Sportsscientists on EPO

[straydog]

Do you have a link to the article stating EPO as an effective treatment for depression?

http://www.ncbi.nlm.nih.gov/pubmed/19185286

This is one....it is not "stating"....it is merely evidential and certainly not proved yet

 

[David Suro]

Straydog,

Cool article. PubMed is awesome.

The article suggests a lot of topics that are worthy of further study. It's important to note that the study was performed on rats. I'm not sure how the researches are able to determine the mood state of a rat, but it seems to have something to do with a "forced swim" test. All seriousness aside, that sounds like a pretty fun experiment to conduct!

If research continues and administration of EPO is found to be an effective componenet of a treatment protocol for depression, then the WADA is going to have to consider implecations of the medical exemption rule.

I guess they could still use the 50% hard ceiling rule for hematocrit to ensure that there is a limit to the abuse of a possible loophole.

There might be a bright financial future for any psychiatrist who wants to be involved in pro cycling.

 

[David Suro]

Regarding elimination of carbon dioxide, there are a couple key points to consider.

When carbon dioxide is produced in the muscle tissue as a result of energy production via the electron transport chain (aerobic pathway), it exists in the muscle tissue in far higher concentrations than in the atmosphere. The atmosphere is less than 1% carbon dioxide. Thus, elimination of CO2 occurs primarily through simple diffusion. The CO2 is dissolved in the blood plasma and readily released from the plasma across the alveolar (lung) membrane.

Getting oxygen to the muscle tissue is a different story. Oxygen is needed in the muscle in higher concentrations than it exists in the atmosphere. The body, therefore, must have a process for concentrating the oxygen and delivering it. Hemoglogin in the RBC's and myoglobin in the muscle tissue are the key molecules in that process.

I do not know of a relationship between elevated hematocrit and increased rate of CO2 elimination. If anyone has a link, I would lilke to read it.

 

[straydog]

Straydog,

Cool article. PubMed is awesome.

The article suggests a lot of topics that are worthy of further study. It's important to note that the study was performed on rats. I'm not sure how the researches are able to determine the mood state of a rat, but it seems to have something to do with a "forced swim" test. All seriousness aside, that sounds like a pretty fun experiment to conduct!

If research continues and administration of EPO is found to be an effective componenet of a treatment protocol for depression, then the WADA is going to have to consider implecations of the medical exemption rule.

I guess they could still use the 50% hard ceiling rule for hematocrit to ensure that there is a limit to the abuse of a possible loophole.

There might be a bright financial future for any psychiatrist who wants to be involved in pro cycling.

Yes it does....how did they "force" them? Gunpoint? A Cat?

There are quite a few other articles on the research being done, (it was the first one I found in a very quick search just to get one for you) on it's anti depressant efficacy....and I believe there are already some clinical (human) trials here in the UK being carried out....and more in the pipeline

And I suspect the 50% ceiling, and the bio passport parameters, will be the practical way forward.

It's amazing what (and for why) some people have TUE's at present....and also will be interesting to see in the future what "experimentative" remedies are granted TUE status.

 

[forty four]

great thread good discussion.

 

[onefastgear]

Hi David, thanks for your comment. I have no evidence for the CO2 theory and was merely 'thinking out aloud' about a potential role, but it seems unlikely given what acoggan said.

As for the O2 part, I was under the impression that despite the muscle's need for high amounts of O2 in aerobic metabolism, it still moves down a concentration gradient to reach muscle - the so-called Oxygen Cascade. The parital pressure of O2 at sea level is 760mmHg x 0.21 = 159mmHg, and this cascades down a gradient to the mictochondria where the partial pressure is 2mmHg, the "Pasteur Point" , where partial pressures below this level means that aerobic metabolism ceases. (Apologies for my non-SI units, but it's what I'm familiar with).

I have always thought in fairly simple terms about the oxygen flux equation and what can be reasonably varied to improve O2 content and thus delivery (ie haemoglobin and cardiac output). A couple of excellent posts between the physiologists on this forum have opened my eyes to many of the other variables that govern O2 uptake and delivery and have even speculated at what may be coming in terms of performance enhancement.

Makes for good reading. Although I must admit the troll threads/posts are great for a laugh.

 

[onefastgear]

Reti production will be stimulated almost "immediately" (as half life of i.v. epoetin alpha is just 6-8 hours). Small doses are even washed out completely during the ca. 10 hours time-window over night. Eris will have matured within a week.

Microdosing should be even more effective unit by unit. Huge amounts of (s.c.) EPO inhibit endogen production much more than small (i.v.) doses because of a) supranormal levels and b) insufficient supply of iron.

Thanks .38 for that answer. The question had come up at work when another anaesthetist asked me what the point of taking EPO during a race, and I hadn't stopped to consider the time-frame it before.

It was speculated in another thread that perhaps EPO is now 'old news', and that riders have 'moved on' to autologous transfusing. The mission now is to look for a reliable marker. I thought 2,3-DPG might hold some promise (as the level falls in stored blood), but the textbooks suggest that it is replenished within hours of re-infusion, so looking for RBCs with differing 2,3-DPG is probably unhelpful.

 

[acoggan]

I was under the impression that despite the muscle's need for high amounts of O2 in aerobic metabolism, it still moves down a concentration gradient to reach muscle - the so-called Oxygen Cascade. The parital pressure of O2 at sea level is 760mmHg x 0.21 = 159mmHg, and this cascades down a gradient to the mictochondria where the partial pressure is 2mmHg, the "Pasteur Point" , where partial pressures below this level means that aerobic metabolism ceases.

Your understanding is essentially correct. The only thing I might add is that:

1) the intracellular pO2 can be even lower than 2 mmHg, especially in the immediate vicinity of the mitochondria (you can think of them as O2 "black holes" ), but even so

2) the rate of mitochondrial respiration generally is not limited by O2 availability...only at exercise intensities approaching/exceeding the maximal VO2 of a particular muscle are anoxic foci detectable.

Finally, note that saying that anoxia is not present is not the same as saying that O2 availability doesn't influence metabolism...and in fact Wilson has presented a fairly strong case for O2 availability to play a role in regulating the rate of mitochondrial respiration even when its availability isn't rate-limiting per se.