RECOVERY AT ALTITUDE INHIBITS MITOCHONDRIAL DEVELOPMENT
Slivka, D., Heesch, M., Cuddy, J., Hailes, W., Dumke, C., & Ruby, B. (2013). Mitochondrial related gene expression is suppressed after simulated high altitude exposure. Medicine & Science in Sports & Exercise, 45(5), Supplement abstract number 2711.
"Short term exposure to altitude/hypoxia (train high / live low) has demonstrated an increase in mitochondrial function whereas chronic exposure (train high/live high) has shown a decrease in mitochondrial function."
This study determined the acute gene response after exercise when exposed to simulated high-altitude during recovery in active males (N = 10). Ss cycled for 90 minutes in laboratory conditions and then either recovered for six hours in laboratory conditions (975 m; normoxia) or at simulated high-altitude (5000 m; hypoxia). Skeletal muscle biopsies from the vastus lateralis were obtained before exercise, after exercise, and six hours after exercise for the measurement of metabolic gene expression and muscle glycogen. Blood oxygen saturation was measured via pulse oximetry before exercise, after exercise, and during recovery. Ss received a liquid carbohydrate beverage immediately after exercise (1.2 g/kgBW) and solid feedings (1.28 g/kgBW carbohydrate, 0.15 g/kgBW fat, and 0.29 g/kgBW protein) at two and four hours into recovery.
Blood oxygen saturation was lower during hypoxia trials than normoxia trials. Muscle glycogen decreased with exercise and increased with recovery with no difference between trials. HIF1alpha, HIF2alpha, OPA1, MFN2, NRF2, SOD, COX, and PGC1alpha gene expressions were suppressed after altitude exposure while FIS1, HO1, PFK, and HK were unaffected by altitude exposure.
Implication. High-altitude exposure during recovery from exercise inhibits gene expression associated with mitochondrial development but does not affect muscle glycogen resynthesis.
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