THERE’S A NEW STUDY from Danish researchers at Aarhus University, published in Experimental Physiology, that explores how the endurance drug of choice, EPO, works.
The simple picture is that EPO stimulates the production of red blood cells, which improves delivery of oxygen from the lungs to the working muscles, which in turn allows you to run (or bike or swim or whatever) faster. In reality, the picture is a little murkier. Any race longer than 10-15 minutes takes place below VO2max – so does increasing your max really improve performance in sub-maximal aerobic exercise? A 2007 study from another Danish group showed that time-to-exhaustion at 80% of VO2max was increased by about 54% after just 4 weeks of EPO. But this raises another puzzle, because over the same time period, VO2max (i.e. maximal oxygen transport) increased by just 12.6%. Where does the extra boost come from, if not from better oxygen transport?
That’s the question the new study addresses. What’s unique about the study design is that they divided their 36 subjects into four groups: one did 10 weeks of training (3 bike sessions per week) and received a placebo; a second trained and received EPO; a third did no training and received a placebo; and the fourth did no training and received EPO. Because EPO and endurance training have many similar effects, there’s always uncertainty about what changes are caused by training itself, EPO itself, or the combination of the two. The aim of this particular study was to see whether EPO helps to stimulate changes in muscle fibres (e.g. size increases, transitions to more slow-twitch) and in the growth of blood vessels within the muscles.
The answer, in short, is that EPO didn’t do anything to muscle fibres and blood vessels. Training (with or without EPO) increased fiber size, capillary density, and several other parameters; EPO didn’t make it better or worse.
On the other hand, EPO did have the expected effect on red blood cells. Here’s a look at the hematocrit (the fraction of red cells in your blood); bear in mind that 50% was the “no start” threshold that cycling instituted to discourage EPO use in the 1990s:
[SP = sedentary/placebo; SE = sedentary/EPO; TP = training/placebo; TE = training/EPO]
It’s interesting that in the non-EPO groups, training actually seems to suppress hematocrit a bit, perhaps because the overall plasma volume is also increasing as a function of training – but EPO reverses that effect pretty quickly! So for anyone who says “Oh, EPO doesn’t really do anything, you still have to do the training…” Well, it’s true that you still have to train, but this graph makes it pretty clear that EPO has powerful effects on its own. Along those lines, VO2max jumped 27% in the training-EPO group, but it also jumped 15% in the sedentary-EPO group. Not too shabby.
So if muscle changes don’t explain the “extra” boost of EPO, what does? There are a number of theories – for example, it apparently influences brain function and improves mood and perceived physical conditioning. But I’m not entirely clear on why there needs to anything extra. Time-to-exhaustion tests generally produce percentage changes that are as much as 10 to 15 times bigger than time trials, so a 54% boost in time to exhaustion compared to a 12% boost in VO2max doesn’t necessarily seem out of line to me. Either way, it’s a powerful drug.
***
