Eight Weeks on Moderate Doses of Erythropoietin (EPO) Build a Bigger Mitochondrial Engine and Shed Some Body Fat, but is That Really Worth Taking the Risk?

Image 1: These EPO containing Recormon vials are highly popular in the French Pyrenees ;-)

Fatty acid oxidation is certainly one of the buzzwords in the supplement industry. Interestingly enough, it is mostly used very indiscriminately for all sorts of physiological processes which are sometime more, sometimes less related to the actual process of β-oxidation, in the course of which the acetyl CoA are liberated from their original molecular bond. In fact, the majority of the currently available "fat burners" (those neat little pills with tons of fat liberating, but not burning stimulants in them) has no effect on the efficacy of this process. In previous posts, as the one on irisin and the utility of exercise induced increases of PGC1-alpha,  I have already hinted at the importance of "building a bigger engine", or, more formally, increasing the oxidative capacity of your mitochondria in your individual battle against your love handles and the global battle against obesity. Today, we are going to have a look at a not exactly kosher, but tried and proven drug everyone who has not deliberately ignored the media coverage of the Tour de France over the past couple of years will have heard of: Erythropoietin - short, EPO!

More red blood cells transport more oxygen to larger mitochondria

About two years ago, a group of researchers from the Duke University Medical Center discovered that the "blood-building" drug Erythropoietin had an unexpected yet not exactly undesirable side-effect: It activated cardiac mitochondrial biogenesis - or, to stick to the previously introduced "terminology" it tuned the lab rats engines (Carraway. 2010). Now, in the latest issue of Frontiers in Physiology a group of European researchers reproduced these results in a group of six healthy young men (21 ± 2 years, 180 ± 1 cm, weight 73± 2 kg) who participated voluntarily (no, the study does not state that those were Tour de France competitors ;-) in an 8-week trial. Over the course of the study period received an additional iron supplement (100mg; was in fact started 2 weeks prior) which, obviously in conjunction with the EPO treatment,

• 1st week: daily subcutaneous injections of 5,000IU of rhEPO
   
• 2nd-7th week: weekly subcutaneous injections of either 0, 2500, or 5000 IU, depending on the subjects' Hct level

was intended to raise their blood hematocrit (Hct) to ∼50% (which is considered still save, i.e. the risk of developing thrombosis is low, and the maximum allowed value in sports!) and to maintain that value throughout the study period. The Hct levels were controlled on a weekly basis and the rhEPO doses were adjusted appropriately:

After the 8 week intervention period, the mean Hct for the whole group was increased significantly to 51 ± 1%. Three of the six subjects received full treatment dosage with a total of 70.000 IU rhEpo over 8 weeks, while two subjects were administered 67.500 and 62.500 IU, respectively. The remaining subject exhibited a strong response to the rhEpo injections, and received a total of 50.000 IU. 

The maximal oxygen consumption of the study participants, which was measured during a standardized exercise protocol (+35W increase in resistance every 60s) on a braked cycle ergometer, increased regardless of the dosage that was required to keep the hematocrit values from 54 to 58ml/kg per minute (cf. figure 1).

Figure 1: Changes in body composition and measures of oxidative capacity in the course of the 8-week treatment period (data calculated based on Plenge. 2012)

Contrary to these 8.3% (+/- 2%) increases in VO2max, the changes in body composition, the scientists had expected based on previous rodent studies (Hojman. 2009) did not reach statistical significance, something I personally would yet not mind if my body fat percentage dropped by 2% after 8 weeks of doing nothing would set me up to shed even more fat. That is all the more true, because the statistical more than significant +22% increase in mitochondrial oxidative phosphorylation and electron transport capacity in the muscle fibers of my vastus lateralis, which are indicative of a profound increase in mitochondrial respiratory capacity, or, the aforementioned tuning of your mitochondrial engines, would set me up for further fat loss in the future.

"Cool, bro! Where can I get this EPO?"

Image 2: You better take their bikes than their drugs.

Yet although all this certainly sounds formidable and "exercise in a pill" always sells way better than real workouts, I guess I better put these results into perspective before you jump to any conclusions. After all, the 4-weeks intervention trial Jennifer L. Trilk and her colleagues from the Department of Kinesiology at the University of Georgia conducted in 2010, is only one out of many examples, which show that "artificial enhancements" like these may be highly beneficial for people performing at already superhuman levels, but comparably ineffective for the average, let alone the formerly sedentary human being (Trilk. 2010).

After all, the overweight women in the Trilk study achieved a +12% increase in VO2Max after no more than 12 HIIT sessions consisting of 4-7 30s all-out sprints on an cycle ergometer, which were seperated by four minutes rest. And let's be honest, if you'd rather take a highly expensive, potentially dangerous drug from the gray market than invest ~90min of your precious weekly TV time into some HIIT exercise, you should not wonder if you are sick and obese.