Affiliation:
1. Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1; and
2. School of Human and Biomedical Sciences, University of Canberra, Canberra, Australian Capital Territory 2601, Australia
Abstract
The hypothesis was tested that exercise-induced changes in plasma composition stimulate unidirectional K+ transport ( J inK) in human red blood cells (RBCs). Ten men performed two 30-s high-intensity leg-cycling tests separated by 4 min of rest. Antecubital venous blood was sampled before exercise and at the end of the second exercise bout. RBCs were separated from true exercise plasma,42K was added to plasma, and RBC K+ transport was studied in vitro at 37°C. In the second part of the study, blood from nine healthy men studied in vitro at 37°C was used to test the hypothesis that exercise-simulated (ES) plasma stimulates net K+ transport and J inK (measured using 86Rb) in human RBCs. The J inK of resting RBCs added to true exercise plasma was 1,574 ± 200 (SE) μmol ⋅ h−1 ⋅ l−1vs. 1,236 ± 256 μmol ⋅ h−1 ⋅ l−1in true resting plasma at 2 min (controls). In true exercise and ES plasma, J inK was increased through activation of the ouabain-sensitive Na+-K+pump and the bumetanide-sensitive Na+-K+-2Cl−cotransporter. Increases in plasma osmolality and K+, H+, and epinephrine concentrations independently and in combination stimulated K+ transport into human RBCs. In a third series of experiments, in which ES plasma K+ concentration was continuously measured during the first 5 min of incubation of RBCs, a 1.6 ± 0.3 mmol/l decrease in plasma K+concentration occurred during the first 2 min. It is concluded that RBCs transport K+ at elevated rates in response to exercise-induced changes in plasma composition.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
12 articles.
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