EPO Helps Mid D More than Long Distance?

You only mention competition. Drugs are very useful (and used more often) in training than in meets. You're supposed to be a coach? Canova you truly are either a drug pusher or the dumbest coach ever. You try and defend your drug supporting by stating measurements that are only relevant in racing. Smoke and mirrors.

Mrr82 wrote:

You only mention competition. Drugs are very useful (and used more often) in training than in meets.

That's the entire focus of doping right now. More recovery, more power out of competition so you can train way beyond a clean athlete.

What makes EPO so wonderful is even micro-dosing is you lay off the stuff a few days before your meet and you get all the benefits and no chance of going positive.

The dumbest coach ever till now won 42 medals in WCh (including all categories) without using any drugs, and this is the first reason because I don't believe in the effects of EPO when there is proper training.

I think that also using microdoses the blood viscosity increases, so the real problem is not to use microdoses for being clean at antidoping controls, but which effect microdoses can have on the performance.

You say microdoses can help athletes in training, and you clearly don't understand what is training.

If training is at low intensity, athletes don't need any microdose.

If training is at high intensity, we have again the same physiological situation

of the competition.

Supposing EPO can help athletes to recover in shorter time, this fact is not important in training, because for every athlete, in the specific period, what ia important is the "external load" of specific training, which must be the same for different athletes if they want to reach the same performances, but this "external load" can have different recovery times, depending on the "internal load" for every different athlete.

Again, coaching is not a science, but an art.

And, of course, who depends 100% from some pseudo-scientific belief, doesn't have the ability and the sensibility for being an artist.

The theory that increased peripheral resistance would slow down blood flow so much that the amount of oxygen transported to the tissues actually actually falls was very much discussed in 1970s and 1980s.

The theory was somewhat valid and based (among other evidence) on test tube ("in vitro") studies performed in 1960s. It was shown that the calculated amount of oxygen increased with the elevation of hematocrit when hematocrit was increased. After the hematocrit reached the figure of 45, the amount transported started declining when the blood flow slowed too rapidly to counteract the increase in the oxygen carrying capacity of the blood.

But based on studies done on real subjects ("in vivo") this is fallacious.

There has almost never been a blood doping study where the cardiac output (Q) fell significantly enough to counteract the increase in hemoglobin concentrationafter the hemoglobin level was elevated. The Swedish team that "discovered" the blood doping in 1971 did another study and pinpointed that there was no fall in Q after reinfusion (nor any change in 2,3DPG level)

A 1987 Swedish study (Celsing, Ebklom et all) concluded that even people whose hematocrit level was naturally very high (~50-55) improved their performance after they were reinfused with five (!) bags of blood. This was even when some hematocrit valued increased above 60.

The measured "in vitro" increase of viscocity was still significant 40 %, so the team concluded only that the in vitro measurement of viscocity is meaningless and has little to do with real life situations.

If you have anything specific you'd care to discuss, please add it to this thread.

Renato Canova wrote:

The dumbest coach ever till now won 42 medals in WCh (including all categories) without using any drugs.

Canova states that his athletes are absolutely, positively, 100% not guilty of doping. That settles it, folks. Nothing to see here. His athletes do not dope. And they certainly don't dope with EPO, because EPO doesn't work.

Also, as you will note, it wasn't Canova's athletes who won medals, it was Canova himself.

Renato, the "blood viscosity" argument is flawed, and needs to be called out.

You are correct in saying that blood flow velocity decreases with increasing hematocrit. However, over a wide range in hematocrit, this decrease in velocity is small, and not nearly enough to compensate for the increased oxygen carrying capacity induced by the extra red blood cells.

http://bja.oxfordjournals.org/content/88/2/277.full

To use your lorry analogy; a low hematocrit would be like using half-empty lorries for transport. Yes, they may be slightly faster than full lorries, but the full lorries more than make up for it, because over a wide range of loads, the velocity of a lorry isn't nearly proportional to the weight of its cargo.

If you've read this post, please stop repeating the blood viscosity argument.

I have no idea if the blood viscosity argument is correct. I do know that the linked article is a few points for a tube that has NOTHING to do with when blood viscosity would be an issue for running.

When blood is flowing through a HUGE tube (for example 0.15 cm internal diameter) the cells don't interact with each other almost at all. When blood flows through a capillary in the body the cells interact with each other constantly and their effective viscosity is MUCH different.

From the article,

Method: Using a transcranial Doppler apparatus, we measured the peak velocity of whole blood cells pumped by a cardiopulmonary bypass (CPB) circuit, through a 0.15‐cm internal diameter segment of rigid tubing. BF and BFV relationships were obtained at temperatures of 19, 28, and 37°C and at Hct of 0.05, 0.22, 0.39, and 0.54, by altering CPB flow over a range from 10 to 100 cc/min. Linear regression analysis was performed.

mrr82 gets the smackdown, but he thinks he knows more than someone who's coached 42 world championship medalists, i.e. far more than the United States has won in the distances from 1983 to the present.

On viscocity I should point the following.

The Swedish 1987 study I referred above tried to find whether there existed an optimal hematocrit level for oxygen transport. Despite the 40 % increase in the test tube viscosity the optimal for oxygen transport was always the highest that could be achieved. The team concluded the following after this phenomenom:

"In conclusion, the results show a close relationship between Vo2MAX and [Hb]. Furthermore, both comparisons between individuals with high and low normal [Hb] as well as the individual response between [Hb] ranges below and abote the normal [Hb] suggest that the influence of viscosity as such on Vo2MAX is negligible...

It is a well-known fact that the peripheral circulation during exercise is different from that at rest since there is a considerable change in blood vessel diameter, blood flow, internal temperature and distribution of blood volume. These adaptations certainly counteract the negative influence of the raised viscosity caused by the increased [Hb]... n vitro methods available for measuring viscosity in humans used in the present study should be extrapolated to physiological conditions (especially during exercise) with great caution."

(Effects of anaemia and stepwise-induced polycythaemia on maximal aerobic power in individuals with high and low haemoglobin concentrations.

Celsing F, Svedenhag J, Pihlstedt P, Ekblom B.,

Acta Physiol Scand. 1987 Jan;129(1):47-54.)

On the question whether EPO helps "Mid D" more than long distance, the answer could be yes in my opinion. There are many more factors affecting the outcome of marathon run than simple Vo2MAX or lactate threshold. These factors include glycogen depletion, heat tolerance etc.

If you look how much marathon speed has improved after the introduction of EPO, the improvement has been somewhat lower when one compares how much 5k and 10k times improved during 1990-1999.

If I am not mistaken, blood doping can also help in shorter distances in ways other than elevating Vo2MAX because elevated red blood cell count could possibly increase the anaerobic capacity because red blood cells act as a lactic acid buffer. Unfortunately there is relatively little literature on this subject (apparently Marion Jones believed in it and used EPO).

Canova, You have said often that EPO does not work for elite athletes. Would you be okay with athletes competing against your athletes to use EPO?

I wonder whether EPO helps a marathoner make the decisive surge late in a race. Rita Jeptoo threw down a 4:48 mile to drop the field and set a massive course record. I would think that those kinds of surges would benefit from EPO in the same way a 1500/5k runner would due to the high VO2 max demand.

I try to teach to the athletes I train to look at themselves. I don't agree when an athlete, for example, says "I'm ready for winning Gold medal" in WCh or OG, because this situation is out of his control. Every athlete can only control his personal situation, and I like to hear athletes saying "my training, and my shape, are better than in the past. Since I had 27' in 10000m, now I know I can run in 26:40".

In my training phylosophy, the higher motivation for an athlete is to improve himself, that is the only thing he can have under control.

In 2005, during WCCCh, in the long run Eliud Kipchoge attacked Kenenisa with two laps to go. Kenenisa followed him easily, and Eliud finished the energy 500m before the finish line, reducing his speed till walking in the last 50 meters. His final position was 5th.

After the race, I spoke with him, asking "Why did you attack Kenenisa 4 km before the end of the race ?", and he answered "I tried my best".

"Sorry Eliud, you are the second in the World, and today your position was number 5. I think second is better than fifth, so you didn't try your best, you did a mistake".

How was possible to think to attack an athlete with WR in 5000, WR in 10000, already practically unbeated in Cross Country, when the PB of Eliud in 10000m was 40 seconds slower ?

You can hope to win a competition only when are very close the performance of the leader. But, when the leader is the best Bolt, or Michael Johnson, or the best Bekele, or the best Shaheen, or the best Isinbayeva, you need to know that your best is to be the second.

In some case, to be the second means to be the best among the Champions, after some "alien", and, if the alien makes some mistake (Kenenisa Bekele in WCCCH 2007 in Mombasa, or Isinbayeva with 3 faults at the first height in WCh), the second can become the winner (Zersenay Tadese or Rogowska).

So, the best thing is to concentrate in themselves. In this case, top athletes with this mentality don't care is the other are doped or not : in this way, also clean athletes with great talent can win Olympics, WCh and better WR.

Training at altitude causes naturally higher production of EPO and therefore RBCs (more oxygen per blood volume). Nearly all distance athletes at a world class level train at altitude. If this method does not work, why are they training at altitude? A runner would tend to train at slower speeds at altitude and be consistently more tired causing lower training volume. So that is 3 strikes against altitude training (Higher RBCs bad, slower speeds, lower training volume). Why is this the standard practice? Because it works. And EPO works in exactly the same way and can work on top of the altitude gains.

Mid D, Long D? Who cares where it is MORE effective. It IS effective. That is why it is used.

I can produce a lot of data, showing that not Always training in altitude causes a higher production of RBC, so this is not a rule.

For example, last year I had the opportunity to stay with all the Chinese Team of middle and long distances in Duoba (2400m high) for a period of about 8 weeks, and, since there is a good lab of physiology, I had blood tests on weekly basis with all the athletes, in order to test not only the difference in their blood values between BEFORE going altitude and AFTER, but the weekly changes (practically, the effects altitude produces, week after week).

After that period, we went Changbaishan (800m high) for the last 18-20 days before Asian Games.

We had some athletes improving dramatically : Ding Changqin (15'55" PB before training in altitude, winning silver in 10000 with 31'53" fruit of 16'20" + 15'33", and 3 days later bronze in 5000m with 15'12"), Zhao Jing (2'02" PB in 2013, without training till beginning of June because studied in the University for achieving the Master in Journalism, after one month at the beginning of July running 2'08" in Jinan, immediately after altitude training, in Changbaishan, 2'40" in 1000m, in Asian Games 1'59"48), Li Zhenzhu (9'53" in steeple in 2013, no competitions in the event in all 2014, winning silver with the last lap in 66" in 9'35"), other athletes remaining on their normal levels.

ALL THE ATHLETES IMPROVING (responders) had values LOWER than before going to altitude, while many athletes competing in Asian Games with higher Hct and Hb were not able to improve their previous performances.

So, it seems clear the reason because the "responders" improved is NOT the higher production of RBC, because this didn't happen.

Which is the reason ? Is the increase of AFFINITY between Hb and O2, that means the possibility to have at disposal more quantity of O2.

There is no doubt that training in altitude, in the 80% of cases, can give some advantage, ma the advantage is not where normally we look at.

Aragon, for understanding the validity of the studies you mentioned, we need to know some particular, that NEVER are clear in ANY research.

For example, when they speak about "performance" for the tested Group, what exactly this performance is ? Is something on teadmill lasting 5 or 10 minutes at max intensity, is an incremental test, or is a Marathon ?

And which is the level of the performance ?

One thing everybody must understand is that the "statistical parameters" for scientists, and for a coach, are completely different.

For researchers, the Group "elite" when they study the effects of running a Marathon includes athletes from the WR holder till 2:45. The Group of generally considered "well trained athletes" is between 2:45 and 4 hours.

The Group of "athletes with moderate training" includes runners between 4:00 and 5:00.

Instead, for a coach, athletes running in 2:11 are part of a totally different Group, as demonstrated by the all-time lists, because till now there are 1189 runners who ran under 2:11.

Personally, I already have problems to consider an athlete running 2:05:42 in the same class of the best, since at the moment this athlete is number 50 all time.

More data the researchers collect around average athletes, more deviation there is from the values of elite athletes.

The reality is that THERE ARE NOT RESEARCHES SPECIFICALLY CARRIED OUT with elite athletes.

In more than 30 years of my activity as coach of athletes of international level (not only African), too many times I saw situation well different from what the "classic" methodology had teached, and I found a lot of data very far from the data produced by the "official" physiology.

I agree that physiology should explain the effects of training, and of doping, on the athletes, but the reality is that almost the totality of scientific investigation are carried out on a sampling very far, and very different, from every elite athlete.

Of course, the human body is Always a human body, like a cas is Always a car. However, also if their mecanical principle are the same, I can't study a Fiat 500 for evaluating a Formula One.

There are too many assertions in the study of the Swedish scientists that are not correct, if referred to elite runners. For example, "the results show a close relationship between VO2 max and Hb" that really doesn't exist, since we have athletes with very high VO2 max but low Hb, and athletes with high Hb and low VO2 max. Not only, but VO2 max, in spite of the fact that physiologists continue to consider it an important parameter, has very little influence on the performance of endurance, of course inside a range very wide, but including high values. For example, the first athletes able running a Marathon under 2:10, the Aussie Derek Clayton, had a VO2 max of 69, very far from athletes who never were able to run so fast.

The fact is that I can't explain with the positions of the official physiology what I often see in training. And is not the training depending on physiology, but physiology depending on training, such as any experimental science.

So, I can describe what happens (this is a fact), and physiologists must explain the reason. The problem is that they are not able to explain what training of high level produces, because they don't know what this training is, and never have the opportunity to study a period of training of the best athletes, since training is a dynamic process, while their tests, following the classic protocolls, are "static pictures" of the final situation.

Renato Canova wrote:

The reality is that THERE ARE NOT RESEARCHES SPECIFICALLY CARRIED OUT with elite athletes.

Of course there is research with elite athletes. It is just not published because it is cheating.

Renato Canova wrote:

Of course, the human body is Always a human body, like a cas is Always a car. However, also if their mecanical principle are the same, I can't study a Fiat 500 for evaluating a Formula One.

But if you add an octane booster to either, the performance gets better because they both work on the same principle. Just as the human body does whether elite or hobby jogger. Performance percentages may vary, but the underlying principle will consistently produce a similar result.

Here is a very detailed explanation/metastudy of gas transport in the blood.

The only thing it doesn't say much about is the role of nitric oxide, which is a bummer because I'm trying to find out if nitro-loading really works. Disgusting red beet juice.

But it very clearly explains why your capacity to deliver oxygen to muscle is highest when you have a concurrent high anaerobic output, e.g. running MD. Which is a good thing, because you're running much faster then and need more power.

sorry try this

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3824146/