Lance v. Lemond - Lemond comes clean?

[Big Doopie]

Personally, I think Greg was totally drugfree. I think that he's honest when he says he loves the sport of cycling very much and hates the fact that there is so much ped use now. Now it's not a matter of 'just' using amphetamines or 'just' steriods, it's the whole package, steroids, testosterone, hgh, epo, and blood transfusions(did I miss anything?).

I think as a fellow American cyclist Greg is particularly disgusted that LA cheats and builds this wild myth of miracles around himself. Look how disgusted many of us are about LA? Think how much more, a CLEAN champion, is P.O.ed and disgusted? I do not see Greg as being bitter at all, except perhaps towards a system contaminated by doping when he did what he did clean.

But, what can we expect when the 'head' of cycling(UCI)is so corrupt?the rest of the body must follow.

I think LA accusing Greg of doping is an act by a desperate narcissistic man.

excellent post. +1.

 

[Ferminal]

Associated Press -
Lance Armstrong's lawyer: 'Stop leaks'



And my favorite part:

Nice use of 'investigation', I guess that proves it's illegitimate.

 

[MacRoadie]

The letter notes that after seeing some of the leaks in the media, Herman requested a meeting with Miller but that the prosecutor refused to discuss investigation theories or general topics.

Didn't ignore the request, refused it.

That would be an eff you.

 

[Krebs cycle]

I would check your equipment because, I have seen much less than 100's, but the ones I have seen were tested by lab groups with a lot of publications, that take a lot of care in what they do.

Here you are accusing the AIS physiology dept of sloppy lab standards.

Yet the variance I have seen is much greater than that. Similarly, if you look at wattage in the off season, that can be 20% (or more) lower than in peak form. You think there is no change in VO2max? It's all threshold increasing as a percentage of VO2max? Lemond himself says it depends on training status in the quote you use. Presumably because he has seen in-season out-of-season variation in his own results. Or perhaps because he has seen it in others.

You are putting words in my mouth. I never said that wattage doesn't vary and I never said that VO2max doesn't vary. What I am saying is that VO2max does not vary by >15% in well trained athletes.

I guess I just imagined seeing an athlete go from ~70 to 81. I guess I fantasised being in the room at the test. I should see a shrink.

Maybe the athlete did not go to max on the first test? Maybe Greg Lemond did not go to max on the treadmill as buckwheat pointed out.

The mode specificity may be part of it. The training status may be part of it. The elevation is probably the bulk of it. Since you're the careful scientist, how did you end up throwing around the allegations of impossibility and doping? Why did you leave it to me to work out that Lemond's initial quote alluded to the location, from which you can deduce the altitude? You don't seem too careful or scientific to me.

Nowhere does it say that the 2nd test was done at sea level, but lets examine that on its own and hypothesize that it was. For starters, I'll repeat it one more time since you are cherry picking comments from my posts to make an argument where it does not exist.... I am not saying that VO2max cannot vary as a function of exercise mode and training status. I AM saying that it doesn't vary by >15%, especially when the higher value is achieved with a modality that engages less muscle mass.


Now if the 2nd test were conducted at sea level, then we are in complete agreement. The altitude has the greatest effect and a 16% difference is to be expected when we take into account the small effects of training and modality.

However, if both tests were conducted at Squaw Valley, then another very suspicious result becomes apparent. At 1900m we would expect a drop of around 10% in VO2max (many published values throughout the literature). We also know that VO2max does not recover at altitude with acclimatisation. Therefore, a score of 92ml/kg at 1900m would mean that sea level VO2max is approaching 100ml/kg.

Try convincing anyone that is physiologically possible without doping.

 

[Krebs cycle]

My point? W/o seeing the data from Lemond's original test, we have no way of knowing whether he did in fact achieve VO2max, such that it is foolish to even speculate.

Exactly correct so why did you accuse me of saying that Lemond doped?

The circumstantial evidence implicating LA goes far beyond anything that implicates Lemond, so whilst I'm 99% convinced that LA is/was a doper, I'm about 1% convinced that Lemond was. That still doesn't mean that it magically makes it possible for an endurance trained athlete to have a 16% change in VO2max.


VO2peak and VO2max are not always the same. You and realist will note that in every post I have focussed my discussion around VO2max. VO2peak is a different story.

 

[lean mean &green]

Nice, very nice. Might have to use that one myself sometime. As a scientist myself I've always considered it part of my role to make science accessible as possible to the layman. In fact even when talking to my colleagues I tend to use common vernacular. Turgid obscure jargon is in my experience largely the realm of social scientists and is a sign of inherent uncertainty. The result seems to be a need to puff up what one does by using a whole lot of bluster. Unfortunately a lot of sports scientists are the product of physical education departments which are directed primarily on pumping out teachers not scientists.

don't be too quick to blame those PE departments. the king of the "puffers" isn't even a product of them.

i mostly agree that bluster is the product of inferiority tho it has more to do with characteristics of the individual than the discipline.

 

[acoggan]

(snip)

Okay, so it appears that your understanding is deeper than implied by your previous post. I'm still waiting, however, for you to explain why you believe that the symorphisis concept applies to a particular species, much less a single individual (since it so obviously does not).

Getting back to the point at hand. Do you really believe that a well trained cyclist who is also a good runner is able to recruit SOOOOO much more muscle mass during cycling than running that it would increase his VO2 from 79 to 92ml/kg?

VO2? Yes. VO2max? Of course not.

 

[acoggan]

\In well trained athletes, VO2max simply does not vary by more than a few percent. 79 up to 92 is a 16% increase. It is an enormous change and anyone that thinks it is remotely possible obviously hasn't spent much time working with elite athletes. This is the kind of change you expect when you take a sedentary person and train them for 6-12 months.

More like a couple of weeks (numerous studies have demonstrated that VO2max increases by 5-10% per week during the initial phases of training).

 

[acoggan]

My working hypothesis is that IMO it is virtually impossible for a well trained cyclist that is also a good runner, to achieve a VO2max that is 16% higher on a bike than a treadmill.

I agree. However, what evidence is there that the results of the first test to which Lemond refers represent a true VO2max, versus a VO2peak?

 

[Realist]

So Lucia's professional cyclists went from 72.6 up to 75.2, an increase of 3.6%. That I can handle. 1.5-2% is the typical variation that one sees in VO2max in elite endurance athletes. If you were to test at the completion of a high intensity training block I wouldn't be surprised to see it go slightly above the typical error. But it is a far cry from 16%.

See this is exactly what you said:

I've tested 100s of athletes in season and out of season. VO2max remains the same or is within 1-2%. AMAZING!!

See some people would say the difference between 1% and 3.6% is 2.6%. I would call it 360%.

Funny you should mention Dave Martin, because he is one the scientists you more or less accused of having sloppy lab standards in your previous post.

I don't think the lab standards were sloppy I think you are playing fast and loose with the truth. You claimed earlier that the repeatability of your measurements is better than the error of the measurements. You are full of crap, not your lab.

I'm sorry if I put words in your mouth re: doping. I might have misinterpreted what you said and I really do take that back.

I should acknowledge that I have been sloppy using VO2max and VO2peak interchangeably - but I did this in the context of Greg Lemond's stated values, which are clearly peak VO2 results in a VO2max test, not necessarily VO2max values per se. Sorry for confusion/inaccuracy caused by this.

 

[Krebs cycle]

Okay, so it appears that your understanding is deeper than implied by your previous post. I'm still waiting, however, for you to explain why you believe that the symorphisis concept applies to a particular species, much less a single individual (since it so obviously does not).

In my mind, the symmorphosis concept characterizes the balance between cardiovascular and respiratory limitations esp. in the elite athlete. Jerry Dempsey has published a number of papers discussing the idea that cardiovascular and peripheral adaptations to endurance training far exceed the capacity of the pulmonary system to adapt. Hence, once you've achieved large increases in capillary density, mitochondrial content, blood volume, left ventricular hypertrophy etc etc you begin to encroach on the pulmonary system's capacity to transport oxygen. At this point, I believe that autonomic neural control of HR and MAP is designed to optimize VO2max given the known central limitations. Therefore, what might appear at first to be disadvantageous for oxygen transport (eg: decreasing %SaO2) might actually serve to maximise oxygen delivery. Whether or not that happens I feel is related to the structural limitations of the pulmonary system. Women tend to have smaller lung volumes compared to weight and height matched men and they also have a higher incidence of EIAH. In this case, a higher maximal HR would be more advantageous.

The point I was making about symmorphosis is that you can't simply keep increasing VO2max by increasing maximal CO and that is a structural limitation of the pulmonary system, not a peripheral metabolic one. What is REALLY interesting is that exogenous EPO and/or blood doping does increase VO2max. So what that implies is that long term feedback mechanisms serves to regulate the increase in blood volume before you reach the upper most ceiling where you simply cannot increase VO2max any further. My guess is that the additional work on the heart is that mechanism. 17 odd heart failure deaths in elite cyclists during the 1990s would appear to corroborate that theory. EPO has been shown to stimulate ANP for example. Other stressors on the heart increases both ANP and BNP. EPO production itself has been proposed to be self limiting and indeed this is part of how the EPO test "off-score" is calculated.

VO2? Yes. VO2max? Of course not.

Realist are you reading this?

 

[Krebs cycle]

See some people would say the difference between 1% and 3.6% is 2.6%. I would call it 360%.

A percent of a percent is a very bad way to express data. Will Hopkins would crucify you on that point.

3.6kg is indeed 360% greater than 1kg, but 3.6% is only 2.6% greater than 1%

Anyway, you are correct that it is possible for VO2max to change outside of the typical error and its my bad for using a little bit of (under) exaggeration re. potential for variability in VO2max.

I don't think the lab standards were sloppy I think you are playing fast and loose with the truth. You claimed earlier that the repeatability of your measurements is better than the error of the measurements. You are full of crap, not your lab.

Que? Repeatability of measurement and error of measurement are analgous terms, so I would never say that one is better than the other because they are essentially opposite sides of the same coin. If I'm telling you that I've seen 100s of tests in elite athletes over many years where the results have been within 2% this implies that the difference was within the typical error. The overwhelming consensus in the literature also supports this observation. However, there is also plenty of support in the literature for short term increases in VO2max to occur which are outside the typical error, resulting from some specific intervention, such as LHTL, or a block of high intensity aerobic training for example, but it doesn't stay elevated indefinately. Most of the studies on EPO doping show increases of around 6-12% in VO2max. To achieve a 16% increase is highly suspicious indeed and therefore, some other explanation likely exists as we have been discussing.

 

[callac]

3.6kg is indeed 360% greater than 1kg, but 3.6% is only 2.6% greater than 1%

Nope, 3.6% is 2.6 percentage points greater than 1%.
In "pure" percent, it's still 360% greater than 1%...
But that's quite OT...

 

[Realist]

A percent of a percent is a very bad way to express data. Will Hopkins would crucify you on that point.

3.6kg is indeed 360% greater than 1kg, but 3.6% is only 2.6% greater than 1%

Anyway, you are correct that it is possible for VO2max to change outside of the typical error and its my bad for using a little bit of (under) exaggeration re. potential for variability in VO2max.

I agree in general re: % of %, but was emphasising the massively different range that gives on the error.

Que? Repeatability of measurement and error of measurement are analgous terms, so I would never say that one is better than the other because they are essentially opposite sides of the same coin. If I'm telling you that I've seen 100s of tests in elite athletes over many years where the results have been within 2% this implies that the difference was within the typical error. The overwhelming consensus in the literature also supports this observation. However, there is also plenty of support in the literature for short term increases in VO2max to occur which are outside the typical error, resulting from some specific intervention, such as LHTL, or a block of high intensity aerobic training for example, but it doesn't stay elevated indefinately. Most of the studies on EPO doping show increases of around 6-12% in VO2max. To achieve a 16% increase is highly suspicious indeed and therefore, some other explanation likely exists as we have been discussing.

Test-retest reliability and error are only synonymous if the underlying thing being measured is completely stable over time. This is the whole debate here so I don't think you can say they are synonymous in this case. It is subtle though, I see how you could argue your way.

Also: apologies for heat in debate. This has got more interesting than I expected, I could have credited you with a little more respect. Mea culpa.

 

[Krebs cycle]

Test-retest reliability and error are only synonymous if the underlying thing being measured is completely stable over time. This is the whole debate here so I don't think you can say they are synonymous in this case. It is subtle though, I see how you could argue your way.

Also: apologies for heat in debate. This has got more interesting than I expected, I could have credited you with a little more respect. Mea culpa.

Me too... yo tambien!!

I suspect we agree on a lot more things than we disagree

Healthy debate is good!

 

[Krebs cycle]

Nope, 3.6% is 2.6 percentage points greater than 1%.
In "pure" percent, it's still 360% greater than 1%...
But that's quite OT...

Enter real values.

A 1% increase in VO2max from a baseline of 75.0 is 75.75ml/kg
A 3.6% increase is 77.7 ml/kg.

77.7 is 2.6% greater than 75.75, not 360% greater.

Get.with.the.program.


Anyway, looking at those values in real terms I have to admit I was being a bit misleading. I've conducted a lot of testing before and after pre-season volume training, but less so directly following the competitive phase because athletes want a month off, not coming into the lab for more testing.

Unless you test the athletes in an unfatigued state (ie: tapered) then the majority would fall within about 2.5% and then a minority would fall within 3-4%. A rare few will improve beyond that (up to around 5-6%) level especially if they were unfamiliar with the testing procedures and it was a learning effect, I was lucky enough to get the timing right with the testing. Once I had a netball player who became an olympic rower. She had an increase of about 10% on her initial rowing VO2max test (had recently started training again after returning from a knee reconstruction), but it took 18months to achieve that, and thereafter for the next 2yrs it stayed about the same.

 

[callac]

77.7 is 2.6% greater than 75.75, not 360% greater.

I totally agree on that. My point was that you cannot say, as you put above, that 3.6% is 2.6% greater than 1%. It's 2.6 percentage points greater...
And 3.6 is 360% greater than 1, whether the unit is kg, m, W or % (though % is not a unit per se, and indeed, should be used carefully... )

 

[Realist]

Enter real values.

A 1% increase in VO2max from a baseline of 75.0 is 75.75ml/kg
A 3.6% increase is 77.7 ml/kg.

77.7 is 2.6% greater than 75.75, not 360% greater.

Get.with.the.program.

Yes, but I was talking about the increase in uncertainty/range not the increase in magnitude of measurement. Thanks for your other comments with this post. Interesting, and we're finding a middle ground.

Because I am a fun guy... I did a little simulation to demonstrate another thing, which is that Lucia's data is reported for mean changes, not individual, and some individuals should have larger changes than in the group data (unless the group changes homogenously).

I used Lucia's reported means and sd's to simulate a group of 13 riders out of season and in season VO2max's (10,000 runs of sim).

I assumed the VO2max's were distributed normally (probably wrong) and then ran 4 sims: one assumes perfect rank matching, so the rider with the worst VO2 at the start has the worst at the end. One assumes completely random matching. This gives upper and lower bounds. Then I also simulated with the standard deviation halved, since maybe you could argue there was more noise in Lucia's data than some other data.

I get:

Rank matched normal SD: 4.43
Rank matched half SD: 3.16
Random match normal: 6.24
Random match half: 3.72

So even if you thought the Lucia had some kind of large source of noise, we expect to see a change of greater than the 2.6 we see in the means. In reality, the change is likely to be substantially bigger. I would bet Lucia's group had a an individual with a change of at least 5% in it.

If I extend the simulation to have 200 individuals, under the most conservative assumption I get not much change, but using Lucia's reported standard deviations I get 5.6 and 8.6 as my largest changes, suggesting that, if their data is approximately accurate and approximately normal, we should see a change of ~10% in at least one or two professional cyclists moving between out of season and in season.

I don't really believe this simulation, but it is somewhat instructive. Comments?

 

[acoggan]

In my mind, the symmorphosis concept characterizes the balance between cardiovascular and respiratory limitations esp. in the elite athlete. Jerry Dempsey has published a number of papers discussing the idea that cardiovascular and peripheral adaptations to endurance training far exceed the capacity of the pulmonary system to adapt. Hence, once you've achieved large increases in capillary density, mitochondrial content, blood volume, left ventricular hypertrophy etc etc you begin to encroach on the pulmonary system's capacity to transport oxygen. At this point, I believe that autonomic neural control of HR and MAP is designed to optimize VO2max given the known central limitations. Therefore, what might appear at first to be disadvantageous for oxygen transport (eg: decreasing %SaO2) might actually serve to maximise oxygen delivery. Whether or not that happens I feel is related to the structural limitations of the pulmonary system. Women tend to have smaller lung volumes compared to weight and height matched men and they also have a higher incidence of EIAH. In this case, a higher maximal HR would be more advantageous.

The point I was making about symmorphosis is that you can't simply keep increasing VO2max by increasing maximal CO and that is a structural limitation of the pulmonary system, not a peripheral metabolic one. What is REALLY interesting is that exogenous EPO and/or blood doping does increase VO2max. So what that implies is that long term feedback mechanisms serves to regulate the increase in blood volume before you reach the upper most ceiling where you simply cannot increase VO2max any further. My guess is that the additional work on the heart is that mechanism. 17 odd heart failure deaths in elite cyclists during the 1990s would appear to corroborate that theory. EPO has been shown to stimulate ANP for example. Other stressors on the heart increases both ANP and BNP. EPO production itself has been proposed to be self limiting and indeed this is part of how the EPO test "off-score" is calculated.

Well if that is your hypothesis then it is no wonder that I (and probably others) were confused by your use of the term "symmorphosis", 'cause what you describe ain't it - in fact, the viewpoint you express is completely the opposite of symmorphosis.

As you may or may not know, Taylor and Weibel introduced the concept of symmorphosis in a series of papers published in Respiratory Physiology in 1981, with this citation probably being the most relevant here:

http://www.ncbi.nlm.nih.gov/pubmed/7232884

In doing so, they hypothesized (or embraced the hypothesis that) all elements of the oxygen transport system are developed in direct proportion to one another, such that no single element can be considered to be rate-limiting. From their perspective (i.e., as comparative physiologists) the concept made a lot of sense, and indeed it does fit with physiological knowledge when considering large differences in body size/metabolic rate, e.g., when comparing an elephant and a shrew. Even in that context, however, there are obvious exceptions, i.e., "athletic" species (e.g., thoroughbred race horses) whose data significantly deviate from the overall trend line. More importantly, though, the concept clearly does not apply at the level of a single species, e.g., humans. This is evidenced by the fact that, e.g., the capacity of the muscles to demand/accept blood flow and consume O2 greatly exceed the capacity of the heart and lungs to provide it. Perhaps most importantly of all, the concept of symmorphosis is completely repudiated ("refudiated" if you're Sarah Palin) at the level of the individual by the observation that with endurance exercise training muscle respiratory capacity increases by 50-100% while skeletal muscle capillarization increases by only about half that amount, maximal cardiac output increases to an even less extent still, and essentially no changes in pulmonary structure or function occur (unless you're a long-term swimmer, perhaps). Obviously this is something you understand well, so I can't for the life of me understand why you introduced the concept of symmorphosis into this discussion.

 

[lean mean &green]

Yes, but I was talking about the increase in uncertainty/range not the increase in magnitude of measurement.

can we all agree to...

1. let percentage-gate go?

2. the discrepancy of lemond's numbers are suggestive of error or at the very least don't follow a predictable pattern.

3. lemond's values aren't solid evidence of ped use or abstinence.

 

[acoggan]

Yes, but I was talking about the increase in uncertainty/range not the increase in magnitude of measurement. Thanks for your other comments with this post. Interesting, and we're finding a middle ground.

Because I am a fun guy... I did a little simulation to demonstrate another thing, which is that Lucia's data is reported for mean changes, not individual, and some individuals should have larger changes than in the group data (unless the group changes homogenously).

I used Lucia's reported means and sd's to simulate a group of 13 riders out of season and in season VO2max's (10,000 runs of sim).

I assumed the VO2max's were distributed normally (probably wrong) and then ran 4 sims: one assumes perfect rank matching, so the rider with the worst VO2 at the start has the worst at the end. One assumes completely random matching. This gives upper and lower bounds. Then I also simulated with the standard deviation halved, since maybe you could argue there was more noise in Lucia's data than some other data.

I get:

Rank matched normal SD: 4.43
Rank matched half SD: 3.16
Random match normal: 6.24
Random match half: 3.72

So even if you thought the Lucia had some kind of large source of noise, we expect to see a change of greater than the 2.6 we see in the means. In reality, the change is likely to be substantially bigger. I would bet Lucia's group had a an individual with a change of at least 5% in it.

If I extend the simulation to have 200 individuals, under the most conservative assumption I get not much change, but using Lucia's reported standard deviations I get 5.6 and 8.6 as my largest changes, suggesting that, if their data is approximately accurate and approximately normal, we should see a change of ~10% in at least one or two professional cyclists moving between out of season and in season.

I don't really believe this simulation, but it is somewhat instructive. Comments?

My comment is that there is no need for simulations when there are other direct data supporting your contention of significant seasonal variations in VO2max among trained cyclists, e.g.:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1858845/

http://www.ncbi.nlm.nih.gov/pubmed/6825246

http://www.ncbi.nlm.nih.gov/pubmed/18641717

Etc.

EDIT: Of course, there is also Table 17.6 of Chris Gore's book "Physiological tests for elite athletes", showing that VO2max is 9.3% higher in relative terms (i.e., in mL/min/kg) and 4.5% higher in absolute terms (i.e., in L/min) when comparing in-season to out-of-season data from members of the Australian Olympic road team...which certainly does make you wonder where this claim originates:

"I've tested 100s of athletes in season and out of season. VO2max remains the same or is within 1-2%. AMAZING!!"

 

[Realist]

My comment is that there is no need for simulations when there are other direct data supporting your contention of significant seasonal variations in VO2max among trained cyclists

Indeed, and thanks for the data. It was quicker for me to simulate off Lucia's data than to do a lit review. Glad I got the order of magnitude about right...

 

[Realist]

can we all agree to...

1. let percentage-gate go?

Ok

2. the discrepancy of lemond's numbers are suggestive of error or at the very least don't follow a predictable pattern.

Depends what you mean error, but sure, in the spirit of goodwill, that's a decent approximation.

3. lemond's values aren't solid evidence of ped use or abstinence.

Yep.

 

[Krebs cycle]

Well if that is your hypothesis then it is no wonder that I (and probably others) were confused by your use of the term "symmorphosis", 'cause what you describe ain't it - in fact, the viewpoint you express is completely the opposite of symmorphosis.

As you may or may not know, Taylor and Weibel introduced the concept of symmorphosis in a series of papers published in Respiratory Physiology in 1981, with this citation probably being the most relevant here:

http://www.ncbi.nlm.nih.gov/pubmed/7232884

snip

I can't for the life of me understand why you introduced the concept of symmorphosis into this discussion.

I really can't be bothered with this. You brought up the maxHR thing. All I'm saying is that in elite endurance athletes structure/function limitations exists which mean that the cardiovascular system is almost perfectly matched to the pulmonary system such that you can't just increase VO2max by increasing the capacity of one element of the system (ie: max HR). If you don't see how the concept of symmorphosis applies directly to that, then I can't help you.

 

[Krebs cycle]

EDIT: Of course, there is also Table 17.6 of Chris Gore's book "Physiological tests for elite athletes", showing that VO2max is 9.3% higher in relative terms (i.e., in mL/min/kg) and 4.5% higher in absolute terms (i.e., in L/min) when comparing in-season to out-of-season data from members of the Australian Olympic road team...which certainly does make you wonder where this claim originates:

"I've tested 100s of athletes in season and out of season. VO2max remains the same or is within 1-2%. AMAZING!!"

That data was from female cyclists 20yrs ago. I'm not a dinosaur and I'm basing my comments on observations from over the past 10yrs on a variety of different sports including cycling, triathlon, rowing, middle distance running and kayaking.

By all means, keep quoting an "off hand comment" that I have already admitted does not contain full disclosure. At least I am honest enough to state that on a public forum. Argue all you want over exactly how much it does change by (which is futile anyway because so many factors are invovled) however, this entire discussion is based on my primary comment that I stand by "VO2max does not vary by more than 15% in well trained endurance athletes". Furthermore, at 1900m altitude, an increase in true VO2max from 79 on a treadmill to 92-93 on a bike is nothing short of astonishing.

You seem to agree on that point and none of your links refute it, so I can only guess that you are trolling and simply trying to belittle me instead of contributing to a healthy discussion.