EFFECT OF PHYSICAL-TRAINING ON EXERCISE-INDUCED HYPERKALEMIA IN CHRONIC HEART-FAILURE - RELATION WITH VENTILATION AND CATECHOLAMINES

Background The exercise-induced rise in arterial potassium concentrati on ([K+](a)) may contribute to exercise hyperpnea and could play a rol e in exertional fatigue. This study was designed to determine whether the exercise-induced rise in [K+](a) is altered in patients with chron ic heart failure (CHF) and whether physical training affects K+ homeos tasis. Methods and Results We evaluated 10 subjects with CHF (ejection fraction, 23+/-3.9%) and 10 subjects with normal left ventricular fun ction (NLVF) who had undergone previous coronary artery graft surgery (ejection fraction, 63+/-8.6%). Subjects performed an incremental cycl e ergometer exercise test before and after a physical training or detr aining program. Changes in [K+](a) and ventilation (V-E) during exerci se were closely related in both groups. Subjects with CHF did less abs olute work and had reduced maximal oxygen consumption (Vo(2)max) compa red with subjects with NLVF (P<.01). Exercise-induced rises in [K+](a) , V-E, norepinephrine, lactate, and heart rate were greater at matched absolute work rates in subjects with CHF than in subjects with NLVF ( P<.01). However, when the rise in [K+](a) was plotted against percenta ge of Vo(2)max to match for relative submaximal effort, there were no differences between the two groups. Physical training resulted in redu ced exercise-induced hyperkalemia at matched submaximal work rates in both groups (P<.01) despite no associated change in the concentration of arterial catecholamines. At maximal exercise when trained, peak inc reases in [K+](a) were unaltered, but peak concentrations of catechola mines were raised (P<.05). The decrease in V-E at submaximal work rate s after training was not significant with this incremental exercise pr otocol, but both groups had an increased peak V-E when trained (P<.01) . Conclusions Exercise-induced; rises in [K+](a), catecholamines, and V-E, are greater at submaximal work rates in subjects with CHF than in subjects with NLVF, Physical training reduces the exercise-induced ri se in [K+](a) but does not significantly decrease V-E during submaxima l exercise with this incremental cycle ergometry protocol. The reducti on in exercise-induced hyperkalemia after training is not the result o f altered concentrations of aterial catecholamines. The pathophysiolog ical significance of the increased exercise-induced hyperkalemia in CH F and the mechanisms of improved K+ homeostasis with training have yet to be established.