RIGOROUS SWIM TRAINING IMPAIRS MITOCHONDRIAL-FUNCTION IN POSTISCHEMICRAT-HEART

The effect of rigorous swim training (6 h day(-1), 5 days week(-1) for an average of 191 h) on mitochondrial respiratory function was invest igated in rat heart subjected to in vivo ischaemia reperfusion (I-R). Mitochondria was isolated from the risk region of the left ventricle s ubjected to 60 min occlusion of the main left coronary artery followed by 30 min reperfusion. Heart weight and heart-to-body weight ratio wa s increased by 21 and 28% (P < 0.01), respectively, in the trained (T, n = 15) vs. control rats (C, n = 20). I-R per se showed minimal effec t on heart mitochondria regardless of training status. In sham, state 4 respiration rate was 26 and 32% (P < 0.05) lower in T vs. C rats, us ing malate-pyruvate (M-P) and 2-oxoglutarate (OG) as substrates, respe ctively. Training also reduced state 3 respiration by 28% (M-P) and 50 % (OG) (P < 0.01). The respiratory control index (RCI) was unaltered i n T with M-P, but decreased with OG (P < 0.01). In vitro exposure to s uperoxide radicals severely reduced state 4 and 3 respiration and RCI, but T hearts showed greater reductions of state 4 and 3 rates than C. Mitochondria from T hearts also revealed a greater state 4 inhibition by H2O2 and HO. compared with C. A lower glutathione content and a hi gher gamma-glutamyl transpeptidase activity (P < 0.05) was observed in T vs. C. it is concluded that rigorous swim training impairs heart mi tochondrial function, making them more susceptible to in vivo and in v itro oxidative stress, and that this damaging effect may be related to a diminished glutathione reserve.