Effects of Hypobaric and Normobaric Hypoxia on Mitochondrial Related Gene Expression

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Environmental stimuli such as temperature and hypoxia can influence cellular signaling in the skeletal muscle. Previously we have reported no changes in gene expression related to mitochondrial development with acute exposure to normobaric hypoxia. However, exposure to hypobaric hypoxia may elicit different physiological responses. PURPOSE: To determine the response of skeletal muscle mitochondrial related gene expression after 4-h exposure to normobaric hypoxia (NH), hypobaric hypoxia (HH) and normobaric normoxia (NN) after exercise. METHODS: Recreationally trained participants (n = 15, age: 24 ± 4 y, height: 178 ± 12 cm, weight: 72.47 ± 13.84 kg, body fat: 14 ± 7%, VO2max: 3.60 ± 0.83 L · min-1, Wmax: 274 ± 72 W) each completed three trials of 1-h cycling at 70% of Wmax. Following exercise, participants sat in an environmentally controlled chamber for a 4-h recovery period in NH (4,420 m), HH (4,420 m), or NN (975 m) environmental conditions. Blood oxygen saturation was measured using pulse oximetry at baseline, 30 min into exercise, immediately after exercise, and 30 min into each hour of recovery. Muscle biopsies were taken from the vastus lateralis pre-exercise and after a 4-h exposure period. Samples were analyzed using qRT-PCR to assess gene expression related to mitochondrial development. RESULTS: Arterial oxygen saturation was lower in HH and NH trials compared to the NN trial (p < 0.001) and lower in the HH compared to NH (p = 0.001). PGC-1α, GABPA, ERRα, and NRF1 mRNA were not different between the three conditions or from pre-exercise (p = 0.804, 0.650, 0.956, 0.563, respectively). TFAM mRNA increased in NH from pre-exercise to post-exercise (p = 0.036) and was higher than NN (p = 0.011). CONCLUSION: These data indicate that gene expression related to mitochondrial development is only marginally affected (TFAM) by the type of hypoxic environment after a 4-h treatment despite differences in arterial oxygen saturation. Funding provided by the Department of Defense United States Army Medical Research and Materiel Command (DOD USAMRMC: W81XWH-15-2-0075).