Exercise training depletes sarcoplasmic reticulum calcium in coronary smooth muscle.

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.