I am a rabid fan of road bike racing.
There, I said it.
I am that person who scans the web at every free moment, looking for tidbits of information regarding the latest race results and updates on my heroes in the peloton. The geek in me loves to gawk at the latest and greatest carbon fiber and titanium machines each spring. I’ve even traveled to some of the big races, including the World Cycling Championships and the Tour de France, to watch as these remarkable athletes whiz – or toil – by.
It is not often that one can convert a pastime into something productive at work, but in 2004, I managed to do just that.
It was July, and Lance Armstrong was competing to win his sixth consecutive Tour de France. Many observers were convinced that he and most of the other favorites were using performance enhancing drugs (PEDs) – a suspicion Lance confirmed last year during an interview with Oprah Winfrey. One of the most powerful PEDs for endurance sports like cycling is injectable erythropoietin, or EPO. A synthetic version of a hormone naturally produced by the kidney, EPO aids performance primarily by stimulating your bone marrow to produce excess red blood cells. These, in turn, carry greater amounts of oxygen from your lungs to your muscles.
Race organizations had already realized that this excess can be dangerous. Several riders died in their sleep in the late 1990s, the blood in their arteries “sludging” due to blood counts far above the normal range. The organizations began testing riders for their blood counts, banning those with counts above a certain limit from starting a race because of safety concerns. By 2001 they had an EPO test, which should have ended the drug’s use. Yet, during the next several years, blood testing revealed that riders’ red blood cell counts appeared to remain steady throughout the grueling three-week Tour, when they should have been falling from continued exertion. The riders, it appeared, were micro-dosing EPO.
Meanwhile, an Outside Magazine reporter decided to test EPO on himself for a story. He found that the drug not only helped him in the grip of exertion but it also allowed his muscles to recover more quickly. Riding hard for four or five days in a row was suddenly possible for this amateur bicyclist.
That made me wonder: Could EPO benefit one’s performance in some way beyond increasing oxygen transit? Was there a direct effect on the heart and skeletal muscle when EPO is injected?
Enter my good friend Dr. Peter Van Buren, a clinical cardiologist and long-distance cross country skier who also directs a research laboratory at UVM. Peter’s primary research interest is in how heart muscle fails. I knew that Peter’s team had been analyzing tiny human heart muscle samples obtained at the time of heart surgery.
I figured that it wouldn’t be too difficult for Peter to test the samples for evidence that human heart muscle had a receptor for EPO – that in effect, the heart was a target for EPO and would respond in some way when stimulated by EPO. Before I spoke to him I did a quick literature search and found my questions had not previously been answered. One day while we were sitting in the echocardiography lab between studies, I told Peter my suspicions, and possibly in part due to his own athletic fandom interests (EPO was heavily abused by professional cross country ski racers at that time as well), he agreed to analyze some of his samples.
Peter came back a couple of weeks later and said that there were definitely EPO receptors on heart muscle cells! However, he wasn’t satisfied with just that (and others soon after did publish the very same findings). Over the next several years, Peter and his team continued their investigation, and eventually published their findings in 2012 in the Journal of Molecular and Cellular Cardiology. Most pointedly, they showed that under the influence of EPO, heart muscle cells seem to contract more forcefully and relax more quickly between contractions. Though there may be no direct correlation between cellular behavior and performance of the entire organ, the finding suggests that EPO possibly improves a heart’s strength, efficiency, and overall function. In other words – to carry the conjecture further – EPO may improve athletes’ endurance performance and recovery because the muscle in their heart and skeleton work more strongly and efficiently under its influence.
Of course, the value of this line of research isn’t just that it may explain how top cheating athletes get an unfair advantage. It may someday lead to the use of EPO-like medications in the treatment of congestive heart failure.
So here I am today, still scanning all the websites and parsing the pirated coverage of bike races all over the world – all for another research idea. (Really!)
Prospero B. Gogo, MD, is Director of the Cardiac Catheterization Laboratory at the University of Vermont Medical Center and Interventional Cardiologist. He is an Associate Professor at the Larner College of Medicine at UVM.
Hefer D, Yi T, Selby DE, Fishbaugher DE, Tremble SM, Begin KJ, Gogo P, Lewinter MM, Meyer M, Palmer BM, Vanburen P. Erythropoietin induces positive inotropic and lusitropic effects in murine and human myocardium. J Mol Cell Cardiol. 2012 Jan;52(1):256-63.