Dan Miller is an MU medical student with an individual National Research Service Award to study molecular diagnostics associated with Human Papillomavirus and head and neck cancer. He's also a state champion mountain biker and nationally ranked cyclocross racer. Miller has been living with metastatic cancer in his lungs and vertebrae since 2005.
In response to Lance Armstrong's recent doping scandal, Miller wrote:
He's a fallen hero.
I'm glad he stepped down from Livestrong. The evidence against him is insurmountable. It's tough, because even though he gave me a lot of hope and he's been a hero of mine since he won his first tour, I still think he's dirty. And sadly, it appears that he denied others a career for not doping while simultaneously forcing others to dope and launching incredible public humiliation campaigns against those who questioned him.
The basic crime is that he was a central player in the most sophisticated doping program in sports history and subsequently grew an empire that even as a cancer survivor myself, seems grandiose and even harmful. I've lost too many strong and young friends to cancer to believe the myth that one can beat cancer with willpower. I hate that their message essentially implies that those who succumb to cancer aren't "strong" enough or are otherwise inadequate.
I also think Nike should give their millions to American Cancer Society, instead of Livestrong.
Miller writes a blog called "Dan's blog" in which he recently posted the following about the science and effects of performance enhancing drugs.
"So, I have a question for all my cycling coach, exercise physiologist, fitness expert friends out there. If one took performance-enhancing drugs and improved their VO2 Max and LT, but then stop taking drugs is it safe to say they may still reap some benefits of the enhanced physiological adaptation brought on by the drugs, even years later?" — Brandon Dwight, of Boulder Cycle Sport.
I've thought quite a bit about this question, and although I'm not credentialed in any of the ways he specifically addresses, I do understand medicine, physiology, pharmacology and have a decent background in exercise phys. So this is all from my humble opinion:
The bottom line is that performance enhancing drugs can't all be grouped into the same category. That is to say that Epo and blood transfusions are completely different than Clenbuterol, diuretics, anabolics and things like growth hormone.
The physical demands of a baseball player are so incredibly different than those of a stage-racer cyclist, which in turn are pretty different than even mountain biking and especially track cycling. In baseball, cheaters want to get bigger, stronger and faster. So their enhancing pharmacology with things like growth hormone, estrogen antagonists and testosterone enhancers all reflect that. And those particular drug regimens definitely alter gene expression in such a way as to produce long-term, performance-enhancing benefits. I would imagine that track cyclists, if interested in the benefits of pharmacology, would utilize similar cocktails.
I'll never forget reading about some cat 2 cyclist from Houston who got busted taking a very advanced (medically speaking) estrogen antagonist and testosterone-enhancing approach. He was on a bunch of breast cancer drugs (which, as a cancer survivor, bike racer and physician-scientist in training, really pissed me off).
I'd predict that his ability to recover from training was enhanced and that he had a noticeable increase in short-duration power outputs on the bike. He probably won more sprints. But in terms of time trialing or stage racing, there's a certain point where there would be diminishing returns and frankly null or even detrimental benefits with that particular pharmacological approach.
That's simply because the demands of endurance sports are so incredibly different than power sports. And size especially, but also to some extent the myofibril adaptations associated with high-power, is/are detrimental to type-I (endurance, skinniness) oxidative fibers. It's literally like comparing the white meat associated with a chicken with the red meat of a buffalo. They're metabolically incredibly different, and everything from training to fuel-source are almost diametrically opposed. And this difference is mainly associated with the bold-faced term and has everything to do with oxidative phosphorylation, mitochondrial efficiency and the physiology associated with getting hydrogen ions away from and oxygen into working muscles.
Oxygen delivery. That's the name of the game in endurance sports. Anabolics and cortisol synthetics don't really affect it. Genetics are huge and effect pulmonary/chest anatomy and physiology in such a way that it's probably the biggest difference between a pro-tour rider and the rest of us. But the genetics of erythropoiesis probably don't factor in much ... which is to say that most people's bone marrow is on pretty similar playing fields. Unless, of course, you alter the kinetics of hematopoeisis. And like most things in physiology, you can increase hematopoesis or decrease it, and these events can occur naturally (you get a bacterial infection, your bone marrow makes more white blood cells) or pharmacologically/iatrogenically (cancer patient gets radiation treatment which damages bone marrow stem cells, so they become deficient in various blood cells).
Just to tie the point back to performance, it is the red blood cells which serve to help buffer hydrogen ions (which isn't always talked about but is a HUGE factor) and deliver oxygen from the lungs (genetically determined) to the working tissues. Measurements of red blood cells often confuse medical students and physicians, so it isn't worth the effort to go through the meanings of Hct, Hgb, MCH, MCV, reticulocyte count, RPI, etc.
But the key to discussing the answer to the question at the beginning of this post is that red blood cells hang out in the blood for around 4 months. So changing the kinetics of RBC production, like with EPO or simple increasing circulating RBC mass, like with autotransfusions have short-lived effects.
So in short, anabolics can have potentially long-term performance-enhancing effects. Drugs and transfusions to affect oxygen delivery almost certainly don't. But, since doping leads to enhanced performance, which can lead to winning races ... then (to quote Adam Myerson) "It can make the ability to return to that higher level easier than it would have if it was done cleanly, and incrementally." But more importantly, the access to better teams, better races, better support, and better money, all lead to an ability to do better preparation and reach a higher level still. So, not exactly the question you asked, but an example of how it can indirectly continue to benefit the level of fitness reached after doping."
To me, the use of EPO in endurance sports is a medical travesty, and if you want to seriously talk about long term effects of EPO use, I think you're getting into the realm of oncology and cancer biology. Synthetic EPO saves lives; mostly for cancer patients and renal failure patients. And like any drug that is ingested or injected, there are effects beyond those associated with the therapeutic benefit.
I was taught in medical school that there is no such thing as drug "side-effects." Biology doesn't work that way, there are only effects. For EPO, it's a mitogenic agent, or something that induces/promotes the cell cycle. Anything that does that, has the potential to facilitate conditions that lead to cancer. So in a sense, a cancer patient or former cancer patient that takes EPO is putting themselves at risk for more cancer. And in another, more abstract sense, spitting in the face of the patients for whom EPO was originally intended.
Personally, I've received enough radiation over the years that my bone marrow has taken a hit. When you measure my white blood cells and red blood cells, you can see that deficiency. Also, I ride and race bikes with active, living tumors in my vertebrae and in my lungs (although those in my lungs are only 5-10mm). I'm clearly not a world class athlete and could never be one, but my point in saying that is that these things effect oxygen delivery in my body, but I'm clearly still capable of having a decent power output at LT and VO2.
My own conclusion, based on understanding my own physiology, is that training can trump anatomy but only to a certain point.
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