Alkalosis increases muscle K(+) release, but lowers plasma [K(+)] and delays fatigue during dynamic forearm exercise

Alkalosis enhances human exercise performance, and reduces K(+) loss in contracting rat muscle. We investigated alkalosis effects on K(+) regulation, ionic regulation and fatigue during intense exercise in nine untrained volunteers. Concentric finger flexions were conducted at 75% peak work rate (similar to 3 W) until fatigue, under alkalosis (Alk, NaHCO(3), 0.3 g kg(-1)) and control (Con, CaCO(3)) conditions, 1 month apart in a randomised, double-blind, crossover design. Deep antecubital venous (v) and radial arterial (a) blood was drawn at rest, during exercise and recovery, to determine arterio-venous differences for electrolytes, fluid shifts, acid-base and gas exchange. Finger flexion exercise barely perturbed arterial plasma ions and acid-base status, but induced marked arterio-venous changes. Alk elevated [HCO(3)(-)] and Pco(2), and lowered [H(+)] (P < 0.05). Time to fatigue increased substantially during Alk (25 +/- 8%, P < 0.05), whilst both [K(+)](a) and [K(+)](v) were reduced (P < 0.01) and [K(+)](a-v) during exercise tended to be greater (P=0.056, n = 8). Muscle K(+) efflux at fatigue was greater in Alk (21.2 +/- 7.6 mu mol min(-1), 32 +/- 7%, P < 0.05, n = 6), but peak K(+) uptake rate was elevated during recovery (15 +/- 7%, P < 0.05) suggesting increased muscle Na(+),K(+)-ATPase activity. Alk induced greater [Na(+)]a, [Cl(-)](v), muscle Cl(-) influx and muscle lactate concentration ([Lac(-)]) efflux during exercise and recovery (P < 0.05). The lower circulating [K(+)] and greater muscle K(+) uptake, Na(+) delivery and Cl- uptake with Alk, are all consistent with preservation of membrane excitability during exercise. This suggests that lesser exercise-induced membrane depolarization may be an important mechanism underlying enhanced exercise performance with Alk. Thus Alk was associated with improved regulation of K(+), Na(+), Cl(-) and Lac(-).