A single session of high‐intensity interval exercise in hypoxia did not change mitochondrial respiration or content in human skeletal muscle biopsies

Abstract

Both high-intensity interval exercise (HIIE) and hypoxia have been suggested to affect mitochondria. However, it is not yet fully elucidated how a single session of HIIE in hypoxia affects mitochondrial respiration and content in human skeletal muscle. In this current study, we investigated the effects of a single session of HIIE combined with simulated hypoxia (3200 m, oxygen fraction of 14%) on mitochondrial respiration and content. We hypothesized that HIIE in hypoxia would induce substantial changes in mitochondrial respiration, but not in mitochondrial content. Ten healthy male participants (age, 28 ± 5 years; BMI, 26.0 ± 3.4) were recruited and completed three HIIE sessions (six 4-minute exercise bouts, separated by 2 minutes of resting) in a random order, separated by at least one week. Exercise sessions include an HIIE in hypoxia (88.4% of peak oxygen uptake (VO2peak) determined in hypoxia), an HIIE in normoxia matched for relative intensity (88.7% of VO2peak determined in normoxia), and an HIIE in normoxia matched for absolute intensity (74.1% of VO2peak determined in normoxia). Skeletal muscle samples were collected prior to, 3 hours, and 24 hours post-exercise to determine mitochondrial respiration and content. Hypoxia decreased VO2peak (by 20.2 ± 9.1%, p < 0.01), peak power output (PPO, by 9.4 ± 2.1%, p<0.01), and lactate threshold (LT, by 13.1 ± 3.0%, p<0.01). In the skeletal muscle biopsies, mitochondrial respiration, measured by Oroboros O2k with high-resolution respirometry, was similar among the three conditions prior to the HIIE interventions (p > 0.05) and remained unchanged both 3 and 24 hours after HIIE interventions performed in different conditions (p > 0.05). Citrate synthase activity, as a marker of mitochondrial content, did not differ prior to, or 3 and 24 hours after HIIE interventions among the three conditions (p > 0.05) . In conclusion, a single session of HIIE in hypoxia did not alter mitochondrial respiration and content. Gene expression and protein content of mitochondrial biogenesis markers are currently being analyzed.