Jan Ullrich

[Trond Vidar]

So Epo only made the "big guys" faster but not the climbers?

see RRs post above.

You can also put into the equation that in a non-EPOed field, a climber would normally put more minutes into a big guy on numerous mountainstages, compared to the fairly short ITTs where the TT/big guys excel.

 

[Zam_Olyas]

So who is gonna start a thread?

 

[Semper Fidelis]

It is clear you do not understand how Oxygen vector doping works or it's effect on tactics. Yes, larger riders received greater benefit from EPO. It also turned huge portions of the peloton into climbers, neutralizing the attacks of climbers that once shattered the field. By 1989 less then 5 riders had broke 45 minutes on Alp d'Huez......in 1997 60 riders broke 45.

Seen it stated before but well worth repeating. "Where did all the Colombian climbers go?"

EPO made them and the job irrelevant in my opinion.

 

[FoxxyBrown1111]

Will anyone tempt to answer this?

After reading trou it all, i´ll do it:
I know RR would disagree, but i´d say Ullrich still (as D´Hont did, for example). I am 100% sure he´d have beaten Bassons, Delion and others. Maybe not by 9 mins, but he still wins all those tours b/c of his ITTs...

 

[Le breton]

By 1989 less then 5 riders had broke 45 minutes on Alp d'Huez......in 1997 60 riders broke 45.

According to Vayer & Portoleau page 19 of "Pouvez-vous gagner le Tour?" :

In 1989 7 riders broke 45 minutes on Alpe d'Huez......in 1997 60 riders broke 45.

 

[Merckx index]

what % is it when you increase from 39% to 50% ?

As I said, maybe in the nineties. But after the EPO test, in the transfusion era, when LA won most of his Tours, a twenty percent increase would require three 5OO ml. blood bags. Correct me if I’m wrong, but I’ve never come across any reference to a rider transfusing that much blood at one time.

You are basing your assumption on one 3rd hand quote

For Ulle, yes. I don’t know what his natural HT was. But LA’s HT data are all over the internet. The average value of what I’ve seen is in the low forties. That is not exceptionally low. There are many other riders with a HT in that range.

And you would be wrong. It was one of the key parts of almost every top doping program of the 90's/00. No surprise that when Armstrong started working with Ferrari he showed up at training camp looking like a linebacker. Did you watch cycling in the 90's? Ever wonder how rider went full gas on climbs with their mouths closed, breathing out their nose?

I’m sure you’re aware that the linebacker quote occurred pre-cancer, at a time when LA still couldn’t even finish a Tour, let alone dominate one. He didn’t look like a LB when he started winning Tours, yet he climbed about as well then as highly doped up riders did in the nineties. Moreover, regardless of any theory about muscle vs. blood flow, LB type of muscle, i.e., upper body weight, would definitely be a disadvantage to a climber.

Over the last several decades I have had many, many, many discussions about this topic with the doctors, directors, and riders you might have read about in the magazines. For them none of what I have written would be new.

I may be wrong about what the goal of these doctors was, but I still very much doubt that this approach makes sense. These doctors for the most part are not real scientists, and don’t necessarily know what they’re talking about. It wouldn’t be the first time the peloton followed some program that had no rational basis in theory and didn’t actually provide much of an advantage.

I repeat, I would like to see an actual study that shows you have to put on muscle to take advantage of an increased HT. The converse is definitely not true. MLB and NFL players put on muscle all the time, and don’t need any extra oxygen to take advantage of that.

It is clear you do not understand how Oxygen vector doping works or it's effect on tactics. Yes, larger riders received greater benefit from EPO.

First you said that riders had to put on more muscle to take advantage of the increased oxygen transport. If that’s the case, smaller riders could do this as well as larger riders. Anyone can put on more muscle. Now you seem to be implying that being naturally large gives you an advantage. Why? What’s the rationale for this?

Common sense ought to tell you the problem with this reasoning. Some of the highest VO twos have been recorded by relatively small, skinny athletes. IOW, their ratio of oxygen transport to muscle mass is far greater than for a larger athlete with a much lower VO two. Obviously there is an enormous possible range of ratios of oxygen availability to muscle mass.

It also turned huge portions of the peloton into climbers, neutralizing the attacks of climbers that once shattered the field. By 1989 less then 5 riders had broke 45 minutes on Alp d'Huez......in 1997 60 riders broke 45.

Yes, and the increased HT is perfectly capable of explaining that, without the added muscle theory. As I noted before, those faster times continued in the next decade, when riders were not bulking up.

If this theory were the case, riders like LA and Ulle should have been able to dominate one-day races, for which they were naturally more suited, even more than GTs. Why was that not the case? LA never won a monument, and only two major classics. In his linebacker years, on relatively flat courses, he should have been destroying the field. Why wasn’t he?

I suppose you might argue that the competition in those races was all big guys, who all had the same doped up edge. But as another poster noted, this advantage should have been even greater for TTng than for climbing. So why weren’t TTs in the nineties far faster than in the following decade, when this bulked up approach was not being used?

 

[Race Radio]

SNIP

Brevity is your friend

Armstrong's off season baseline was 39, sometimes 38. Of course this is just one element of a riders response to PED's.

Yes, riders had Hct close to 50 in the 00's, Landis was 48.5 in the 3rd week of the Tour. Lance was consistently close to 50 during the tour thanks to a mixture of EPO, Blood bags, and fun drugs.

 

[Tyler'sTwin]

As I said, maybe in the nineties. But after the EPO test, in the transfusion era, when LA won most of his Tours, a twenty percent increase would require three 5OO ml. blood bags. Correct me if I’m wrong, but I’ve never come across any reference to a rider transfusing that much blood at one time.

Maybe not at one time, but over a 3 week Tour, definitely. And the decline in HT is due to volume expansion, not a decline in RBC mass.

I've heard the yield is only 0.72, so three 500ml bags would not be close to 20%. More like 12-15%. But when you factor in the EPO, 20% up in the 3rd week looks very likely and probably conservative.

 

[Merckx index]

Brevity is your friend

In light forum banter, yes, in discussions about scientific matters, usually not.

Armstrong's off season baseline was 39, sometimes 38. Of course this is just one element of a riders response to PED's.

Then why wasn't he flagged by the passport when he had all those lower forties when he came back after retirement?

Yes, riders had Hct close to 50 in the 00's, Landis was 48.5 in the 3rd week of the Tour. Lance was consistently close to 50 during the tour thanks to a mixture of EPO, Blood bags, and fun drugs.

What was Floyd's baseline HT? If LA's HT was close to fifty during the seven wins, then he definitely was doping less during the come back, since none of the values made public during that period is close to that.

Again,though, whether it was twenty percent or less is really a minor issue. You still have not provided any documentation of your thesis, that more muscle is required to make use of a large increase in HT. Understand I'm not saying it's flat-out wrong. I'm just saying I would have to see some evidence before I would buy into it.

Maybe not at one time, but over a 3 week Tour, definitely. And the decline in HT is due to volume expansion, not a decline in RBC mass.

If it isn't at one time, you aren't going to get the full twenty percent. I didn't say the decline was due to changes in RBC mass. Since HT, or percent, is what is measured, not mass, the underlying reason for the decline is irrelevant.

I've heard the yield is only 0.72, so three 500ml bags would not be close to 20%. More like 12-15%.

Which makes my point even more strongly.

But when you factor in the EPO, 20% up in the 3rd week looks very likely and probably conservative.

Really? Again, can you provide a link to this? In the transfusion era, EPO is mostly micro-dosed, and used to counteract the decrease in retics following transfusion. It's not primarily used to raise HT, for the very good reason that this increase needs to be masked as much as possible. Even before the passport, there was the off-score.

 

[Race Radio]

Then why wasn't he flagged by the passport when he had all those lower forties when he came back after retirement?

Dude, you jump around like a rabbit.

First you wrote

But after the EPO test, in the transfusion era, when LA won most of his Tours, a twenty percent increase

and now you jump to the 09/10 season?

On average an undoped riders Hct will drop 13% during the course of a 3 week Tour. It is a massive advantage for a rider whose natural Hct is 39 to enter the 3rd week with a 48.5......massive.

We can go back and forth forever on this but the facts remain that oxygen vector doping effects each rider in vastly different ways. from 1993-2005 a rider's reaction to these drugs was one of the primary reasons for success.

Armstrong, Riis, Jan, and others never would have won a GT. Never.

 

[Tyler'sTwin]

If it isn't at one time, you aren't going to get the full twenty percent.

Why not? Are the gains from the previous BB's gone by the time you get to the third one?

I didn't say the decline was due to changes in RBC mass. Since HT, or percent, is what is measured, not mass, the underlying reason for the decline is irrelevant.

It's not irrelevant because RR claimed guys were getting 20% increases in RBC mass and you disputed that by pointing out that intra-GT BB's may only counteract the decline in HT. Since the decline likely had nothing to do with RBC mass, those BB's meant an increase in RBC mass.

Your objection was irrelevant.

Really? Again, can you provide a link to this? In the transfusion era, EPO is mostly micro-dosed, and used to counteract the decrease in retics following transfusion. It's not primarily used to raise HT, for the very good reason that this increase needs to be masked as much as possible. Even before the passport, there was the off-score.

It's almost impossible to trigger an >132 off-score unless you allow your retics to totally crash when at a borderline HT.

Post EPO-test Lance used more EPO per week than Ashenden used to increase Hb mass by 10%. Lance used smaller doses daily and Ashenden used larger doses 2/week. I don't know if that matters. I also don't know if it matters that his subjects had less total Hb than Lance to begin with.

Here's JV describing the evolution of EPO-use:

For post 50-percent rule, the standard [dose] … gets a guy from 39 percent to 48 percent in four weeks or so and will stabilize it there in a three-week [grand tour].

Now, once the EPO test came into play, initially, the dosage… didn’t change, just the method, from subcutaneous to IV. In a 70kg rider, [this dose] will clear in 24 hours. So, take the shot straight after the stage, it’s out by the time you could get tested the next day.

Once OOC [out-of-competition] testing was introduced and they could come anytime other than between 10:00 p.m. and 7 a.m., a quicker clearance was needed, hence the ‘Micro Dose’ intravenous method.

And commentary from Veloclinic:

A quick calculation confirms that the EPO dosing described for the Armstrong era was equal to or greater than the dosing in the Ashenden (2011a) study. Therefore, a 10-percent increase in Hgb mass derived from the Ashenden (2011a) study stands as a safe estimate for the effect of EPO.

 

[Merckx index]

Dude, you jump around like a rabbit.

First you wrote


and now you jump to the 09/10 season?

A natural HT is not supposed to change over the years. If he had a natural HT of 38-39 in 99-05, it should have been the same in 09/10. In which case, I believe many of his published values in 09/10 should have been flagged.

We can go back and forth forever on this but the facts remain that oxygen vector doping effects each rider in vastly different ways. from 1993-2005 a rider's reaction to these drugs was one of the primary reasons for success.

I'm not disputing that it affects riders differently, though I would dispute that the differences are "vast". More specifically, I'm disputing the theory that a) one has to put on extra muscle to take full advantage of an increased HT, and b) naturally heavier riders had an advantage in this respect. You said that you spent many hours talking with doctors and others who formulated their programs based on this. What exactly was their rationale? Give me a summary of what they said. Something more substantial than "this extra oxygen is wasted if there isn't more muscle mass".

I'm not afraid to admit I'm wrong, and I will if you provide convincing evidence. But one of the first principles of science is that you don't make arguments based on authority. The fact that so-and-so made these claims is an interesting point on which to start a discussion, but evidence has to follow.

Armstrong, Riis, Jan, and others never would have won a GT. Never.

I'm not disputing this, or more precisely, I'm agnostic on the question. I don't know. But even if that's the case, this extra muscle theory doesn't necessarily follow. It still looks to me more like a rationale for the fact that they did win doping.

It's not irrelevant because RR claimed guys were getting 20% increases in RBC mass and you disputed that by pointing out that intra-GT BB's may only counteract the decline in HT. Since the decline likely had nothing to do with RBC mass, those BB's meant an increase in RBC mass.

Your objection was irrelevant.

OK, I see your point. I was thinking in terms of testing. But HT is not irrelevant here. The amount of oxygen delivered to tissues at any moment depends on the concentration in the blood, which is HT. If you increase your Hb mass by 20%, but the HT is only increased, say, 10% over baseline, the oxygen delivery will be 10% greater, or something proportional to that 10% greater, than during baseline. Not 20%. It will only increase more than 10% as the extra fluid is absorbed over time.

But in a GT, absorption of extra fluid is opposed by plasma expansion. So the original point that plasma expansion reduces oxygen transport is relevant here.

Now it may be that extra muscle alters this equilibrium, so that more oxygen can be delivered at a given HT level. This is the kind of evidence that might support RR's theory. I suspect that is what the doctors were basing their arguments on, and if so, I would like to see some studies supporting it.

But if that were the case, one would expect to see significant changes in efficiency, which apparently don't occur. Or I would expect that Coyle/Coggan would have suggested this as an explanation for their claim that LA's efficiency increased, since it would be a much simpler rationale than changes in type I/II fiber proportion. And in any case, even if this effect does occur, it would still not affect the relationship of HT to oxygen delivery, nor would it explain why heavier riders have an advantage over smaller ones.

A quick calculation confirms that the EPO dosing described for the Armstrong era was equal to or greater than the dosing in the Ashenden (2011a) study. Therefore, a 10-percent increase in Hgb mass derived from the Ashenden (2011a) study stands as a safe estimate for the effect of EPO.

Yes, which is what I estimated before, maybe 10%.

But again, this is a side issue. If some riders post-EPO test raised their HT or Hb 20%, fine. The major point is still whether only large riders who bulked up could take advantage of this.

 

[Tyler'sTwin]

Net haemoglobin increase from reinfusion of refrigerated vs. frozen red blood cells after autologous blood transfusions.
Ashenden M, Some Danish Fellow Who Is Not An Anti-Doping Expert.
Science and Industry against Blood Doping, Gold Coast, Queensland, Australia.

Abstract

BACKGROUND AND OBJECTIVES  Two main blood storage procedures can be used for storing red blood cells: refrigeration and freezing. Nevertheless, the efficiency of these procedures measured as the increase in haemoglobin after reinfusion compared with baseline has never been examined. The main objective was to examine which storage procedure yielded the largest increase in circulating haemoglobin after reinfusion compared to baseline. MATERIALS AND METHODS  Equal volumes of blood from 15 men were withdrawn and stored either frozen or refrigerated as packed red blood cells. Serial measures of circulating haemoglobin by carbon monoxide rebreathing provided an opportunity to monitor recovery from anaemia, as well as the net increase in circulating haemoglobin after transfusion. RESULTS  The post-thaw yield of haemoglobin in the bags was 72% after refrigerated storage compared with only 52% after freezing. Nevertheless, frozen storage allowed haemoglobin to fully recover before reinfusion, while the haemoglobin was 10% lower in the refrigerated group compared with baseline. After reinfusion, the haemoglobin levels were 11·5% higher than the baseline values in the group reinfused with frozen blood, while for the refrigerated group, haemoglobin levels were only 5·2% higher than baseline. CONCLUSION  The relatively larger recovery from anaemia in the frozen group during storage more than compensated for the larger loss of haemoglobin during freezing and resulted in a larger net gain in haemoglobin. Based on the average 23 g per week recovery of haemoglobin, extending refrigerated storage to 7-8 weeks may yield sufficient time for patients to fully replenish harvested haemoglobin from three bags of blood without reliance on frozen storage of RBC.

 

[Race Radio]

JV has said a lot about these topics. While JV is one of the better educated people in the sport I have had this same conversion, in more detail, with multiple DS', Doctors, and riders over the last couple decades

Originally Posted by Jonathan Vaughters
Also, an old Finnish study (if you can find it) found that athletes with higher Vo2 maxes benefitted less from EPO use than those who started with lower Vo2 maxes. The more talented athlete were (generally) benefitting less. Another observation of that study was that ectomorphic body types showed less increase than mesomorphic types. So, the variables on the exact advantage are endless and vary person to person (A BIG counterpoint to the argument that just letting everyone dope is fair). I read this study in about 1995 and haven't seen it anywhere since, so i cant find a link, sorry...

 

[Tyler'sTwin]

Based on the average 23 g per week recovery of haemoglobin

Do you think this is true regardless of Hb mass? If so, 0.6-07L would've been the sweet spot pre EPO and Freezing. Unless they could speed up recovery by going to altitude.

 

[Race Radio]

SNIP

You are jumping around again.

More then willing to engage on the topic, but let me know when you stop the filibuster.

 

[Merckx index]

RR, you can skip this post, because it isn't brief. Someone else may find something of interest in it, though.

Plasma expansion results in a lower HT, which means a lower oxygen concentration in the blood. The conventional view has been that this means that the V02 max should be reduced. IOW, it is HT, and not Hb mass, which determines oxygen intake and power. If this is the case, then plasma expansion and the accompanying reduction in HT is very relevant to the issue of how much increased oxygen intake there is following an increase in Hb mass by transfusion during a GT.

However—and I didn’t know this before, I find it surprising and unexpected--several studies have shown either no change or even an increase in V02 following plasma expansion, e.g.,

http://jap.physiology.org/content/101/3/707.long

The authors of the linked study (who cite other work consistent with their results) used a plasma volume expander to lower average HT in their subjects from 44 to 41. This means Hb mass remained the same, but in a larger volume. But V02 max actually increased an average of about 5%.

Why? They assumed there had to be a compensatory process that over-rode the lower oxygen concentration, and came to the conclusion that it was probably a larger stroke volume, perhaps because of the reduced viscosity of the blood. Interestingly, in support of this, there are other studies (not noted by these authors, I believe) that show a negative correlation between HT and V02. I.e., individuals with lower HTs tend to have higher V02 maxes (though just to underscore the variable results in this area, an article cited above in this thread reported that individuals with higher V02 maxes tended to benefit less from EP0). While there are many factors that could go into this, it certainly is consistent with the possibility of greater stroke volume.

Thus this and some other studies suggest that plasma expansion might not only not reduce oxygen intake during a GT, but even increase it. IOW, you might get a performance enhancement just by taking saline, and not just to counteract dehydration. However, several caveats:

1) they noted that any compensatory mechanisms are likely to have a limit, and that limit is likely to be breached by a large degree of plasma expansion. Thus they suggested that the compensation might not occur in elite athletes, which AFAIK have not been studied in this manner. As RR noted, plasma expansion can be very large in riders. In fact, they experience a large degree of plasma expansion simply as a result of training, then a further increase if they ride a GT. Thus they might have exceeded the limits of compensatory processes. FWIW, work by Coyle and Coggan suggests that reduction of HT by 5-10% eliminates the increase in V02 seen with a lower reduction of HT, though the above study was conducted with an 8% decrease in HT.

2) Transfusion changes the situation. If a rider transfuses packed cells, the HT increases, which presumably would counteract the effects on stroke volume, IOW reduce the compensatory processes. OTOH, if the rider transfuses whole blood, which has little effect on the HT, there is a further large increase in blood volume, which would further stress any compensatory mechanisms. So it needs to be emphasized that we don’t know what the effect on V02 would be of plasma expansion of elite racers, whether in fact all of any hypothetical 20% increase in Hb mass would translate into increased oxygen intake.

3) An increased V02 does not necessarily translate into more oxygen use by muscles. The authors of the above study cited a much earlier study that showed changes in V02 were paralleled by changes in oxygen getting into the leg muscles, which were measured by comparing the concentration of oxygen in arterial and venous blood. However, even if more oxygen is getting into the muscle, it does not establish that this extra oxygen is actually being used. AFAIK, this has never been established. I raised this point with Andy Coggan in another thread, because Coyle’s conclusion of greater mechanical efficiency rests on this assumption. Everyone in the field seems to assume that V02 is an accurate measurement of oxygen metabolism. That might not always be the case.

Originally Posted by Jonathan Vaughters
Also, an old Finnish study (if you can find it) found that athletes with higher Vo2 maxes benefitted less from EPO use than those who started with lower Vo2 maxes. The more talented athlete were (generally) benefitting less. Another observation of that study was that ectomorphic body types showed less increase than mesomorphic types. So, the variables on the exact advantage are endless and vary person to person (A BIG counterpoint to the argument that just letting everyone dope is fair). I read this study in about 1995 and haven't seen it anywhere since, so i cant find a link, sorry...

Great, a study almost two decades old, can't find the link.

How about this?

Subjects had an average HT of 42.7% at the outset of the study. After 30 days or less of EPO, they were all over 50% (average of 50.8%). Sounds like LA and Ulle. V02 max increased by an average of 7.5%. Sure, that's a huge increase, definitely helps them win races. But does it suggest the need for added muscle mass? According to the study cited by JV, subjects in this study (who were described as well-trained athletes, but I don't believe were active elite riders) should have benefitted more from EPO than even an average pro, so the 7.5% increase should be an overestimate of the benefit someone like LA or Ulle should get.

Or is your point that adding muscle mass would increase V02 max? Or that there is a correlation between body weight of subject and V02 max increase? That would be very interesting, and would support your hypothesis, but I would like to see a study demonstrating that.

While you're at it, maybe you could explain where the cut-off is. You have strongly implied that less talented riders like (according to you) LA and Ulle could benefit more from the same doping program than more talented riders. Not simply improve more beyond their baseline than the more talented riders could, but shift their baseline from below the baseline of the more talented riders to above it. IOW, clean, LA and Ulle were inferior climbers to certain other riders. On the same doping program (yes, I know, the view is their program was better, but much of your argument implies that it didn't have to be), LA and Ulle were superior to the same climbers, doped to the same degree.

If that's true, where do you draw the line? I mean, I'm inferior naturally to LA and Ulle, does that mean if I doped on the same program as they did, I could beat them? And if not, why not? Because I'm not as muscular? OK, what about some football player who was more muscular than they were? Could he have dominated them climbing just by going on the same doping program? And if not, why not?

The problem with this kind of reasoning--why it leads to conundra like this--is that you aren't merely stating that they improved more than the lighter climbers, but they caught up to them and surpassed them. With that kind of logic, you predict that the worse the athlete is without dope, the better he will be with it.

Another point to add: EPO administration does not increase plasma volume, so any effect of diluting the increase in Hb mass on stroke volume does not occur.

 

[Benotti69]

So Epo only made the "big guys" faster but not the climbers?

If you consider how much Pantani was taking, his hct was above 60%, yes if they all EPO'd to 50% the climbers were gone.

 

[Fearless Greg Lemond]

After reading trou it all, i´ll do it:
I know RR would disagree, but i´d say Ullrich still (as D´Hont did, for example). I am 100% sure he´d have beaten Bassons, Delion and others. Maybe not by 9 mins, but he still wins all those tours b/c of his ITTs...

You dont think Ullrich got a little help from Edgar Allen Poe in his TT'ing?

 

[Bratam]

Tyler Hamilton speaks glowingly about Jan Ullrich in his book. Tyler says he "rode the 1997 Tour and survived. Riis was heavily favoured to win, but to the world's surprise, he was surpassed by a teammate, a wide-eyed, muscled 23yo German named Jan Ullrich. Ullrich was genuine phenomenon, with a fluid pedal stroke and incredible power for such a young rider. Watching him, I agreed with most observers: Ullrich was clearly Indurain's successor, the guy who was going to dominate the tour for the next decade."

 

[Bratam]

Tyler goes on to write that

"Ullrich was like a superman -or, to be more accurate, a super-boy. He'd come up training in East Germany, where the coaches lived by the maxim -throw a dozen eggs against a wall, and keep the ones that don't break. Ullrich was the unbreakable egg, a Cold War kid who, like Lance, had grown up without a father and, with the help of the East German state had turned his energy into the single most impressive physique in cycling history. Ullrich's body was unlike any other riders I'd ever seen. I'd sometimes try to ride next to him just so I could watch: you could actually see the muscle fibers moving. He was the only rider I've ever seen whose veins were visible under the lycra"

Sounds like seriously low body fat, with some muscle behind it.

 

[acoggan]

3) An increased V02 does not necessarily translate into more oxygen use by muscles. The authors of the above study cited a much earlier study that showed changes in V02 were paralleled by changes in oxygen getting into the leg muscles, which were measured by comparing the concentration of oxygen in arterial and venous blood. However, even if more oxygen is getting into the muscle, it does not establish that this extra oxygen is actually being used. AFAIK, this has never been established. I raised this point with Andy Coggan in another thread, because Coyle’s conclusion of greater mechanical efficiency rests on this assumption. Everyone in the field seems to assume that V02 is an accurate measurement of oxygen metabolism. That might not always be the case.

You're barking up completely the wrong tree here: the O2 stores of the body are quite small, such that VO2 as measured at the mouth is equal to the whole-body rate of O2 utilization over all but the smallest time interval.

Moreover, since gross mechanical efficiency during exercise reflects the metabolism of the body as a whole, whether or not the O2 is being used by the muscles or by other tissues matters not one whit.

 

[Merckx index]

You're barking up completely the wrong tree here: the O2 stores of the body are quite small, such that VO2 as measured at the mouth is equal to the whole-body rate of O2 utilization over all but the smallest time interval.

Moreover, since gross mechanical efficiency during exercise reflects the metabolism of the body as a whole, whether or not the O2 is being used by the muscles or by other tissues matters not one whit.

I called your attention to this thread, and suggested you comment on the theory that larger, bulked up riders make better use of EPO. You completely ignore this and focus on a side issue related to another thread. So who’s barking up the wrong tree?

In the context of this thread, whether or not oxygen is being fully utilized by the muscles is critical. RR claims that naturally heavier riders obtain a much greater advantage from blood doping than lighter, classic climbing types, and that by bulking up they obtain an even greater advantage. Since he can’t or won’t provide any specific studies to back up this claim—other than a reference by JV to some paper that apparently no one can find--I have no idea whether he means by this that heavier riders obtain a far larger increase in V02 as a result of blood doping, or whether they make better use of oxygen intake with the same V02.

I imagine you are better qualified to evaluate this theory than anyone else in this forum. I wish you would.

 

[Race Radio]

I called your attention to this thread, and suggested you comment on the theory that larger, bulked up riders make better use of EPO. You completely ignore this and focus on a side issue related to another thread. So who’s barking up the wrong tree?

In the context of this thread, whether or not oxygen is being fully utilized by the muscles is critical. RR claims that naturally heavier riders obtain a much greater advantage from blood doping than lighter, classic climbing types, and that by bulking up they obtain an even greater advantage. Since he can’t or won’t provide any specific studies to back up this claim—other than a reference by JV to some paper that apparently no one can find--I have no idea whether he means by this that heavier riders obtain a far larger increase in V02 as a result of blood doping, or whether they make better use of oxygen intake with the same V02.

I imagine you are better qualified to evaluate this theory than anyone else in this forum. I wish you would.

You might do better if you actually read what I wrote instead of attributing things to me I never said. I said nothing about naturally heavier riders, I wrote clearly that riders with greater muscles density will benefit more from Oxygen vector doping. JV said the same. Neither of us said anything about weight, but you repeat it over and over. some 300 doughboy is going to get little benefit.

Given your filibusterer posting style convincing of this means nothing to me, you do not have to believe it is true.

 

[Merckx index]

You might do better if you actually read what I wrote instead of attributing things to me I never said. I said nothing about naturally heavier riders, I wrote clearly that riders with greater muscles density will benefit more from Oxygen vector doping. JV said the same. Neither of us said anything about weight, but you repeat it over and over. some 300 doughboy is going to get little benefit.

Given your filibusterer posting style convincing of this means nothing to me, you do not have to believe it is true.

In response to another poster’s “So Epo only made the "big guys" faster but not the climbers?” you replied:

Yes, larger riders received greater benefit from EPO

Not "more densely muscled" (yes, you did say that at one time, too), but simply "larger". When you make both kinds of statements, I think someone can be forgiven for not understanding you mean one but not the other. Also, JV's quote refers to mesomorphic body types. Mesomorphs are not necessarily more densely muscled, they simply have more muscle, and a classic V-shaped body type. The distinction is clearly illustrated by Pantani. You refer to him as an example of someone densely muscled, but he was not a classic mesomorph. More mesomorphic than other climbers, very possibly, but almost any pro athlete in, say, MLB or the NFL, would be more mesomorphic than Pantani.

But I'm not going to quibble over "larger" vs. "more densely-muscled". I'm happy going with the latter. I'm still asking you to provide evidence of this, in support of statements like these:

every DS in the 90/00's understood the Hct/Vo2 formula. They also understood that when your body suddenly has 20% more RBC that unless you have muscles to absorb that additional oxygen that it is wasted.

Now add in the cocktail of drugs, under expert supervision, that when administered correctly and on schedule add lean muscle mass that can put that additional RBC to good use.

I assume what you really meant here is "unless you have densely packed muscles..." and "add densely packed lean muscle mass", and that we are further to understand that only densely muscled riders, among whom you identify without any evidence but statements you claim others made to you, LA and Ulle, can take full advantage of this program.

In any case, this is what I'm asking AC to comment on.