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Journal of Applied Physiology, Vol 71, Issue 5 1764-1773, Copyright © 1991 by American Physiological Society
ARTICLES |
L. Stehno-Bittel, M. H. Laughlin and M. Sturek
Department of Physiology, School of Medicine, University of Missouri, Columbia 65211.
We examined the effects of chronic exercise training on sarcoplasmic reticulum (SR) Ca uptake, spontaneous SR Ca release, and whole-cell currents in coronary smooth muscle cells. Single coronary artery smooth muscle cells demonstrated increases in intracellular free Ca (Cai) during depolarization (measured with fura-2) that were abolished by diltiazem (10(-4) M). Diltiazem significantly inhibited (80%) refilling of the SR Ca store. The SR Ca store of exercise-trained pigs was 64% less after 11 min vs. 2 min of recovery, whereas cells from sedentary pigs showed no depletion. Exercise-training-induced depletion of the SR Ca store was abolished when ryanodine (10(-5) M) was applied during the recovery, but depletion was enhanced by low concentrations of ryanodine (10(-8) M). In smooth muscle from sedentary pigs, 10(-8) M ryanodine mimicked the effects of exercise training by depleting the SR Ca store during 11 min of recovery (54% depletion). When allowed a longer recovery without ryanodine (14 min or without prior depolarization), the SR Ca store in cells from exercise-trained pigs returned toward peak levels. The outward K current vs. voltage relationship did not differ in cells from exercise-trained or sedentary pigs. Exercise training reduced the number of spontaneous transient outward currents normally found in cells from sedentary pigs. We introduce a model that provides a rational basis to explain the results obtained in this study.
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