Normobaric Hypoxia Preserves Skeletal Muscle Oxidative Capacity but Impairs Microvascular Responsiveness Following Short-Duration, Low-Intensity Exercise

Abstract

Introduction: Skeletal muscle oxidative capacity can be influenced by oxygen availability, yet the specific impact of reduced microvascular oxygen pressure during submaximal exercise remains unclear. Prior work using blood flow occlusion to reduce oxygen availability suggests that low tissue saturation impairs muscle oxygen consumption recovery kinetics, though metabolite accumulation may confound these findings. Therefore, the purpose was to compare skeletal muscle oxidative capacity in a normoxic and hypoxic environment. Methods: Using a counter-balanced method, ten participants completed both experimental conditions with normobaric hypoxia set at 12.3% oxygen simulating 4,300 meters. A near-infrared spectroscopy device was placed on the biceps brachii to assess tissue saturation index (TSI) and skeletal muscle oxidative capacity. Following acclimation, a baseline assessment of muscle oxygen consumption was performed. 60 seconds of bicep exercise was then administered, followed by a skeletal muscle oxidative capacity assessment. Results: Despite a 5% reduction in muscle TSI in hypoxia (p = 0.003), there is no impact on skeletal muscle oxidative capacity (K-constant = 1.44 ± 0.37 min-1 for normoxia and 1.38 ± 0.37 min-1 for hypoxia; p = 0.322). However, there was a greater microvascular responsiveness in normoxia compared to hypoxia (10.3 s vs 15.4 s; t = 2.53, p = 0.032). Conclusions: Moderate hypoxia does not impair mitochondrial recovery kinetics but does impair microvascular responsiveness following low‑intensity exercise. This investigation also introduces a standardized approach for removing erroneous data points when analyzing the K‑constant.