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Why does EPO work even below VO2max?

Dec 6, 2020
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Hey,

I was wondering this: if I am working at a steady-pace at, say, 90% VO2max, then it seems oxygen delivery is not a limiting factor.

Why then whould taking EPO make me faster, since I don't need more oxygen?

Thanks
 
Being below V02 max doesn't mean that oxygen isn't a limiting factor. I guess it depends on how you define limiting. At 90% V02max, you can sustain your effort for, let's say, one hour. You don't need any more oxygen to maintain that effort over that period. But if you take EPO, your V02max will increase, and so, therefore, will your 90% V02 max. So now you can sustain a greater effort for that period of one hour. Another way to put it is that with EPO, since your V02max is higher, the level of performance that was previously 90% V02 max is now lower, say, 85% V02max. You can sustain 85% V02max even longer than 90% V02max, so EPO also allows you to sustain your previous effort even longer.
 
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Hey,

I was wondering this: if I am working at a steady-pace at, say, 90% VO2max, then it seems oxygen delivery is not a limiting factor.

Why then whould taking EPO make me faster, since I don't need more oxygen?

Thanks
The intuition of Merckx index is sound and essentially accurate, but perhaps it should be added that it isn't automatic that an athlete who could maintain a 90 % pace of Vo2Max for an hour can maintain exactly also 90 % pace of the new and higher Vo2Max after EPO/blood doping.

In absolute term, he gets a boost of course.
 
Dec 6, 2020
2
1
15
The intuition of Merckx index is sound and essentially accurate, but perhaps it should be added that it isn't automatic that an athlete who could maintain a 90 % pace of Vo2Max for an hour can maintain exactly also 90 % pace of the new and higher Vo2Max after EPO/blood doping.

In absolute term, he gets a boost of course.

That is what I don't understand. By which mechanism does an athlete able to sustain 90% vo2max for an hour is likely to do the same at a higher vo2max? Why having a pace become 85% of vo2max make it easier to sustain?
 
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That is what I don't understand. By which mechanism does an athlete able to sustain 90% vo2max for an hour is likely to do the same at a higher vo2max? Why having a pace become 85% of vo2max make it easier to sustain?
Here is from the ACSM position stand on blood doping from experts such as Michael Joyner, Michael Sawka and Lawrence Spriet of whom two have researched blood doping themselves in experimental studies:
When VO2max is increased following blood doping, a given absolute power output represents a lower percentage of the new Vo2Max... Consequently, many investigations report unchanged Vo2, lower heart rates, lower venous and arterial lactate, and higher venous and arterial pH values at standardized submaximal power output following blood doping. This reduced physiological strain should contribute to improved submaximal performance after blood doping.
It is noteworthy that Michael Sawka measured also lower body temperatures after blood reinfusion in one of his papers from the late 1980s, which might also give some extra boost and delay the onset of total exhaustion.
 
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Can similar VO2 usage levels (including VO2max) be obtained REGARDLESS of the amount of muscle fatigue?
Does EPO (or other PEDs) reduce the effect of muscle fatigue, and allow the muscles to maintain their VO2 usage (and power output) for a longer time?
 
Being below V02 max doesn't mean that oxygen isn't a limiting factor. I guess it depends on how you define limiting. At 90% V02max, you can sustain your effort for, let's say, one hour. You don't need any more oxygen to maintain that effort over that period. But if you take EPO, your V02max will increase, and so, therefore, will your 90% V02 max. So now you can sustain a greater effort for that period of one hour. Another way to put it is that with EPO, since your V02max is higher, the level of performance that was previously 90% V02 max is now lower, say, 85% V02max. You can sustain 85% V02max even longer than 90% V02max, so EPO also allows you to sustain your previous effort even longer.
Same climbing speed that used to be say 180bpm clean, with EPO might drop to 170 bpm or even 160 bpm. Providing you trained that zone properly, it should become lots easier.

I say trained the zone, because:
I used to train way too specifically as a lad, quite frequent 5km solo attempts at a 600m track that barely required lifting for the corners. I barely had lactate even at threshold, it was quite hard to determine the zones for my trainer. 15-20 bpm below threshold, I'd be dying of lactate pain. Could barely finish a medium interval in that zone. I'd slip out of the zone on the top side and the lactate could flush for relief.
Trainer then gave me more of those medium zone intervals to do and I became capable of doing longer rides. 2-3 hours races are no fun with a lactate peak so high 15-20 bpm under threshold.
 
That is what I don't understand. By which mechanism does an athlete able to sustain 90% vo2max for an hour is likely to do the same at a higher vo2max? Why having a pace become 85% of vo2max make it easier to sustain?

As tuck pointed out, lactate is key. FTP, functional threshold power, is often defined as the power a rider can maintain for an hour. I think Andy Coggan, who used to post here, coined the term, or at least has promoted it. It more or less coincides with the power at which lactate is produced at the same rate at which it's removed--IOW, if you exceed that power, lactate accumulates, and you go into the red.

Let's say that your lactate threshold, LT, is at 90% V02 max. If you increase your V02max, the LT also goes up. Why?

Lactate is produced from pyruvate, which in turn is produced from glucose in the process known as glycolysis. If there is enough oxygen, pyruvate does not get converted into lactate, but rather enters the Krebs cycle, where it results in the production of ATP, the energy molecule necessary for muscular contraction. So you can sustain power up to the LT, which in this example, we're saying is 90% of V02 max.

If you increase V02 max, the concentration of lactate at which fatigue sets in will not be changed. But because you are taking in more oxygen, that level will be reached at a higher power output. More pyruvate is able to go to the Krebs cycle, so less of it is being converted to lactate. The LT will still be reached when you are taking in 90% of the oxygen that was taken in during your original V02 max, but since your V02 max is now higher, that will correspond to a lower % of V02 max. Or as Aragon's quote notes, at 90% of the new V02 max, the lactate concentration will be lower, hence now below the threshold..

An interesting implication of this, though, which hadn't occurred to me before, is that your FTP or LT should be reached at a lower % of V02 max than was the case with your original V02 max. That is, assuming EPO or other forms of blood doping don't affect the concentration of lactate at which fatigue sets in, they should lower your FTP as a % of V02 max.
 
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There is also some experimental evidence that the relative sustaineable power (% of Vo2Max) doesn't remain the same after blood doping. One paper of interest is the Thomsen et al paper titled Prolonged administration of recombinant human erythropoietin increases submaximal performance more than maximal aerobic capacity in which Vo2Max was elevated by 11-12 % with EPO, and time-to-exhaustion fixed at 80 % of the pre-EPO Vo2Max watts was increased by 54 % (which was of course only 71-72 % of the new higher Vo2Max).

It is interesting when they tested for how long the subjects could cycle at 80 % of the new Vo2Max watts, their performance time was 27 % worse than before the EPO-treatment.
 
time-to-exhaustion fixed at 80 % of the pre-EPO Vo2Max watts was increased by 54 %

Yes, that study was quoted a lot back then, by Ross Tucker particularly.

It is interesting when they tested for how long the subjects could cycle at 80 % of the new Vo2Max watts, their performance time was 27 % worse than before the EPO-treatment.

i assume you mean that it was 27% worse than performance at 80% of the original V02 max. The doped subjects were sustaining more power, just the same amount of power relative to the V02 max.
 
i assume you mean that it was 27% worse than performance at 80% of the original V02 max. The doped subjects were sustaining more power, just the same amount of power relative to the V02 max.
That is precisely correct, and the term "worse" is also very misleading from my part, because 27 % shorter duration in a TTE test with 12-13 higher watts isn't qualitatively worse in any meaningful metric. Here is chart to clarify the three tests (there was also a fourth one, but is is essentially the same as the TTE 2)

TTE 1 - baseline
W at Vo2Max= 330
W at test = 264 (80 % of the initial w at Vo2Max)
Time = 22 min

(EPO treatment, Hb jumps from 146 to 160 g/l)

TTE 2 - Post-EPO
W at Vo2Max = 374
W at test = 264 (80 % of the initial w at Vo2Max, 71 % of the new w at Vo2Max)
Time = 34 min

TTE 3 - Post-EPO
W at Vo2Max = 371
W at test = 297 (80 % of the new w at Vo2Max, 90 % of the initial "clean" W at Vo2Max)
Time = 16 min

It also looks as if the subjects really gave their best in the TTE 3, because the max lactate is on average 12 mmol/l whereas it is between 10 and 11 in all the other tests in the paper. (strange anecdote: the authors write that the relative intensity is 68 % in the TTE 2, but their own numbers of 264 / 374 give 70.6 %.