Dying to Win: Memories of Doping and Duping : Current Sports Medicine Reports

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Pearls and Pitfalls

Dying to Win

Memories of Doping and Duping

Eichner, E. Randy MD, FACSM

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Current Sports Medicine Reports 12(1):p 3-4, January/February 2013. | DOI: 10.1249/JSR.0b013e31827dc0e3
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The disgrace of cyclist Lance Armstrong brings back memories of doping and duping. This sad saga may hold lessons for those of us in sports medicine. Or if not lessons, it can bring at least dilemmas for us to ponder. Let me begin the story with a benchmark event 22 years ago.

The “Dying to Win” Session

At the Annual Meeting of the American College of Sports Medicine (ACSM) in 1991, I took part in a Current Issue session: “Dying to Win: rEPO, Blood Doping, and Athletics.” Up to 800 persons attended. I keyed on a recent spate of deaths in elite European cyclists. I noted that recombinant erythropoietin (rEPO) appeared in Europe in 1987, and the unusual deaths began soon thereafter. From 1987 to 1991, up to 20 competitive cyclists died suddenly and unexpectedly. Autopsy results were elusive, but cycling authorities said the deaths were from “heart attack,” “cardiac arrest,” or “cardiac failure.” To me, however, about 15 of the deaths seemed to fit a profile that suggested another explanation: They were young and improving fast, “rising stars” who died not during a race but at rest before or after a race. I recalled that at our ACSM meeting in 1990, a team physician with long experience with Dutch cyclists said he knew that some in the peloton were using rEPO. I suggested that this spate of atypical sudden deaths in top European cyclists was largely from the abuse of rEPO. I implied they were doping to win, and some were dying to win (3).

As soon as that session ended, I was accosted verbally by two angry European team cycling physicians who said my charges were reckless and baseless and I was “slandering the dead.” I replied: “Time will tell.” Now, 22 years and additional tragic deaths later, time has told. Let me explain.

From Blood to Mud

The rationale for abusing rEPO in competitive cycling is that by raising the hematocrit without unduly raising blood viscosity, one can enhance aerobic performance by enhancing oxygen delivery to muscles. By 1990, the first experiment on the effects of rEPO on athletes had been done, and the lead researcher was quoted to the effect that rEPO might enable an elite athlete to shave 30 s off a 20-min racing time (7). This is one point for sports scientists to ponder: How best to convey their research to the public without feeding the fire. That study was published in 1991 (5). Other studies followed, including a controlled study that also showed a performance benefit from rEPO (2). The abuse of rEPO continued in the peloton, and so did the deaths.

The problem is that the higher the hematocrit, the greater the risk of clots. Blood clots are the proximate cause not only of pulmonary emboli but also of many strokes and heart attacks. Coagulability hinges partly on blood viscosity, which is set by the plasma fibrinogen level, the deformability of red cells, and the hematocrit. Hematocrit also influences platelet adhesion, the first step in arterial thrombosis. Hematocrit, then, modulates the flow, fluidity, and coagulability of blood. As hematocrit increases toward 60% as in mountaineering, for example, blood clots can become a menace.

In 1991, a warning appeared in a prestigious medical journal on how fast hematocrit can rise with large doses of rEPO and how rEPO abuse by athletes could drive hematocrit to “dangerously high levels” (1). To oversimplify, it warned of “blood to mud,” ending up with blood too thick to pump and too easy to clot. This warning did not end the deaths. By 2007, after esteemed studies in patients with renal disease, cancer, and other major illnesses tied higher dosing of rEPO to greater risk of death from thrombotic events (heart attack, stroke, or venous thromboembolism) or heart failure, the Food and Drug Administration issued a black box warning on these risks from rEPO. Even this did not end the abuse of rEPO by athletes — or the deaths. Cyclists continued to dope, dupe, and die.

Sudden Deaths in Swedish Orienteers

A spate of deaths in orienteers paralleled the cycling deaths. Suddenly, among young, elite orienteers (but in no other Swedish sports), the death rate spiked to 1% a year for 3 years in a row. From 1989 to 1992, seven elite-level orienteers, all from the same small area of central Sweden, died during or after competitions or training. They knew one another and occasionally trained together. All performed very well shortly before they died; some placed near the top in national competitions. The last, Melker Karlsson, 24, was a rising star who died after a training run and sauna. His death was the final straw that led to a meeting of Swedish health experts to probe potential causes and solutions. As in the cyclists, the deaths were considered “cardiac,” and a popular hypothesis was a transmissible myocarditis, ascribed first to Chlamydia and then to Bartonella (9). Their supporting evidence, however, is not compelling and does not dissuade skeptics, including me, from speculating that a culprit in this spate of sudden deaths in top Swedish orienteers was abuse of rEPO.

High Hematocrits and More Dead Cyclists

Evidence from many believable anecdotes, from sworn testimony to the United States Anti-Doping Agency (USADA), and from police raids at the 1998 Tour de France and before the 2006 Tour de France shows that cyclists continue to abuse rEPO. Indeed, top South African cyclist David George was caught on rEPO (and admitted it) in August 2012. The culture of competitive cycling dies hard; despite the deaths and the black box warning, rEPO abuse in cycling has endured for 25 years.

In his affidavit to USADA, Stephen Swart, a teammate of Lance Armstrong in 1994 to 1995, said that their Motorola Team used rEPO for the 1995 Tour de France, and that most riders, including Lance Armstrong, had a hematocrit over 50% (8). It is widely reported that Marco Pantani abused rEPO and had a hematocrit of 60% in a 1995 race (4). And as noted in Tyler Hamilton’s recent tell-all book, Bjarne Riis won the 1996 Tour de France on rEPO, and his peak hematocrit was an astonishing 64% (6). For cyclists who abuse rEPO, there may be a thin line between winning and dying.

Alas, the deaths continue. From early 2003 to early 2004, eight more European cyclists died, and as I see it, up to five fit the profile of a likely rEPO death. Notable were French cyclist Fabrice Salanson, 23, found dead in his hotel room just hours before he was to start the Tour of Germany, and Belgian cyclist Johan Sermon, 21, who went to bed early to rest up for a planned 8-h training ride the next day, but was found by his mother dead in bed at dawn. In early 2009, the promising Belgian cyclist Frederick Nolf, 21, died at night in his Ritz-Carlton hotel room, after the fourth stage of the Tour of Qatar. He went to bed laughing and happy and never woke up. No autopsy was done.

How the autopsy results on Salanson were described to the press may come closest to the truth in this long, sad saga. Dr. Jan Dressler of the University of Dresden Medical Institute said the death was probably caused by the heart enlarging and the coronary vessels failing to pump enough blood. In other words, his blood was mud and was hard to pump and his heart stopped. Now that Lance Armstrong has fallen from grace and some of his army of conspirators and enablers have been exposed, maybe the fallout finally will change the culture of cycling and the rEPO deaths will end. We can hope.


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6. Hamilton T, Coyle D. The Secret Race New York: Bantam Books; 2012, p. 283.
7. Mantell ME. EPO: cycling’s atomic bomb. VeloNews. 1990; 19: 17–9.
8. Swart S. Affidavit to USADA, Sept. 17, 2012. Available at: http://d3epuodzu3wuis.cloudfront.net/Swart%2c+tephen%2c+Affidavit.pdf. Accessed Nov. 10, 2012.
9. Wesslen L, Ehrenborg C, Holmberg M, et al.. Subacute bartonella infection in Swedish orienteers succumbing to sudden unexpected cardiac death or having malignant arrhythmias. Scand. J. Infect. Dis. 2001; 33: 429–38.
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