Dose-response of hypoxia on mitochondrial related gene expression
Advisor Information
Dustin Slivka
Location
Dr. C.C. and Mabel L. Criss Library
Presentation Type
Poster
Start Date
7-3-2014 9:00 AM
End Date
7-3-2014 12:00 PM
Abstract
Mitochondrial function is increased in repeated short term exposure to hypoxia. However, chronic hypoxia exposure has been shown to decrease mitochondrial function. It is unknown if a dose-response relationship between mitochondrial gene expression and magnitude of hypoxia impacts this paradox in mitochondrial function between acute and chronic hypoxic exposure. PURPOSE: To determine the mitochondrial related gene response to incremental levels of hypoxia. METHODS: Recreationally-trained male cyclists completed a 60-minute ride at 70% of Wmax at an altitude of 975 m, followed by 6 h of recovery at four different simulated altitudes (0 m, 1667 m, 3333 m, or 5000 m). Blood O2 saturation was measured via pulse oximetry every hour during the 6 h recovery period. Muscle biopsies were obtained from the vastus lateralis pre- and 6 h post-exercise for analysis of mitochondrial related gene expression. RESULTS: Blood O2 saturation decreased with increasing simulated altitude during recovery (0 m: 98 ± 1%; 1667 m: 94 ± 1%; 3333 m: 90 ± 1%; 5000 m: 79 ± 2%; p < 0.05). Expression of PGC-1α, HK, and SOD increased significantly with exercise (p < 0.05), but were not different between trials. There was a tendency for expression of HIF-2α to increase with exercise, although this did not reach statistical significance (p = 0.089). CONCLUSION: These data demonstrate no dose-response relationship between magnitude of hypoxic exposure and mitochondrial gene expression. Therefore, the paradox of mitochondrial function in response to acute and chronic exposure to hypoxia cannot be explained by the magnitude of hypoxia.
Dose-response of hypoxia on mitochondrial related gene expression
Dr. C.C. and Mabel L. Criss Library
Mitochondrial function is increased in repeated short term exposure to hypoxia. However, chronic hypoxia exposure has been shown to decrease mitochondrial function. It is unknown if a dose-response relationship between mitochondrial gene expression and magnitude of hypoxia impacts this paradox in mitochondrial function between acute and chronic hypoxic exposure. PURPOSE: To determine the mitochondrial related gene response to incremental levels of hypoxia. METHODS: Recreationally-trained male cyclists completed a 60-minute ride at 70% of Wmax at an altitude of 975 m, followed by 6 h of recovery at four different simulated altitudes (0 m, 1667 m, 3333 m, or 5000 m). Blood O2 saturation was measured via pulse oximetry every hour during the 6 h recovery period. Muscle biopsies were obtained from the vastus lateralis pre- and 6 h post-exercise for analysis of mitochondrial related gene expression. RESULTS: Blood O2 saturation decreased with increasing simulated altitude during recovery (0 m: 98 ± 1%; 1667 m: 94 ± 1%; 3333 m: 90 ± 1%; 5000 m: 79 ± 2%; p < 0.05). Expression of PGC-1α, HK, and SOD increased significantly with exercise (p < 0.05), but were not different between trials. There was a tendency for expression of HIF-2α to increase with exercise, although this did not reach statistical significance (p = 0.089). CONCLUSION: These data demonstrate no dose-response relationship between magnitude of hypoxic exposure and mitochondrial gene expression. Therefore, the paradox of mitochondrial function in response to acute and chronic exposure to hypoxia cannot be explained by the magnitude of hypoxia.