Physical activity is a key component of our environment that is a major contributor to the prevention of many chronic diseases that plague our society. Dr Frank Booth and colleagues have argued on numerous occasions that the human body evolved to expect and respond to high levels of physical activity, whereas currently our society provides us with technical innovations that encourage low levels of physical activity.1 The unfortunate result is that people are less physically active than ever and there are epidemic elevations in various chronic diseases. Numerous publications have shown that reduced physical activity significantly and unequivocally increases an individual’s risk for developing conditions such as type 2 diabetes, cardiovascular disease, and obesity.2^–6 The data are so convincing that the Center for Disease Control lists physical inactivity as a potential cause for a number of chronic diseases.7 Contrary to the viewpoints of some, there are no medications that are as effective as regularly performed exercise for preventing conditions such as type 2 diabetes.8 Therefore, it is imperative that we continue to work to unravel the mechanisms that control phenotypic changes in response to alterations in physical activity state.

In this issue of the British Journal of Sports Medicine, Drs Booth and Roberts propose that the elite athlete represents a model that is most similar to our physical activity ancestry and can therefore help researchers understand molecular mechanisms for chronic disease prevention through physical activity.9 However, they also emphasise not only that physical inactivity in this population may help us identify unknown mechanisms underlying chronic disease, but that the detrained elite athlete may be more susceptible to inactivity-related increases in disease risk.

Interestingly, when communicating the importance of regular physical activity physicians and researchers refer to average individuals whose physical activity levels are far below the recommended exercise dose of 20–60 minutes of continuous aerobic activity 3–5 days per week at an intensity of 55–90% of maximal heart rate.10 An often overlooked group is the highly competitive athlete, who during times of training and competition is clearly very active and often easily exceeds the minimum activity values prescribed for the prevention of chronic disease. In fact, if one examines the risk of various chronic diseases in this population, the risks appear to be very low.11 12 However, the effect of inactivity for the elite athlete may be significantly pronounced.

There is mounting evidence that physically inactive athletes become susceptible to various chronic diseases such as diabetes and cardiovascular disease. In the early 1990s a survey conducted on retired National Football League players revealed that linemen have 52% greater risk of cardiovascular-related death than the general population.13 Recently, retired linemen were found to have a greater incidence of metabolic syndrome with significantly greater BMI, low HDL, and elevated fasting plasma glucose compared with non-linemen.14 Detraining studies on athletes have demonstrated that cessation of regular exercise for athletes leads to changes in insulin sensitivity, plasma lipids, and body composition consistent with the metabolic syndrome. Short-term detraining (10–30 days) has been associated with decreases in insulin sensitivity in both master athlete-level runners15 and young elite kayakers.16 Further, 1 week of detraining was related to a significant increase in fasting and postprandial plasma triglyceride concentration.17

Drs Booth and Roberts have provided us again with a valid argument for why physical activity levels should be considered by doctors as part of their normal examinations. However, they are now providing even more rationale that even former competitive athletes should be included, because upon retirement, if they adopt a lifestyle that does not include a significant amount of physical activity, their risk of chronic disease increases dramatically. Something that we need to remain aware of is that highly competitive athletes train for many years to reach the elite level, and when the high-level regular training stimulus is removed a significant strain is placed on the molecular/cellular/biochemical profile of the muscle. In other words, if athletes hope to remain in a state that is advantageous to preventing chronic disease, they must refrain from being inactive and continue to exercise, albeit at a potentially lower level. Booth and Roberts afford us with evidence that athletes who continue to train are still at an advantage due to increased levels of physical activity; however, those who stop all forms of physical activity develop the same, if not greater, risk for a number of chronic diseases as subjects who have been mostly sedentary all their lives.