward to your thoughts.

Not enough time now to address all points in detail but it seems as though you are looking for a "specific limiter" both in your own arguments and also those of those of others (eg: Dr Coggan and myself). I think this somewhat misrepresents the position that I suggested, which is that there is NO specific limiter and depending on the circumstances, the dominant limiter can change. This point can be illustrated easily as Wagner states.... "if blood flow is zero, then VO2max must also be zero".

However, there is a maximal mitochondrial rate at some point, you cannot simply continue increasing O2 supply forever and achieve a corresponding increase in mitochondrial VO2.

Have a read of the JAP point counter point series on this topic.....

Bengt Saltin, José A. L. Calbet & Peter Wagner
Point: Counterpoint "in health and in a normoxic environment, VO2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow".
Journal of Applied Physiology February 2006 vol. 100 no. 2 744-748

All of the big hitters in this field (Wagner, Saltin, di Pramprero, Gonzalez-Alonso, Richardson, Calbet etc) are undeniably in agreement that convective O2 supply plays a major role in VO2max, however I think one argument stands out by di Pramprero which goes a long way to explain several of your questions posed (in particular why is VO2max different for different exercise modalities incorporating different active muscle mass?) which is this....

The greater the active muscle mass involved the more dominant the role of O2 supply. The smaller the muscle mass the greater the role that peripheral O2 diffusion + maximal mitochondrial rate plays. For whole body large muscle group exercise di Pramprero estimates that O2 supply accounts for 70% of the limitation for 2 legged exercise and this drops to 50% for one legged exercise.

Wager also makes an important point (which again, addresses some of your questions about trained vs untrained). In order to make use of enhanced O2 supply, you need to have the appropriate peripheral mechanisms sufficiently developed or else it won't help.

edit: so to answer the question about x-country skier > runners > cyclists, then according to di Pramprero, a x-country skier is mainly limited by O2 supply, whereas the same individual performing a VO2max test on a cycle ergometer will experience a slightly greater peripheral diffusion limitation which thus offsets any "extra" cardiac output that has become available since there is less active muscle mass. Thus they cannot raise their leg VO2 enough in order to maintain VO2max at the same level achieved during xc skiing.

finally, I'm interested to read your thoughts on why the single knee extensor model (ie: leg VO2 increases) is evidence of a peripheral limitation. That just doesn't make sense to me. How is it possible that during whole body exercise peripheral O2 diffusion + maximal mitochondrial rate can be the limiter if those two things can be INCREASED during single leg exercise?? For them to be limiting at maximal whole body exercise, they must also be operating at their maximal physiological limit, therefore under no experimental circumstances should we see an increase beyond the rate achieved in whole body exercise, but that isn't what the evidence shows. The same cannot be said for cardiac output though.... at VO2max in whole body exercise, CO is also operating at, or near its maximal physiological capacity.

So in whole body large muscle group exercise there is a close relationship between VO2max and COmax, whereas there is a dissociation between VO2max and maximal muscle diffusing capacity + mitochondrial VO2max.

 

[Krebs cycle]

Very basically, VO2 = oxygen consumption and VO2max = maximal oxygen consumption. So everything you need to know about the limiters to VO2max are in the VO2 equation.

VO2 = gas properties x surface area x (PAO2 - PcapO2)/thickness of air-blood barrier.

Elapid that looks like "Fick's law of diffusion" not the Fick principle as shown below....

The fick eqn:

VO2 = CO x (CaO2 - CvO2).

 

[FrankDay]

Not enough time now to address all points in detail but it seems as though you are looking for a "specific limiter" both in your own arguments and also those of those of others (eg: Dr Coggan and myself). I think this somewhat misrepresents the position that I suggested, which is that there is NO specific limiter and depending on the circumstances, the dominant limiter can change. This point can be illustrated easily as Wagner states.... "if blood flow is zero, then VO2max must also be zero".

There is always a specific limiter, depending upon circumstances. For instance, in constrictive pericardititis the limiter might be the pericaridium restricting stroke volume. In asthma, it might be minute ventilation. In pneumonia it might be alveolar diffusion or ventilation perfusion mismatch. As a physician I learned it is always important to understand the mechanisms behind what is being observed as proper understanding of the underlying mechanism leads to more appropriate treatment. However, in this instance, I think we should be discussing what is going on in the normal individual. IMHO, the better one understands the details of the mechanisms behind what is being observed the better one understands how to move forward.

However, there is a maximal mitochondrial rate at some point, you cannot simply continue increasing O2 supply forever and achieve a corresponding increase in mitochondrial VO2.

Agree. I mean you could continue to increase O2 delivery but then you meet another limit. Afterall, there is only so much room in the muscle. Increasing the number of mitochondria may mean reducing the number of contracting elements. Doesn't do much good to make more ATP if the muscle can't use it. So, we are stuck discussing they way things normally are.

Have a read of the JAP point counter point series on this topic.....

Bengt Saltin, José A. L. Calbet & Peter Wagner
Point: Counterpoint "in health and in a normoxic environment, VO2 max is/is not limited primarily by cardiac output and locomotor muscle blood flow".
Journal of Applied Physiology February 2006 vol. 100 no. 2 744-748

All of the big hitters in this field (Wagner, Saltin, di Pramprero, Gonzalez-Alonso, Richardson, Calbet etc) are undeniably in agreement that convective O2 supply plays a major role in VO2max, however I think one argument stands out by di Pramprero which goes a long way to explain several of your questions posed (in particular why is VO2max different for different exercise modalities incorporating different active muscle mass?) which is this....

The greater the active muscle mass involved the more dominant the role of O2 supply. The smaller the muscle mass the greater the role that peripheral O2 diffusion + maximal mitochondrial rate plays. For whole body large muscle group exercise di Pramprero estimates that O2 supply accounts for 70% of the limitation for 2 legged exercise and this drops to 50% for one legged exercise.

Wager also makes an important point (which again, addresses some of your questions about trained vs untrained). In order to make use of enhanced O2 supply, you need to have the appropriate peripheral mechanisms sufficiently developed or else it won't help.

edit: so to answer the question about x-country skier > runners > cyclists, then according to di Pramprero, a x-country skier is mainly limited by O2 supply, whereas the same individual performing a VO2max test on a cycle ergometer will experience a slightly greater peripheral diffusion limitation which thus offsets any "extra" cardiac output that has become available since there is less active muscle mass. Thus they cannot raise their leg VO2 enough in order to maintain VO2max at the same level achieved during xc skiing.

What bothers me about this paper is that "all of the big hitters" seem to be missing the point that when at or near VO2max one is always beyond the anaerobic threshold. Why are all of these people ignoring this fact and the possible implications of anaerobic metabolism on the elements necessary (mitochondria, skeletal muscle, cardiac muscle) to produce work.

finally, I'm interested to read your thoughts on why the single knee extensor model (ie: leg VO2 increases) is evidence of a peripheral limitation. That just doesn't make sense to me. How is it possible that during whole body exercise peripheral O2 diffusion + maximal mitochondrial rate can be the limiter if those two things can be INCREASED during single leg exercise?? For them to be limiting at maximal whole body exercise, they must also be operating at their maximal physiological limit, therefore under no experimental circumstances should we see an increase beyond the rate achieved in whole body exercise, but that isn't what the evidence shows. The same cannot be said for cardiac output though.... at VO2max in whole body exercise, CO is also operating at, or near its maximal physiological capacity.

So in whole body large muscle group exercise there is a close relationship between VO2max and COmax, whereas there is a dissociation between VO2max and maximal muscle diffusing capacity + mitochondrial VO2max.

I think there are a couple of ways to explain this finding, assuming I understand it. Remember, there is a susbtantial difference between how VO2max is determined between running/cycling testing and single leg extension testing. cycling/running testing involves a ramp test with a cycle rate of about 90/minute at low intensity and relatively long periods above threshold. Such a testing protocol is unlikely to open all of the capillary beds. Further, we don't even know which muscles are the first to go anaerobic. Any muscle going anaerobic is going to have a total body affect as HCO3 is consumed and excess CO2 produced (per ATP) in buffering the lactate production. This relatively slow change in the total body milieu means that as one gets closer to "VO2max" one is closer to the point where enzymes are functioning efficiently and energy production cannot keep up with demand.

In the single leg extension test I presume the cycle rate is slow and there is a rapid increase to maximum. Further, since a single muscle mass is being exercised other weaker muscles cannot interfere with this muscles function by going anaerobic sooner and once this muscle does go anaerobic it will take longer for the total body milieu changes since the buffering effects are spread though out the entire body mass.

It blows my mind that these so-called heavy hitters are ignoring the fact that VO2max always occurs above the anaerobic threshold and ignoring the possible physiologic effects of this fact. I will say this, in the referenced article they do say this

However, in all these conditions, peak V̇o2 is increased if the limitation is somehow overcome and more O2 is made available to the mitochondria (6, 14, 22, 25).

Of course, increasing the availability of O2 to the mitochondria delays the onset of anaerobic metabolism. These folks don't seem to be able to see the forest for the trees.

One has to be able to explain the drop in CO at VO2max. IMHO, that can only be explained by a decrease in the efficiency of the metabolic pathways from a change in the cardiac cell milieu due to anaerobic metabolism occurring in the exercising muscle.

edit: Perhaps these exercise physiologists can be excused for missing this as they have never dealt with a patient is shock and seen the effects of acid-base abnormalities on physiologic function. After all, all of these pH changes seen during exercise are very transient.

 

[Krebs cycle]

edit: Perhaps these exercise physiologists can be excused for missing this as they have never dealt with a patient is shock and seen the effects of acid-base abnormalities on physiologic function. After all, all of these pH changes seen during exercise are very transient.

Well I guess us exercise physiologists can excuse a cardiologist who deals with patients characterized by chronic acid-base derangements for overestimating the role that metabolic acidosis plays on limiting whole body VO2 in healthy individuals


Now if you want to discuss acid-base physiology I assume you've read Peter Stewart's book?

 

[FrankDay]

finally, I'm interested to read your thoughts on why the single knee extensor model (ie: leg VO2 increases) is evidence of a peripheral limitation. That just doesn't make sense to me. How is it possible that during whole body exercise peripheral O2 diffusion + maximal mitochondrial rate can be the limiter if those two things can be INCREASED during single leg exercise?? For them to be limiting at maximal whole body exercise, they must also be operating at their maximal physiological limit, therefore under no experimental circumstances should we see an increase beyond the rate achieved in whole body exercise, but that isn't what the evidence shows. The same cannot be said for cardiac output though.... at VO2max in whole body exercise, CO is also operating at, or near its maximal physiological capacity.

So in whole body large muscle group exercise there is a close relationship between VO2max and COmax, whereas there is a dissociation between VO2max and maximal muscle diffusing capacity + mitochondrial VO2max.

I have been thinking about this a bit more and I have this observation.

In the single leg model just what is it, do you think, that makes the athlete say "I can't go on." Surely it isn't cardiac output because CO is surely less than we know the athlete can do when using all the muscles. Yet, the athlete has reached VO2max for the muscle mass being exercised. Hence, CO or delivery cannot be the limiter, making the athlete stop - something else has to be it. What could it be?

 

[Krebs cycle]

I have been thinking about this a bit more and I have this observation.

In the single leg model just what is it, do you think, that makes the athlete say "I can't go on." Surely it isn't cardiac output because CO is surely less than we know the athlete can do when using all the muscles. Yet, the athlete has reached VO2max for the muscle mass being exercised. Hence, CO or delivery cannot be the limiter, making the athlete stop - something else has to be it. What could it be?

Well we need to get one thing straight first.... where do you place O2 diffusion (from capillary to mitochondria)? Is this part of O2 supply (ie: #2) or do you see it as part of O2 extraction and utilisation (#3)?

I think a distinction needs to be made which is that O2 diffusion from blood to mitochondria is part of the O2 supply chain whereas maximal mitochondrial rate is what sets the upper limit for O2 utilsation. ie: supply vs demand.

You appear to be arguing in favour of both #2 and #3 though because previously you said that peripheral O2 diffusion is the main limiter, but you are also saying that metabolic acidosis secondary to anaerobic metabolism inhibits maximal mitochondrial rate and this limits VO2 in whole body exercise.


To get you started on the single leg model studies try these.....

Oxygen transport: air to muscle cell.
Richardson RS.
http://www.ncbi.nlm.nih.gov/pubmed/9475644


What governs skeletal muscle VO2max? New evidence.
Richardson RS.
http://www.ncbi.nlm.nih.gov/pubmed/10647536

 

[FrankDay]

Well we need to get one thing straight first.... where do you place O2 diffusion (from capillary to mitochondria)? Is this part of O2 supply (ie: #2) or do you see it as part of O2 extraction and utilisation (#3)?

I really don't see it as either. I see it as a cascade, similar to the blood coagulation cascade, many components acting in series/parallel to achieve a certain end. The rate of oxygen delivery is determined and controlled by the rate of demand (extraction). The delivery rate will follow the demand rate until one component of the delivery cascade cannot achieve that rate. Whatever the limit is, be it breathing (asthma), lung diffusion (pneumonia), heart (heart disease), blood (anemia), etc. the marker that this limit has been reached is called the anaerobic threshold. So, I guess this is a "delivery" problem but, calling it a delivery problem isn't very helpful or useful since there are so many elements involved in the delivery. Then, we get to the "problem" of what to call diffusion of oxygen from the capillary to the mitochondria. The average person simply ignores this part of the cascade thinking that once the oxygen has been delivered to the "muscle" that is all that need be done. So, if the person thinks that delivery means delivering oxygen from the lungs to the muscle via blood then diffusion is extraction. But, if delivery doesn't stop until oxygen is in the mitochondria, then diffusion is delivery. Since most people don't think of this oxygen diffusion in the muscle problem I think if we are going to use this term that extraction is probably the best term to use even though I don't like it. Whatever we call it we know that once the athlete is past the anaerobic threshold that the oxygen delivery does not equal the energy demand. The only thing left to be determined is how far beyond the anaerobic threshold is the athlete which will determine how long the athlete can continue before they are forced to stop and can do no more. This is VO2max for this particular situation, be it running, cycling, or a single leg condition. The number will depend upon the training state of the exercised muscles and the mass of the exercised muscles, along with the other variables in the cascade. But, the mechanism of what "stops" the athlete at this point most surely has to be the changes in the ability to extract oxygen (muscle enzyme and electrolyte changes) and deliver (cardiac enzyme and electrolyte changes) due to pH changes occurring due to anaerobic metabolism.

I think a distinction needs to be made which is that O2 diffusion from blood to mitochondria is part of the O2 supply chain whereas maximal mitochondrial rate is what sets the upper limit for O2 utilsation. ie: supply vs demand.

Again, I prefer discussing the cascade or system. I think we can agree though that demand controls the system, at least below the anaerobic threshold.

You appear to be arguing in favour of both #2 and #3 though because previously you said that peripheral O2 diffusion is the main limiter, but you are also saying that metabolic acidosis secondary to anaerobic metabolism inhibits maximal mitochondrial rate and this limits VO2 in whole body exercise.

Well, I do believe it is diffusion that sets the anaerobic threshold limit. Even if the heart or lungs are bad, the diffusion problem follows those limits and is still more limiting.

Anyhow, I don't like using the terms delivery or extraction for this discussion and I think we should talk about whether the system is supplying the need and if not, why not (what is the weakest link), can anything be done about it?, and what else happens when supply doesn't meet need. (we are able to increase VO2 beyond anaerobic threshold. What prevents us from increasing indefinitely?)

To get you started on the single leg model studies try these.....

Oxygen transport: air to muscle cell.
Richardson RS.
http://www.ncbi.nlm.nih.gov/pubmed/9475644


What governs skeletal muscle VO2max? New evidence.
Richardson RS.
http://www.ncbi.nlm.nih.gov/pubmed/10647536

I will try to take a look at those today.

 

[FrankDay]

Oxygen transport: air to muscle cell.
Richardson RS.
http://www.ncbi.nlm.nih.gov/pubmed/9475644

My argument with Noakes/Coggan has usually NOT come down to a "supply" "demand" argument but, rather, the location of the limiter, Central neural (Noakes), Central Cardiac (Coggan), Peripheral (me). I especially enjoyed this support for my view in this abstract

2) the role of O2 diffusivity in determining the maximum O2 flux rate (VO2max);

What governs skeletal muscle VO2max? New evidence.
Richardson RS.
http://www.ncbi.nlm.nih.gov/pubmed/10647536

And this support for my view from Richardson

In summary, these investigations illustrate 1) the importance of the diffusion gradient from blood to muscle cell;

 

[Tapeworm]

How does thermal stress factor as a limiter?

 

[FrankDay]

How does thermal stress factor as a limiter?

I am not sure what you are asking exactly. But, I will make a few comments along this line to see if this helps.

Temperature can have a variable effect. It is clear that warming skeletal muscle can improve performance but significant deviations in core temperature can reduce performance.

A couple of principles that come to mind that could influence the ultimate effect.

Increasing temperature should increase diffusion rate of oxygen.

enzymes seems to work best in a narrow range of temperature.

I did find this discussion and this study that seems to address some of these questions.

 

[Krebs cycle]

My argument with Noakes/Coggan has usually NOT come down to a "supply" "demand" argument but, rather, the location of the limiter, Central neural (Noakes), Central Cardiac (Coggan), Peripheral (me). I especially enjoyed this support for my view in this abstract And this support for my view from Richardson

It doesn't support your view at all! You've categorically stated that peripheral O2 diffusion has an upper limit which occurs at VO2max in whole body exercise hence preventing it from going any higher, but that isn't what is quoted. It says...

"1) the importance of the diffusion gradient from blood to muscle cell;"

The diffusion GRADIENT my friend, is determined by the PcapO2 - PmO2. Since PmO2 is always about 0.5-1mmHg (except in hyperoxia), then this value is largely determined by PaO2.

The very next sentence says "2) illustrate that even in functionally isolated trained skeletal muscle the highest recorded metabolic rates can be increased by increasing O2 supply"

What this means is that the diffusion gradient is not the only thing that affects diffusing capacity (indeed Fick would turn in his grave if you said it was). If you increase convective O2 supply by say, increasing muscle blood flow (to a small muscle group instead of a large one), then you can increase diffusing capacity and consequently mitochondrial VO2 goes up.

In the other review Richardson concludes "Finally, the proportionate relationship between myoglobin associated PO2 and VO2max in conditions of normoxia and hypoxia additionally supports the hypothesis that maximal respiratory rate of muscle cells is limited by O2 supply."

Notice the difference? "Importance of" versus "IS limited by" ??

On the same page if you follow the links you find....

we conclude that, in normoxic conditions of isolated KE exercise, KE VO2 max in trained subjects is not limited by mitochondrial metabolic rate but, rather, by O2 supply."
http://www.ncbi.nlm.nih.gov/pubmed/10066722

If you flick forward a few years we continue to find evidence of the same thing.....

During whole-body exercise in severe acute hypoxia and in chronic hypoxia, peak Q and LBF are blunted, contributing to the limitation of maximal oxygen uptake (Vo2max). During small-muscle exercise in hypoxia, PGE is less perturbed, Cao2 is higher, and peak Q and LBF achieve values similar to normoxia. Although the Po2 gradient driving O2 diffusion into the muscles is reduced in hypoxia, similar levels of muscle O2 diffusion are observed during small-mass exercise in chronic hypoxia and in normoxia, indicating that humans have a functional reserve in muscle O2 diffusing capacity, which is likely utilized during exercise in hypoxia. In summary, hypoxia reduces Vo2max because it limits O2 diffusion in the lung.
http://www.ncbi.nlm.nih.gov/pubmed/19555296

A "functional reserve" means just that.... at VO2max during whole body exercise at sea level, peripheral diffusing capacity is NOT maxed out. O2 supply clearly is though and if you supply more oxygen by increasing one or all of the following: CaO2, CO or muscle blood flow, then diffusing capacity goes up, the mitochondria gets more oxygen, it is able to utilize it and so oxygen consumption goes up. This is what the evidence shows. Nowhere do we see evidence that diffusing capacity and VO2max stay constant despite increasing O2 supply which is what your theory predicts.

I agree entirely with the "cascade" approach and I agree that peripheral diffusion plays a role in limiting VO2max, but basically what you are saying is that a downstream step in the cascade (ie: peripheral diffusion) has nothing to do with what occurs upstream. It's an outdated and incorrect viewpoint. You can go on and on for days or months reading dozens upon dozens of studies which all lead to the same conclusion which is something I did years ago.

I can forgive you for being a clinician, but if you want to play science with a scientist then you had better not cherry pick results just because they "support your views" without looking at the overall weight of evidence. That is naughty little boy science and I think you know it

 

[JayKosta]

Are there studies that measure blood O2 content changes at maximum whole-body exercise?

If blood O2 content remains high or increases, would that mean that the 'diffusing capacity at the mitochondria' is the limiter FOR THAT INDIVIDUAL ?

At some level of exertion is it the production of 'blood waste products' that prevent further O2 diffusion when additional O2 is available in the blood?

Is there a significant difference among indivduals in the ratio of O2 usage and blood 'waste product content' at maximum whole-body exercise? Perhaps due to genetics, or training?

For highly trained aerobic athletes, does the blood O2 content lessen when whole-body VO2max is approached?

Jay Kosta
Endwell NY USA

 

[FrankDay]

It doesn't support your view at all! You've categorically stated that peripheral O2 diffusion has an upper limit which occurs at VO2max in whole body exercise hence preventing it from going any higher, but that isn't what is quoted. It says...

"1) the importance of the diffusion gradient from blood to muscle cell;"

The diffusion GRADIENT my friend, is determined by the PcapO2 - PmO2. Since PmO2 is always about 0.5-1mmHg (except in hyperoxia), then this value is largely determined by PaO2.

No, sorry. Here is what really happens. Oxygen diffuses out of the capillary along its entire length in which, of course, the PcapO2 is decreasing along the entire length as oxygen diffuses out. The first mitochondria to go anaerobic will be the one that is furthest from the capillary being fed by the end capillary oxygen tension. Under normal conditions the body regulates caplillary blood flow to keep end capillary oxygen tension high enough to prevent any mitochondria from becoming anaerobic. This only becomes an issue at high demand where further capillaries cannot be recruited. At this point, the diffusion gradient of concern is not PaO2-PmitO2 but PendcapO2-PmitO2. This gradient varies with demand once one is past the anaerobic threshold. The further one is past the anaerbic threshold and closer one is to VO2max the more mitochondria become hypoxic, more lactic acid is produced, and the faster acid-base conditions will deteriorate not only locally but throughout the entire body.

The very next sentence says "2) illustrate that even in functionally isolated trained skeletal muscle the highest recorded metabolic rates can be increased by increasing O2 supply"

That does support my view. Increasing supply delays the point where anaerobic conditions are met at the end capillary.

What this means is that the diffusion gradient is not the only thing that affects diffusing capacity (indeed Fick would turn in his grave if you said it was). If you increase convective O2 supply by say, increasing muscle blood flow (to a small muscle group instead of a large one), then you can increase diffusing capacity and consequently mitochondrial VO2 goes up.

I don't say it is the only thing that affects diffusing capacity. I am simply saying it is, under normal conditions, the rate limiting element of the oxygen delivery cascade that leads to anaerobic conditions in the cell of the exercising athlete. It is because the diffusion gradient decreases as more oxygen is extracted and the diffusing distance cannot be decreased if all available capillaries are open. There is also the issue that the capillaries are empty of blood when the muscles are contracted during high intensity exercise (where the intramuscular pressure exceeds arterial pressure). This further degrades the ability to diffuse oxygen to the mitochondria because time is also lessened.

In the other review Richardson concludes "Finally, the proportionate relationship between myoglobin associated PO2 and VO2max in conditions of normoxia and hypoxia additionally supports the hypothesis that maximal respiratory rate of muscle cells is limited by O2 supply."

Notice the difference? "Importance of" versus "IS limited by" ??

Of course, maximum O2 metabolism is limited by supply since the supply involves the entire chain from the trachea to the mitochondria. What I am trying to address is which element of the chain is the rate limiting step.

On the same page if you follow the links you find....

we conclude that, in normoxic conditions of isolated KE exercise, KE VO2 max in trained subjects is not limited by mitochondrial metabolic rate but, rather, by O2 supply."
http://www.ncbi.nlm.nih.gov/pubmed/10066722

That doesn't contradict anything I have said.

If you flick forward a few years we continue to find evidence of the same thing.....

During whole-body exercise in severe acute hypoxia and in chronic hypoxia, peak Q and LBF are blunted, contributing to the limitation of maximal oxygen uptake (Vo2max). During small-muscle exercise in hypoxia, PGE is less perturbed, Cao2 is higher, and peak Q and LBF achieve values similar to normoxia. Although the Po2 gradient driving O2 diffusion into the muscles is reduced in hypoxia, similar levels of muscle O2 diffusion are observed during small-mass exercise in chronic hypoxia and in normoxia, indicating that humans have a functional reserve in muscle O2 diffusing capacity, which is likely utilized during exercise in hypoxia. In summary, hypoxia reduces Vo2max because it limits O2 diffusion in the lung.
http://www.ncbi.nlm.nih.gov/pubmed/19555296

A "functional reserve" means just that.... at VO2max during whole body exercise at sea level, peripheral diffusing capacity is NOT maxed out. O2 supply clearly is though and if you supply more oxygen by increasing one or all of the following: CaO2, CO or muscle blood flow, then diffusing capacity goes up, the mitochondria gets more oxygen, it is able to utilize it and so oxygen consumption goes up. This is what the evidence shows. Nowhere do we see evidence that diffusing capacity and VO2max stay constant despite increasing O2 supply which is what your theory predicts.

Diffusing capacity certainly is maxed out for the conditions being encountered. If one artificially increases the ability to diffuse more then, of course, it can be increased (this is what EPO does for the athlete). But, at some point, again, the diffusing capacity will mix out. The fact that some mitochondria are anaerobic while others are not is proof that the diffusing capacity is an issue. This anaerobic threshold limit is normally reached well below VO2max. How can you explain this finding using a mechanism other than diffusing capacity being the rate limiting step in the oxygen delivery cascade?

I agree entirely with the "cascade" approach and I agree that peripheral diffusion plays a role in limiting VO2max, but basically what you are saying is that a downstream step in the cascade (ie: peripheral diffusion) has nothing to do with what occurs upstream. It's an outdated and incorrect viewpoint. You can go on and on for days or months reading dozens upon dozens of studies which all lead to the same conclusion which is something I did years ago.

I can forgive you for being a clinician, but if you want to play science with a scientist then you had better not cherry pick results just because they "support your views" without looking at the overall weight of evidence. That is naughty little boy science and I think you know it

Why don't you ask yourself as to what are the conditions at the anaerobic threshold that means that all of the energy required cannot be met through aerobic metabolism? Of course it is a supply issue. The question is not whether it is a supply issue but where in the supply chain is the issue. And then, ask yourself what happens as one continues to increase demand beyond the anaerobic threshold? And, then ask yourself, what causes to athlete to say "I can push no further" when continuing to increase above the anaerobic threshold to what we call VO2max? And, then ask yourself why athletes can recover from this "I can do no more" condition in only 1-2 minutes to be able to, essentially, repeat the effort again. I think if you ask and answer these questions you will reach the exact same conclusion I have.

It isn't cherry picking. It is simply trying to come up with a mechanism that explains all of the observable real world results. (How do you explain the decline in cardiac output observed at VO2max?) If you think there is another rate limiting step let's hear what it is and your evidence to support that thesis. It is unsatisfactory to me to lump all the steps together and say "supply" is the problem. Of course "supply" is the problem. Let's break it down.

 

[FrankDay]

Are there studies that measure blood O2 content changes at maximum whole-body exercise?

Yes. What happens, of course, depends upon where it is measured. And, the values are skewed generally because of mixing. Arterial blood oxygen concentration will frequently drop at high exercise intensity levels, not because oxygenation at the lungs is reduced but because there is always some shunt through the lungs that doesn't get fully oxygenated and as venous blood levels drop due to increased extraction in the exercising muscle this lowered oxygen content of the shunted blood will lower the total arterial oxygen content from what is seen with normal venous shunting. And, venous levels don't always reflect what is going on in the muscle because, again, of mixing from blood returning from the skin or other organs that extract very little oxygen. The skin component can be fairly high when cooling efforts are at a maximum.

If blood O2 content remains high or increases, would that mean that the 'diffusing capacity at the mitochondria' is the limiter FOR THAT INDIVIDUAL ?

As long as the individual is at an aerobic level diffusion is adequate. If at an anaerobic level it is inadequate. One of the effects of training is to manufacture more capillaries, which lowers the diffusion distance, increasing diffusion capacity. This is probably the major reason anaerobic threshold and VO2max increase with training.

At some level of exertion is it the production of 'blood waste products' that prevent further O2 diffusion when additional O2 is available in the blood?

Diffusion is a passive process, it is not affected by accumulation of blood waste products or anything else. IMO it is the rate of production of lactate that limits further exertion. Lactate is bufferred by the HCO3 buffer system to produce excess CO2 and to reduce pH. It is the excess CO2, that causes the breathlessness as we go past the anaerobic threshold as we cannot increase minute volume enough to expel CO2 at th CO2 production rate so it accumulates and CO2 is the prime driver for respiratory rate, causing us to feel breathless. Concurrent pH changes affect muscle function and as it changes muscles cannot continue to function at the same level, causing both the skeletel muscles and the cardiac muscle to have reduced efficiency, explaining why cardiac output drops at VO2max. Of course, as soon as you stop exercising, the lactate production stops, the excess CO2 is blown off pretty quickly and the athlete quickly returns to a "ready to exercise" state since all these changes are very transient.

Is there a significant difference among indivduals in the ratio of O2 usage and blood 'waste product content' at maximum whole-body exercise? Perhaps due to genetics, or training?

No, as far as I know. Of course, there are some disease states of genetic conditions that might affect this to some degree. I am talking about differences in the usual "normal" athlete.

For highly trained aerobic athletes, does the blood O2 content lessen when whole-body VO2max is approached?

Except as noted above due to an effective pulmonary shunt and mixing O2 should not drop at high intensity exercise. Those who do see a drop it is usually small and because of the oxyhemoglobin dissociation curve oxygen content delivered to the artery is hardly affected at all despite a small drop in PaO2.

Because everyone has an anaerobic threshold well below VO2max and because all of the other variable elements in the oxygen delivery cascade (lung diffusion, minute ventilation, cardiac output) are capable of increasing beyond where they are when this limit is reached I think we can safely conclude that capillary to mitochondrial oxygen diffusion is the rate limiting step in all normal exercising mammals. Want to increase anaerobic threshold or VO2max? Train to increase your capillary density.

 

[Rip:30]

Training, experimental manipulation and drugs increase O2 supply (and utilization) at the end of the chain (mitochondria) because the existing delivery capacity of physiochemical structure of the capillary system is not saturated in most cases, even for trained athletes. Therefore you can view cardiorespiratory supply as a rate limiting step for a given experiment. There is no "one rate limiting step" though. You can change the equation however you want: you could extract more O2 with a different type of hemoglobin, decrease the diffusion distance, ect...

To say something is rate limiting from an experiment assumes that when you manipulate one variable, the others are held constant at values that represent maximum (or normal) values for the natural conditions you want to study. Thus depending on how you define the variables and measurments it is possible to have multiple limiting steps. The question becomes further bogged down in semantics when you start to consider what maximal or normal values for the controlled variables really should be, and how those relate to distributions across natural populations.

I think the fact that trained athletes show the ability to use more O2 when it is delivered points partially to the fact that it's more easy to manipulate that variable that it is to augment diffusion capacity in capillary beds. It does rule out mitochondrial utilization as a limiting step though and so it boils down to perspective and whether it makes sense to separate the capillary issues, or bundle them into supply (vs use).

 

[FrankDay]

Training, experimental manipulation and drugs increase O2 supply (and utilization) at the end of the chain (mitochondria) because the existing delivery capacity of physiochemical structure of the capillary system is not saturated in most cases, even for trained athletes. Therefore you can view cardiorespiratory supply as a rate limiting step for a given experiment. There is no "one rate limiting step" though. You can change the equation however you want: you could extract more O2 with a different type of hemoglobin, decrease the diffusion distance, ect...

I am sorry, the broad term "cardiorespiratory supply" does not qualify as a rate limiting STEP! The rate limiting STEP of the oxygen delivery cascade is the single component that limits all the others. And, of course there is a single rate limiting step unless you can point to the fact that all of the elements have an equal capability, which is silly since we know that single elements can be manipulated to affect the end result. How on earth do you explain the fact that there is a difference in oxygen delivery rate between anaerobic threshold and VO2max? And, we know that VO2max is the limit for the circumstances at the time. What exactly prevents the athlete form going further? IMHO, all the evidence points to that rate limiting step in most circumstances as being the diffusion of oxygen from the end/mid capillary to the furthest mitochondria. Only in the case of something like asthma can a case be made for another mechanism (but, even then, it is the diffusion step and anaerobic metabolism that keeps the athlete from going beyond VO2max. If you have evidence that points to another element of the cascade being the limiting step (or that all the elements are equal) please put it forth and make your argument.

To say something is rate limiting from an experiment assumes that when you manipulate one variable, the others are held constant at values that represent maximum (or normal) values for the natural conditions you want to study. Thus depending on how you define the variables and measurments it is possible to have multiple limiting steps. The question becomes further bogged down in semantics when you start to consider what maximal or normal values for the controlled variables really should be, and how those relate to distributions across natural populations.

In any given trial the elements are what they are. Therefore, even though it may be possible to manipulate some of the elements through the use of doping practices changing HB or blood volume or cardiostimulatory drugs or inspiratory oxygen concentration the fact remains that in each situation there will be an anerobic threshold, a VO2max, and a rate limiting step.

I think the fact that trained athletes show the ability to use more O2 when it is delivered points partially to the fact that it's more easy to manipulate that variable that it is to augment diffusion capacity in capillary beds. It does rule out mitochondrial utilization as a limiting step though and so it boils down to perspective and whether it makes sense to separate the capillary issues, or bundle them into supply (vs use).

i didn't know it was possible to augment diffusion capacity in capillary beds, at least acutely. It is, of course, possible to augment capillary diffusion capacity quite easily as that comes from simple aerobic conditioning. The difficulty comes from trying to further augment this capability once an excellent capillary density is established. Anyhow, if one is truly interested in understanding physiology one shouldn't be trying to "bundle things together" but, rather, to tease them apart to understand each component and how they interact. If you want to say that "oxygen supply" is the limiter you will get no argument from me. Where you will get an argument from me is if you try to claim that such a statement is an indication that you understand what is really going on.

 

[Krebs cycle]

No, sorry. Here is what really happens. Oxygen diffuses out of the capillary along its entire length in which, of course, the PcapO2 is decreasing along the entire length as oxygen diffuses out. The first mitochondria to go anaerobic will be the one that is furthest from the capillary being fed by the end capillary oxygen tension. Under normal conditions the body regulates caplillary blood flow to keep end capillary oxygen tension high enough to prevent any mitochondria from becoming anaerobic. This only becomes an issue at high demand where further capillaries cannot be recruited. At this point, the diffusion gradient of concern is not PaO2-PmitO2 but PendcapO2-PmitO2. This gradient varies with demand once one is past the anaerobic threshold. The further one is past the anaerobic threshold and closer one is to VO2max the more mitochondria become hypoxic, more lactic acid is produced, and the faster acid-base conditions will deteriorate not only locally but throughout the entire body.
That does support my view. Increasing supply delays the point where anaerobic conditions are met at the end capillary.I don't say it is the only thing that affects diffusing capacity.

For starters you are again describing an O2 "supply" limitation to the mitochondria since changing O2 supply variables is what alters venous PO2

see here textbook stuff..... http://bit.ly/YCFGGm

All 3 panels show that at VO2max under normal circumstances PvO2 is about 20mmHg.
Panel A shows that if you decrease diffusing capacity by 50% then VO2max drops from about 3.63 L/min to 2.6 L/min
Panel B shows that if you maintain diffusing capacity at normal levels but reduce blood flow by 50% then convective O2 supply drops and you get a larger drop in VO2max down to 2.3 L/min.
Panel C shows that if you drop PaO2 by about 50% down to 40 mmHg whilst maintaining diffusion normal then VO2max drops to 2.9 L/min.

According to you, panels B and C in the textbook are wrong.


Secondly, the bit in bold italics about capillary recruitment is an out of date viewpoint...

Dynamics of muscle microcirculatory and blood-myocyte O(2) flux during contractions.
Poole DC, Copp SW, Hirai DM, Musch TI.

This emergent picture calls for a paradigm-shift in our understanding of the function of capillaries by de-emphasizing de novo' capillary recruitment'.

http://www.ncbi.nlm.nih.gov/pubmed/21199399

What this above review discusses is the fact that at higher muscle blood flow, the surface area for diffusion increases. The single leg studies show that when you increase muscle blood flow even higher than what occurs in whole body exercise, diffusing capacity still increases. As stated previously, it isn't maxed out at VO2max in whole body exercise.

Thirdly, your view of the "anaerobic threshold" is very out of date, nearly 30yrs in fact. You are stuck a long long way in the past dear sir.....

1985....

Med Sci Sports Exerc. 1985 Feb;17(1):22-34.
Anaerobic threshold: review of the concept and directions for future research.
Brooks GA.

Recent studies on dog gracilis muscle in situ clearly indicate that lactate production occurs in contracting pure red muscle for reasons other than an O2 limitation on mitochondrial ATP production.In addition to failure of the essential assumption of the anaerobic threshold [T(an)] hypothesis that there exist limitations on O2 availability in muscles of healthy individuals during submaximal exercise, several groups of investigators have produced results which indicate that parameters associated with changes in pulmonary minute ventilation [i.e., the ventilatory threshold, T(vent)] do not always track changes in blood lactate concentration. Therefore, the T(an) hypothesis fails on the bases of theory and prediction

The "anaerobic" theory FAILS.

from 1990....

Adv Exp Med Biol. 1990;277:825-33.
Experimental support for the theory of diffusion limitation of maximum oxygen uptake.
Wagner PD, Roca J, Hogan MC, Poole DC, Bebout DC, Haab P.

While at this point in time phenomena such as perfusion heterogeneity and muscle shunts cannot be quantitatively taken into account in such analyses, the remarkable concurrence between expectations of the hypothesis and experimental data continue to lend support to the basic idea that maximum VO2 is not limited by any single step of the oxygen transport pathway from atmosphere to mitochondria, but rather by the way in which each and every step combines with every other step to determine OXYGEN SUPPLY.

As stated previously, yes peripheral O2 diffusion plays a role in limiting O2 supply to mitochondria, but it is not THE rate limiting step because it can change depending on what happens upstream. Look at the "milestone of discovery" on page 312 of the ACSM textbook page link above. It says....

evidence supporting the interaction between convection and diffusion.. on VO2max

Once again, it appears that you are implying that a downstream phenomena (ie: metabolic acidosis) is actually what "limits" VO2max at the mitochondria and you are ignoring the role the upstream components play. If you say you're not ignoring the role those upstream components play, well then you are agreeing that convective O2 supply also plays a role in "limiting" VO2max.

If you claim that at a typical muscle pH at VO2max in whole body exercise is associated with the maximal mitochondrial rate then prove it and link to a review article which concludes as much. So far I've linked to original research, review articles, a JAP point:counterpoint discussion and a textbook chapter. Now it's your turn to back up what you say with evidence, preferably something that isn't 30yrs out of date.

 

[Dear Wiggo]

I think the fact that trained athletes show the ability to use more O2 when it is delivered points partially to the fact that it's more easy to manipulate that variable that it is to augment diffusion capacity in capillary beds. It does rule out mitochondrial utilization as a limiting step though and so it boils down to perspective and whether it makes sense to separate the capillary issues, or bundle them into supply (vs use).

Are capillaries considered "peripheral", or only mitochondria? Or does it go back further still?

 

[Krebs cycle]

I dunno Dr Frank, maybe we are actually agreeing and its just a matter of semantics? In your response to me you seem to agree with the concept of a cascade (of multiple steps) in the O2 transport pathway, but then in your response to Rip:30 you imply that the ONLY step in that pathway that is rate limiting is peripheral diffusion. Just because it is the last step in the pathway doesn't mean that it is the rate limiting step.

You keep saying "all the evidence" points to that but you haven't linked to any studies whatsoever to support that contention. I've linked to an entire body of research which demonstrates that your view is incorrect. Not just one or two studies, but a vast array of work spanning 20-30yrs. As stated by Peter Wagner in the JAP point:counterpoint article, if you limit ANY step in the pathway then it has a downstream effect which ultimately reduces peripheral O2 diffusion to the mitochondria and VO2max. Conversely, if you acutely increase any number of steps in the pathway other than peripheral diffusion then you increase VO2max. That completely disproves the theory that peripheral diffusion is 100% rate limiting.

Imagine if you are pouring water into a bucket at 5 L/min through a sieve. The sieve limits the rate at which the water can flow into the bucket by 1 L/min so the water flows into the bucket at 4 L/min. When you turn the tap on stronger and pour more water onto the sieve, then more water flows into the bucket.

What is limiting the amount of water flowing into the bucket? The sieve or the tap or both? The answer is BOTH.

Now, let say you turn the tap up to V(dot)H2Omax. The sieve is still limiting the flow of water into the bucket. But now you pour MORE water onto the sieve (say from a glass or some other container), and guess what.... more water flows into the bucket!!

So what was limiting the amount of water flowing into bucket before you added the glass of water? The tap or the sieve or both?

The answer is still BOTH.

Anyway, thanks for the discussion. I don't have the time to continue it so please don't find my lack further responses as a sign of disrespect. I read many of the articles that I have linked to years ago and I thank you for re-invigorating my interest in this area. IMHO you have a bit of catching up to do though on a few seminal topics in exercise physiology.

In addition to what I've already posted, I suggest the following.....

Slow component of VO2 kinetics: mechanistic bases and practical applications.
http://www.ncbi.nlm.nih.gov/pubmed/21552162

Control of oxygen uptake during exercise.
http://www.ncbi.nlm.nih.gov/pubmed/18379208

Oxygen uptake kinetics: historical perspective and future directions.
http://www.ncbi.nlm.nih.gov/pubmed/19935845


Anaerobic threshold: the concept and methods of measurement.
"there is no evidence that lactic acid production above the AnT results from inadequate oxygen delivery"
http://www.ncbi.nlm.nih.gov/pubmed/12825337

 

[FrankDay]

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.

 

[JayKosta]

As a side-note, there seems to be confusion in some situations about the term 'VO2max'.

I think it basically breaks down to 2 major items:

1) The maximum O2 usage for an individual when an individual is exercising in manner to achieve maximum O2 usage. Which probably means exercising in such a way as to maximize the greatest amount of muscle usage - for that individual.

2) The maximum O2 usage for an individual when an individual is exercising in a PARTICULAR manner, such as cycling, running, step-test, etc. In this situation, fewer muscle groups are involved than in #1, and probably the O2 usage will be less than in #1 because of less overall muscle usage.

I think I've also seen versions of O2-usage being discussed at various 'physiological thresholds' - such as 'aerobic threshold', 'lactate threshold', 'HR-thresholds', etc.

I mention this because it is critical to know what type of O2-usage terminology, measurements, and comparisons are done for particular studies, tests, trials, articles, etc.

Jay Kosta
Endwell NY USA

 

[JayKosta]

...
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.

=========================
Frank,

just guessing here, but perhaps there is a physiological 'limiter' that discourages cardiac output from continuing at its maximum amount in order to prevent damage that could result if output remained at the max. This could probably be tested by doing some sort of 'buffering' or 'masking' to blood chemistry, or neurology.

Jay Kosta
Endwell NY USA

 

[FrankDay]

=========================
Frank,

just guessing here, but perhaps there is a physiological 'limiter' that discourages cardiac output from continuing at its maximum amount in order to prevent damage that could result if output remained at the max. This could probably be tested by doing some sort of 'buffering' or 'masking' to blood chemistry, or neurology.

Jay Kosta
Endwell NY USA

You are now talking about the Noakes Central limiter theory. The problem with this IMO is this is a "black box" theory with no theorized mechanism to sense when one is approaching damage or to prevent one from going beyond this limit nor does it address all the physiological changes seen at VO2max (such as the drop in CO at Vo2max). This theory fails on way too many levels to have much credibility.

Edit: I got to thinking about this a little bit. The Noakes Central Limiter theory is the only one that carries a name that I know of. I think this is because he is pretty much alone in the world (there are others but it seems they all trained with him) in advocating for this limiter. It seems I am the only one in the world advocating for the peripheral limiter theory. Perhaps I might propose we call it the Day Peripheral Limiter Theory. Someday I might become "famous" (in a very limited circle I am afraid) if I am ever proved right. LOL

 

[JayKosta]

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