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Endurance training attenuates the bioenergetics alterations of rat skeletal muscle mitochondria submitted to acute hypoxia:Role of ROS and UCP3

BO Hai, Wang Yihe, Li Haiying, Zhao Juan, Zhang Hongying, Tong Changqing

Department of Physiology and Pathophysiology,Medical College of Chinese People's Armed Police Force.Tianjin 300162；China；Science and Research Department,General Hospital of Chinese People's Armed Police Force.Beijing 100039

Abstract

The physiological significance of skeletal muscle mitochondrial uncoupling protein 3(UCP3) in hypoxia is elusive.In the current study,UCP3 mRNA and protein expressions were investigated along with mitochondrial respiratory function,reactive oxygen species(ROS) generation,as well as manganese superoxide dismutase(MnSOD) expression in rat skeletal muscle with or without endurance training after an acute and severe hypobaric hypoxia exposure for different time.Acute hypoxia induced a series of impairments in skeletal muscle mitochondrial bioenergetics.In untrained rats,UCP3 protein content increased by 60% above resting level at 4 h hypoxia,whereas MnSOD protein content and activity were unaltered.UCP3 upregulation increased mitochondrial uncoupling respiration thus reducing O_(2)~(.-) generation,but inevitably decreased ATP production.Training decreased acute hypoxia-induced upregulation of UCP3 protein(67% vs 42%) in rat skeletal muscle.ROS production in trained rats also showed a dramatic decrease at 2 h,4 h and 6 h,respectively,compared with that in untrained rats.MnSOD protein contents and activities were significantly(50% and 34%) higher in trained than those in untrained rats.Training adaptation of MnSOD may enhance the mitochon-drial tolerance to ROS production,and reduce UCP3 activation during severe hypoxia,thus maintaining the efficiency of oxidative phosphorylation.In trained rats,mitochondrial respiratory control(RCR) and P/O ratios were maintained relatively constant despite severe hypoxia,whereas in untrained rats RCR and P/O ratios were significantly decreased.These results indicate that(1) UCP3 mRNA and protein expression in rat skeletal muscle are upregulated during acute and severe hypobaric hypoxia,which may reduce the increased cross-membrane potential (#DELTA##psi#) and thus ROS production;(2) Endurance training can blunt hypoxia-induced UCP3 upregulation,and improve mitochondrial efficiency of oxidative phosphorylation due to increased removal of ROS.

Key words: muscle mitochondria;training;Hypoxia;uncoupling protein 3;Reactive oxygen species

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Citing This Article：

BO Hai, Wang Yihe, Li Haiying, Zhao Juan, Zhang Hongying, Tong Changqing. Endurance training attenuates the bioenergetics alterations of rat skeletal muscle mitochondria submitted to acute hypoxia:Role of ROS and UCP3. Acta Physiol Sin 2008; 60 (6): 767-776 (in Chinese with English abstract).