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Saturday, June 23, 2007

Know your drugs - understanding the Tour de France

OK, we promise that when the race starts, we'll start focusing on the cyclists and give you detailed analysis and discussion about the riders in the race. Then we'll talk about why Vinokourov is better on the shorter climbs than the longer ones, why Boonen is such a great sprinter and why the guys who time-trial well are often nowhere to be seen on the climbs.

But for today, in keeping with our previous post on drugs, we thought we'd give you the scientific low-down (in every day language) on what the drugs that have been in the news actually do. In otherwords, in keeping with our quest on The Science of Sport, we aim to explain the HOW and WHY? behind sports performance. And unfortunately, that includes drugs and doping.

So we look here at two commonly used drugs, both of which have been in the news quite heavily in the recent past.

1) EPO

EPO, short for erythropoeitin, is a hormone that is normally produced by the kidneys. It then has its effect on the bone marrow, which produces more red blood cells. So the effect of injecting synthetic EPO is to increase the body's natural production of red blood cells. Why would you want to do this? Well, the theory is that the red blood cells, which carry oxygen, are an important determinant of performance ability. That's because the oxygen is required by the muscles and the theory for fatigue during exercise is that if your muscles do not get sufficient oxygen, they rapidly fatigue. Connecting the dots, you get the logic that if you can increase the body's oxygen carrying capacity, you increase the ability to exercise before fatiguing.

And this is probably correct, but it might be a little over simplified. Why, for example, does EPO have it's greatest effects during endurance exercise like a Tour stage, where the cyclist is not really riding very close to their aerobic limit? In otherwords, if EPO was improving performance by increasing oxygen delivery to the muscle, then it would be most effective in the event where oxygen delivery is the potentially limiting factor. And when is oxygen potentially limiting? During shorter, higher intensity exercise, like 1500 m running events, perhaps up to about 15 minutes of exercise. Longer than this, and oxygen supply is not really limiting. So anyone who's ever ridden for 5 hours will tell you that you never really hit that limit, because you don't exercise near your maximum level. So we believe that EPO must have some other effect in addition to the one it has on the blood and oxygen levels.

Bottom line though - EPO works, and so that's why cyclists use it. The problem is that the more red blood cells you have, the thicker the blood becomes - it becomes more viscous. Imagine adding flour to a mixture of milk and water when you are baking. Eventually it gets so thick that it's difficult to mix. The heart has to do the 'mixing' for the blood and so if the red blood cell count is too high, then the heart has to work harder. There was a spate of sudden deaths during the night in young, fit European cyclists about 5 years ago - these were all rumoured to be linked to EPO use, because the cyclist's hearts were just not able to pump the blood anymore.

I once saw the most chilling quote in a book - it spoke of how some cyclists would actually set their alarms to go off a few times a night, and they would then wake up, cycle for 10 minutes on the indoor rollers and then go back to bed. The idea was that they would increase the heart rate and 'protect' the heart from having to pump too much per contraction. The quote was that "Cyclists would live to ride during the day, and then ride to stay alive at night".

EPO has now become much easier to detect, though there are of course still problems. However, i suspect that there are other, similar but undetectable drugs being used. Remember the BALCO scandal of five years ago? Just because someone has not tested positive does not mean they are not using - some drugs are created specifically to ensure that they are not detectable. So I think there may well be drugs out there that will be discovered in maybe 10 years, but which are improving performance now.

2) Testosterone

The second drug we look at is the male sex hormone, testosterone. This was a super famous drug in the 1980's, when, together with similar anabolic drugs, it became widely used by sprinters and field athletes, particularly those from East Germany and other Eastern Bloc countries (where many of these synthetic hormones were created). In general, anything ending in -one or -ol is an anabolic, used by athletes to increase muscle mass and promote recovery. Ben Johnson famously broke the 100 m world record in Seoul 1988, only to be stripped of the title and record for use of Stanozolol, an anabolic steroid.

More recently, testosterone hit the news after Floyd Landis tested positive after the 2006 Tour, specifically a stage where he heroically clawed back a huge deficit to claim the yellow jersey.

Testosterone, as we've said, is an anabolic agent, which increases muscle mass when used in conjuction with training. So why would a cyclist in the Tour de France wish to use it? For one thing, cyclists need to be small, so that they can climb 10% gradients on mountain passes without having to haul too much mass up the climb. Secondly, testosterone is used best over long periods, in conjuction with training. It would have little effect when used once.

So either we have an anomaly, or perhaps Landis (and others, perhaps?) are using it every day, but not being detected. It's important to remember that one is only picked up if the ratio of testosterone to another hormone, epitestosterone exceeds 4, then they do further investigation. So it's possible to use both testosterone and epitestosterone in the right amounts and never be picked up by this screening process.

But we still haven't answered why a cyclist would use it? Some fascinating research from Spain has showed that during the course of the three-week Tour, a cyclist's testosterone levels, together with other hormone levels, decrease progressively. This decrease has been linked to an impairment in performance - the final time-trial in the Tour de France, for example, is always quite a bit slower than the first time-trial. So performance goes down over the course of the race, and so do the hormones. The theory is that the stress of riding 5 or more hours every day puts the body into what is called a "catabolic" state - everything is breaking down. Now, in theory, the use of testosterone, which is "anabolic", prevents this and allows the cyclist to recover better. And so this is why it would be used - it prevents the normal decline in hormone levels and performance over the course of the race.

So that's an overview of two of the drugs that have been (and seem to be, and probably will be) used for cycling. Let's hope that the 2007 Tour is not affected by these or any other doping products, and that we can enjoy writing about the cyclists instead of the doctors for three weeks in July!

Ross

7 Comments:

Lei said...

Fascinating post! I didn't know that EPO is erythropoietin. But why do athletes take EPO (and risk side-effects and being caught) when the same effect can be achieved by training at altitude? Training at altitude stimulates the body to increase EPO production naturally.

Thank you for the comment on my blog, too. I've been reading your blog in awe for a little while now! I admire what you do. Keep up the great work!

RunnerGirl said...

Wow - this is a really good and intereting blog. Such an intereting post!

LuckyLab said...

It would seem most riders have now adopted the training at altitude method (or sleeping at altitude in tents, which also seems to help). The benefit of training and sleeping at altitude is that it seems to provide a natural upper limit to hematocrit levels, unlike synthetic EPO, and can keep you at the upper end of normal without putting you dangerously above. Taking EPO now is just the lazy way to do it.

Normal hematocrit range is on the order of 36-45% red blood cells of whole blood volume (the rest is plasma, white blood cells and platelets). This can be pushed slightly higher or significantly lower due to natural events. Chemotherapy can push hematocrit levels dangerously low, so low that not enough oxygen gets to the brain and other vital organs. However, due to blood viscosity problems, which can cause clots and cardiovascular stress among other things, hematocrit levels don't often naturally exceed 55%.

Hematocrit levels by themselves are also a very poor method of detecting doping as the actual volume of red blood cells is not going to vary much while the plasma volume can flucuate wildly due to dehydration. A drop in plasma will bump up the hematocrit level. It can be used to prescribe further testing, but by itself is not an ironclad indicator of a doper.

A somewhat interesting assumption is that a 20% increase in hematoctrit levels is equal to a 20% increase in performance. Since there are other factors to performance than blood's oxygen carrying capacity, EPO use is likely to be substantially less effective than is assumed by many. The performance numbers of "former" dopers seem to bear that out, assuming they are not, in fact, continuing to dope.

Ross Tucker and Jonathan Dugas said...

HI Lei, Runnergirl and LuckyLab

Thank you for your posts and kind words. They are very stimulating. As you have seen below, I have put a couple of new posts up in response, to try to answer the questions, inspired by your posts!

LuckyLab, you make some excellent points and much of what I write in a new post is repeating what you've raised here, with some other ideas perhaps.

But thanks again and hopefully my response posts cover some of the questions and issues!

Ross

Ed said...

In your discussion of EPO you speculate that EPO must have other benefits independent of its O2 carrying capacity: Not necessarily! Actually the increase in oxygen carrying capacity could also help those in events longer than 15 min. In both biking in hills and virtually all xc skiing events the terrain is uneven calling for bursts of increased effort. A higher O2 carrying capacity would help in these situations all through the race, no matter how long it is. Your speculation, ie. reg. benefit for the first 15 minutes only, would seem to apply only for a continuously even running marathon or road bike event.

Ross Tucker and Jonathan Dugas said...

Hi Ed

Fair point, but EPO still has its biggest effect on performance during steady-state exercise. For example, when Tour de France riders climb up a mountain like Alp d'Huez, they sustain a power output that is close to a ventilatory threshold, which usually corresponds to about 80% of their maximum oxygen carrying capacity (it's about 6W/kg, their max is usually about 7w/kg.

There are some shifts in this power, but if you look at the power output profiles, it's not great. An attack which lasts 30 seconds picks the power up to about 650 W, but then it drops down right away to 400-450W for the rest of the climb.

Yet this is where EPO has its most profound effect - a study from Denmark found a 54% improvement in performance at a sustained power output, for example. And this doesn't make sense if EPO's sole benefit was to increase the oxygen carrying capacity. It must therefore act elsewhere as well, or is mediated via its effect on how the brain regulates performance in response to oxygen capacity of the blood.

Ross

Anonymous said...

Thanks for this post, very interesting effects of EPO usage. Any idea how this translates to marathon running? Most tests results seem to be concluded and published on cyclists where a cyclists ability to perform at the highest level is a mix of aerobic ability and power/strength. A marathon runner though is less concerned with power and more concerned with lowering his/her lactate threshold pace .