EPO Helps Mid D More than Long Distance?

longjack wrote:

EPO was used three days per week during the "corrective phase", which is the first two weeks of a cycle. Typically, it was on Mondays, Wednesdays and Fridays. It was only used once per week during the "maintenance phase" thereafter, typically this was every Wednesday. The dosage was 4,000 IU per injection. The purpose was to increase the red blood cell count and enhance oxygen uptake and utilization. This substance provides a big advantage to sprinters because it enables them to do more track repetitions and obtain a much deeper training load during the off season.

that makes no sense. Sprinters don't do aerobically intense workouts, they take long recoveries. No matter how many reps they do it won't tax them aerobically nor in terms of pH.

More logically, the benefit of EPO to sprinters would be to allow their muscles to contract more forcefully and to clear acids more quickly. Greater training load is the steroids' gig.

Back before the passport the elite athletes were merely trying to avoid failing an epo test and weren't concerned with microdosing

Renato is correct when he says many blood samples are now needed to prove doping under the ABP system

The fluctuations evident in the older pre-ABP era samples examined are much wilder and reliably indicate doping as ashenden has concluded,so Renato is incorrect here imo when he concludes that 1-2 older samples can't prove doping

Renato Canova wrote:

Webby, the statistics say that 77 Kenyan samples have hematocrit levels four standard deviations above the mean and well Beyond what altitude training can produce, but we don't know who are the owner of these 77 samples.

I already explained that the only way for understanding if an athlete is doped or not, using the BP, is to have clear "longitudinal" informations about his behaviour for a period of 2-3 years, with not less than 8-10 blood tests.

And also I explained that blood values are individual, and to try to relate the blood values of one athlete with a statistic mean is a big methodological and scientific mistake..

Exactly. Why does it surprise anyone that athletes who are at least 5-6 sigma anomalies performance-wise to have natural hematocrit levels that are 4 sigma anomalies?

That's the reason for longitudinal studies, aka biological passport. But if you have an athlete that has access to an on-clubhouse medical lab , and whose coach has been admitted to have done illegal testoterone studies on his own son, you have a lot to be suspicious of him when his T values are consistently at the borderline of what is considered "allowable"

Just sayin, I don't agree with your last opinion.

With 2 samples it's not possible to have any suspicion of doping, because you can't know which of the two samples is the "basic clean value" of the athlete.

Before WCCCh, I had one of the Chinese athletes with values as 9.8 Hb and 29.6 Hct. This was a clear case of anaemia, in fact she was practically not able to run fast : Always tired, no recovery and no muscle strength.

Few days ago, she ran the best chinese time of the season in 1500m, and the second chinese performance (and PB after 8 years) in 5000m.

Of course, her blood values are very different compared one period to the other. In this case, the values before WCCCh were so low that everybody understand she was sick. But suppose she was only a little under her usual values, because of some deficit of iron, for example, and she could have an antidoping test in this occasion. Comparing this value, with the value she can have when in shape, we can find a big gap, but... which of the two values we decide is the "normal value" ?

It's not possible to have only a simple idea, if we don't have at least 6 tests, but only comparing 8-10 tests we can have a good picture of the real situation.

Renato,

Thanks for your reply. I always enjoy your contributions, and always defer to you on matters related to coaching. And often on matters related to drugs. In this case, however, you admit that you are not a scientist. I am a scientist. A statistician, specifically. And since the leaked data have come out, I think your arguments about the effectiveness of doping on elite athletes is too far-fetched to warrant any further consideration.

Yes, the 77 samples may belong to 77 athletes or 20 athletes, but we know that 1/3 of medalists have hematocrit that is absolutely off the charts high. So high that many doctors will never come across numbers like these in their careers. So we know that either athletes with high levels are drawn to the sport because they are better, or something that they do or take creates high levels. Nothing that you have ever argued about the physiology of top athletes could explain what we have learned from this leak.

On the other hand, blood doping that leads to improved performance explains it perfectly.

hypothetically speaking wrote:

Renato Canova wrote:

Webby, the statistics say that 77 Kenyan samples have hematocrit levels four standard deviations above the mean and well Beyond what altitude training can produce, but we don't know who are the owner of these 77 samples.

I already explained that the only way for understanding if an athlete is doped or not, using the BP, is to have clear "longitudinal" informations about his behaviour for a period of 2-3 years, with not less than 8-10 blood tests.

And also I explained that blood values are individual, and to try to relate the blood values of one athlete with a statistic mean is a big methodological and scientific mistake..

Exactly. Why does it surprise anyone that athletes who are at least 5-6 sigma anomalies performance-wise to have natural hematocrit levels that are 4 sigma anomalies?

Renato wrote this week that having high hematocrit levels does not predispose an athlete to better performance.

Just a few random thoughts on the ABP-IAAF debate, because I don't want to ”troll” on every subject and because I haven't followed the issue too closely.

It should be emphasized that the debate on the OFF-scores, ”natural values” and ABP is far from over, so there should be at least some caution before accepting any claims of Ashenden/Parissotto if there is no further data made available.

For instance, Danish blood doping specialist Rasmus Damsgaard has the opinion that there was actually no conclusive evidence that either Lance Armstrong (2009-2010) or speed skater Claudia Pechstein (2009) had blood doped when they were stripped of their achievements based solely on blood parameters.

Pechstein lost in two sport arbitration hearings and Lance lost his 2009 TDF bronze based on the somewhat vague claim that Armstrong's blood values were ”consistent” with blood doping (low reticulocyte + not falling Hct during Tour + relatively quick changes in parameters). It was claimed that there was one in million possibility for these occurring naturally, a charge that Damsgaard – who supervised some of the blood testing – disagrees with.

And here is also a somewhat troubling quote from a few years old research paper on blood doping referring to Mr. Ashenden's study:

”Ashenden and co-workers... performed a study where ‘microdoses’ of rhEpo were injected in healthy volunteers for up to 12 weeks... ABP software did not flag a single subject as being suspicious of doping... A further concern raised by the study was that one sample before any rhEpo injections had occurred was designated 'abnormal'.”

Without questioning the claim that blood doping has been prevalent, it would be interesting to know on which parameter(s) Ashenden/Parisotto have based their judgments (hematocrit, OFF-score or...?). I think that high OFF-score is the only one where a single test could be suspicious and even this can't totally exclude the possibility of low erythropoiesis due to illness or fall of androgens (overexhaustion etc).

wejo wrote:

We were talking today and I was saying I thought I had seen a thread saying EPO would help mid-distance runners more than long distance runners because they are competing closer to their max.

Does anyone remember the thread or the concept? Am I off base?

Also, I think there was something about how EPO would help cyclists more than 10,000m runners or vice versa. It obviously can help everyone but helps some more than others.

This is just hypothetical but I have tried some "theoretical" numbers in the past.

Let's consider a primary 800 guy of 1'44.00 ability

His 400 speed say is 47.00

He may or may not have any 1500 ability, but those 2 numbers can give us a theoretical line of fit :

47.00 / 1'44.00 ->

3'32.00

7'41.51

13'35.24

29'15.48

2"21'42

Now, the crucial aspect is what is going to happen to the 800/400 when he dopes up on EPO

Let's say, he gets it down to 1'43.00.

My quite experienced eye reckons obviously his 400 will also improve as it has an aerobic component, but not as much as the 800, which has much more improvement

( It would be down to ~ 46.55 if it did )

My best guess is that you would be looking at 1/3s improvement over 400 -> 46.67

46.67 / 1'43.00 ->

3'29.55

7'35.33

13'23.37

28'47.50

2"19'07

Theoretically, I reckon a "proper" amount of EPO doping will improve distances by as follows :

400m - ~ 0.7%

800m - ~ 1.0%

1500m - ~ 1.2%

3000m - ~ 1.4%

5000m - ~ 1.5%

1000m - ~ 1.6%

M - ~ 1.9%

( I've done bit of rounding up/down )

EPO should improve performances for increasing race distance by ~ those % age amounts if used properly

( obviously more if you really ramp it up to dangerous dosages )

So the data shows that 2/3 of the medalists were not suspicious? Maybe hematocrit level isn't connected to performance the way we once thought it was.The data from the IAAF haven't been leaked to the public. The public could put the argument to rest, because they have been arguing without data all along.

webby wrote:

Now that the statistics from IAAF have leaked, I think we can put this argument to rest. Or can someone here explain how 1/3 of medalists (and 77 Kenyan samples) have hematocrit levels four standard deviations above the mean and well beyond what altitude training can produce? (Keep in mind RC's view that people with naturally high hematocrit don't have an advantage.)

Does winning cause hematocrit to rise?

As I have mentioned, blood doping (at least in theory) increases also the anaerobic capacity, so it could have a positive effect on anaerobic performance also. And there does exist some effects that blood doping can have on performance independent of the increases of Vo2MAX. These include::

1) Increased oxygen flow do brain enhances mood, motivation and subjective well-being. ”If there were handlebars attached to the earth, I would lift it”, boasted one Finnish runner right after a transfusion.

2) In one study, noradrenalin concentration of subjects doubled after the EPO administration. This could be helpful particularly during marathon because it could fight the effects falling dopamin/serotonin – ratio and central fatigue (I hope someone wiser than me can clarify if this is indeed the case). The hormone also enhances mood and is hypothetized to be the cause of so-called ”runner's high”.

3) Increased heat tolerance. One literature review on the subject concluded this on the phenomenom some 26 years ago:

”In many forms of endurance exercise, particularly in hot conditions, a significant part of the cardiac output is involved in heat dissipation with blood being shunted through the superficial layers of the skin to dissipate this heat. This part of the cardiac output is therefore not available for the transport of oxygen to the exercising muscle; thus, performance is limited. If, because of a raised haematocrit from blood doping, a smaller proportion of the total cardiac output can supply the same amount of oxygen to exercising muscle, this releases a larger component of the output for this secondary role of heat dissipation which can therefore be more efficient and will allow a higher work rate in unfavourable environmental conditions.”

(M Jones and D S Tunstall Pedoe: "Blood doping--a literature review", Br J Sports Med. 1989 Jun; 23(2): 84–88.)

There are now and then other possible effects also listed. These include, for instance, that EPO binds iron and thus protects cells and that EPO changes the muscle type from faster to slower (one rodent study). All the above are very underresearched subjects and overshadowed by the elevation of the oxygen carrying capability of blood, which is indeed the most significant effect in my opinion.

When one thinks the increase of the noradrenalin level, it is interesting to speculate whether microdosers of EPO got an edge over their competitors during Tour de France via this pathway also.

I don't think that anyone ever argued that you had to have doped blood to win. Only that it helps So 1 in 3 medalists having blood stats that put them at the far reaches of the distribution does anything but indicate that "hematocrit level isn't connected to performance the way we once thought it was."

I can accept that you may not choose to convict any individual based on extremely suspicious blood from one test. What I'm talking about is the certainty that you don't get results in a sample of 5000 athletes that look like this if there isn't systematic doping. And the fact that the pattern changes dramatically after the biological passport rule took effect makes the conclusion even more obvious.

Honestly, I'm surprised that there is so much debate among smart posters.

A big part of the reason for "debate", is that there is so little real data, for the subject population, that it supports a broad array of interpretations.

You claimed that "doping for performance" explains the 1/3 value quite well -- but fail to see that it doesn't explain the other 2/3. A model that explains 1/3 of the results needs more work.

Maybe you can talk about this 4 standard deviations of hematocrit. I didn't see the source of this claim anywhere -- where can I find it? That way I could be sure that I'm not responding to something you just over-interpreted.

When looking at blood profiles, the scientists measure 7 variables: "hemoglobin, hematocrit, red blood cell count, mean corpuscular volume, mean corpuscular hemoglobin, mean cell hemoglobin concentration, and reticulocyte percentage", which help form the conclusions of "suspicious" or "likely doping".

The "suspicious" values would be dependent on many other factors besides hematocrit. Help me understand why you are not oversimplifying this.

rekrunner wrote:

You claimed that "doping for performance" explains the 1/3 value quite well -- but fail to see that it doesn't explain the other 2/3. A model that explains 1/3 of the results needs more work.

It's not supposed to explain the other 2/3 because it doesn't claim to describe all doping, just blood doping.

Most of these blood tests are years old anyhow. There's something new going on, some sort of metabolic accelerator that allows some elites to compete at a weight that would normally lead to injury or overtraining. And/or a new stimulant. Only the poorer countries are still recklessly using blood boosters.

I am intentionally using shorthand. My point stands. And I didn't say that it explains 1/3 of the values. I said it explains perfectly all of the findings, in which 1/3 are classified as outrageously off-the-scale implausible, and the rest are . . . we don't know yet.

What we do know is that if you were to take the 100 best clean athletes in the sport and add in 50 doped athletes, you could end up with 1/3 of medalists being doped. The same could happen if you added 100 or 500 doped athletes to the mix. Not sure why you see a 1/3 - 2/3 split as inconsistent.

What is clear is that you don't get 1/3 of medalists with blood values occur 0.1% of the time (or less) in the general population unless either the values are artificial or the sport selects for people with those values to a degree that we have not seen with any other aspect of physiology.

When you use shorthand, I can't be sure you are not getting things wrong.

What does it mean for 1/3 of the medalists having a hematocrit value four standard deviations from the mean?

I found a reference that says 3 standard deviations corresponds to 53% hematocrit. Yet you claim (a shorthand equivalent) that 1/3 of the medalists, and 77 Kenyan results, would have had one standard deviation more than 53% hematocrit.

The point I made about performance and the relation to blood values -- if the 1/3 athletes and the 2/3 athletes have statistically the same performance, then another perfect explanation is that the changes in blood parameters didn't make a significant difference in performance.

The key word and the interesting word in the subject is "MORE".

I thought "no way", but look at former ADMITTED EPO drug cheat Christian Hesch.

What did he improved more in comparatively? Clearly he improved more in the mile. He went sub-four, which blows away all other equivalents.

Most of his results are vacated, but if you take them to McMillan, you could say he improved most at Mid D.

I agree with point one.

In point two, if noradrenalin increased after EPO administration, that would be a performance enhancing effect. Does that mean that the EPO caused the increase in noradrenalin? No, it doesn't. The increase is a product of our emotional response to stress.

With point three, an increase in blood plasma volume over a period of hours and days is a normal response to heat stress. With EPO administration, the plasma volume is lower, so less is avalable for heat dissipation through sweating. If the EPO doped athlete is also using a plasma expander, then this would negate the supposed benefits reasoned by the authors.

With regards to your point about noradrenalin, there is no doubt that noradrenalin is a performance enhancer, since it increase both cardiac output and concentration on the skills required for improved performance. What I am saying is that there is no drug that can improve this ability. It really is all in your head.

To make a long story short, the study I referred has the following data:

During maximal exercise, arterial noradrenalin concentration of the test group was 1.042±0.343 mol/l before EPO administration, whereas it was 2.136±0.6 after the subjects had been treated with EPO for a few months. Authors do mention this only in passing and the cause and effect is not clear.

I don't know much more about the world of stimulants than average person, but I know that there is this substance called amphetamine. The Encyclopedia of Sports Medicine tells us the following: ”Amphetamine and its derivatives are sympathomimetic amines, chemical analogues to the natural endogenous catecholamine hormones epinephrine, norepinepihrine [=noradrenalin] and dopamine... amphetamine appears to potentiate the activity of the natural catecholamines.”

I went quickly through the 1987 Sawka study where the heat mechanism was tested. Here is a summary of the most significant findings:

Our data indicate that polycythemia provides a small thermoregulatory advantage for euhydrated nonheated-acclimated individuals. The rate of heat storage values, as calculated from esophageal temperatures, were lower postreinfusion for 11 of 12 observations... We can hypothesize a potential physiological mechanism for improved sensible heat exchange after erythrocyte infusion, namely, that the elevated arterial O2 content allowed a reduced skeletal muscle blood flow and thus increased cutaneous blood flow at a given cardiac output during submaximal exercise...

Our data indicate several new findings concerning acute polycythemia: 1) the increased erythrocyte volume was associated with a reduction in plasma volume to maintain the same blood volume as during the preinfusion measurements; 2) polycythemia reduced total circulating protein but did not alter F-cell ratio, plasma osmolality, plasma protein content, or plasma lactate at rest or during exercise-heat stress; 3) polycythemia did not change the volume of fluid entering the intravascular space from rest to exercise-heat stress; and 4) polycythemia tended to reduce the rate of heat storage during exercise-heat stress.

Even I had a some trouble focusing on the study, but there you have it, my friend.

By the way, plasma expansion doesn't necessarily negate the Vo2Max increase associated with blood doping. There has been for some time this debate whether plasma expanders increase or decrease performance (ie. whether the increase in Q can (over)compencate the lower hemoglobin level). If my memory is right, after reviewing the literature, blood doping specialist Norman H. Gledhill came to the conclusion that ”volume loading” didn't alter Vo2MAX to one way or another significantly.

But as I mentioned in my original post, all of these "non-oxygen carrying" effects of transfusions/EPO are still somewhat unproven.

The second of my sentences should read:

"During maximal exercise, arterial noradrenalin concentration of the test group was 1.042 +/-0.343 mol/l before EPO administration, whereas it was 2.136 +/-0.6 after the subjects had been treated with EPO for a few months. Authors do mention this only in passing and the cause and effect is not clear."