The effects of heavy long-term exercise on ventricular myocyte shortening and intracellular Ca2+ in streptozotocin-induced diabetic rat

ObjectiveThis study investigated whether exercise training, initiated at the onset of diabetes, could preserve the contractile properties of ventricular myocytes.Research Design and MethodsThe effects of a heavy exercise training program on shortening and intracellular Ca2+ in unloaded ventricular myocytes from streptozotocin (STZ)-induced diabetic rats were examined. Animals were divided into four groups: control sedentary (CS), diabetic sedentary (DS), control heavy exercise (CHE), and diabetic heavy exercise (DHE). Exercise protocol: 5×60 min/week, 18 m/min, 5% gradient. Exercise training began 1 week after STZ treatment and continued for 12–23 (mean 17.5) weeks.ResultsDiabetes induced prolongation of time-to-peak (TPK) shortening (124±2 ms in DS compared to 97±2 ms in CS rats), which was further increased by exercise (133±3 ms in DHE and 112±2 ms in CHE myocytes). Diabetes had no significant effects on time-to-half (THALF) relaxation of shortening (61±2 ms in DS compared to 56±2 ms in CS myocytes). Exercise induced significant prolongation of THALF in control (66±3 ms) but not in diabetic (69±3 ms) myocytes. Diabetes, though not exercise, significantly prolonged TPK (76±3 ms in DS compared to 64±2 ms in CS) and THALF recovery (160±5 ms in DS compared to 118±4 ms in CS) of the Ca2+ transient. Neither diabetes nor exercise had significant effects on the amplitude of myocyte shortening and the Ca2+ transient.ConclusionsHeavy long-term exercise alters the dynamics but not the amplitude of unloaded myocyte contraction in the STZ-induced diabetic rat.