Long term effects of doping

[JimmyFingers]

When chambers got caught he told the truth. He said it's not possible to win 100m races without doping. Did anyone take him seriously? Was anything done. Did the press take this up?

No, they told him to **** off.

If chambers is doping again I can't condemn him. It's not a sport you can win clean in, but everyone is too busy making money off the superhuman performnces the average Joe wants to see.

poetic that he's with conte, who also told them how it was and was also told his contributions are unwanted.

You're very right of course, but sprinting is the goose that lays the golden egg, they're not going to rock the boat.

Without sarcasm his performances don't exactly indicate continued doping. Britain has a good tradition of sprinting but our sprinters are seconds off world class pace these days, including Chambers. We're half decent in the relays though.

 

[lean mean &green]

Yes I agree. I know it will be impossible in the near future to get this officially going, but why not release the data to the public at least. I know the APB is a joke and that's sort of my point, Lance released his 2009 data and we could clearly see that he was still manipulating his blood. The OFF-score that the APB is using should be much lower. Re. WADA, I agree.



This is not true. Endogenous EPO production doesn't work via a negative feedback loop, such as your endocrine system, i.e. your body doesn't detect excess EPO and shuts endogenous production down. Instead, feedback regulation is based on the tissue O2 pressure, which, for the most part, depends on the Hb concentration. The most appropriate site for controlling EPO production are the kidneys, because pO2 remains relatively stable here. When [Hb], and thus pO2, are low it acts as a direct stimulus for endogenous EPO release. Of course when rhEPO is administered [Hb] is higher and there is no stimulus for endogenous EPO release, so it 'shuts down', but the moment [Hb], and thus pO2, falls back to normal, endogenous EPO release resumes as normal. (1)

I have also heard that they are worse off, but I would prescribe this entirely to placebo, they don't remember how bad they were.

(1) http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0609.2007.00818.x/full

nice link, looks like a great survey article that could become a good reference. i've got some light reading to do today, thanks.

IMO quasi expert opinion PEDS don't lead to "permanent" change but adaptations ARE what I'll call "lasting". the benefits, depending upon the drug/method might last for a period of years. realistically, an advantage might be gained for 5 or more years. hypothetically, some changes could be almost permanent.

you could make a sound argument that this justifies lifetime bans but i just don't see it as practical. it raises the stakes and makes cover-ups MORE likely and false positives, though EXTREMELY rare, do occur.

 

[D-Queued]

nice link, looks like a great survey article that could become a good reference. i've got some light reading to do today, thanks.

IMO quasi expert opinion PEDS don't lead to "permanent" change but adaptations ARE what I'll call "lasting". the benefits, depending upon the drug/method might last for a period of years. realistically, an advantage might be gained for 5 or more years. hypothetically, some changes could be almost permanent.

you could make a sound argument that this justifies lifetime bans but i just don't see it as practical. it raises the stakes and makes cover-ups MORE likely and false positives, though EXTREMELY rare, do occur.

Don't usually find myself arguing with your point, but please indulge me.

No permanent change?

Cover-ups more likely?

Like when teams invoke mandatory termination clauses? You know, like SKY?

Dave.

 

[Briant_Gumble]

When chambers got caught he told the truth. He said it's not possible to win 100m races without doping. Did anyone take him seriously? Was anything done. Did the press take this up?

No, they told him to **** off.

If chambers is doping again I can't condemn him. It's not a sport you can win clean in, but everyone is too busy making money off the superhuman performnces the average Joe wants to see.

poetic that he's with conte, who also told them how it was and was also told his contributions are unwanted.

I agree with this, I'm not condemning Chambers for continuing to dope I'm just talking about the scientific effects of long term doping which is relevant to the post I quoted.

I don't see Chambers as someone who is retaining the benefits from past doping but rather someone continuing to dope.

 

[lean mean &green]

Don't usually find myself arguing with your point, but please indulge me.

No permanent change?

Cover-ups more likely?

Like when teams invoke mandatory termination clauses? You know, like SKY?

Dave.

haha, slight miscommunication. i just meant i think the "permanent" benefits or performance enhancements would be minimal after someone stopped using drugs/methods for a few years. ie probably not enough to justify lifetime ban.

in lyle's case the complications could be very permanent.

 

[Briant_Gumble]

Plus he swore on telly after he won the Olympic qualifying race.

Chambers working with Conte is the same as Lance working with Ferrari.

Except I find the two C's more likeable.

It's like an alcoholic going to a bar because he says he likes to buy bags of peanuts.

 

[JimmyFingers]

Chambers working with Conte is the same as Lance working with Ferrari.

Except I find the two C's more likeable.

It's like an alcoholic going to a bar because he says he likes to buy bags of peanuts.

I'm not going to defend Chambers, but if he was doping on his come back, it didn't do him much good

 

[Netserk]

I'm not going to defend Chambers, but if he was doping on his come back, it didn't do him much good

Do you know how well he would do without?

 

[JimmyFingers]

Do you know how well he would do without?

I'm going to take a stab at worse than with

 

[DirtyWorks]

This is not true. Endogenous EPO production doesn't work via a negative feedback loop, such as your endocrine system, i.e. your body doesn't detect excess EPO and shuts endogenous production down. Instead, feedback regulation is based on the tissue O2 pressure, which, for the most part, depends on the Hb concentration. The most appropriate site for controlling EPO production are the kidneys, because pO2 remains relatively stable here. When [Hb], and thus pO2, are low it acts as a direct stimulus for endogenous EPO release. Of course when rhEPO is administered [Hb] is higher and there is no stimulus for endogenous EPO release, so it 'shuts down', but the moment [Hb], and thus pO2, falls back to normal, endogenous EPO release resumes as normal. (1)

I have also heard that they are worse off, but I would prescribe this entirely to placebo, they don't remember how bad they were.

(1) http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0609.2007.00818.x/full

Ok, so I don't make the same mistake twice, I read your reply as follows:

Old-fashioned EPO, the body "rebalances" EPO levels once the external administration stops almost immediately.

rhEPO, there is a temporary period where the body doesn't produce EPO, but it kicks off once the blood parameters return to normal.

No wonder they liked the stuff. Using steriods is far more complicated with the on/off cycles. That's not even including the masking efforts.

 

[hiero2]

I wanted to put up someone who we know was doing EPO, I have looked at the retirement age of the greats of the past, it tends to be prior to 35 years of age.

There may be other reasons of course why people are going on longer, so it is just a thought.

Occam's Razor: economics, pure and simple. A star of yesteryear made about what a peloton rider makes today, even adjusted for inflation etc. You wanted a family, or the benefits of a "normal" life, you got a "real" job.

. . . I would think that androgens or other anabolic drugs leads very much to a long- to permanent advantage, doesn't it? You won't lose the extra gained muscle mass, . . .

This is not true - or only partially true, and misleading. You do lose the extra gained muscle mass, by and large. You keep up to what you could have built up without the doping boost. Otherwise, Tammy would still be bulked up and shaving. Body builders are quite aware of this loss of mass.

. . . (1) . . .(2), I would think that these new vessels and mitochondria should provide at least a long term improvement in training adaptations, shouldn't it? . . .

(1) http://ndt.oxfordjournals.org/content/20/6/1025.full
(2) http://circres.ahajournals.org/content/106/11/1722.full

. . .
Even with testosterone or any steroid doping, the beneficial impacts can clearly provide a permanent benefit.

Dave.

Wrong. Sorry, but wrong. The bulking of testosterone gives an advantage maybe lasting weeks. Also, use of testosterone leads to long term dependence on artificial T. The quip on weight-building forums is that TRT (testosterone replacement therapy) is forever. T does not lead to permanent advantage beyond what the person could do without the T supplementation.

Those 2 studies on EPO are very nice, but they do NOT specify, nor indicate, any long term advantage. They are specifically measuring events during administration of EPO. None of the advantageous cell developments looked at are long term. See answer #2, to dirtyworks, below.

. . .
Interesting bit on bbc news the other day. Discusses how steroids are being used to STAY YOUNG.

Quite a good segment on the old guy in the gym - using steroids.

Also a bit where a doctor says they don't yet know the long term effects of steroids - but do know it increases TUMOUR GROWTH IN THE PROSTATE.....Mr Armstrong springs to mind.
. . .

Actually, if the doc said that, he was either disingenuous, or the quote was misleading. Quite a few long term effects are known, in the form of increased risk for various issues. The doc could have said that, meaning "that not MUCH is known, but there are risks that are known".

Also, they could be talking about simple maintenance hormonal therapy - which would have long-term beneficial effect for some people. In other words - our patient, Mr. X, produced 100mg of testosterone naturally when he was 25. Today he is 40, and only producing 10mg of testosterone. We add 90mg of supplemental T, and voila, Mr. X regains more performance ability. So, IF Mr. X has lowered levels of natural T, compared to what he once produced naturally, THEN yes, we can extend the number of years in which he can be active and productive at more youthful levels. If Mr. X does NOT have a lowered level of T, then no, we can not do this. Testosterone is self-limiting in natural production.

Depending on the drug, yes.

Two examples:

1. EPO use does it's magic, then when the athlete stops, their body's EPO production is practically shut off and they are temporarily worse off until their body makes it again. Someone can correct me if I've summarized that wrong.

2. Imagine the difference in fitness over 60 days if you can recover 1% better than a natural athelete. All without testing positive. There are peptide combinations for doing just that now and without the complications of on/off steriod cycles.

One research paper published long ago had the benefits of transfusions going out for weeks. Weeks!

#1 above - this is pretty much also my understanding of the mechanisms. It IS true of steroids. Idk about EPO. For EPO, I think you need to use your #2 - benefit fades in a short term timeframe.

#2 - weeks, yes. But this is short term, not long term. This means you could have a better season, or even a better year, but it does NOT mean you would get next year better as a result.

You could make an argument, and to an extent I would agree, that an athlete's long term performance is enhanced because they are able to maintain training regimens better over the long-term. I could see this, but I think this would be little different from what they COULD do naturally, IF they had the mental strength, internal discipline and drive.

 

[sideshadow]

I'm going to take a stab at worse than with

I think we can ask, would he be where he is now if he used no drugs at all?

Ok, so I don't make the same mistake twice, I read your reply as follows:

Old-fashioned EPO, the body "rebalances" EPO levels once the external administration stops almost immediately.

rhEPO, there is a temporary period where the body doesn't produce EPO, but it kicks off once the blood parameters return to normal.

No wonder they liked the stuff. Using steriods is far more complicated with the on/off cycles. That's not even including the masking efforts.

Correct. You might have read that drug tests showed so and so stopped producing natural EPO, but it's because of high [Hb], not due to exogenous rhEPO, as would be the case when using androgens. When the blood parameters return to normal, EPO production resumes as normal, as you said.

 

[Briant_Gumble]

@Hiero2. Great post!

 

[lean mean &green]

This is not true - or only partially true, and misleading. You do lose the extra gained muscle mass, by and large. You keep up to what you could have built up without the doping boost. Otherwise, Tammy would still be bulked up and shaving. Body builders are quite aware of this loss of mass.

TT is an extreme case, i don't know that it's instructive.

body builders are able to maintain some hypertrophy beyond they're natural gains even when they cycle "off" which they must do to overcome burnout/disaster. this is in fact, the real determinant of a successful program. adding mass while using anabolic androgenic steroids for a few weeks is actually the easy part, success is really measured by how well losses are limited when drugs are removed from the equation to restore some hormonal balance. female hormones are even sometimes added to limit side effects and to kick start the production of natural male hormones ie saving as many ill gotten gains as possible. after a short period of time the cycle begins again, probably with a different or percieved to be better cocktail of anabolics, followed by an off cycle, and so on and so on...

i think (my opinion) adaptations are more lasting than it appears through your posts but i could be misinterpreting your meaning. my thinking is that if someone uses AAS's skillfully for 10 years it may be a few years until the PE/hypertrophy/etc have completely faded if, and this is a very important if, they continue dedicated training.

 

[sideshadow]

This is not true - or only partially true, and misleading. You do lose the extra gained muscle mass, by and large. You keep up to what you could have built up without the doping boost. Otherwise, Tammy would still be bulked up and shaving. Body builders are quite aware of this loss of mass.

I suppose due to the negative feedback, that might occur, this could happen, but I don't think if you do it correctly and conservatively that you will return completely to baseline levels if you keep training. What do you think about GH/IGF-1?

Those 2 studies on EPO are very nice, but they do NOT specify, nor indicate, any long term advantage. They are specifically measuring events during administration of EPO. None of the advantageous cell developments looked at are long term.

Mmm, what would be the point of an study on the effects of EPO without administration of EPO? Those studies simply show that EPO produces effects, other than simply increasing [Hb], which of course will return to baseline when rhEPO is discontinued. The question is, in the context of a professional athlete, who has used rhEPO for years and who has a training stimulus nearly every day, will these changes (increased mitochondrial mass and increased vessel density) return to the levels they once were? If we had a study showing it either way I wouldn't ask. Neither mitochondria nor endothelial cells need continuous EPO stimulation, above baseline levels, to prevent destruction or to keep functioning. So why should it reverse?

I will accept that if those changes do occur they won't allow the athlete to perform supra-physiologically (>6w/Kg) but they could possibly get as close as possible, possibly closer than they ever could've without it.

You could make an argument, and to an extent I would agree, that an athlete's long term performance is enhanced because they are able to maintain training regimens better over the long-term. I could see this, but I think this would be little different from what they COULD do naturally, IF they had the mental strength, internal discipline and drive.

Thanks. I'm not saying I'm sure one way or the other, just asking the question.

 

[hiero2]

Two very good responses -

TT is an extreme case, i don't know that it's instructive.

body builders are able to maintain some hypertrophy beyond they're natural gains . . .

Ok. KEY to this statement is "beyond their (sic) natural gains". We don't really know that this is true. Neither do the body builders. We can, imo, take it as truth if amended by the modifier "during that time period". I.e. if they cycle a gain period for 6 weeks - at 12 weeks they could still have more mass than they would have had if they had only done the same sets and reps over the 12 weeks naturally. Feel free to correct the timeframes, I'm speaking hypothetically. What I am saying is that eventually, with continued training they would have gotten to the same spot naturally. Another way to look at it is this: eventually, even WITH the supplemented gain period, AND with continued training, their mass will return to the level that their natural hormone production levels will support.

. . .even when they cycle "off" which they must do to overcome burnout/disaster. this is in fact, the real determinant of a successful program. adding mass while using anabolic androgenic steroids for a few weeks is actually the easy part, success is really measured by how well losses are limited when drugs are removed from the equation to restore some hormonal balance. female hormones are even sometimes added to limit side effects and to kick start the production of natural male hormones ie saving as many ill gotten gains as possible. after a short period of time the cycle begins again, probably with a different or percieved to be better cocktail of anabolics, followed by an off cycle, and so on and so on...

i think (my opinion) adaptations are more lasting than it appears through your posts but i could be misinterpreting your meaining. my thinking is that if someone uses AAS's skillfully for 10 years it may be a few years until the PE/hypertrophy/etc have completely faded if, and this is a very important if, they continue dedicated training.

Btw - very good description of the gain process. Now, note the highlighted portion. Ok - and maybe so. You think they might maintain some hypertrophy for a few years. I don't think any such gain (the unnatural, supplemented portion) would last that long. I'm saying weeks, or at best, a few months. But, this is not my field, and I am not aware of any long-range studies of this. You might be.

I suppose due to the negative feedback, that might occur, this could happen, but I don't think if you do it correctly and conservatively that you will return completely to baseline levels if you keep training. What do you think about GH/IGF-1?

Notice I didn't comment on growth hormones. I think, from what I've read, this is the most promising area, when looking for long-term results and benefits. However, also from what I've read, we ain't there yet. Not by a long shot. Our knowledge of how this stuff works is woefully inadequate to insure a long-term low risk benefit. It's like interferon - supposedly we have refined and duplicated a natural occurring body substance. But, our knowledge of how it works is so incomplete that administering interferon is still "chemotherapy" - therapy by chemicals - with results far less positive than one would have thought 50 years ago when it was first played with. Does it help? Yes. Is it as good a discovery as penicillin? No way. The same with growth hormones. A lot of promise, not a lot delivered, and no real surety of WHAT is delivered long-term.

. . .Mmm, what would be the point of an study on the effects of EPO without administration of EPO? Those studies simply show that EPO produces effects, other than simply increasing [Hb], which of course will return to baseline when rhEPO is discontinued. The question is, in the context of a professional athlete, who has used rhEPO for years and who has a training stimulus nearly every day, will these changes (increased mitochondrial mass and increased vessel density) return to the levels they once were? If we had a study showing it either way I wouldn't ask. Neither mitochondria nor endothelial cells need continuous EPO stimulation, above baseline levels, to prevent destruction or to keep functioning. So why should it reverse?

I will accept that if those changes do occur they won't allow the athlete to perform supra-physiologically (>6w/Kg) but they could possibly get as close as possible, possibly closer than they ever could've without it.



Thanks. I'm not saying I'm sure one way or the other, just asking the question.

Notice I specified that these results were detailed DURING the administration of EPO. It is clear from your response, that you understand this, but many other readers will not, if it is not clear.

You say you see no reason for those changes that occur to revert. And, that you are not aware of studies looking at these changes long-term. Neither am I. However, normal cell death, while apparently reduced during the study, still occurs. Why would the new replacement cells imitate the artificially enhanced cells? Even according to the evidence referred to by this study, one would not expect that to happen. So, best possible situation would be that the changes stuck around so long as some of the cells that got changed stuck around and functioned. As those cells die and get replaced, part of the natural process, one would expect regression to the natural, pre-enhancement, levels, yes? The question, and I think you said the same thing, pretty much, is then - which cells get changed, and how long do they normally live? I know, for red blood cells, this is normally a fairly rapid process (rbc life cycle ~ 105-120 days). Similar for liver cells. Muscle cells go for years.

Actually, thinking about the cell aging process - I might have to change my opinion. Above, lean mean & green thinks that the reversion process might take years. If some of the hypertrophy adaptation to

gtg - I'll finish this later.
Back. Srry. Ok - had to tcob. Now, to stop and think WHY I originally came to the conclusions I've held to. It is because we know, through what research exists, and practical experience, that most of the effect of steroids and O2 vector doping is gone within weeks of cessation. Most is gone within days. Given that we have decades worth of testing that could still be done - in other words we don't have a lot of answers yet that we could have - I will grant the possibility that SOME benefit may be retained for years. I am still very sceptical, but it could be. I would have to estimate 10% or less, but that could still be significant in certain cases. But this could account for my experience and reading indicating benefit retention measured in weeks, and L M & G's experience and reading leading him to believe there is some benefit that could be measured in years.

 

[IndianCyclist]

while i am certainly not an expert, logically speaking, EPO would boost blood's oxygen carrying capacity. This would help to increase the exercise done by the leg's red muscles thereby increasing the red muscle mass. even after removal of EPO treatment the muscle gain would remain for long time.

 

[sideshadow]

However, normal cell death, while apparently reduced during the study, still occurs. Why would the new replacement cells imitate the artificially enhanced cells? Even according to the evidence referred to by this study, one would not expect that to happen. So, best possible situation would be that the changes stuck around so long as some of the cells that got changed stuck around and functioned. As those cells die and get replaced, part of the natural process, one would expect regression to the natural, pre-enhancement, levels, yes?

The one study only shows inhibition of apoptosis after organ injury and not normal cell death, but the point of that reference was just to show EPO-R are not confined to the erythroid lineage. The second one is more interesting which showed increased mitochondrial mass and increased vessel formation. It's purpose was also just to show that there are still effects that these drugs have, that we don't know of yet, whose to say there aren't more, and therefore should guys be allowed back after a two year ban if these drugs, and the increased training it allows for, could still have a residual effect?

Cardiac myocytes for the most part don't undergo death and regeneration, such as skin cells, and are classically thought of as a terminally differentiated organ. Only recently has it been shown that regeneration is possible following organ injury. This is the same with skeletal muscle cells and the change in size is largely due to changes in cell size and not number. An increase in death of these cells is usually pathologic, and under normal circumstances shouldn't occur in a healthy young adult.

@IndianCyclist. I don't think EPO will lead to an increase in muscle size, other drugs are better, and as for the second part of your question, that is what we are trying to find out.

 

[Dear Wiggo]

This is not true. Endogenous EPO production doesn't work via a negative feedback loop, such as your endocrine system, i.e. your body doesn't detect excess EPO and shuts endogenous production down. Instead, feedback regulation is based on the tissue O2 pressure, which, for the most part, depends on the Hb concentration. The most appropriate site for controlling EPO production are the kidneys, because pO2 remains relatively stable here. When [Hb], and thus pO2, are low it acts as a direct stimulus for endogenous EPO release. Of course when rhEPO is administered [Hb] is higher and there is no stimulus for endogenous EPO release, so it 'shuts down', but the moment [Hb], and thus pO2, falls back to normal, endogenous EPO release resumes as normal. (1)

Is it as simple as: for a fixed altitude (assuming constant atmospheric oxygen pressure [??]]) as Hgb concentration goes up, EPO goes down? Or is there more to it and if so do you mind expanding?

 

[Krebs cycle]

Mmm, what would be the point of an study on the effects of EPO without administration of EPO? Those studies simply show that EPO produces effects, other than simply increasing [Hb], which of course will return to baseline when rhEPO is discontinued. The question is, in the context of a professional athlete, who has used rhEPO for years and who has a training stimulus nearly every day, will these changes (increased mitochondrial mass and increased vessel density) return to the levels they once were? If we had a study showing it either way I wouldn't ask. Neither mitochondria nor endothelial cells need continuous EPO stimulation, above baseline levels, to prevent destruction or to keep functioning. So why should it reverse?
.

The question is whether those changes shown in the studies you linked to which are not involved in increasing O2 supply (eg: cardiac mitochondrial density), are capable of enhancing performance on their own in the absence of the EPO induced red cell mass increase.... regardless of whether or not those changes happen to be permanent.

Carsten Lundby has stated "there is no evidence indicating that EPO should increase exercise performance by mechanisms other than increasing oxygen transport capacity."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3082090/

It is very clear that blood volume returns to normal after cessation of EPO administration, so I would say that, definitely, once you stop blood doping and your blood volume returns to normal then VO2max does too since blood volume is one of the major limitation to VO2max. The published evidence shows this pretty clearly also. However, if long term use of EPO results in significant angiogenesis (which is thought to play a role in the %VO2max that can be sustained ie: lactate threshold) which remains for a long time after EPO use has stopped, then maybe it is possible that a former EPO doper can maintain a higher than normal (for them) %VO2max at LT than otherwise. That would confer a performance benefit. Capillarisation and mitochondrial density are plastic though and inactivity results in a decrease in these. So I doubt that someone who was not on supra-normal O2 transport would maintain supra-normal mechanisms of O2 extraction forever.

 

[sideshadow]

The question is whether those changes shown in the studies you linked to which are not involved in increasing O2 supply (eg: cardiac mitochondrial density), are capable of enhancing performance on their own in the absence of the EPO induced red cell mass increase.... regardless of whether or not those changes happen to be permanent.

Carsten Lundby has stated "there is no evidence indicating that EPO should increase exercise performance by mechanisms other than increasing oxygen transport capacity."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3082090/

It is very clear that blood volume returns to normal after cessation of EPO administration, so I would say that, definitely, once you stop blood doping and your blood volume returns to normal then VO2max does too since blood volume is one of the major limitation to VO2max. The published evidence shows this pretty clearly also. However, if long term use of EPO results in significant angiogenesis (which is thought to play a role in the %VO2max that can be sustained ie: lactate threshold) which remains for a long time after EPO use has stopped, then maybe it is possible that a former EPO doper can maintain a higher than normal (for them) %VO2max at LT than otherwise. That would confer a performance benefit. Capillarisation and mitochondrial density are plastic though and inactivity results in a decrease in these. So I doubt that someone who was not on supra-normal O2 transport would maintain supra-normal mechanisms of O2 extraction forever.

Yes, I agree with your post. Thomsen et al. showed that prolonged administration of rhEPO shows an even greater increase in submaximal performance than maximal aerobic capacity (1), as you've said the sustainable %VO2max could improve.

So if we assume CO to be adequate (delivering necessary O2) during submaximal exercise then surely rhEPO must improve performance by alternative mechanisms than by simply increasing [Hb] and maximum oxygen delivery to the exercising muscles? And then as you asked, will these effects remain? There of course is no proof. But, as it is sub-maximal performance that also benefits it seems that with correct training it might. At the very least EPO seems to provide a huge shortcut to achieving genetic potential faster, doesn't it?

(1) http://link.springer.com/article/10.1007/s00421-007-0522-8
(sorry couldn't find one with full free access)

@Wiggo. Yes that's right. If Hb goes up, with rhEPO administration, and pO2 is high you won't release endogenous EPO. Stopping rhEPO, [Hb] comes back down, pO2 goes down and EPO release resumes.

 

[Dear Wiggo]

@Wiggo. Yes that's right. If Hb goes up, with rhEPO administration, and pO2 is high you won't release endogenous EPO. Stopping rhEPO, [Hb] comes back down, pO2 goes down and EPO release resumes.

I am curious why it is normal for pro cyclists in the off season to have high Hgb AND high retic%?

Plasma volume contraction would be the norm, as they take time off or ease off the intensity over the off season. ie the cessation of high intensity training and/or racing that lead to plasma volume expansion means it is now reversed.

As plasma volume contracts, surely Hgb as a g/dL increases and endogenous EPO release and subsequent retic% would decrease, I would have thought?

 

[Dear Wiggo]

Yes, I agree with your post. Thomsen et al. showed that prolonged administration of rhEPO shows an even greater increase in submaximal performance than maximal aerobic capacity (1), as you've said the sustainable %VO2max could improve.

This is what we observe in Bjarne Riis, who bumped his Hgb off the charts, but still couldn't win the prologue. But when it came to a sustained climb he pretty much dropped everyone.

 

[Krebs cycle]

Yes, I agree with your post. Thomsen et al. showed that prolonged administration of rhEPO shows an even greater increase in submaximal performance than maximal aerobic capacity (1), as you've said the sustainable %VO2max could improve.

So if we assume CO to be adequate (delivering necessary O2) during submaximal exercise then surely rhEPO must improve performance by alternative mechanisms than by simply increasing [Hb] and maximum oxygen delivery to the exercising muscles? And then as you asked, will these effects remain? There of course is no proof. But, as it is sub-maximal performance that also benefits it seems that with correct training it might. At the very least EPO seems to provide a huge shortcut to achieving genetic potential faster, doesn't it?

(1) http://link.springer.com/article/10.1007/s00421-007-0522-8
(sorry couldn't find one with full free access)

.

Remember though that in that study they increased [Hb]. Thus CaO2 was also increased meaning that O2 convective flux at submax workloads is enhanced. In the Thomsen study they tested time to exhaustion at 80% of the pre EPO VO2max (ie: same absolute workload). So if VO2max goes up, this % goes down and of course you expect Texh to increase. In this case it is still a consequence of the enhanced O2 flux. They did one test at the same relative workload (ie: 80% of the wk 11 VO2max) and the time to exhaustion actually went down. That shouldn't happen if EPO stimulated non-haematologic adaptations that enhanced performance, so the results of that study actually support the conclusion that the main driver of improved performance following EPO doping is enhanced O2 transport capacity.

Carsten Lundby wouldn't be making such statements in later review articles if his earlier work (ie: he is the final author on the Thomsen paper) showed otherwise. The jury is still out IMO. It's possible there are other performance enhancing adaptations that remain months of years after the EPO use has stopped but at present if Lundby thinks there is no evidence of it, then that's good enough for me because he is probably one of the world's leading experts on the subject.

ps: don't worry about the fulltext access.... I've got that one covered ;-)

 

[sideshadow]

Remember though that in that study they increased [Hb]. Thus CaO2 was also increased meaning that O2 convective flux at submax workloads is enhanced. In the Thomsen study they tested time to exhaustion at 80% of the pre EPO VO2max (ie: same absolute workload). So if VO2max goes up, this % goes down and of course you expect Texh to increase. In this case it is still a consequence of the enhanced O2 flux. They did one test at the same relative workload (ie: 80% of the wk 11 VO2max) and the time to exhaustion actually went down. That shouldn't happen if EPO stimulated non-haematologic adaptations that enhanced performance, so the results of that study actually support the conclusion that the main driver of improved performance following EPO doping is enhanced O2 transport capacity.

Carsten Lundby wouldn't be making such statements in later review articles if his earlier work (ie: he is the final author on the Thomsen paper) showed otherwise. The jury is still out IMO. It's possible there are other performance enhancing adaptations that remain months of years after the EPO use has stopped but at present if Lundby thinks there is no evidence of it, then that's good enough for me because he is probably one of the world's leading experts on the subject.

ps: don't worry about the fulltext access.... I've got that one covered ;-)

Thanks KrebsCycle, you have been most informative. I am still not fully convinced, but time will tell I guess . Thanks.

@Wiggo. I'm not sure.