Presentation Title

Effects of Simulated High Altitude Exposure on Mitochondrial-Related Gene Expression

Advisor Information

Dustin Slivka

Location

Dr. C.C. and Mabel L. Criss Library

Presentation Type

Poster

Start Date

3-3-2017 2:15 PM

End Date

3-3-2017 3:30 PM

Abstract

Short term exposure to altitude/hypoxia stimulates an increase in mitochondrial function whereas chronic exposure has shown a decrease in mitochondrial function. PURPOSE: To determine the acute gene expression response after exercise when exposed to simulated high altitude during recovery. METHODS: Ten recreationally active males (25 ± 2 yrs, 78.9 ± 8.6 kg, 178 ± 8 cm, 13.1 ± 4.5% fat, 4.3 ± 0.6 L·min-1 VO2 max) cycled for 90 min in laboratory conditions and then recovered for 6 hours in either normoxia (975 m) or hypoxia (5000 m). Skeletal muscle biopsies from the vastus lateralis were obtained before exercise, after exercise, and 6 hours after exercise for the measurement of metabolic gene expression and muscle glycogen. Blood oxygen saturation was measured before exercise, after exercise, and during recovery. RESULTS: Blood oxygen saturation was lower during hypoxia trials than normoxia trials (p < 0.05). Muscle glycogen decreased from 116 ± 23 mmol·kg-1 wet wt. to 47 ± 17 mmol·kg-1 with exercise and then increased to 77 ± 18 mmol·kg-1 during recovery with no difference between trials (p > 0.05). HIF1α, HIF2α, OPA1, MFN2, NRF2, SOD, COX, and PGC1α gene expression were suppressed after altitude exposure (p < 0.05) while FIS1, HO1, PFK, and HK were unaffected by altitude exposure (p > 0.05). CONCLUSION: High altitude exposure during recovery from exercise inhibits gene expression associated with mitochondrial development without affecting muscle glycogen re-synthesis. These data may explain the mechanism by which mitochondrial function is reduced after extended stays at altitude.

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COinS
 
Mar 3rd, 2:15 PM Mar 3rd, 3:30 PM

Effects of Simulated High Altitude Exposure on Mitochondrial-Related Gene Expression

Dr. C.C. and Mabel L. Criss Library

Short term exposure to altitude/hypoxia stimulates an increase in mitochondrial function whereas chronic exposure has shown a decrease in mitochondrial function. PURPOSE: To determine the acute gene expression response after exercise when exposed to simulated high altitude during recovery. METHODS: Ten recreationally active males (25 ± 2 yrs, 78.9 ± 8.6 kg, 178 ± 8 cm, 13.1 ± 4.5% fat, 4.3 ± 0.6 L·min-1 VO2 max) cycled for 90 min in laboratory conditions and then recovered for 6 hours in either normoxia (975 m) or hypoxia (5000 m). Skeletal muscle biopsies from the vastus lateralis were obtained before exercise, after exercise, and 6 hours after exercise for the measurement of metabolic gene expression and muscle glycogen. Blood oxygen saturation was measured before exercise, after exercise, and during recovery. RESULTS: Blood oxygen saturation was lower during hypoxia trials than normoxia trials (p < 0.05). Muscle glycogen decreased from 116 ± 23 mmol·kg-1 wet wt. to 47 ± 17 mmol·kg-1 with exercise and then increased to 77 ± 18 mmol·kg-1 during recovery with no difference between trials (p > 0.05). HIF1α, HIF2α, OPA1, MFN2, NRF2, SOD, COX, and PGC1α gene expression were suppressed after altitude exposure (p < 0.05) while FIS1, HO1, PFK, and HK were unaffected by altitude exposure (p > 0.05). CONCLUSION: High altitude exposure during recovery from exercise inhibits gene expression associated with mitochondrial development without affecting muscle glycogen re-synthesis. These data may explain the mechanism by which mitochondrial function is reduced after extended stays at altitude.