Exercise prevents diabetes-induced impairment in superficial buffer barrier in porcine coronary smooth muscle.

In healthy coronary smooth muscle cells, the superficial sarcoplasmic reticulum (SR) buffers rise in intracellular Ca(2+) levels. In diabetic dyslipidemia, basal Ca(2+) levels are increased, yet Ca(2+) influx is decreased and SR Ca(2+) uptake is increased. Exercise prevents diabetic dyslipidemia-induced increases in basal Ca(2+) levels and decreases in Ca(2+) influx. We tested the hypothesis that diabetic dyslipidemia impairs Ca(2+) extrusion via a decrease in superficial SR and that exercise will prevent these losses. Male Yucatan swine were maintained in four treatment groups: control, hyperlipidemic, diabetic dyslipidemic, and diabetic dyslipidemic plus aerobically exercise trained. Intracellular Ca(2+) levels were measured during depolarization-induced Ca(2+) influx and caffeine-induced SR Ca(2+) release. Na(+)/Ca(2+) exchanger and plasmalemmal Ca(2+)-ATPase activity were assessed by inhibition with low extracellular Na(+) and 5,6-carboxyeosin, respectively. Superficial SR was quantified using the internal membrane dye 3,3'-dihexyloxacarbocyanine iodide (DiOC(6)) and novel analysis techniques. We found that, in diabetic dyslipidemia, Ca(2+) extrusion was impaired and superficial SR was decreased. Exercise prevented the diabetic dyslipidemia-induced decrease in superficial SR and restored plasmalemmal Ca(2+) extrusion. On the basis of these results, we conclude exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca(2+) regulation.