In other words, the ability of the mitochondria to process oxygen far exceeds oxygen supply. Which is why blood packing works a treat, and so does dosing with EPO.
Some LetsRunners are just learning today what grade nine science students have been taught for decades! Oh, the excitement.
Aghast wrote:
The limiting factor is delivery NOT the rate at which the mitochondria can reduce oxygen
http://www.ncbi.nlm.nih.gov/pubmed/10647532
End of thread, troll diffused
Aghast wrote:
The limiting factor is delivery NOT the rate at which the mitochondria can reduce oxygen
http://www.ncbi.nlm.nih.gov/pubmed/10647532
In mostly untrained individuals that is true. Most EPO users don't fit that group. It is true that VO2Max at lower levels is mostly not limited by mitochondrial processes, however long term improvement in VO2Max does tend to come from improvements in this area, rather than O2 delivery/cardiac output.
It seems reasonable to assume that the type of athletes that use EPO have already maxed out the non-peripheral VO2Max mechanisms and are in the area where mitochrondrial processes DO become part of the limitations on further increases.
From the full article:
"there is some evidence that the increase in mitochondria play a permissive role in allowing V ̇O2max to increase. Holloszy and Coyle (44) note that the lowest value for SDH activity in the elite runners studied by Costill (16) was still 2.5-fold greater than that found for untrained individuals in the same study. The increase in muscle mitochondria may allow a slightly greater extraction of O2 from the blood by the working muscles, thus contributing in a minor way to increased V ̇O2max"
In other words in elite athletes who have presumably close to maxed out their Vo2max, mitochrondria are at least somewhat limiting, otherwise increasing their number would not increase Vo2max at all.
And from the wikipedia article on v-o oxygen difference (an indication of the rate at which oxygen is extracted from the blood, i.e. peripheral efficiency):
"Research has shown that following the commencement of exercise there is a delay in the increase of the a-vO2 diff, and that a-vO2 diff only has a marginal impact in the total change in VO2 in the early stages of exercise. The bulk of the early increase in oxygen consumption after a sudden change in exercise levels results from increased cardiac output.[4] However it has also been found that the increase in the maximal a-vO2 diff resulting from adaptations to a physical training program can account for most of the difference in VO2 max in subjects participating in sub-maximal exercise"
So again, as vo2max reaches maximum, it is not cardiac output/oxygen carrying properties of the blood, but the rate of the extraction of that oxygen that becomes most important.
The fact is, that from a scientific research point of view, the verdict is still out on whether elite athletes get significant performance benefits from EPO administration.
However, EPO is highly recommended for sedentary runners with Kidney disease if they want to run a decent 5000m in a few weeks :-)
Aghast wrote:
This basic stuff- how can you not understand?
Oxygen delivery = cardiac output x the arterial oxygen content
At rest oxygen delivery greater than oxygen requirements.
During exercise oxygen requirments increase so oxygen delivery is increased by increasing cardiac output. However if arterial oxygen content is higher to begin with then cardiac output does not have to be increased as much to deliver the same amount of oxygen.
In other words, with EPO you can do the same amount of work with a lower heart rate.
So we agree that exogenous EPO lowers the heart rate for a given oxygen uptake.
However, that also means that maximum heart rate is lowered also, thus there is no net gain.
So the question still remains: what is the supposed mechanism by which exogenous EPO improves performance?
Your logic is faulty. From where are you drawing the conclusion that the max heart rate is decreased?
unbrainwashed wrote:
So we agree that exogenous EPO lowers the heart rate for a given oxygen uptake.
However, that also means that maximum heart rate is lowered also, thus there is no net gain.
So the question still remains: what is the supposed mechanism by which exogenous EPO improves performance?
Aghast wrote:
The limiting factor is delivery NOT the rate at which the mitochondria can reduce oxygen
http://www.ncbi.nlm.nih.gov/pubmed/10647532
It has to be oxygen demand by the muscles, not delivery.
Also, the authors are using circular reasoning to say that blood doping increases VO2max. As does everyone who says that blood doping/EPO doping increases oxygen delivery.
The dogma runs thus:
Q: How does blood doping/EPO doping increase oxygen delivery?
A: Because there are more red blood cells delivering oxygen?
Q: And how does more RBCs than normal deliver more oxygen?
A: Because more RBCs carry more oxygen in the blood?
Sadly it seems that almost everyone is brainwashed by this dogma, but unable to explain the supposed mechanism without resorting to circular reasoning.
Mob wrote:
Your logic is faulty. From where are you drawing the conclusion that the max heart rate is decreased?
unbrainwashed wrote:So we agree that exogenous EPO lowers the heart rate for a given oxygen uptake.
However, that also means that maximum heart rate is lowered also, thus there is no net gain.
So the question still remains: what is the supposed mechanism by which exogenous EPO improves performance?
The max heart rate is decresed by the increase in blood volume.
remind us again why elite cyclists use EPO. for the placebo effect?
Sadly you didn't read the abstract because you don't understand the authors logic. It is frustrating arguing with fools / trolls.
unbrainwashed wrote:
Aghast wrote:The limiting factor is delivery NOT the rate at which the mitochondria can reduce oxygen
http://www.ncbi.nlm.nih.gov/pubmed/10647532It has to be oxygen demand by the muscles, not delivery.
Also, the authors are using circular reasoning to say that blood doping increases VO2max. As does everyone who says that blood doping/EPO doping increases oxygen delivery.
The dogma runs thus:
Q: How does blood doping/EPO doping increase oxygen delivery?
A: Because there are more red blood cells delivering oxygen?
Q: And how does more RBCs than normal deliver more oxygen?
A: Because more RBCs carry more oxygen in the blood?
Sadly it seems that almost everyone is brainwashed by this dogma, but unable to explain the supposed mechanism without resorting to circular reasoning.
Why does it have to be oxygen demand and not delivery? Why can't delivery be insufficient to supply the oxygen demand?
unbrainwashed wrote:
Aghast wrote:The limiting factor is delivery NOT the rate at which the mitochondria can reduce oxygen
http://www.ncbi.nlm.nih.gov/pubmed/10647532It has to be oxygen demand by the muscles, not delivery.
Also, the authors are using circular reasoning to say that blood doping increases VO2max. As does everyone who says that blood doping/EPO doping increases oxygen delivery.
The dogma runs thus:
Q: How does blood doping/EPO doping increase oxygen delivery?
A: Because there are more red blood cells delivering oxygen?
Q: And how does more RBCs than normal deliver more oxygen?
A: Because more RBCs carry more oxygen in the blood?
Sadly it seems that almost everyone is brainwashed by this dogma, but unable to explain the supposed mechanism without resorting to circular reasoning.
From the article posted earlier are studies which totally destroys your arguments:
This pulmonary limitation in highly trained athletes can be overcome with O2-enriched air. Powers et al. (65) had highly trained subjects and normal subjects perform two VO2max tests. In one test the subjects breathed room air and in the other they breathed a 26% O2 gas mixture. On hyperoxic gas, the highly trained group had an increase in VO2max from 70.1 to 74.7 mL·kg-1·min-1 and an increase in arterial O2 saturation (SaO2) from 90.6% to 95.9% during maximal work. None of these changes were observed in normal subjects (VO2max = 56.5 mL·kg-1·min-1).
Gledhill (35,36) completed comprehensive reviews of 15–20 studies that have examined the effects of blood doping. Reinfusion of 900–1,350 mL blood elevates the oxygen carrying capacity of the blood. This procedure has been shown to increase VO2max by 4–9% in well designed, double-blind studies (35,36)
Pulmonary limitation? What pulmonary limitation? And why does this have to be overcome? Well trained athletes have the oxygen carrying capacity they need. If they needed more, then surely they would produce more red blood cells wouldn't they?
Tell my why elite athletes naturally have hematocrits of 42% or less? Go on tell me, I insist you give me a seriously considered answer. Tell me why Haile Gebreselassie and Renato Canova's athletes have hematocrits of 40%?
Yes hyperoxic gas will increase oxygen uptake and those figures you quoted are proportional to the 02 saturation level, and hypoxia will reduce it oxygen uptake but that is irrelevant to low altitude racing.
As for studies showing increased VO2max with blood reinfusion, I am sure that is the result they were looking for, but did you know that VO2 fluctuates at a given pace and often goes down during the early acceleration of incremental tests? Why is that?
Aghast wrote:
From the article posted earlier are studies which totally destroys your arguments:
This pulmonary limitation in highly trained athletes can be overcome with O2-enriched air. Powers et al. (65) had highly trained subjects and normal subjects perform two VO2max tests. In one test the subjects breathed room air and in the other they breathed a 26% O2 gas mixture. On hyperoxic gas, the highly trained group had an increase in VO2max from 70.1 to 74.7 mL·kg-1·min-1 and an increase in arterial O2 saturation (SaO2) from 90.6% to 95.9% during maximal work. None of these changes were observed in normal subjects (VO2max = 56.5 mL·kg-1·min-1).
Were you aware that the "highly trained" group was deliberately selected based on the fact they showed EIH (exercise induced hypoxia), i.e. their %SaO2 was less than or equal to 92% during exercise? This seems to select for a group that is most likely to benefit from O2 supplementation, and not surprisingly they saw Vo2Max increases. Note that at Av Vo2Max of 70.1 , the highly trained group is very fit, but still probably sub-elite, although elite's can have Vo2Max in that range, but that is partly why Vo2Max is a poor predictor of race performance.
There is no question that cardiac output/blood oxygen availability is part of what limits Vo2Max, the question these studies don't answer is, at the elite level where drug use starts to matter, is this still a significant limiter?
Consider
http://www.ncbi.nlm.nih.gov/pubmed/22567828"When PO2 (Plasma O2) approaches plateau of the VO2-PO2 relationship, an increase of VO2 is restricted by mitochondria capacity to accumulate oxygen and augmented oxygen delivery will not lead to a significant increase of muscle VO2". In other words there is a point at which blood O2 level increases plateau Vo2max, and further blood o2 stops increasing Vo2max. It is not unreasonable to assume that elite level athletes may well have reached this plasma O2 plateau, in which case EPO or any other method of increasing plasma o2 carrying ability may indeed be a placebo.
noce wrote:
remind us again why elite cyclists use EPO. for the placebo effect?
Probably not, but if it was, it wouldn't be the first time elite athletes took "supplements" that had no real impact on their performance.
Cyclists who compete in multi-day tour like events are the endurance athletes MOST likely to benefit from methods which improve the O2 carrying ability of blood. These athletes , when undoped, exhibit reduced hematocrit volumes through the period of their event. This means that like other populations with compromised hematocrit levels (such as those EPO is medically used on), they will likely receive some benefit by maintaining the oxygen carrying ability of their blood across the course of the event. The ability to maintain high hematocrit across a tour is one of the flags the drug testers look for.
Similar issues might apply to endurance runners, and their training, and in theory a runner could train at a higher level across time by doping, avoiding the easy/hard modulation of training clean runners are forced to use, but the oxygen carrying system isn't the only one, and other parts of the body might break under such a long term training strategy. Of course there are different drugs for those bits :-)
hammer and tongs wrote:
Reminder: Cathal Lombard, admitted EPO cheat, improved from 30:30 to 27:30 in the 10k and 14:30 to 13:18 in the 5k at age 28, after already training at a high level for many years. Cite all the scientific jargon you want. Any rational person realizes this kind of improvement cannot be due to placebo.
If given a choice between placebo or the drug, this level of improvement can only be due to placebo. If EPO was this effective basically any D1 runner could be making US olympic teams.
This is either really funny or you are a shockingly ignorant person.
EPO is that effective. Not many, if any, D1 athletes are willing to cheat, let alone able to cheat. What is so hard to understand about that? There are dozens of cyclists who have had Cathal Lombard type improvement due to EPO, blood packing, and other doping protocols. I'm sure none of that stuff works, though. It's just the placebo effect.
common, you are just repeating the dogma. EPO works as a placebo, it's all in the athletes head.
As Henry Ford said: Whether you think you can, or you think you can't--you're right.”
Repeating your opinion ad nauseum does not count as making an argument.
unbrainwashed wrote:
common, you are just repeating the dogma. EPO works as a placebo, it's all in the athletes head.
As Henry Ford said: Whether you think you can, or you think you can't--you're right.”
You should give your info to Armstrong. That would be a great defense.
"Yes I took EPO, but look it's really makes NO DIFFERENCE it's just a placebo! I could just have been shooting up sugar water and had the same effect."
unbrainwashed wrote:
common, you are just repeating the dogma. EPO works as a placebo, it's all in the athletes head.
As Henry Ford said: Whether you think you can, or you think you can't--you're right.”
You are obnoxiously persistent. Fine, let's skip to the big question. If EPO provides ONLY a placebo effect (not sure if you've every blatantly said that but you seem to be implying it) then should it be banned from international competition or not?
