Acute influence of mild hyperbaric oxygen at 1.25 atmospheres absolute with normal air on mitochondrial enzymes and PGC-1α mRNA levels in rat skeletal muscle

نویسندگان

  • Naoto Fujita
  • Tomoka Tomioka
  • Miharu Ono
  • Masataka Deie
چکیده

Recent findings on hyperbaric oxygen treatment suggest potential usefulness in enhancing mitochondrial function and number in obese individuals with weightinduced osteoarthritis and lower-back pain. Therefore, if hyperbaric oxygen should enhance metabolic function of mitochondria in skeletal muscle, it might serve as an alternative to exercise to reduce obesity. The purpose of the present study was to investigate the effects of mild hyperbaric oxygen on mitochondrial content and biogenesis in skeletal muscle. Eight-week-old male Wistar rats were randomly assigned to hyperbaric-oxygen or non-hyperbaric-oxygen (control) groups. Rats in the hyperbaric-oxygen and control groups were exposed to 1.25 atmospheres absolute and normal atmospheric pressure, both with normal air, respectively. At 1hof exposure to mild hyperbaric oxygen, the extensor digitorum longus and soleus muscles were removed and analyzed. In both the muscles, regardless of the muscle cell type, the activities of citrate synthase and succinate dehydrogenase were not altered due to exposure to the mild hyperbaric oxygen. Moreover, the expression level of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) protein remained unaltered; however, the mRNA level for PGC-1α was significantly higher in the hyperbaric-oxygen group than in the control group. These results suggest that although mild hyperbaric oxygen does not enhance mitochondrial content acutely, regular treatment might lead to mitochondrial biogenesis over time. Correspondence to: Naoto Fujita, Department of Musculoskeletal Functional Research and Regeneration, Graduate School of Biomedicine and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan, Tel: +81-82-257-5423, Fax: +81-82-257-5423; E-mail: [email protected]

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تاریخ انتشار 2016