The effect of long exercise training on the indexes of the func­tional state isolated by Lanhendorf rat hearts during ischemia-reperfusion, the sensitivity of calcium-induced mitochondrial permeability transition pore (MPTP) opening as well as the mitochondrial uncoupling protein 3 (UCP3) expression were investigated. The obtained results indicate the positive effect of long exercise training on the heart functional state. Reperfusion injurings of the heart contractile function and its myocardial oxygen metabolism were less pronounced in adapted to exercise loading rats (trained rats). It was shown that the sensitivity of mitochondrial permeability transition pore open­ing to its inductor Ca2+ in the trained rats heart decreased compared with control animals. Thus, in the trained rat heart mitochondria had a significant increase in cNOS activity (al­most twice), slight increase in the iNOS activity compared with control, and a slight increase in the hydrogen peroxide level. Under adaptation to the long exercise training, the ex­pression level of UCP3 in rat heart mitochondria was reduced by 65 % compared with the control. These results suggest that the decrease in the expression level of UCP3 in the adaptation of animals to exercise training may play the certain role in the complex mechanism of adaptive response of the heart, that may be aimed mainly on the efficiency of oxidative phospho­rylation in mitochondria and, consequently, to increase in the ATP synthesis. Thus, long exercise training contributes to the improvement of the heart functional state, namely, its contrac­tile function, and also increases the resistance to reperfusion injury, reducing the sensitivity of the MPTP opening to the action of calcium ions by increasing the activity of mitochond­rial constitutive NOS and synthesis of nitric oxide, an endog­enous inhibitor of MPTP opening.