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 concentration ([K+](a)) may contribute to exercise hyperpnea and could play a role in exertional fatigue. This study was designed to determine whether the exercise-induced rise in [K+](a) is altered in patients with chronic heart failure (CHF) and whether physical training affects K+ homeostasis. Methods and Results We evaluated 10 subjects with CHF (ejection fraction, 23+/-3.9%) and 10 subjects with normal left ventricular function (NLVF) who had undergone previous coronary artery graft surgery (ejection fraction, 63+/-8.6%). Subjects performed an incremental cycle ergometer exercise test before and after a physical training or detraining program. Changes in [K+](a) and ventilation (V-E) during exercise were closely related in both groups. Subjects with CHF did less absolute work and had reduced maximal oxygen consumption (Vo(2)max) compared 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 percentage of Vo(2)max to match for relative submaximal effort, there were no differences between the two groups. Physical training resulted in reduced 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 increases in [K+](a) were unaltered, but peak concentrations of catecholamines were raised (P<.05). The decrease in V-E at submaximal work rates after training was not significant with this incremental exercise protocol, 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 rise in [K+](a) but does not significantly decrease V-E during submaximal exercise with this incremental cycle ergometry protocol. The reduction in exercise-induced hyperkalemia after training is not the result of altered concentrations of aterial catecholamines. The pathophysiological significance of the increased exercise-induced hyperkalemia in CHF and the mechanisms of improved K+ homeostasis with training have yet to be established.