Presentation Title

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.

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COinS
 
Mar 7th, 9:00 AM Mar 7th, 12:00 PM

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.