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AJP - Regulatory, Integrative and Comparative Physiology, Vol 270, Issue 6 1347-R1354, Copyright © 1996 by American Physiological Society
ARTICLES |
J. Hallen, B. Saltin and O. M. Sejersted
Department of Physiology, National Institute of Occupational Health, Oslo, Norway.
Infusion of the beta 2-adrenoceptor agonist terbutaline will cause an activation of the Na(+)-K+ pump that leads to lowering of plasma K+ concentration and intracellular Na+ concentration. The present study examines whether these changes will affect the K+ homeostasis during subsequent exercise. Two-legged knee-extension exercise was carried out at low (40 W) and high (75 W) power for 8 min in six healthy, male subjects before (control) and during intravenous infusion of terbutaline (priming dose 500 micrograms, sustained dose 4.1 micrograms/min). Catheters in the femoral vein and artery allowed blood sampling and continuous recording of femoral venous plasma K+ concentration ([K+]fv) by means of a pliable, K(+)-sensitive electrode. Leg blood flow was measured by bolus injections of indocyanine green. Terbutaline decreased arterial K+ concentration by 0.83 mmol/l. The femoral veno-arterial concentration difference for K+ and loss rates of K+ were not significantly affected by terbutaline, but leg blood flow during steady-state exercise increased by approximately 0.5 l/min (P < 0.05). However, at cessation of exercise terbutaline significantly attenuated the rate of fall of [K+]fv at high power from 63 +/- 6 to 38 +/- 6 micromol. l-1.s-1, indicating a reduced reuptake rate of K+. The loss rate of K+ from the leg peaked after around 40 s of exercise, pointing to a rapid activation of reuptake rate of K+. We conclude that, during terbutaline infusion, the reuptake rate of K+ in exercising muscles is attenuated.
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