The thing that amazes me is the fact that all the "experts" that are posting on this subject have soooo much time on their hands. If we look at the frequency of their posts, these people must not work (or posting while being paid by others), do not enjoy training, and must not have much else going on in their day to day lives. So sad.

jIM

Rip, I thought the highest attainable VO2 uptake, by your definition, was VO2 Peak. VO2 max, by your definition, again is the highest possible VO2 uptake and delivery. How does one measure this and assure onself that it cannot be increased 5 or 10 ml per minute. Many studies have shown that this value can be changed by people encouraging the athlete. VO2 uptake is limited primarily by cardiac output. How does one know that the subject is at the highest cardiac output possible for them. What if they were at their supposed VO2 max and were administered a little beta stimulant. If they were would the CO go up or go down. Only if it went down is the subject at max CO. Unless one has tested for this one doesn't know if the subject has really reached max CO or max O2 uptake.

"I did as much as i could and got all out of breath", whether someone is "encouraging" them or not, is not a very satisfactory end point in my opinion as I can do that to people on the PC's in my booth and they are WAY below their oxygen uptake capacity, and they know it.

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Frank,
An original Ironman and the Inventor of PowerCranks

can someone do a study on why i have subjected myself to 10 pages of this?

it's making me want to injure myself...

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f/k/a mclamb6

LOL

What seemed to be a flip-flop. I thought it was consistent to my position that the limiter to exercise is local and not cardiac. Maybe I was inprecise. Where did I confuse?

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Frank,
An original Ironman and the Inventor of PowerCranks

Too slow Wrote: "Come on, with all of those studies cited surely someone can tell me, what is the average level of efficiency of the cycling subjects studied?"

Mr. Slow, the book called bicycling science by Whitt and Wison addresses cycling efficiency. In general, overall cycling efficiency will vary (energy to wheel divided by energy expended) from about 16 and 23%, with the pros having the higher numbers. 20% is a good number for most people. So, if you are riding at 200 watts you are probably burning about 1000 watts of fuel. The simple efficiency of the contracting muscle is about 40-45% so the pedaling efficiency (work to wheel divided by work done by muscle) of cyclists can vary from about 30 to 55%. These numbers certainly suggest there might be lots of room for improvement there if only the inefficiencies could be found and corrected. :-)

You are also right on the energy loss from the constant acceleration and deceleration from uneven force application, although this is probably small. I think I tried to calculate the energy loss from this and it was worth a second or so per mile, if I remember correctly. But, sometimes, seconds count.

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Frank,
An original Ironman and the Inventor of PowerCranks

 
If a hand cranking trike rider switched to HAND
POWERCRANKS he probably would not find any
difference because the pulling and pushing powers
of his hands are equal, which is why he is already
pulling and pushing when powering his trike
When using the legs, things are very different and
here unweighting the pedals has more to offer than
serious attempts at producing pulling up power.
PC's are an excellent training tool for developing
the unweighting trechnique because you are forced
to use the pulling up technique on all training rides.
Single leg pedaling is only used for brief periods.
But once unweighting is perfected, the PC's work is
done.
Rowers use their legs to increase and extend the
application of arm power, with a few simple biomechanical changes when pedaling cyclists can
reverse this process and gain many advantages both
from the medical and performance aspects of cycling.
But cycling's long term problem has been the fact
that there are too many doctors or scientists involved
with the mentality of Dr Coggan who believe that
pedaling technique is unimportant, so improvement
must come from other means.

I found a few Pubmed articles addressing helium-oxygen mixtures and measuring exercise tolerance. One concluded that hyperoxygenated helium mixtures improved maximal aerobic exercise duration. The most recent one concluded that it wasn't the hyperoxygenation that did the "trick" of improving exercise duration, but it was the decrease in "normal noxious" effects (local airway sensation factors) associated with the high rate of ventilation during exercise that limits ventilation. In other words, the first study said delivering higher FIO2 (even if it had to be done by using helium) improved exercise (thereby inferring that O2 diffusion in the lung was a limiter to exercise) whereas the recent (April, 2004) study said...hold on...it is the body's "Normal" reaction to the fast-moving air in the airways that limits the ability to exercise at higher levels...maybe this is why higher FIO2 isn't always associated with better exercise tolerance.

It's this kind of banter that makes science interesting.

Perhaps this discussion about local factors vs. Cardiac output as a limiter to exercise gets off track depending upon consideration of the length and intensity of exercise. Maybe at some intensity/durations cardiac output is the limiter. At other intensity/durations...local muscle factors are the limiters. At still other intensity/durations it is something else. I think we could all agree that at certain temperatures/water loss situations that HEAT would be the limiting factor.

Where I have the firm idea that local muscle factors are THE limitation to exercise is this: Whether it is dehydration, intensity, fuel delivery, waste removal, A-V oxygen content/delivery/diffusion/capacity, cardiac output, cyanide poisoning, innervation, etc., no matter what the contributing reasons may be...when energy at the local muscle cell is no longer sufficiently available to produce a contraction forceful enough to allow the person to continue to exercise at a given level...the exercise is then limited. I think this points to mitochondrial function and subsequent energy transport systems as THE limiter to exercise.

I agree there are intensity/durations of exercise wherein an individual's current blood flow through the muscle bed is insufficient to allow the mitochondrial function and energy transport systems to supply the material required for a muscle cell to function. Still, even at these intensities/durations of exercise, cardiac output isn't necessarily at 100%.

In these cases: if cardiac output isn't at 100% when the exercise intensity is unable to be sustained, therefore it isn't cardiac output that is the limiter....even if it were blood flow through the muscle that is the limiter.

But, if cardiac output is at 100% when the exercise intensity is unable to be sustained, then perhaps it could be cardiac output that is the limiter...but, the question isn't over...is cardiac output limited because of secondary reasons...i.e., is is because of dehydration? Cardiac muscle fatigue? Vasodilation in other areas due to attempts at heat radiation/severe embarrassment/ or histamine release from an allergic reaction? Decreased venous return? Decreased stroke volume due to dehydration/decreased venous return/excessive rate? Or is it inadequate training of the heart to acheive higher cardiac outputs in these conditions? Depending upon the answer, cardiac output may not have really been the primary limitation even if cardiac output were at 100% of it's current capacity when exercise intensity decreased.

Where does this differ from your supposition? Are we in agreement on any/some/much of this?

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

You want see the Fank vs. Rip measure off too. A BATTLE TO SEE WHO IS THE BIGGEST!!!

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customerjon @gmail.com is where information happens.

yaqui,

Several points I have been thinking about and your post goes to some of them.

First, let me say I think this debate is strictly about what keeps people from increasing the overall energy expenditure of their exercise when everything is optimum and that we shouldn't complicate things by adding heat, dehydration, etc. etc. into the mix, otherwise this thread may go on forever. Anyhow, I guess it is possible that, under certain circumstances that cardiac could be the limiter to increasing energy expenditure. the certain circumstances is when every muscle in the body is equally aerobically adapted and used to the exact same degree in the exercise such that they all approach anaerobic threshold at once. However, I think the above situation never occurs and it is more likely that some muscles are better trained than others and how we use the muscles is not so well controlled that some groups may be used more intensely than others so that as we approach our limit some muscles go anaerobic while others are fine. It is these anaerobic muscles that are the limiter because anaerobic metabolism produces lactate, which is buffered by the bicarbonate system (if it weren't we would stop exercising almost immediately after reaching this point) and this buffering produces a LOT of CO2, which then overwhelms the lungs ability to expel CO2, and it is this "problem" that forces us to stop. Want some "proof"? Just come by my booth at any expo and watch novices ride the PC's. Watch experienced cyclists start huffing and puffing after about 15 seconds, their heart rate go up, and be unable to continue pedaling after 30-60 seconds despite the fact they are at a cadence of 70 and the resistance of the unit is 100 watts. These people clearly are not at VO2 max but I managed to overwhelm their lungs and a few local muscles by making them go anaerobic. One muscle going anaerobic enough can stop the whole machine. Want to delay this process, then one needs to better train that limiting muscle or develop techniques to use it less. By the way, putting helium in the inspired air changes the characteristics of the air such that turbulent flow occurs later so the maximum ventilatory volume can be increased to get rid of more of that obnoxious "lactate produced CO2", allowing the athlete to last a little longer.

The other problem that the "cardiac limitor" proponents have that hasn't been addressed is that of the normal respiratory variation of cardiac output with ventilation. Most people don't realize that the cardiac output of the right and left side of the heart varies and are out of synch, that is there is a substantial variation in CO if measured during inspiration or expiration. (for all you lurkers out there, you can check this for yourself by feeling your pulse during quiet breathing, then take a slow deep breath and feel the pulse rate change, then change again as you exhale) Take the right heart, it is higher during inspiration and lower during expiration. The left heart is just the opposite. In the operating room, it is important, when measuring CO to always do it at the same part of the respiratory cycle or the numbers will be all over the place and it will be impossible to make any good clinical judgments about the numbers.

So, if the heart has no reserve at VO2 Max, what happens to the normal ventilatory variation when at VO2 max? Does it go away? How can it go up and down if the heart is at it's very max? Exactly what is the limiter, is it stroke volume cannot increase any more or HR or both? It must be both, but respiratory ventilation variation changes both, how can this be?

Maybe Dr. Winkle can point us to one of his vaunted Pub Med studies that has looked at this "problem" that will answer the question for us.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

oh god....

find a happy place, find a happy place....

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f/k/a mclamb6

Rats, caught in a plausibly clever argument. Unfortunately, I don't understand how the argument is constructed. Perhaps you could enlighten me. I just thought I was pointing out a physiological problem with their analysis. They have yet to give a mechanism for what is limiting the heart from increasing CO, it is just stated as fact.

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Frank,
An original Ironman and the Inventor of PowerCranks

Kraig,

Let me rephrase my question to Dr. Winkle, so as to not be quite so "devious".

Dr. Winkle, or anyone else, please give me a mechanism for the healthy heart being the limiting factor at VO2 max. Don't just say it can't go any faster or increase stroke volume any more but give me the mechanism as to what prevents it from doing so. Does it run out of energy? Is it impossible for the contractile elements to contract any faster? Does turbulence restrict blood flow to a certain amount? Is it primarily a left heart or right heart problem?

I have a mechanism for the local muscles being the limiter (they go anaerobic). If you have a mechanism for the heart being the limiter please tell me, and the world. I would also be interested if there is any experiemental data to support your hypothesis. I am not interested in your "evidence" that the heart is the limiter, I want your hypothesis as to WHY it is the limiter and any supporting evidence for that hypothesis, if it exists.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

You are correct, and especially the younger anesthesiologists seem to not realize the effect ventilation has on cardiac output. Since right sided cardiac output varies more due to ventilitory pressure changes than left sided cardiac output (in someone with left-side reserve), and they are always measuring the right side...they tend to get numbers all over the place. I call the cardiac output monitor the "random number generator" when they do this. A couple of times I bet one of them 20 dollars I could get higher results than him every time...I simply cycled the ventilator every time he injected. He learned quickly, and I got to go out to eat that night.

I'm recovering from pneumonia/bronchitis, but went for an easy ride today. My HR never got above 150, partly because if I went hard enough to require that much effort my respirations would deepen to the point I would begin to cough. So, I just rode relatively easy compared to usual. After about 30 miles, my quads began to cramp when pushing up steep hills. I had been no where near my maximum cardiac output at any time all day, yet, my muscles were tired and cramping as a result. I even stood up a couple of times and worked them a little harder, they cramped more. But, as long as I eased the workload enough, they were fine. I had no signs of tetany in any other muscles (during or after exercise), and had taken a few Endurolytes prior to and over the course of the ride, drank an appropriate amount of water, so I think my electrolytes were fine. I can only surmize that local muscle factors limited my exercise rate, it certainly wasn't cardiac output limiting my exercise rate. I think it is this kind of thing that limits exercise rates in many examples.

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Quid quid latine dictum sit altum videtur
(That which is said in Latin sounds profound)

Being an anesthesiologist doesn't mean one knows everything about this stuff. Depends upon what their training is like or what they have specialized in (cardiac is much more "aware" of this stuff than Ob-GYN specialists). Anyhow, learning can come from all sorts of areas and I'll bet that anesthesiologist who lost the bet will never forget that "trick". Question is, does he realize this variation occurs in the healthy also (or the sick who are spontaneously ventilating), except it is backwards. Right heart output is lowest when the ventilator is causing inspiration and highest when the diaphragm is causing inspiration. It is all about intrathoracic pressure (higher intrathoracic pressure reduces venous return) and pulmonary vascular resistance (which is increased with higher intrathoracic pressure). BTW, the only way to get a true CO in the ICU is to disconnect the ventilator and do the measurement (that was our routine), the next best way is to do the measurement just before the ventilator fires.

OK, all you guys here now know something your doctor doesn't. Don't get too smug.

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Frank,
An original Ironman and the Inventor of PowerCranks

One correction to your statement yaqui. You said: "Since right sided cardiac output varies more due to ventilitory pressure changes than left sided cardiac output (in someone with left-side reserve)"

That really isn't true (at least in the healthy heart) since the totality of the variations have to be the same, otherwise, blood would back up in the body or in the lungs. The extra blood that is given to the lungs when right sided output is greater than left, is eventually given to the left causing it to increase and right sided output to fall. The thing is, this is a respiratory variation and not so much associated with each beat so individual stroke volume can vary widely and since the inspiration phase is usually shorter than the exhalation phase (at least at rest and when a patient is on the ventilator), the slope and magnitude of the various changes is seen as greater on one side than the other. Perhaps that is what you meant, not the totality.

Another way to minimize the impact of this effect in the ICU is to use High frequency ventilation with very low tidal volumes, where intrathoracic pressure essentially remains constant and ventilation occurs primarily through diffusion. Enough medicine. Only you, yaqui, probably cares about this stuff. But it is nice to know that there is someone out there who knows I am not just spouting stuff.

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Frank,
An original Ironman and the Inventor of PowerCranks

kay, this is my last word on the subject. For reference, you can find much of the following information in Costill (1999), Chapter 7, entitled Cardiovascular Control During Exercise. It can also be found in Astrand, and some of it in Guyton (my med school text…sorta weak on the phys of exerecise, but usefull none the less).

Cardiac output is determined by a few factors: preload (how much venous return blood is hitting the heart) Contractility (which is how hard the heart is squeezing), and afterload (the blood pressure in the aorta which the heart must overcome to eject blood).

Cardiac output is increased in a few ways as exercise is increased. When muscle units are activated, they are perfused with blood. The heart must respond to maintain blood pressure in the face of an increased volume. Cardiac input increases by increased contractility, by increased rate via the sympathetic system, and also because afterlaod has been reduced, allowing the heart to eject more blood. Finally, the heart begins to receive more blood per unit time because of increased return. This stretches the heart more, and by the frank-starling mechanism, the heart ejects what is put into it. This is that part frank has been harping on.

Frank's argument would hold water IF and only IF the heart was able to increase it's output indefinitely. He keeps talking about "reserve". The problem is this: As heart rate increases, and the heart stretches to accept more blood, there is a problem. The heart is beating so fast that it does not have time to fully fill any more. Thus, cardiac output levels off. There is a nice graph of this on page 228 in Costill, where cardiac output is graphed against treadmill speed for a runner from 4 km/hr to 30 km/hr. Around 14 km/hr, cardiac output begins to level off, maximal output is finally reached at 17 km/hr, and then cardiac output finally begins to FALL because it is beating so fast that it is not filling fully anymore.

Vo2 max occurs somewhere around the point of maximal cardiac output, and certainly BEFORE the point that cardiac output begins to fall because the rate has gone too high. The reason why muscles are going anaerobic and generating high levels of lactate is because the heart is unable to provide them with any more oxygen, because it has reached it's maximum output. They are thus less reliant on oxidative phosphorylation, and more reliant on anaerobic metabolism.

Now, frank may propose whatever he likes to argue with this. This will be his opinion. It is not what is accepted in the field of physiology, and is not what I or any other physician or physiologist I know to be based on data. I refuse to argue the point any more. Please note I am not arguing about powercranks. I stated my position earlier, which is that I have no position until I see a good study. I am arguing that Frank is obviously not familiar with what is understood about the physiology of exercise. If he does not belive this information is true, he is free to argue his opinion and write his own treatise on the subject, after doing the appropriate research. He will then most likely win a nobel prize because he will have undone quite a bit of previous work and revolutionized the science.

Please frank, tell me I am wrong. I have gone through my texts and written a thorough response. I'm on call today, and I have the whole medical library of my hospital at my disposal. I would LOVE to read things that contradict what I just wrote. Problem is, I can't find any, because all three phys texts texts I have access to agree on this. So do the anesthesisologist and cardiologist I had lunch with.



Over and Out,

Philbert.

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Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!

A couple hundred posts back or so Brodsky made the following statement...

"Motor units are perfused with blood when they are activated by the nervous system. The limiter is cardiac output; perfusion of muscle must be balanced against systemic blood pressure. If you suddenly and maximally perfused all possible motor units, you'd be on the floor because of low blood pressure. So, in fact, the ultimate exercise limiter is cardiac output. If you could endlessly increase your cardiac output, your criticism might be understandable at least.

This point is demonstrable by testing oxygen uptake while exercising a small muscle mass. I'll try to find one of the papers if you need a citation...a physician friend of mine is writing a book and turned me onto it. Basically, O2 uptake (and local blood flow) is higher when you exercise a small muscle mass because the heart is able to perfuse that muscle more, because maintaining systemic bp is easier."

It took about a hundred posts to do it, but Rip supported it. You guys are now dancing around it.

You also never addressed:


http://www.ncbi.nlm.nih.gov/...mp;list_uids=3057322

and

http://www.ncbi.nlm.nih.gov/...mp;list_uids=3414535

Though this process can often be painful to participate in and watch, I certainly learned a lot and I'm one of those geeks who will actually sit down and read a physiology text. My thanks to all who participated in and contributed to this train wreck.

JustCurious,

Thanks for your contributions. I just posted my last commentary immediately before you did. This thread is too long.

Philbert

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Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!

Dr. Philbert writes: "Vo2 max occurs somewhere around the point of maximal cardiac output, and certainly BEFORE the point that cardiac output begins to fall because the rate has gone too high. The reason why muscles are going anaerobic and generating high levels of lactate is because the heart is unable to provide them with any more oxygen, because it has reached it's maximum output. They are thus less reliant on oxidative phosphorylation, and more reliant on anaerobic metabolism."

Thanks for the support. If VO2 max occurs before the peak, then there is reserve. If it occurs at the peak then there is not but we don't know why it falls. What is the mechanism. Perhaps, the mechanism is that the pH has changed from the peripheral muscles going anaerobic and the lungs unable to exhale the CO2 load. I have never said the ability of the heart to increase was infinite. What I have said is the limiter to exercise is not the heart but theperiphery. Give me a mechanism for that drop off. What is it? I agree it occurs. But you haven't given me a mechanism for its occurance. I propose it is accumulated pH change from peripheral anaerobic metabolism (this occurs slowly because CO2 is water soluble so is distributed through all of the body water so it takes a significant burden to change pH, although it probably doesn't take a big pH change to significantly effect cardiac contractility. Hmm, I wonder why we treat acidosis in the ICU? What is your proposed mechanism? Just give me a mechanism that originates in the heart, that is what the debate is about.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

Curious,

It is easy to rebut those articles because they do not go to the issue. The fact that blood flow can increase in isolated muscle does not give me a mechanism for failure of the heart to provide adequate flow when the whole body is exercising. Give me the mechanism for the heart failing to be able to increase CO further that lies primarily in the heart (when the periphery is producing lactic acid like crazy). You do agree the periphery is producing lactic acid before one reaches VO2 max, don't you? Actually, I don't expect you to give me a mechanism as you are a lay person. But, until someone can give a mechanism for this failure that is heart specific and originates in the heart, then all these "the limitation to exercise is cardiac" pronouncements are just that, pronouncements without a basis.

Since Philbert is on call today and has the entire medical library (and some others who are capable of thinking deeply about this problem) at his disposal we will await his report (unless he gets overwhelmed with patients in the interim.

Frank

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Frank,
An original Ironman and the Inventor of PowerCranks

Sorry, I was trying to be brief and left a little bit out. Let me be precise.

Vo2 max occurs somewhere around the point of maximal cardiac output, and certainly BEFORE the point that cardiac output begins to fall because the rate has gone too high. What happens before it starts to fall is that it LEVELS OFF. There is no reserve to be had, because the output is not changing appreciably one way or the other within those few beats per minute, at least not in any meaningful way we can measure.

I am giving you a mechanism. I am saying that HR increases to the point that the ventricles have balanced filling perfectly with rate, as much as is possible and as much as we can tell with our technology. This is V02 max. As the heart futily tries to provide more blood, rate increases and the ventricles no longer fill completely. Thus CO cannot increase any more. The failure of the muscle is secondary to the primary problem of the heart to provide any additional oxygenated blood. Which part of this don't you get? That sounds like a problem with the heart to me, doesn't it to you?

But really, Frank, it isn't up to me to prove my position with mechanisms. I am merely stating what is obvious from the texts. You are the one proposing mechanims that differ from the established literature. It is up to YOU to provide us with data or literature to back up your points. So far, you have not provided a mechanism that has any backing other than your say-so, and your knowledge of anesthesia that you brought up earlier. I have provided citations to support my case. Don't beat around the bush. The reason you are is that you cannot provide any citations to back up yours. I have tried to find some to back up your mechanism, but I can't. That makes it your opinion, which you are entitled to but which is not defensible via literature. Period.

Now I really AM through with this.

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Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!

Lay person to Reverend Day,

Philbert provided the mechanism. "Frank's argument would hold water IF and only IF the heart was able to increase it's output indefinitely. He keeps talking about "reserve". The problem is this: As heart rate increases, and the heart stretches to accept more blood, there is a problem. The heart is beating so fast that it does not have time to fully fill any more. Thus, cardiac output levels off. There is a nice graph of this on page 228 in Costill, where cardiac output is graphed against treadmill speed for a runner from 4 km/hr to 30 km/hr. Around 14 km/hr, cardiac output begins to level off, maximal output is finally reached at 17 km/hr, and then cardiac output finally begins to FALL because it is beating so fast that it is not filling fully anymore."

I may not be an MD, but I am an engineer. Let me put this in engineering terms. You're claiming the pump is essentially oversized - that it's the 'network' it supplies that limits output. Your logic is implying that limitations in the 'network' the pump feeds is limiting the pump's output (limited capillary density, etc.). If the 'network' can accept or handle more flow (a proven training adaptation), you argue that the pump can handle it (it in fact even also gets bigger through training). It simply speeds up as needed to meet momentary demand. As a 'lay' person before this and some of the previous related discussions on this subject, I would have agreed with you. It makes some of the concepts of those who worship in the 'temple of the heartrate monitor' easier to explain... Things such as demonstrated maximum heartrate seems to be sport or activity specific --> involve more muscle mass and max attainable HR seems to be slightly higher.

What the evidence presented seems to show is that the pump is indeed 'undersized'. At VO2max, the network has the theoretical ability to open up to a point that could exceed what the pump is able to provide in terms of flow. That was demonstrated when flow increased to greater levels when active muscles were worked in isolation than when contributing to an effort at systmemic VO2max. Undersized pump, oversized network being fed --> output pressure would drop off to dangerous levels if our bodies didn't have a built in protection mechanism that closed off that network enough to maintain pressure. As this is a closed system, that restriction to maintain pressure limits the heart's ability to refill between beats. Increase capillary density of the working muscles? Effective, but only to the point where that same training that induces an increase in capillary density also increases cardiac output. Short term effort at VO2max --> It's still your heart that maxes out before the effects of anearobic metabolism begin limiting the effort. If your heart had the ability to put out more, the reliance on and affect of anaerobic metabolism would be lessened. At least that's what mainstream scientific evidence seems to say.

What am I missing?

Sorry Philbert. I should be letting you handle this. We seem to by typing at the same time.