Increased levels of physical activity are known today to be one of the most powerful protective factors against cardiovascular disease and its progression.
There are a wide variety of epidemiologic and interventional studies demonstrating that a physically active lifestyle is related to a reduced incidence of cardiovascular disease development, an improved prognosis in patients with established disease, and an improved functional capacity.
Nevertheless, bad things occasionally happen during exercise. A number of individuals either die or have a myocardial infarction after exercise. It is above all unaccustomed heavy exertion which is related to the triggering of acute myocardial infarction, with the risk being mostly during the exertion itself or in the hour after exertion. The risk from heavy exertion is thereby strongly influenced by the individual's habitual exercise pattern. Individuals who exercise frequently are much less likely to trigger a myocardial infarction than individuals who are relatively sedentary. Habitual exercise strongly decreases the risk that unaccustomed vigorous exertion would trigger sudden death.
Patients at risk for exertion-related complications are those with a relatively well preserved exercise capacity which allows them to perform vigorous exercise, those with significant ischemia during exercise testing and those who frequently violate the target heart rate limit during exercise training. The large proportion of deaths occurs in individuals who exercise infrequently or has only recently begun to exercise. Once initial weeks of exercise are completed, more intense exercise is of less relative risk. The two primary strategies for minimising risk are therefore appropriate screening of prospective exercisers to identify individuals at risk and appropriate control of exercise intensity, particularly during the first few weeks of an exercise program.
Even in patients with severely reduced left ventricular function, regular aerobic exercise training has been shown to be of important benefit. Moderate aerobic training in these patients is safe and besides the amelioration of exercise capacity also contributes to an amelioration of the left ventricular function and diameter. In these patients, exercise training should be started under supervision, ideally in a structured rehabilitation program. This allows them to accustom themselves to regular physical exercise, to learn about their physical limits and to reliably determine the adequate exercise intensity.
In athletes with coronary artery disease, two levels of risk are defined:
Mildely increased risk:
- preserved left ventricular systolic function (ejection fraction > 50%)
- normal exercise tolerance for age, demonstrated during treadmill or cycle ergometer exercise testing
- absence of exercise-induced ischemia or complex ventricular arrhythmias
- absence of hemodynamically significant stenosis in any major coronary artery
- successful myocardial revascularization.
Substantially increased risk:
- Impaired left ventricular systolic function at rest (ejection fraction less than 50%)
- Evidence of exercise-induced myocardial ischemia or complex ventricular arrhythmias
- Hemodynamically significant stenosis of a major coronary artery (>50% or more lumen diameter narrowing).
Athletes in the mildly increased risk group can participate in low dynamic and low/moderate static competitive sports (classes IA and IIA) but should avoid intensely competitive situations. Athletes in the substantially increased risk category should generally be restricted to low-intensity competitive sports (class IA). Athletes should be informed of the nature of prodromal symptoms (such as chest, arm, jaw and shoulder discomfort, unusual dyspnea) and should be instructed to cease their sports activity promptly and to contact their physician if symptoms appear.
Classification of sports. This classification is based on peak static and dynamic components achieved during competition. The increasing dynamic component is defined in terms of the estimated percent of maximal oxygen uptake (Max O2) achieved and results in an increasing cardiac output. The increasing static component is related to the estimated percent of maximal voluntary contraction (MVC) reached and results in an increasing blood pressure load. The lowest total cardiovascular demands (cardiac output and blood pressure) are shown in green and the highest in red. Blue, yellow, and orange depict low moderate, moderate, and high moderate total cardiovascular demands.