Abstract

After 4 weeks swimming course of rats we observed in myocardium the increased of H2S synthesized enzymes expression (in 1,5-5 times), which accompanied with increased H 2 S content in myocardium (31,6. ± 1.3 vs 12,6. ± 0,3) in cardiac mitochondria (10,5. ± 1,2 vs 4,2. ± 1,1) and in plasma (3,75. ± 0,2 vs 2,4. ± 0,08 nmol/mg protein in control). Using isolated rat heart by Langendorf preparation we have shown that swimming course improved heart function: heart rate was decreased, contractile activity (dP/dt max, developing isovolumic LV pressure) and coronary flow were increased by 20% and 33% respectively. Equal volume stretching of balloon in left ventricle provoked greater contraction in trained comparing to untrained hearts, demonstrating extended functional reserves. Furthermore, training significantly increased mitochondrial membrane potential in isolated mitochondria. The mitochondrial permeability transition pore (MPTP) in trained heart was detected at higher concentration of calcium that reveals extended calcium capacity of mitochondria and lesser sensitivity of MPTP to its inductor – calcium. Blockade of H2S synthesis increased but its high level decreased of MPTP sensitivity to calcium. High level of myocardial H2S increased Frank–Starling reaction too. Thus, heart adaptation to physical training and extending of heart functional reserves are provided by endogenous H2S production and its effects on MPTP sensitivity to calcium.

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