EPO: Duration of effect and recovery protocol?

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I haven't responded because I don't know the answers to your questions, and have a couple of my own.

You are right that it can take a couple of weeks for erythrocytes to go through the maturation process once EPO is given. In an average person the lifetime of an erythrocyte is about 120 days. So does that mean once you reach your desired hematocrit, it will remain there for 120 days until the "extra" red blood cells die off?

Also, in athletes training hard does the 120 day lifetime still apply? Is the lifetime shorter because the blood cells are being pumped through the body faster to supply the oxygen needed by working muscle?

During your recovery phase it sounds like you are assuming that you will have a low hematocrit, presumably because you are assuming the EPO will work in a negative feedback manner to suppress natural erythropoietin production. I don't think that is the case, but I could be wrong. I have never heard that it does.

Posted by: Nandi12

I haven't responded because I don't know the answers to your questions, and have a couple of my own.

You are right that it can take a couple of weeks for erythrocytes to go through the maturation process once EPO is given. In an average person the lifetime of an erythrocyte is about 120 days. So does that mean once you reach your desired hematocrit, it will remain there for 120 days until the "extra" red blood cells die off?

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I don't think so. I think RBC life is shorter in athletes. As well I think exo EPO only exerts its effect for 4-6 weeks.

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Also, in athletes training hard does the 120 day lifetime still apply? Is the lifetime shorter because the blood cells are being pumped through the body faster to supply the oxygen needed by working muscle?

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These are good questions. My hcrit is high year round, probably due to a constant high volume of endurance training. I assume (know) there is a constant cycle of cell creation and destruction, as there is in all systems. Training stresses the body so it adapts by raising natural EPO levels. Very high volume training and/or prolonged high intensity (ie long stage races or prolonged frequent racing) tends to suppress natural hematocrit. During the Tour riders hcrits actually drop due the incredible stress of the race. They have done a few studies that back this up. An athlete probably reaches his natural EPO levels during normal training and then needs a bout of high altitude training, frequent racing or a stage race (balanced with rest) to induce EPO levels to rise as part of the adaptation response. I know that the increased RBC effects from these three scenarios last about 30 days (personal experience). I think the life of RBCs may be shorter in high level endurance athletes, probably due to the stress of extended training. Increased energy metabolism probably accelerates RBC destruction along with the stress of extended endurance training.

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During your recovery phase it sounds like you are assuming that you will have a low hematocrit, presumably because you are assuming the EPO will work in a negative feedback manner to suppress natural erythropoietin production. I don't think that is the case, but I could be wrong. I have never heard that it does.

I read a study or clinical info which stated that exogenous EPO has a negative feedback effect on natural EPO production. I'll try to get this study out tomorrow. It was pretty reliable. Also I've gotten some anecdotal info that corresponds with this.

FHG

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I read a study or clinical info which stated that exogenous EPO has a negative feedback effect on natural EPO production. I'll try to get this study out tomorrow. It was pretty reliable. Also I've gotten some anecdotal info that corresponds with this.

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I'm sure that while you are on EPO your natural production is reduced, since hypoxia is the primary stimulus for natural EPO production, and hopefully you won't experience as much hypoxia while doped (that's the goal). But do the erythropoietin producing cells in the kidney atrophy (like LH producing pituitary cells during an AAS cycle) so that after your EPO cycle natural production is lowered? That's what I'm curious about.

While I don't have anything to document this, I really don't think that exEPO has a similar negative feedback relation to natural EPO production as AS does to natural test production.

Cyclists stay on EPO far longer than most athletes stay on AS. Also, most of the cyclists that I know who have used EPO have come off of it without any problems whatsoever, and while retaining impressive amounts of endurance...they can still smoke me anyday.

AS gains seem to be less permanent.

Once again...just my opinion...I've never used EPO.

Posted by: Nandi12

I'm sure that while you are on EPO your natural production is reduced, since hypoxia is the primary stimulus for natural EPO production, and hopefully you won't experience as much hypoxia while doped (that's the goal). But do the erythropoietin producing cells in the kidney atrophy (like LH producing pituitary cells during an AAS cycle) so that after your EPO cycle natural production is lowered? That's what I'm curious about.

Here is the study was referencing. Once again those jacked up rats come into play...

Funny...the study was done in Belgium-they should've just studied people rather than rats. There are plenty of Belgians on EPO! There are some crazy drug experiments racing the Belgian kermesse circuit.

Piron M, Loo M, Gothot A, Tassin F, Fillet G, Beguin Y.

Department of Medicine, Division of Hematology, and the Department of Clinical Biology, Division of Laboratory Hematology, University of Liege, Liege, Belgium.

Little information is available on the evolution of erythropoiesis after interruption of recombinant human erythropoietin (rHuEpo) therapy. Iron-overloaded rats received 20 daily injections of rHuEpo. During treatment, reticulocytes, soluble transferrin receptor (sTfR), and hematocrit increased progressively. This was accompanied by a substantial expansion of spleen erythropoiesis but a decrease in the bone marrow. Five weeks after treatment, rats developed a significant degree of a regenerative anemia. Erythropoietic activity, as assessed by reticulocytes, sTfR, erythroid cellularity, iron incorporation into heme, and the number of erythroid colonies, was severely depressed 3 weeks after cessation of rHuEpo. This was followed by regeneration of erythroblasts and reticulocytes at weeks 6 to 7 post-Epo, but erythroid progenitors recovered only partially by that time. The anemia was definitely corrected 2 months after cessation of rHuEpo treatment. Serum Epo levels remained elevated for several weeks, but the sensitivity of marrow erythroid precursors to Epo was preserved. No rat antibodies to rHuEpo were detected, and serum from post-Epo animals did not exert any inhibitory activity on erythropoiesis. In conclusion, after cessation of intensive rHuEpo therapy, there was a strong inhibition of erythropoietic activity with secondary anemia followed by late recovery. This was not due to antibodies or other soluble inhibitory factors, a defect in endogenous Epo production, or a loss of sensitivity to Epo. This may rather represent intrinsic erythroid marrow exhaustion, mostly at the level of erythroid progenitors but also at later stages of erythropoiesis.

PMID: 11154221 [PubMed - indexed for MEDLINE

FHG

That's a great reference, fhg. So it's not like feedback inhibition, but rather the exhaustion of erythrocyte precursors. AAS might help recovery. I had posted a couple of abstracts earlier on an EPO thread that showed AAS work upstream from EPO on the most primary class of progenitors. But then again, EPO's effect probably stresses even the most basic progenitors by virtue of forcing development of their progeny. Very interesting. Thanks for posting that.

Now we need to figure out how to get around it. Old fashioned Lasse Viren style doping would certainly help during recovery.

Posted by: Nandi12

That's a great reference, fhg. So it's not like feedback inhibition, but rather the exhaustion of erythrocyte precursors. AAS might help recovery. I had posted a couple of abstracts earlier on an EPO thread that showed AAS work upstream from EPO on the most primary class of progenitors. But then again, EPO's effect probably stresses even the most basic progenitors by virtue of forcing development of their progeny. Very interesting. Thanks for posting that.

Now we need to figure out how to get around it. Old fashioned Lasse Viren style doping would certainly help during recovery.

So would my protocol of increased iron and B12 be useful in EPO recovery? What other components/precursors would be needed?

FHG

I just pulled out a physiology text and read that indeed when Fe falls to < 50 mcg erythropoiesis is impaired, but it does not say at what level. If it is downstream from the BFU and CFU precursors, Fe might not help. I need to find a hematology text to check.

Posted by: Nandi12

Old fashioned Lasse Viren style doping would certainly help during recovery.

Reinfusion of RBCs (yours or a friend's)-yes? Was Lasse a XC skiier or speekskater? I thought he was a winter athlete (obviously by the name!)? Whoever he was he was very very sneaky-well not too sneaky since we now know what he did.

FHG

He was a runner. He denies doing it, claiming that training at altitude was responsible.

Posted by: Nandi12

He was a runner. He denies doing it, claiming that training at altitude was responsible.

Whether he blood doped or not is moot (in regards to his critics or his need to deny it). It was legal before 1985 (at least in cycling-I supposed running may have had different rules and banned substances). It may have been 'unethical' or 'very strongly not recommended' but it wasn't outlawed until 1985. The 1984 US cycling team participated in blood doping and was investigated. During the investigations the team medical staff said they did indeed blood dope and the riders did acknowledge this. However no one was sanctioned as it was not a banned method. The UCI (international cycling governeing body) and IOC and USOC couldn't sanction them. However blood doping was prohibited in the years after the '84 games. Seems pretty inocuous now compared to all the drugs out there.

FHG

Current tests will catch you for blood doping as easy as they will catch you for AS use.

If you RBC is above a certain number (it varies) then your guilty of blood doping.

You can make the "my special diet" argument just like johann mulegg, but they will still rake you over the coals.

However RBC is so easy to test and controll that athletes probably dope just enough to stay slightly below the cutoff.

Austrians were caught this year with blood doping paraphenalia. None were caught.

I think they used either the sick grandma or sick dog excuse.
Priceless.

nandi,
I'm not sure why...but every time I have blood work my coach is always focused on my ferritin levels. If they aren't high enough (really fucking high), then he makes me double my iron supplement. Luckilly, its free, so no big deal.

how high was your ferritin levels?

when i was taking feosol (oral iron from savons) and doing my hypoxic tent, my ferritn was like 1,200! but my rbc was 5.0, hgb 16!, hct 49! and no AS or epo. Also it is a tricky thing to read blood work , cause you also got to take in acct:

MCV,MCHC,RDW, plt count.

also my doody was dark-sign of possible too much iron.