I’m going back to Maxwell’s equations and Schrodinger now
I’ll take Occhams Razor for 600, Alex.
Frank, first you said:
For those of you who advocate that exercise is limited by the heart and lactate has nothing to do with it how do you explain this finding?
Then you said:
VO2 max is VO2 max because it is limited by something
I boldfaced some of those words for clarification. I agree with Dr. Coggan that you can’t seem to decide what you’re arguing about. Is it VO2 max (a measure of how much oxygen your body can suck out of the air) or athletic performance (athletic performance). They are not the same thing.
What is the limiter that determines VO2 max? That is the question. Now, some might argue that VO2 max plays a role in determining athletic performance (edit: and VO2 max is determined during exercise), but that is not the question. What happens that prevents the athlete from exercising harder to further increase how much oxygen they can uptake and burn. What is the limiter? What starts the cascade towards failure?
Have you guys see Liar Liar with Jim Carey? Remeber the scene where he’s in the bathroom beating himself up, slamming the toilet seat on his head, running into the wall, putting soap in his own eyes, etc. The other guy comes in and says “what are you doing?” and he replies in a crazy voice, “I’m Kicking my ass”…
Sometimes people start a new thread and I envision that scene 
No I am not.
Last time I checked the heart was an “organ”, not “tissue” or “cells”.
And organs are generally made up of different tissues and cell types. And only a small fraction of those are “Exposed” to blood.
A little complicated, I know
Boy, was my medical school education lacking. Thank you for pointing that out to me again. Perhaps you could enlighten me as to some of the tissues and cell types that are are not “exposed” to blood. And, at the same time enlighten me as to how they stay alive. Thanks in advance for the lesson.
I usually make it to page 2 before ignoring these threads, but this is the first time I’m bailing after 3 posts…
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e’s not dead. e’s resting…
LOL… classic.
frank,
here is a paper from the JAP that you might be interested in reading. deals with art-hypoxemia, cycling and peripheral muscle fatigue.
i’ve uploaded it to yousendit @ http://download.yousendit.com/6A6DF1110FE69B0C if you want to read the fulltext. otherwise, here is the name:
Arterial oxygenation influences central motor output and exercise performance via effects on peripheral locomotor muscle fatigue in humans - Markus Amann, Marlowe W. Eldridge, Andrew T. Lovering, Michael K. Stickland, David F. Pegelow and Jerome A. Dempsey J. Physiol. 2006;575;937-952; originally published online Jun 22, 2006; http://jp.physoc.org/cgi/content/full/575/3/937
I happen to work with one of the authors, in case you have any further questions. Maybe some reading on other papers by Stickland would help clear things up, as he’s done a lot of work on art-hypoxemia and cycling
my favourite part is figure 3 - where by eliminating arterial hypoxemia, they increase time to fatigue…which goes to show that maybe o2 might just have a role to play in exercise performance…
frank,
here is a paper from the JAP that you might be interested in reading. deals with art-hypoxemia, cycling and peripheral muscle fatigue.
i’ve uploaded it to yousendit @ http://download.yousendit.com/6A6DF1110FE69B0C if you want to read the fulltext. otherwise, here is the name:
Arterial oxygenation influences central motor output and exercise performance via effects on peripheral locomotor muscle fatigue in humans - Markus Amann, Marlowe W. Eldridge, Andrew T. Lovering, Michael K. Stickland, David F. Pegelow and Jerome A. Dempsey J. Physiol. 2006;575;937-952; originally published online Jun 22, 2006; http://jp.physoc.org/cgi/content/full/575/3/937
I happen to work with one of the authors, in case you have any further questions. Maybe some reading on other papers by Stickland would help clear things up, as he’s done a lot of work on art-hypoxemia and cycling
my favourite part is figure 3 - where by eliminating arterial hypoxemia, they increase time to fatigue…which goes to show that maybe o2 might just have a role to play in exercise performance…
I look forward to reading it. However, let me say this before I read it.
Of course, O2 saturation drops at high intensities. Increased extraction at the periphery will magnify any ventilation perfusion defects in the lungs and increasing inspired oxygen of course will increase the amount of oxygen delivered to the tissues and extend the amount to time to failure (just as reversing the acidemia increased time to failure as reported by Nielsen: “When infusion of sodium bicarbonate maintains a stable blood buffer capacity, acidosis is attenuated and SaO2 increases from 89% to 95%. This enables exercise capacity to increase, an effect also seen when O2 supplementation to inspired air restores arterial oxygenation. In that case, exercise capacity increases less than can be explained by VO2 and CaO2. Furthermore, the change in muscle oxygenation during maximal exercise is not affected when hyperoxia and sodium bicarbonate attenuate desaturation.”). But, increasing the arterial oxygen content doesn’t prevent failure so that suggests to me that the initiator of this problem is not the drop in oxygen concentration but something else. What is that something else? So, can’t we conclude, the drop in oxygen concentration is a symptom, not the cause? Can’t we conclude, since the muscle oxygen concentration doesn’t change when acidosis is corrected or oxygen desaturation is corrected, that the problem really is mitochondrial oxygen concentration which is determined by the combination of end (or near end) capillary oxygen concentration (not arterial oxygen concentration delivered to the muscle), the need for oxygen, and the diffusion distance (what is the capillary concentration?).
**
“you could enlighten me as to some of the tissues and cell types that are are not “exposed” to blood. And, at the same time enlighten me as to how they stay alive. And, at the same time enlighten me as to how they stay alive…”
All I can say is:
Wow!
Sure, you make me a firm believer in the fact that every single cell in your body has its own blood supply.
Your brain must be ouzing lactic acid right now
a line from the paper i cited before:
“the exercise-induced HbO2 de saturation was primarily due to a rightward shift in HbO2 de saturation curve, 57% of which can be accounted for by progressive metabolic acidosis, and the remainder by the increase in temperature”
i see your point about how it (increased SaO2) doesn’t stop fatigue; however, it does prevent fatigue (delayed onset). I think we’re trying to over-simplify the whole discussion down to a single factor, while in all actuality, it’s a hell of a lot more complicated (hence why there are researchers still employed)
are you familiar with O2 conformer and the Net Drive effects? (a way of tying metabolism into the big picture)
*"*Can’t we conclude, since the muscle oxygen concentration doesn’t change when acidosis is corrected or oxygen desaturation is corrected, that the problem really is mitochondrial oxygen concentration which is determined by the combination of end (or near end) capillary oxygen concentration (not arterial oxygen concentration delivered to the muscle), the need for oxygen, and the diffusion distance (what is the capillary concentration?)."
isn’t capillary o2 content determined by arterial o2 content? increased artery o2 content = increased gradient = increased content in capillaries - this flows down to increased mitochondrial o2 content. flow modeling would predict this.
just some thoughts
a line from the paper i cited before:
“the exercise-induced HbO2 de saturation was primarily due to a rightward shift in HbO2 de saturation curve, 57% of which can be accounted for by progressive metabolic acidosis, and the remainder by the increase in temperature”
i see your point about how it (increased SaO2) doesn’t stop fatigue; however, it does prevent fatigue (delayed onset). I think we’re trying to over-simplify the whole discussion down to a single factor, while in all actuality, it’s a hell of a lot more complicated (hence why there are researchers still employed)
are you familiar with O2 conformer and the Net Drive effects? (a way of tying metabolism into the big picture)
I have spent a little time reading the paper. I am not familiar with all the tests they are doing so it is a struggle for me to make sense of some of what they are doing. However, I do have some substantial criticism of the paper. What they wanted to do seemed worthwhile but they missed a big opportunity I think. Why on earth they didn’t measure end tidal CO2 bothers me. It would have been very simple to do in view of their set up, probably only had to turn on an instrument, or it may have even been there and they decided it wasn’t important. VCO2 as it relates to VO2 would have been interesting to know here. Second, I am not sure why they chose FIO2=1 in their hyper state. An FIO2 of 1 can actually worsen lung function. And, why did they measure SaO2 when transcutaneous oxygen concentration probes are both accurate (under most instances) and readily available. that data would be much more valuable here. further, I don’t understand how they came to make this statement on page 121: “However, with FIO2 1.0 vs. FIO2 0.21, both determinants contributed about equally to CaO2: 1.1 ml/dl was gained by maximizing Hb saturation, and 1.5 ml/dl was gained by the increase in PaO2”. I have been away from this for awhile but I calculated the increase from dissolved oxygen to be less than .3 ml/dl, not 1.5 ml/dl. Dissolved oxygen is usually considered to be such an insignificant number it can be effectively ignored even at 100% O2.
I am not familiar with the terms O2 conformer and Net Drive effects but I suspect I understand the theory as my way of looking at this problem certainly requires analyzing metabolism.
*"*Can’t we conclude, since the muscle oxygen concentration doesn’t change when acidosis is corrected or oxygen desaturation is corrected, that the problem really is mitochondrial oxygen concentration which is determined by the combination of end (or near end) capillary oxygen concentration (not arterial oxygen concentration delivered to the muscle), the need for oxygen, and the diffusion distance (what is the capillary concentration?)."
isn’t capillary o2 content determined by arterial o2 content? increased artery o2 content = increased gradient = increased content in capillaries - this flows down to increased mitochondrial o2 content. flow modeling would predict this.
Capillary O2 content varies along the length of the capillary as diffusion out occurs along the entire length. Only at the very beginning before any oxygen diffuses out is capillary oxygen content equal to arterial oxygen content. The limiting factor for cellular respiration is the capillary oxygen content at the end of the capillary where oxygen content is lowest and then combined with the distance to the furthest mitochondria, combined with the demand for oxygen. Oxygen is delivered through this distance by diffusion. The amount that can be delivered is limited by the gradiant from the lowest concentration in the capillary along it’s length and the diffusion distance to the furthest mitochondria. When this is exceeded anaerobic metabolism will begin, even though most mitochondria will still be aerobic. As one continues to push things, more and more mitochondria go anaerobic until the burden exceeds the bodies ability to compensate. One effect of training of course is to make new capillaries. The higher the capillary density the less the distance to the furthe so more oxygen can be delivered (my, isn’t it interesting that one of the effects of training is capillary density goes up with training, as does performance).
just some thoughts
Thanks for your thoughts. it is nice to be able to discuss some of these issues on what the literature actually says without getting into a pissing contest as to what it is supposed to say.
o2 conformer and net drive, as a summary, basically state that with more O2 present, more force is produced (at constant motor unit recruitment). This is mainly due to the fatigue-inducing byproducts that are produced (La-, NADH- and ADP) as a result of anaerobic metabolism. (i have some ppt lectures from last year that explain it much better than i ever could)
in a voluntary exercise, you can increase motor drive, which will allow the same force production, but will also increase fatigue markers (those same metabolic byproducts). or, you can keep the same motor drive (same RPE), but will be slower (decreased force). essentially what the study shows - with more O2, you’re faster.
so…essentially, reduced O2 (due to cardiac function, reduced partial pressure, decreased Hb/Hb saturation) leads to increased fatigue-inducing byproducts (La-, NADH-, ADP - byproducts of anaerobic metabolism), which will result in decreased force/performance, increased fatigue (or RPE @ the same work rate), and therefore, decreased performance.
I think the biggest problem with the thread is that the title isn’t actually correct…as I said before, human performance is limited by a whole number of factors that all tie in together.
increased fitness = increased Hb content (o2 carrying cap), increased capillary density (increased SA for diffusion), increased pulmonary and cardiac function, increased La- clearance, and a whole whack of other things. Trying to pin “performance” in general on any one of those things is a pretty big task, and I don’t think that it can or will be done any time soon. It’s not exactly a simple issue.
As for the issues with the paper, I’m not super familiar with their study protocol yet, but will hopefully become familiar in the coming months and will be able to share some insight as I start my own research in (hopefully) a similar area…at which point I’ll be able to shed some more light on the issue!
No I am not.
Last time I checked the heart was an “organ”, not “tissue” or “cells”.
And organs are generally made up of different tissues and cell types. And only a small fraction of those are “Exposed” to blood.
A little complicated, I know
I think small fraction is a gross oversight on your part. More like damn near all cells are exposed to O2.
Last time I checked, O2 was pretty essential to aerobic metabolism, the major source of energy in the human body.
I’ve got nothing to add but my friend Yucko does!!
LOL… I got banned for less, let’s watch…
It wasn’t me… my friend Yucko has a BIG problem with Frank and his incredibly transparent, uninformed, predictable posts.
I, on the other hand, find his posts incredibly illuminating, mentally stimulating, and right on target.
Drunken clowns have a lot of baggage!
o2 conformer and net drive, as a summary, basically state that with more O2 present, more force is produced (at constant motor unit recruitment). This is mainly due to the fatigue-inducing byproducts that are produced (La-, NADH- and ADP) as a result of anaerobic metabolism. (i have some ppt lectures from last year that explain it much better than i ever could)
in a voluntary exercise, you can increase motor drive, which will allow the same force production, but will also increase fatigue markers (those same metabolic byproducts). or, you can keep the same motor drive (same RPE), but will be slower (decreased force). essentially what the study shows - with more O2, you’re faster.
so…essentially, reduced O2 (due to cardiac function, reduced partial pressure, decreased Hb/Hb saturation) leads to increased fatigue-inducing byproducts (La-, NADH-, ADP - byproducts of anaerobic metabolism), which will result in decreased force/performance, increased fatigue (or RPE @ the same work rate), and therefore, decreased performance.
Thanks for the reply. I hope my response is not too rambling or impossible to understand. I am not sure I understand the practical significance of the O2 conformer or net drive theories for the athlete as cellular oxygen concentration is almost impossible to legally manipulate. Further, how can such a theory explain all of the world records that are set at altitude, where cellular oxygen concentrations would be lower than at sea level. It would seem to me that it could just as easily be argued that “fatique-inducing byproducts” are not so much a interfering with performance because low oxygen caused them to be there but, rather, poor perfusion does not take them away rapidly. Of course, both conditions (low oxygen and poor flushing of by products) are caused by the same condition, poor perfusion. Which is more important?
I think the biggest problem with the thread is that the title isn’t actually correct…as I said before, human performance is limited by a whole number of factors that all tie in together.
increased fitness = increased Hb content (o2 carrying cap), increased capillary density (increased SA for diffusion), increased pulmonary and cardiac function, increased La- clearance, and a whole whack of other things. Trying to pin “performance” in general on any one of those things is a pretty big task, and I don’t think that it can or will be done any time soon. It’s not exactly a simple issue.
As for the issues with the paper, I’m not super familiar with their study protocol yet, but will hopefully become familiar in the coming months and will be able to share some insight as I start my own research in (hopefully) a similar area…at which point I’ll be able to shed some more light on the issue!
The thread got its name from several long and heated discussions of this very topic with one group taking the view that the heart is what stops further increases in VO2 uptake (based upon evidence that the CO drops at VO2max even though they could not give a mechanism for such a drop, the drop alone was all they needed to make this claim) whereas I argued the view that the changes that cause the cardiac output to drop at VO2max come from the periphery, specifically from exercising muscle that have gone anaerobic.
While I tend to agree that what is going on is multifactorial it seems to me that we are rarely so balanced that all of these potential sources of failure would fail at the exact same time but, rather, it seems to me, that it is more likely that one element would fail first and as other elements try to compensate for this failure, they are also thrown into failure. Something has to initiate the cascade. I believe the most obvious explanation for what occurs is anaerobic metaboism overwhelming buffer and compensatory mechanisms causing changes in pH resulting in reduced muscular function. That is how i would explain the drop in CO seen at VO2max.
One other thing, increasing fitness does not usually result in increasing Hb concentration. Plasma volume does increase which will normally decrease Hb concentration. Anyhow, all of the changes tend to increase the ability to deliver oxygen to the cells and increase the ability to remove byproducts of metabolism.
I must say the article does set me thinking I might be wrong in one aspect in my theory. Table two on page 124 indicates that minute ventilation at VO2 max is 25% greater for the hypoxic condition than normoxic (although the absolute numbers seemhigh for what I thought remember). Anyhow, I had previously theorized that the end condition came about because of lactic acid being bufferred by the bicarbonate system, increasing the production of CO2 beyond what could be exhaled, causing a change in ph and, hence, a change in muscle function. If it is really possible to increase minute ventilation 25% over what can be done at VO2max during normoxia then that is clearly wrong. I am not sure I am convinced such increases are really possible but that is what the table says. It might be possible if the reduction in oxygen occured because of reduced atmospheric pressure and normal oxygen concentrations (or if helium is substituted for nitrogen) but I doubt these investigators did this.
I was looking back at some lecture notes from this year titled Convective and Diffusive O2 Transport Limitations to Peak Muscle Aerobic Power Output (I’ve sent them to you in a PM)
But the major points on slide 3 are:
1.Peak convective oxygen delivery to the exercising muscle in whole body exercise is ultimately limited by the capacity of cardiac output to match exercising muscle vasodilation (Blood Pressure Regulation)
2.Peak diffusive oxygen flux to the mitochondria is ultimately limited by factors determining the diffusive conductance for oxygen, and the O2 pressure gradient for diffusion from capillaries into the muscle fibres
3.Peak oxygen consumption CAPACITY is ultimately limited by the number of mitochondria (i.e. if there is no limitation to substrates, then the number of enzymes determines the rate of a reaction)
where convective delivery is heart-to-muscle via arteries, and diffusive flux is capillaries to cell
Additionally:
Determinants of Peak Cardiac Output •Heart rate increases linearly with exercise intensity
•Stroke volume increases linearly with exercise intensity up to ~50% peak exercise intensity. Thereafter it may plateau, continue to increase at a lower SV per work rate change, or even decline from heavy to peak exercise intensity
•Peak heart rate can vary between individuals but cannot be altered within an individual
•Heart size and structural characteristics determining end diastolic volume can vary between individuals and can be altered
the limitation on SV to increase will limit CO at Vo2max, and at very close to maximal exercise, may cause a decrease in CO (less filling time at high HR = less SV @ same HR = less CO) - due to the pericardium (again, see lecture notes - lecture 16, slide11 …i’d copy and past the link to the study, but it’s late, and i can’t paste the graphic.)
anyway…that’s a start…now i’m rambling.