Regular exercise enhances cardiac function and modulates myocyte growth in healthy individuals. The talk will describe studies designed to assess contractile function and expression of selected genes associated with intracellular Ca²⁺ regulation after intensity controlled aerobic endurance training in the rat. Female Sprague-Dawley rats were randomly assigned to sedentary control (SED) or treadmill running (TR) 2 h per day, 5 days per week for 2, 4 or 13 weeks. Rats ran for 8 min intervals at 85-90% of V_O2,max separated by 2 min at 50-60%. At the end of the training period, the animals were killed by cervical dislocation and the hearts were removed and ventricular myocytes isolated by perfusion with collagenase-containing solutions. Myocyte length, intracellular Ca²⁺ (fura-2), and intracellular pH (BCECF) were measured in dissociated cells in response to electrical stimulation at a range of stimulation rates. The increase in V_O2,max plateaued after 6-8 weeks, 60% above SED. After 13 weeks, left and right ventricular weights were 39 and 36% higher than in SED. Left ventricular myocytes were 13% longer, whereas width remained unchanged. After 4 weeks of training, myocyte contractility was approximately 20% higher in TR, whereas peak systolic intracellular Ca²⁺ and time for the decay from systole were 20-35% and 12-17% lower, respectively. These results suggest that increased myofilament Ca²⁺ sensitivity is the dominant effect responsible for enhanced myocyte contractility in TR. Western blot analysis indicated 21 and 46% higher myocardial SERCA-2 and Phospholamban, but unaltered Na⁺/Ca²⁺ exchanger levels. In conclusion, this study strongly indicates that physical exercise induces adaptive hypertrophy in cardiac myocytes with improved contractile function in marked contrast to the pathological hypertrophy and associated decreased contractile function associated with congestive heart failure.