Aging is associated with mitochondrial dysfunction and alterations in heart function. A hallmark of mitochondrial dysfunction is the formation of highly conductive megachan- nels – mitochondrial permeability transition pores (mPTPs), the prevention of which may be an effective method of car - dioprotection. Moderate exercise training reduces risk factors and protects the heart from ischemic damage. However, the effects of exercise training on cardiovascular function during aging still need to be studied. This study aimed to investigate the expression of genes encoding potential mPTP components and ATP-sensitive potassium (K ATP ) channel subunits in the heart during ageing and under conditions of moderate exercise training. mRNA expression levels were determined by re- verse transcription and RT-PCR analysis. An increase in the expression of two mPTP components in the heart of old rats was shown, namely: mRNA of the Vdac1 gene, which encodes a voltage-dependent anion channel 1 (VDAC1), by 2.7 times, and mRNA of the Ppif gene, which encodes cyclophilin D, by 2.7 times compared to adult animals, as well as a significant decrease in their expression during moderate exercise training, which is considered a mitoprotective effect. With aging, mRNA expression of structural subunits of mitochondrial (SUR1) and sarcolemmal (SUR2 and Kir6.2) K ATP channels is reduced in heart tissues, indicating a weakening of cardioprotective potential. An increase in the expression of cardiac Kir6.2 and vascular Kir6.1 subunits, which form the channel's conduc- tion pore, and the regulatory component SUR2, under training conditions, may contribute to an increase in the heart's resis- tance to ischemic effects and endurance to exercise training. At the same time, increased expression of the mitochondrial K ATP channel subunit SUR1 may contribute to mitochondrial resistance to adverse factors. Thus, exercise training during aging promotes cardioprotection through modulation of K ATP channels and restoration of mitochondrial function.