The effects of heavy long-term exercise on ventricular myocyte shortening and intracellular Ca 2+ in streptozotocin-induced diabetic rat

Abstract

Objective This study investigated whether exercise training, initiated at the onset of diabetes, could preserve the contractile properties of ventricular myocytes. Research Design and Methods The effects of a heavy exercise training program on shortening and intracellular Ca 2+ 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. Results Diabetes 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 Ca 2+ transient. Neither diabetes nor exercise had significant effects on the amplitude of myocyte shortening and the Ca 2+ transient. Conclusions Heavy long-term exercise alters the dynamics but not the amplitude of unloaded myocyte contraction in the STZ-induced diabetic rat.