[Arginase-nitric oxide synthase system changes due to adaptation to swimming in adult and aged rat hearts]

We tested the physiological indices of adult rat heart beat for the adaptation to prolonged physical exercise (swimming). It was shown that the stimulation of NO-production in the heart mitochondria of trained adult rats improves both systolic and diastolic heart function. In adult rats trained by swimming the activity of both de novo and salvage enzymes of nitric oxide synthesis studied (iNOS, cNOS, nitratreductase) were increased in heart mitochondria, whereas in the old rats only the activity of oxidative de novo enzymes. Training reduced the nitrate pools only in the mitochondria from adult rats and the urea pools in mitochondria from old rats. Intramitochondrial nitrite pools were unchanged. In adult rats, mitochondrial H2O2 pools increased after training, whereas in the old rats they were reduced, the level of uric acid (a marker ofxanthinoxydase activity) in ageing rats after training period was declined. Swimming training resulted in a significant increase in the value of "oxygenation index" in mitochondria of adult rats and decreased the activity of mitochondrial arginase II. The results suggest that swimming is one of the methods of physical load stimulates NO production in the mitochondria of adult and old rats and therefore could be considered as an effective non-pharmacological tool for correction of mitochondrial dysfunction in adults and aging heart.