The physiology thread

[FrankDay]

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

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

Sure it does because the buffering of the alternatively produced lactic acid by the bicarbonate system results in a CO2 molecule. If CO2 production was reduced or eliminated with anaerobic metabolism we would require less minute ventilation to maintain CO2 around 40mmhg, instead we become breathless.

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

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

I believe it is produced in the local tissues but regardless, it is produced and needs to be taken care of.

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

PaCO2 is reduced at VO2max? link please

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

Huh? Acidosis occurs because of anaerobic metabolism is my point. And, this acidosis affects the physiology of a lot of things that are going on at the same time. Don't you find it a bit strange that all of the papers you linked to ignored the effects of acidosis, as if it were a non-issue?

Yes, metabolic acidosis occurs during high intensity exercise.

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

Likely? is there any doubt? Edit: actually, fatigue and performance are two different things. I am mostly referring to performance, not, necessarily, to fatigue. Acidosis may, of course, contribute to fatigue but I don't know much about that.

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

Well then, what is it that causes the athlete to stop? You still haven't given your thoughts on this question.

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

I am trying to come up with a mechanism that explains why cardiac output starts to drop at VO2max. A drop in cardiac contractility as pH drops due to the accumulation of acid products from the buffering of produced lactic acid and the inability to blow off the resulting over production of CO2 would explain this finding. The fact that your review papers ignore the possible effects of anaerobic metabolism at VO2max does not mean I am wrong. If I am wrong, give me "the correct" mechanism to explain this finding.

Oh, and give me a component in the oxygen delivery cascade, other than capillary density affecting oxygen diffusion in the tissues, that can explain how training can and does, reliably, increase VO2max. While other components can affect VO2max, they probably do so, it seems, by affecting oxygen diffusion gradients at the tissue level. The only reasonable conclusion as to what is the limiting factor in the oxygen delivery cascade is the oxygen diffusion component.

 

[FrankDay]

I'm just going to leave this here.

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

Happy reading Frank.

Irrespective of the specific model that describes the process, the physiologic changes associated with lactate accumulation have significant import for cardiopulmonary performance. These include metabolic acidosis, impaired muscle contraction, hyperventilation, and altered oxygen kinetics, all of which contribute to an impaired capacity to perform work. Thus, any delay in the accumulation of blood lactate which can be attributed to an intervention (drug, exercise training, surgical, etc) may add important information concerning the efficacy of the intervention. A substantial body of evidence is available demonstrating that lactate accumulation occurs later (shifting to a higher percentage of VO2max) after a period of endurance training. In athletes, the level of work that can be sustained prior to lactate accumulation, visually determined, is an accurate predictor of endurance performance.

The only real issue I have with this paper is they fail to address the role of capillary density and oxygen diffusion in their analysis. I believe once this is considered everything falls into place and what is going on can be, pretty much, fully understood.

 

[acoggan]

Edit: it is a shame that you have taken the A. Coggan approach to internet "discussion." That is to simply declare the opposition wrong without saying why or what the correct answer really is.

Frank, I've explained more things to more people than you'll ever be able to miseducate in your lifetime, no matter how much you continue to try.

 

[FrankDay]

Frank, I've explained more things to more people than you'll ever be able to miseducate in your lifetime, no matter how much you continue to try.

LOL. Perhaps, but not on the internet.

So, why don't you start now by joining the discussion and "properly educating" the folks (including me) as to what is really going on rather than appearing now to simply put me down and build yourself up.

 

[FrankDay]

That was not an ad hominem.

From the Wikipedia article on ad hominem

A subtle way of ad hominem is attributing minor properties that are hard to argue because of their subjective nature. This type of ad hominem distinguishes itself from other forms by not being the base of the argument, but rather subtly implying such properties exist. This method of ad hominem is usually used to further convince something is true, without being the essential point of the argument, therefore a valid argument could contain this type of ad hominem. In other cases, attributing negative qualities to people or ideas can be used to further confirm oneself's beliefs even though the qualities have no relevance to the belief or idea.

By simply declaring me wrong and himself right comforms to the above, IMHO.

 

[Rip:30]

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.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 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.

You just need to slow down and do some of the math... If you sit down, write out each individual variable carefully and observe the connection mathematically between the way you are breaking apart the reaction kinetics at different points in the supply chain you will see that you are just arguing with yourself about arbitrary semantics in a really idiotic way. Have you ever conducted a publishable experiment? Obviously you can read & write, but you're being overly argumentative about nothing. Slow down and think objectively.

 

[Tapeworm]

The only real issue I have with this paper is they fail to address the role of capillary density and oxygen diffusion in their analysis. I believe once this is considered everything falls into place and what is going on can be, pretty much, fully understood.

You should write to them, maybe you could educate them a little.

 

[FrankDay]

You just need to slow down and do some of the math... If you sit down, write out each individual variable carefully and observe the connection mathematically between the way you are breaking apart the reaction kinetics at different points in the supply chain you will see that you are just arguing with yourself about arbitrary semantics in a really idiotic way. Have you ever conducted a publishable experiment? Obviously you can read & write, but you're being overly argumentative about nothing. Slow down and think objectively.

Wouldn't it be more useful to this discussion if instead of just pointing out that you believe I am wrong you were to actually make a comment as to what you thought was the correct interpretation of the data? Your comment tries to make you look very smart and me look very dumb without you actually committing to anything. Good job!

 

[FrankDay]

You should write to them, maybe you could educate them a little.

No, that was published in the 90's. Too old to be "relevant" in the eyes of the editors. (BTW, I have written many letters to the editors in situations such as this that have been published when I was "active" in medicine) Someone, who cares about his resume, will someday get it right and submit something that finally sees the forest. My guess is it won't come from the exercise physiologist community as their experience is way too limited. Notice the article you referenced was from the physician community in a physician journal. Of course, the exercise physiologists won't notice as they don't read this stuff.

 

[Krebs cycle]

Sure it does because the buffering of the alternatively produced lactic acid by the bicarbonate system results in a CO2 molecule.

No Frank Day, the CO2 is "produced" via bicarbonate buffering, it is not produced during anaerobic metabolism.

I believe it is produced in the local tissues but regardless, it is produced and needs to be taken care of.

You believe wrong. This is textbook human physiology. I teach this at undergraduate level.

Here you say that the "anaerobic" CO2 is produced in the muscle and combined with your previous statement "the production of CO2 becomes much larger than the consumption of oxygen" this would imply that within the muscle fibre more CO2 is produced than oxygen consumed.

That would mean that the RQ is greater than 1.0, which is physiologically impossible.

PaCO2 is reduced at VO2max? link please

Figure 10.6, page 256. Chapter 10: The Respiratory System. ACSM's Advanced Exercise Physiology. Dempsey, Miller and Romer.

Again.... textbook physiology.

Acidosis occurs because of anaerobic metabolism is my point.

As stated previously, this was disproven nearly 30yrs ago.

If you keep repeating an error it won't magically become correct some day.

And, this acidosis affects the physiology of a lot of things that are going on at the same time. Don't you find it a bit strange that all of the papers you linked to ignored the effects of acidosis, as if it were a non-issue?

Blah blah blah same old story. For starters, none of the papers I have linked to ignore it. In every study ever conducted on VO2max, metabolic acidosis was occurring during exercise and thus the effects of acidosis on muscle contractile function are inherently included in the experimental protocol.

Secondly, if acidosis limits VO2max via inhibiting contractile function then this would imply that VO2max would increase during bicarbonate ingestion, but this doesn't happen.

Thirdly, you clearly haven't read any of literature on the limits to VO2max so how would you even know?


The fact that you do not understand high school level human biology leads me to believe you simply cannot be a medical doctor. No qualified MD could possibly think that "more CO2 gets produced in the muscle than oxygen consumed". It's akin to saying that you "believe" 2+2=13 and then telling everyone you're a mathematician so you must be right because you're the only one in the whole world who understands numbers.

IMO you cannot be a doctor. You're just some fraud on the internet pretending to be one. If you google Frank Day MD it comes up with a guy from UCLA Dept of Emergency Medicine, but he isn't an anesthetist. If you google Frank Day anesthetist or anesthesiology then there are no hits at all. So either that is you and you're lying about your qualifications and experience, or that isn't you and you don't exist on the internet which would be rather surprising, or Frank day is not your real name and we've got no way of knowing.

All we do know is that a high school human biology student understands basic physiology better than you do.

 

[Krebs cycle]

Well then, what is it that causes the athlete to stop? You still haven't given your thoughts on this question.

The topic has been about limits to VO2max. This here is a different question.

The answer is that a complex array of factors including peripheral mechanisms and afferent feedback to the CNS arising from many parts of the body produces a sensation that is perceived by the individual as as "fatigue".

Oh, and give me a component in the oxygen delivery cascade, other than capillary density affecting oxygen diffusion in the tissues, that can explain how training can and does, reliably, increase VO2max.

I already did. Hypervolemia.

While other components can affect VO2max, they probably do so, it seems, by affecting oxygen diffusion gradients at the tissue level. The only reasonable conclusion as to what is the limiting factor in the oxygen delivery cascade is the oxygen diffusion component.

Again, repeating the same thing as before which has already been disproven 15yrs ago.

This is a joke. You are not a doctor at all. You've been outed here.

Frank Day = FRAUD.

No point responding any further to such an obvious B#llsh!tter

 

[FrankDay]

Well then, what is it that causes the athlete to stop? You still haven't given your thoughts on this question.

The topic has been about limits to VO2max. This here is a different question.

Wow, I must have completely misinterpreted the way of the usual VO2 max test. I always thought that it was pretty much at VO2max that the athlete soon was saying they couldn't go on and quit the test. I had thought they were pretty much related.

The answer is that a complex array of factors including peripheral mechanisms and afferent feedback to the CNS arising from many parts of the body produces a sensation that is perceived by the individual as as "fatigue".

But, this discussion is not about fatigue

Oh, and give me a component in the oxygen delivery cascade, other than capillary density affecting oxygen diffusion in the tissues, that can explain how training can and does, reliably, increase VO2max.

I already did. Hypervolemia.

Forgive me for falling back on some of my physician (despite your low opinion of me - see below - I do qualify to put MD after my name) training and definition of words but it is your contention that "hypervolemia" explains the improvement in VO2max seen with training? First, let me say that most people, when they start a VO2max test, are "normovolemic" by definition. Second, I am unaware that volume status was even considered a component of the oxygen delivery cascade. Third, I look forward to seeing an explanation somewhere in the literature as to how training affects blood volume and how these changes lead to improvements in VO2max. I am ready to learn. Fourth, perhaps you could tell me how much you think the volume status of the athlete changes with training. Fifth, are you saying that if I were to withdraw that amount of volume from someone like Lance or Fabian that this would return their VO2max status back to what it in in an untrained individual?

This is a joke. You are not a doctor at all. You've been outed here.

Frank Day = FRAUD.

Finding a need to continue with the ad hominen attacks for some reason?

 

[FrankDay]

No Frank Day, the CO2 is "produced" via bicarbonate buffering, it is not produced during anaerobic metabolism.

But, it is still present as CO2 and changing the partial pressure and the body doesn't care how it got there, the effect is the same.

You believe wrong. This is textbook human physiology. I teach this at undergraduate level.

Under graduate physiology is "wrong" at so many levels. It is a good basis to start learning physiology but it misses so many nuances.

Here you say that the "anaerobic" CO2 is produced in the muscle and combined with your previous statement "the production of CO2 becomes much larger than the consumption of oxygen" this would imply that within the muscle fibre more CO2 is produced than oxygen consumed.

It implies no such thing. It is simply a fact that more CO2 shows up in the body than would normally be seen if the equivalent amount of ATP were produced using aerobic metabolism. It comes about because of the buffering of the lactic acid by the bicarbonate buffering system, the main buffering system in the body. If it weren't for this buffering the athlete would have to stop much sooner than they do now with any acid production. It is the buffering system that allows him to continue as long as he does. It isn't that difficult to understand.

That would mean that the RQ is greater than 1.0, which is physiologically impossible.

No it doesn't. It appears because of the buffering - notice an H+ on the right side of the equation pushes the balance to the left to produce a CO2 on the left side of the equation. How much "extra" CO2 is produced this way depends upon how much acid is being produced and buffered. A small amount won't be real noticeable. A large amount should be. There are huge stores of CO2 in the body in the form of HCO3. All that is happening is some CO2 is being released from these stores as acid is produced.

Figure 10.6, page 256. Chapter 10: The Respiratory System. ACSM's Advanced Exercise Physiology. Dempsey, Miller and Romer.

Again.... textbook physiology.

Thanks for that link. There are several items in that data that makes me believe those tests do not go all the way to VO2max. Even if they do they do not discount my basic contention, that the real issue is one of pH changes. What bothers me about that data. First, he shows arterial oxygen pressure below 90 at lower efforts and above 90 at the highest effort. Those are not normal oxygen pressures for healthy people at low efforts. Normal people should always have a PaO2 >90, closer to 95. Second, one would expect arterial oxygen pressure to drop at or near VO2max because of increased end capillary extraction and a lower mixed venous oxygen pressure lowering arterial oxygen pressure due to mixing from the normal shunt. We do not see that, it goes the wrong way suggesting the peripheral tissues are not maximally extracting oxygen yet. Third, he is showing a PaCo2 of 28 at his max. In order to achieve this requires a minute ventilation of over 140% above what would be required to just get rid of the produced CO2 load. While, I guess, not impossible, it does seem improbable that this is possible at VO2max in view of normal airway flow characteristics (link) due to the occurrence of turbulent flow. Such flow rates are essentially impossible to achieve in the operating room when trying to manipulate PaCO2 (something done quite regularly in brain surgery). ("In turn, expiratory flow limitation presents a significant mechanical constraint to exercise hyperpnea" link) Fourth, it is not clear this data represents the type of subject we are talking about here, the athlete and specifically the elite athlete. elite athlete frequently see a drop in PaO2 at or near VO2 max. link1 link2 link3 As noted above, that would be my expectation due to the extra extraction occurring in the capillaries causing "dilution" as it mixes with the arterial blood due to physiological shunt. So, to say that the chart out of your undergraduate textbook represents the case I am discussing simply isn't the case. I will admit that this data does suggest that the cause and effect cascade of pH dropping due to an increase in CO2 (from an inability to increase minute ventilation enough) as I originally proposed is probably not true. That having been said, it does seem that the basics of what I proposed is true, that is, the pH still changes due to the acid load from the anaerobic metabolism because of an inability to blow off enough CO2 to compensate for the acid load resulting in debilitating pH changes. The body tries but it fails. That having been said, I would like to see what the pCO2 is doing in those elite athletes who are seeing reduced oxygen at VO2max before I submit completely on this question though.

Acidosis occurs because of anaerobic metabolism is my point.

As stated previously, this was disproven nearly 30yrs ago.

Disproven is such a strong word when it comes to science. Perhaps you might enlighten us all as to where the acidosis is coming from.

If you keep repeating an error it won't magically become correct some day.


Blah blah blah same old story. For starters, none of the papers I have linked to ignore it. In every study ever conducted on VO2max, metabolic acidosis was occurring during exercise and thus the effects of acidosis on muscle contractile function are inherently included in the experimental protocol.

Ugh, if it isn't mentioned in the paper it is being ignored.

Secondly, if acidosis limits VO2max via inhibiting contractile function then this would imply that VO2max would increase during bicarbonate ingestion, but this doesn't happen.

No it doesn't. You don't seem to understand how much CO2 load is carried in the HCO3 buffer system and how tiny the amount one can ingest relative to that such that changes in pH are imperceptible. You can cause bigger changes in pH when you vomit out all that good gastric acid. Don't forget the pH scale is a log scale.

Thirdly, you clearly haven't read any of literature on the limits to VO2max so how would you even know?

I wouldn't say I haven't ready any of it. I would say I have applied what I know about physiology to my assessment.

The fact that you do not understand high school level human biology leads me to believe you simply cannot be a medical doctor. No qualified MD could possibly think that "more CO2 gets produced in the muscle than oxygen consumed". It's akin to saying that you "believe" 2+2=13 and then telling everyone you're a mathematician so you must be right because you're the only one in the whole world who understands numbers.

You ought to read what I have said. I have never claimed that. Although i would agree with your assessment, my understanding of physiology is not on the high school level.

IMO you cannot be a doctor. You're just some fraud on the internet pretending to be one. If you google Frank Day MD it comes up with a guy from UCLA Dept of Emergency Medicine, but he isn't an anesthetist. If you google Frank Day anesthetist or anesthesiology then there are no hits at all. So either that is you and you're lying about your qualifications and experience, or that isn't you and you don't exist on the internet which would be rather surprising, or Frank day is not your real name and we've got no way of knowing.

LOL, If you say so.

All we do know is that a high school human biology student understands basic physiology better than you do.

If you say so. LOL

 

[Krebs cycle]

Finding a need to continue with the ad hominen attacks for some reason?

It's not an attack. I think you're probably a really nice guy in real life and you enjoy discussing physiology like me. I'm just stating my opinion that you cannot be a medical doctor because I've never met a medical doctor whose understanding of basic human physiology is so bad and who so steadfastly refuses to accept the scientific literature on a range of core topics in exercise physiology.

edit: I suppose you could be a medical doctor, but just with a rather confused grasp of physiology, especially exercise physiology.

 

[JayKosta]

Can someone give a list of the 'cascade' of events regarding O2 usage which spans the range from:
- low O2 usage (e.g. at rest)
- initial point of VO2max
- failure to maintain VO2max

Or, do you know of an online reference where I can find this?

Jay Kosta
Endwell NY USA

 

[FrankDay]

It's not an attack. I think you're probably a really nice guy in real life and you enjoy discussing physiology like me. I'm just stating my opinion that you cannot be a medical doctor because I've never met a medical doctor whose understanding of basic human physiology is so bad and who so steadfastly refuses to accept the scientific literature on a range of core topics in exercise physiology. (edit: I must admit it has been many many years since I dealt with this on a daily basis so it would not surprise me if I have forgotten a few things or if something new has been discovered but, I haven't seen much evidence of that and, if it is the case, I am willing to learn but I need more than "you are wrong".)

edit: I suppose you could be a medical doctor, but just with a rather confused grasp of physiology, especially exercise physiology.

Sure it is an attack. It is an argument against me personally rather than addressing the issues. Your problem is you haven't met many MD's (or anyone) who is willing to challenge your knowledge regarding physiology. I'll admit most MD's don't particularly care about physiology to the degree I do (it was my FAVORITE class in first year medical school, it seemed so "easy" when combined with my engineering background) then I became an ultra-marathoner and anesthesiologist (perhaps I was drawn to anesthesiology because of its strong association with physiology) and my interest continued.

Anyhow, you continue to ignore the issues of this discussion preferring to talk about me personally. You have yet to explain what you believe is going on at VO2max that prevents the athlete from going further. You have failed to explain how it is you believe that our ability to improve VO2max with training is explained by "hypervolemia". Really? And you accuse me of having a poor understanding of basic physiology.

 

[FrankDay]

Can someone give a list of the 'cascade' of events regarding O2 usage which spans the range from:
- low O2 usage (e.g. at rest)
- initial point of VO2max
- failure to maintain VO2max

Or, do you know of an online reference where I can find this?

Jay Kosta
Endwell NY USA

I am not sure exactly what you are looking for. I will list some of the issues related to the cascade.

First, from the air to the lungs. This involves mass transport through a tubing network. Don't forget what is called the "dead space". The driving force is the pressure difference between the air and the alveoli caused by diaphragmatic movement. Oh, and when ispiring and thoracic pressure goes down the tubes will get a little wider and when expiring and thoracic pressure is increased the "tubes" will get narrower. And, the larynx and trachea is "rough". Don't forget that adding water to the inspired air will dilute the amount of inspired oxygen. There is a lot going on. Anyhow, once the air gets to the bronchioles it moves with diffusion.

Next, the alveoli. While it seems this is pretty straightforward, it is not. Oxygen cannot diffuse accross an alveoli unless there is oxygen in the alveoli and there is also blood flow in that alveoli. This also is not so simple because blood flow and alveolar ventilation varies throughout different areas of the lungs. At low blood flows there is no blood flow at the top of the lungs so any ventilation there is wasted. Oh, and some alveoli will be collapsed so any blood flow there is wasted. This issue is called the ventilation-perfusion mismatch and can affect oxygenation and that blood flow where there is no ventilation is called a right to left shunt. Oxygen is not very soluble in blood so most of the oxygen is carried in the RBC's. Breathing 100% oxygen hardly increases the amount of oxygen in the blood at all. In the lungs, the oxyhemoglobin dissociation curve also helps in the transfer but in any case,
in the alveoli where there is a balance of alveolar oxygen and blood flow the transfer of oxygen is usually complete regardless of cardiac output. Anyhow, it usually works pretty well but you can see it is complicated.

Once we have oxygen in the blood we have to get it to the tissues. This is what the heart does. While there are lots of issues that affect the ability of the heart to pump blood, in most cases the heart simply pumps the amount of blood that the tissues demand. It is a self regulating system and the heart only fails to meet the volume demand at VO2max.

Once the blood is at the tissues it is now time to get the oxygen to the mitochondria and the CO2 back into the blood for transport back to the lungs for exhalation. This occurs by diffusion at the capillaries (the walls of the arteries and arterioles are too thick for diffusion to occur efficiently). The tissues generally have more capillaries than the tissues require so, to stay efficient, most of them are closed at rest, increasing the diffusion distance but keeping the work of the heart down. In general, this is controlled by the pre-capillary spincter and these open or close to keep the saturation of the blood leaving the tissue to be around 75%. It is all controlled locally and these are always opening and closing to distribute the blood around. At high demand "all" of the capillaries will be open which means blood flow through the muscle will increase as will the amount of blood pumped by the heart. One other thing that happens at high demand is blood pressure will also increase which most likely helps ensure maximum blood flow through all available capillaries when demand is high. Regardless, if demand keeps increasing beyond the ability of the tissue to get more blood through then extraction will increase to provide more oxygen reducing the venous blood to below the 75% normal saturation. The oxyhemoglobin dissociation curve plays a role here again. At this point more and more mitochondria will be supplied with inadequate oxygen and anaerobic metabolism will start to become significant and apparent.

Anyhow, there are many other things going on also. For instance, highly contracting muscle will push all the blood out of the muscle if the intramuscular pressure is greater than the arteriole pressure. This further limits the amount of time the oxygen has to diffuse to the tissues. Or, temperature and pH affect the oxyhemoglobin dissociation curve helping or hurting delivery of oxygen to the tissues. In most cases these all work pretty well together but understanding all that is going on usually isn't found in undergraduate physiology texts.

Hope this helps.

 

[FrankDay]

The lactic acid question thread

Let me add a new physiology topic to be discussed. This has been alluded to in the VO2max thread but it really is a different topic in my opinion. Anyhow, as mentioned in the VO2max thread there is almost always a low level of lactic acid around even under what is considered fully aerobic conditions. The question is: How does one explain this? Is there a biochemical pathway in the cells that can result in lactic acid being formed that doesn't require anaerobic metabolism? I haven't heard of one. If there is, what is it? If there isn't, how does one explain the formation of lactic acid in the absence of anaerobic conditions? (I think I can do it but I will await the explanation of others.)

 

[CoachFergie]

Krebs, seeing you clearly have an excellent and up to date understanding of exercise physiology I am wondering if you have any thoughts on the underlying physiology of some of the metrics used in racing and training with a power meter such as Normalized Power, Training Stress Score, Chronic and Acute Training Load and Training Stress Balance.

 

[JayKosta]

Let me add a new physiology topic to be discussed. This has been alluded to in the VO2max thread but it really is a different topic in my opinion. Anyhow, as mentioned in the VO2max thread there is almost always a low level of lactic acid around even under what is considered fully aerobic conditions. The question is: How does one explain this? Is there a biochemical pathway in the cells that can result in lactic acid being formed that doesn't require anaerobic metabolism? I haven't heard of one. If there is, what is it? If there isn't, how does one explain the formation of lactic acid in the absence of anaerobic conditions? (I think I can do it but I will await the explanation of others.)

-
Wouldn't 'fast-twitch' muscles be expected to do some amount of anaerobic metabolism through glycolysis, and produce lactic acid, even if the 'overall condition' is CONSIDERED to be 'fully aerobic'?

Jay Kosta
Endwell NY USA

 

[Krebs cycle]

Sure it is an attack. It is an argument against me personally rather than addressing the issues. Your problem is you haven't met many MD's (or anyone) who is willing to challenge your knowledge regarding physiology. I'll admit most MD's don't particularly care about physiology to the degree I do (it was my FAVORITE class in first year medical school, it seemed so "easy" when combined with my engineering background) then I became an ultra-marathoner and anesthesiologist (perhaps I was drawn to anesthesiology because of its strong association with physiology) and my interest continued.

Anyhow, you continue to ignore the issues of this discussion preferring to talk about me personally. You have yet to explain what you believe is going on at VO2max that prevents the athlete from going further. You have failed to explain how it is you believe that our ability to improve VO2max with training is explained by "hypervolemia". Really? And you accuse me of having a poor understanding of basic physiology.

I have addressed the issues comprehensively. You have addressed nothing with science. You just keep repeating the same errors over and over and when you try to argue that the science is wrong you make more errors. You are the one who has left yourself open to attack by not supporting your views with published science, then posting many statements regarding physiology that are grossly incorrect, then when people point out those errors you criticize their understanding of physiology and refer to yourself as an expert whose knowledge and training is better than everyone else.

As I stated before, it makes no difference whether I am qualified or you are, on an internet forum we might aswell assume nobody is qualified, so the best way to discuss a scientific topic such as the limits to VO2max is BY REFERRING TO THE SCIENTIFIC LITERATURE. You keep refusing to do that.

I have referred to the science on many occasions and your only response is that the scientists conducting the research don't know what they are talking about. So in essence you making an ad hominen attack on those scientists.

Pot kettle black. You can't say that someone else doesn't understand the physiology, then cry foul when someone else points out that YOU don't understand the physiology yourself.

 

[Krebs cycle]

Let me add a new physiology topic to be discussed. This has been alluded to in the VO2max thread but it really is a different topic in my opinion. Anyhow, as mentioned in the VO2max thread there is almost always a low level of lactic acid around even under what is considered fully aerobic conditions. The question is: How does one explain this? Is there a biochemical pathway in the cells that can result in lactic acid being formed that doesn't require anaerobic metabolism? I haven't heard of one. If there is, what is it? If there isn't, how does one explain the formation of lactic acid in the absence of anaerobic conditions? (I think I can do it but I will await the explanation of others.)

The problem is that you keep referring to "anaerobic metabolism" as if it means that this only occurs when there isn't enough oxygen around. Without bothering to go to the literature and read about the mechanisms that underlie the lactate threshold, you decided to make up your own little story about it.

So you invented this little "explanation" about the end capillary pO2 dropping to zero and hence those muscle fibres being perfused by the end capillary start going "anaerobic".

But there is no evidence for this little imaginary story you invented in the scientific literature. It is very easy to disprove though by asking the question "is venous pO2 zero above the lactate threshold?". The answer to that question is a definitive NO. We could also ask is venous HbO2 saturation zero? The answer to that question is also a definitive NO.

The reality is that the term "anaerobic metabolism" does not even refer to a scenario in which the pO2 in the end capillary or the muscle fibre is zero. It does not mean there is NO OXYGEN present. What this term actually means is that oxygen is NOT REQUIRED to produce the ATP. A biochemist would refer to this as "substrate level phosphorylation" whereas they would call aerobic ATP synthesis "oxidative phosphorylation".

The question you are really asking is the following:

What causes the rate of substrate level oxidation to rapidly increase while in the presence of oxygen?

2 events occur here 1) PCr breakdown supplies enough ATP for a few seconds of "anaerobic ATP synthesis" and 2) increased glycolytic flux... which results in elevated lactate production

So the question thus becomes... what increases the glycolytic flux and therefore lactate production?

The answer is NOT a lack of oxygen. The correct answer is increasing sympathetic activation. This is a feedforward mechanism. The conscious effort required to exercise at higher intensity increases sympathetic activation, this in turn increases glycolytic flux and lactate production. If we recruit fast twitch fibres which have very high level of glycolytic enzymes but low mitochondrial density, then there is going to a lot of pyruvate being formed and not enough mitochondria around to oxidise it. This mismatch doesn't occur because oxygen supply to the mitochondria starts to decrease as a result of your fairy world end capillary zero pO2 hypothesis, it occurs because the rate of glycolysis is simply too high and the mitochondrial density is too low.

 

[Krebs cycle]

Krebs, seeing you clearly have an excellent and up to date understanding of exercise physiology I am wondering if you have any thoughts on the underlying physiology of some of the metrics used in racing and training with a power meter such as Normalized Power, Training Stress Score, Chronic and Acute Training Load and Training Stress Balance.

All of these training load metrics use the same basic premise that was originally proposed by Banister when he came up with his TRIMP idea... ie: apply some weighting factor to higher intensity exercise.

In each case the weighting factor is curvilinear, as you know, normalized power for example raises the wattage by the power of 4, averages it and then takes the quad root. Thus any time spent at higher power is given a much higher weighting. Other methods use a 3rd order polynominal which approximates the shape of a lactate curve (see Mujika et al. Modelling training responses in swimmers. MSSE 1996).

The difficulty with all training metrics is knowing whether the shape of this curvilinear relationship between power output and physiological stress accurately reflects the actual physiological stress on any given individual. What I suspect is that the shape of the intensity weighting curve can be different for different individuals and also different within an individual depending on the training history. It could be different within an individual depending on recovery or illness and I definitely think it is different for different modes of exercise eg: running vs cycling. Clearly there is a biomechanical impact load in running that isn't present in cycling.

Furthermore, it is obvious that two different training sessions with the same normalized power or training stress score may not induce the same physiological adaptation ie: a 150km aerobic base ride isn't the same as a high intensity interval session despite having the same TSS score. I think useful measures are things like the total amount of time spent above FTP or VO2max power and then make decisions based on the training history of the athlete.

At the end of the day, there is no training metric that is better at telling you how fatigued or fresh your athlete is than simply asking the athlete themselves. For all the cutting edge sport science monitoring that is going on around the world (esp professional team sports), creating a culture of honesty in subjective reporting is critical. The only place that literally ALL of the physiological information is being compiled is inside the individual's brain. Get into the habit of asking what the RPE is during training on a regular basis... like every training session basically.

 

[CoachFergie]

At the end of the day, there is no training metric that is better at telling you how fatigued or fresh your athlete is than simply asking the athlete themselves. For all the cutting edge sport science monitoring that is going on around the world (esp professional team sports), creating a culture of honesty in subjective reporting is critical. The only place that literally ALL of the physiological information is being compiled is inside the individual's brain. Get into the habit of asking what the RPE is during training on a regular basis... like every training session basically.

Many thanks, that is some excellent advice.

 

[sciguy]

Frank,

You've alluded to your "Engineering background" a number of times in the past. Do you hold a degree in engineering and if so what branch and from what institution? Just trying to understand where you're coming from a bit better.

Hugh