Barlow C W, Qayyum M S, Davey P P, Conway J, Paterson D J, Robbins P A
Laboratory of Physiology, University of Oxford, UK.
Circulation. 1994 Mar;89(3):1144-52. doi: 10.1161/01.cir.89.3.1144.
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.
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 (VE) during exercise were closely related in both groups. Subjects with CHF did less absolute work and had reduced maximal oxygen consumption (VO2max) compared with subjects with NLVF (P < .01). Exercise-induced rises in [K+]a, VE, 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 VO2max 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 VE at submaximal work rates after training was not significant with this incremental exercise protocol, but both groups had an increased peak VE when trained (P < .01).
Exercise-induced rises in [K+]a, catecholamines, and VE 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 VE 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 arterial 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.
运动引起的动脉血钾浓度（[K⁺]a）升高可能促成运动性呼吸急促，并可能在运动性疲劳中起作用。本研究旨在确定慢性心力衰竭（CHF）患者运动引起的[K⁺]a升高是否改变，以及体育锻炼是否影响钾稳态。
我们评估了10例CHF患者（射血分数，23±3.9%）和10例左心室功能正常（NLVF）且曾接受冠状动脉搭桥手术的患者（射血分数，63±8.6%）。受试者在体育锻炼或停训计划前后进行递增式自行车测力计运动试验。两组运动期间[K⁺]a和通气量（VE）的变化密切相关。与NLVF患者相比，CHF患者完成的绝对工作量更少，最大耗氧量（VO₂max）降低（P<.01）。在匹配的绝对工作率下，CHF患者运动引起的[K⁺]a、VE、去甲肾上腺素、乳酸和心率升高幅度大于NLVF患者（P<.01）。然而，当将[K⁺]a升高幅度与VO₂max百分比作图以匹配相对次最大运动量时，两组之间无差异。尽管动脉儿茶酚胺浓度无相关变化，但体育锻炼导致两组在匹配的次最大工作率下运动引起的高钾血症减轻（P<.01）。在最大运动量时，训练后[K⁺]a的峰值升高未改变，但儿茶酚胺的峰值浓度升高（P<.05）。采用此递增运动方案时，训练后次最大工作率下VE的降低不显著，但两组训练后峰值VE均增加（P<.01）。
在次最大工作率下，CHF患者运动引起的[K⁺]a、儿茶酚胺和VE升高幅度大于NLVF患者。体育锻炼可降低运动引起的[K⁺]a升高，但采用此递增式自行车测力计运动方案时，在次最大运动期间不会显著降低VE。训练后运动引起的高钾血症减轻并非动脉儿茶酚胺浓度改变所致。CHF患者运动引起的高钾血症增加的病理生理意义以及训练改善钾稳态的机制尚待确定。
