Antiarrhythmic mechanisms during exercise

Abstract

Exercise disturbs cardiac sympathovagal and ionic balance. In arterial blood, vigorous exercise can double plasma K(+), decrease pH by 0.4 unit, and raise catecholamines 15-fold. If any of these changes are experienced at rest, there is an increased risk of arrhythmia and cardiac arrest, yet in exercise they are usually tolerated. How the heart is protected from the chemical stress caused by exercise is not fully understood but may be related to a collective antiarrhythmic effect of these chemical changes, so when they combine there is a mutual antagonism. Catecholamines can offset the harmful cardiac effects of hyperkalemia and acidosis in isolated hearts and whole hearts in vivo and improve action-potential characteristics in K(+)-depolarized ventricular myocytes. This results from an increase in the inward Ca2(+) current that is modulated by both adrenergic and nonadrenergic hormones. Conversely, hyperkalemia can reduce or abolish the incidence of norepinephrine-induced arrhythmias. The efficacy of the mutual antagonism is reduced when the combination of acidosis, hyperkalemia, and high levels of norepinephrine are superimposed on a heart with regional ischemia or a small infarct. However, the heart may be at greatest risk in the postexercise period when plasma K(+) is low and the adrenergic tone is high. Little is known about this period, but abnormal regulation of electrolyte and cardiac sympathovagal balance may increase the incidence of arrhythmia, especially if there is underlying ischemia. Although regular physical activity can reduce the incidence of sudden cardiac death, recent epidemiological studies show that vigorous exercise can trigger myocardial infarction and sudden cardiac death, especially in habitually sedentary subjects with coronary artery disease. This may be partly related to disruption of the normal protective mechanism that allows the heart to cope with the chemical stress caused by exercise.