Exercise restores endogenous H₂ S synthesis and mitochondrial function in the heart of old rats

Ageing is accompanied by a decrease in endogenous hydrogen sulphide (H₂ S) synthesis and the development of mitochondrial dysfunction. The aim of our work was to study the possible participation of exercise training-induced regulation of endogenous H₂ S production in the restoration of mitochondrial function in old rats.

Male rats were divided into three groups: adult, old and exercise-trained old. Exercise training of old rats was performed for 4 weeks. The mRNA expression cystathionine-γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST) were determined using reverse transcription and real-time polymerase chain reaction analysis. Mitochondrial dysfunction was determined by mPTP opening, which was investigated by spectrophotometric registration of the swelling of mitochondria isolated from the rat heart. We also studied the effect of exercise on H₂ S content, oxidative stress and mtNOS activity.

Exercise training in old animals significantly increased the expression of H₂ S-synthesizing enzymes CSE and 3-MST and restored endogenous H₂ S production in cardiac tissue and cardiac mitochondria to levels of adult animals. In addition, the training significantly reduced oxidative stress in old rats, in particular the rate of formation of •O₂ ^- and H₂ O₂ , diene conjugates and malondialdehyde levels in the mitochondria of the heart. Simultaneously, in the hearts of these animals, resistance of mPTP to the inducer of its opening of calcium ions was increased.

Thus, exercise training restores endogenous H₂ S production, and significantly reduces oxidative stress in cardiac mitochondria of old rats that are associated with the inhibition of calcium-induced mPTP opening as an indicator of mitochondrial dysfunction.