Acute versus habitual exercise, thrombogenesis and exercise intensity.

Engaging in regular exercise lowers the risk of coronary heart disease (CHD), and most recommendations suggest at least 30 minutes of moderate intensity physical activity on most (and preferably all) days as a primary-prevention strategy for CHD in the general population (1). However, much has also been made of the higher transient risk of sudden death from myocardial infarction during or shortly after exercise, particularly in sedentary individuals who are not accustomed to regular strenuous physical stress (1). Indeed, recent data from the Physicians’ Health Study suggests that vigorous exercise (defined as 30 minutes of 6 MET or more) could simultaneously increase the short-term risk of sudden death during and up to 30 minutes after vigorous exertion [a relative risk of-sudden death of 16.9 (95% CI 10.527.0; P<0.001)] and also offer protection from this risk in those who habitually engage in vigorous exercise (2); however, the absolute risk of sudden death during any particular episode of vigorous exertion was extremely low (1 sudden death per 1.51 million episodes of exertion). Reassuringly, habitual vigorous exercise did attenuate the relative risk of sudden death that was associated with an episode of vigorous exertion. What might be the underlying mechanisms responsible for this ‘paradox’ of vigorous versus habitual exercise? Albert et al (2) postulated that episodes of vigorous exertion activate the sympathetic nervous system and promote rupture of vulnerable atherosclerotic plaques, whereas habitual exercise could enhance the electrical stability of the myocardium by increasing vagal tone, thereby protecting against fatal ventricular arrhythmias. However, the possibility also arises that the ‘two-edged sword’ of vigorous exercise may relate to activation of the haemostatic system, leading to enhanced thrombogenesis.