Objective     To investigate the effects of training under hypobaric hypoxia on rat myocardial mitochondrial function.      Methods     Thirty-two Wistar rats were randomized into 4 groups: normal control (C)

hypoxic group (H)

exercise group (E)

hypoxia combined with exercise group (HE). Rats of H and HE groups were subjected to hypobaric hypoxia simulating 5 000-meter altitude for 5 weeks (24 h/d)

and the rats in HE group were descended to 4 000 m to swim ceaselessly (1 h/d

6 d/week). The rats in C group and E group were kept under normobaric conditions. The swimming program for E group was the same as HE group. Twenty-four hours after the last bout of exercise training

the rats were sacrificed at simulated 4 000-meter condition (H and HE groups) or at 500 m over sea level (C and E groups). Myocardium from ventricles was collected and mitochondria were isolated. Mitochondrial oxidative respiratory function was measured by Clark oxygen electrode and the protein expression of ATP synthase α subunit was detected by Western blotting.      Results     Compared with H group

the expressions of ST3 and ATP synthase α subunit increased in HE group.      Conclusion     The exercise training at high altitude induced the increase of ATP production capacity

which may be a mechanism of mitochondrial acclimation to high-altitude hypoxia.