Ca2+ regulatory systems in rat myocardium are altered by 24 weeks treadmill training

The present study was conducted to investigate the effects of long-term exercise training on the main components involved in excitation-contraction coupling and relaxation in rat myocardium. Twenty male Wistar rats were divided into sedentary (S) and treadmill-trained (T) groups. Group T was trained for 24 weeks, 5 days/week (25 m/min, 45-60 min, 0% slope). 48 h after the last exercise session, animals were killed and ventricular and soleus muscle homogenates were obtained. The citrate synthase activity in soleus muscle was significantly increased (163%) in T compared with S rats (P < 0.01), confirming the exercise training efficacy. Although heart weight and cardiac oxidative capacity were not modified by exercise training, the binding of [H-3] ryanodine and the dihydropyridine [H-3]PN200-110 to cardiac homogenates, and sarcoplasmic reticulum Ca2+-ATPase activity were increased significantly in the ventricular homogenates from T compared with S animals (P < 0.01). Western blot analysis of ventricular homogenates failed to show significant alterations in dihydropyridine receptor and Ca2+-ATPase levels in T animals, but revealed an increase of ryanodine receptor density in this group (P < 0.01). The activity of the ectoenzymes 5'-nucleotidase and Mg2+-ATPase was not affected by training (P > 0.05). In conclusion, long-term treadmill training induces adaptive changes in some of the components of myocardial rat excitation-contraction coupling and relaxation systems that could contribute to the improvement of cardiac function.