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October 27, 2010
There is no doubt that moderate exercise is good for you. Exercise reduces your risk of heart attacks, stroke, diabetes and some cancers. The promotion of exercise as a positive and powerful health intervention has never been more important given the explosive increase that we are seeing in disease states which are related to under-activity such as obesity and diabetes. In proportion to its importance, I should spend the next 10 pages discussing the need for all people to undertake moderate exercise but I will instead discuss the relatively small amount that we know about the benefits of exercise in the amounts commonly performed by competitive endurance athletes. There are few studies which adequately address this topic and this is somewhat surprising given the massive increase in endurance sport participation over the past few decades.
From the viewpoint of a keen athlete, I would like to first address the “who cares?” factor. The lay press and medical journals like to focus on the stats. Do athletes live a year longer or a year less? Are they 0.1% more or less likely to suddenly die of a heart attack? These are important scientific questions but will the answers influence my decision as to whether I go running in the forest this Sunday? All athletes know that their motivations for sport practice are not based on statistics but from the immediate satisfaction that comes from it. You are more likely to be killed by a car when riding than you are of dying of a heart attack and yet cyclists do not spend all of their cycling hours avoiding this risk on a wind trainer.
On the other hand, my job is to assess athletes who have developed heart problems and so the question as to whether sport may have contributed becomes important. With current evidence, I would not advise that any level of exercise is unhealthy. At the same time, I think that it is important to recognize that some things remain unanswered.
What is strenuous exercise?
Here is the first major problem with the medical literature. Numerous studies report improved health outcomes as a result of regular strenuous exercise. For example, in a widely quoted study (Blair et al., 1989) longer overall survival was attributed to “high levels of fitness” but it was also concluded that these benefits may not be seen in those performing exercise above a level of 10 metabolic equivalents (METS). So, what is 10 METS? This is the equivalent of exercising at an oxygen consumption of 35 ml/kg/min which is about 50% intensity for a well-trained athlete, jogging, riding a bike at 20km/h etc. Put simply, it is way below that which competitive athletes do in training on a regular basis. This same problem is true of nearly all of the large studies that have assessed exercise benefit – they all set maximal exercise at a level way below that appropriate for athletes. Thus, the current evidence base can be summarized as follows:
Figure 1: The benefit of exercise is likely to extend to high levels of exercise but is there a point where the benefits start to plateau or even reverse? Note, however, that it is unlikely that any level of exercise will increase risk to the level of a sedentary person.
It is likely that the benefits of exercise extend beyond the fairly conservative range which has been studied but the controversy involves whether there is a point where ‘extreme’ amounts of exercise may increase the risk of some heart problems.
There are some well-conducted studies from Scandinavia which have looked at health outcomes in ex-Olympic athletes and the results have been very reassuring (Sarna, Sahi, Koskenvuo, & Kaprio, 1993) Olympic athletes live longer and develop fewer health complaints. However, they are also wealthier, smoke and drink less and are likely to have better diets etc. – all of which may account for the differences in health that were reported. Thus, whilst it seems clear that being an athlete is healthy, these studies do not enable analysis as to whether benefits are due to lifestyle factors, exercise, or a combination of both.
What evidence is there to suggest that extreme exercise may have unwanted effects on the heart?
Greater amounts of exercise (at least 3 hours/week) are associated with “re-building” of the heart. This is of benefit for the athlete because a larger heart enables more blood to be pumped during exercise. The more blood that is pumped the greater the amount of oxygen that gets to the muscles for use.
Mostly the heart enlargement that occurs is quite mild and goes away completely if the athlete stops training. This is called ‘physiological remodeling’ and simply reflects enlargement of the muscle just as your biceps enlarge with curls.
However, in more extreme endurance exercise, the heart enlargement can be dramatic (see figure below) and it may not resolve when the athlete stops training. For example, in a study of nearly 150 Tour de France riders (Abergel et al., 2004), hearts size was greatly increased and, when studied 3 years later, the riders’ hearts were larger still. In a recent study from Switzerland (Baldesberger et al., 2008), ex-professional cyclists had persisting enlargement of the heart despite having retired from sport 30+ years earlier. This would suggest that something other than simple muscle enlargement was occurring because otherwise it would have returned to normal size once the load of exercise ceased. This might not seem a big deal but there are only a few things in the heart – muscle, the connective tissues which hold the muscle in place and the electrics of the heart. If there is an increase in the connective tissue part then it can interfere with muscle or electric function. Therefore, the failure of heart size to return to normal MAY be a cause for concern.
Figure 2: Comparison of the heart size in two 23 year olds – a non-athlete and a young professional cyclist. Note the 10cm marker as a reference. The non-athlete’s heart is approximately 15 x 12cm vs. 25 x 18 for the athlete!
This is a very contentious statement and not at all proven. As stated above, the heart enlargement is mostly due to ‘hypertrophy’ (enlargement) of the muscle fibres themselves but there is some suggestion that the connective tissue may also increase following extreme training. This connective tissue is also called ‘scar tissue’ and it has the potential to cause heart rhythm problems. It is very difficult to be certain about whether extreme exercise can cause scar because it is usually only diagnosed under the microscope on heart muscle tissue. As you can imagine, this is hard to get. We are therefore left with reports of single cases or small groups of athletes in which scar was found (La Gerche et al., 2010; Mottram et al., 2004; Whyte et al., 2008) and these do not provide definitive answers.
In one recent high profile case, Ryan Shay died during the 2008 US marathon trials and the cause of this death was never established. His autopsy result was stated as “Cardiac arrhythmia due to cardiac hypertrophy with patchy fibrosis of undetermined etiology. Natural causes.” In other words, he had heart muscle enlargement (completely expected for an elite athlete) with small areas of scar (definitely abnormal in athletes) and the conclusion…natural causes. It is surprising that this finding did not stimulate debate as to why a fit young athlete had patches of scar in his heart. Was exercise the cause? We do not know. But, we will never know if the question is not asked. This is shaky ground, however, because a balance has to be struck between investigating issues such as these and yet not creating disproportionate hysteria within the media and wider community. We must always remember that the death of a young athlete is very, very rare.
There are multiple types of heart rhythm problems (arrhythmias) which range from completely safe through to life threatening. As far as we know, exercise does NOT cause an increase in life threatening arrhythmias. However, there is increasing evidence that some benign arrhythmias are more common. This is well summarized in a review by Lluis Mont (Mont, 2010) for those who are interested and is beyond the scope of the discussion here. However, please remember that these are “nuisance arrhythmias” rather than life threatening ones.
This is a lot of information and may well seem somewhat confusing. I will try to summarise all of this information in some simple points.
Remember, the scale of any potential issues related to sport are miniscule against the massive benefits of exercise.
Abergel, E., Chatellier, G., Hagege, A. A., Oblak, A., Linhart, A., Ducardonnet, A., et al. (2004). Serial left ventricular adaptations in world-class professional cyclists: implications for disease screening and follow-up. J Am Coll Cardiol, 44(1), 144-149.
Baldesberger, S., Bauersfeld, U., Candinas, R., Seifert, B., Zuber, M., Ritter, M., et al. (2008). Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists. Eur Heart J, 29(1), 71-78.
Blair, S. N., Kohl, H. W., 3rd, Paffenbarger, R. S., Jr., Clark, D. G., Cooper, K. H., & Gibbons, L. W. (1989). Physical fitness and all-cause mortality. A prospective study of healthy men and women. JAMA, 262(17), 2395-2401.
Kujala, U. M., Tikkanen, H. O., Sarna, S., Pukkala, E., Kaprio, J., & Koskenvuo, M. (2001). Disease-specific mortality among elite athletes. JAMA, 285(1), 44-45.
La Gerche, A., Robberecht, C., Kuiperi, C., Nuyens, D., Willems, R., de Ravel, T., et al. (2010). Lower than expected desmosomal gene mutation prevalence in endurance athletes with complex ventricular arrhythmias of right ventricular origin. Heart, 96(16), 1268-1274.
Mont, L. (2010). Arrhythmias and sport practice. Heart, 96(5), 398-405.
Mottram, P. M., Haluska, B., Leano, R., Cowley, D., Stowasser, M., & Marwick, T. H. (2004). Effect of aldosterone antagonism on myocardial dysfunction in hypertensive patients with diastolic heart failure. Circulation, 110(5), 558-565.
Sarna, S., Sahi, T., Koskenvuo, M., & Kaprio, J. (1993). Increased life expectancy of world class male athletes. Med Sci Sports Exerc, 25(2), 237-244.
Whyte, G., Sheppard, M., George, K., Shave, R., Wilson, M., Prasad, S., et al. (2008). Post-mortem evidence of idiopathic left ventricular hypertrophy and idiopathic interstitial myocardial fibrosis: is exercise the cause? Br J Sports Med, 42(4), 304-305.