Impact of progressive hypoxic exposure, with or without exercise, on muscle and peripheral oxygen saturation in athletes

Abstract

Introduction: Hypoxic exercise is increasingly used to enhance training adaptations and mitigate injury risk. However, it is unclear whether peripheral capillary oxygen saturation (SpO2) accurately reflects muscle oxygen saturation (SmO2) in proportion during rest and resistance exercise. Objective: To examine acute SmO2 and SpO2 responses to different levels of hypoxia during rest and low-load resistance exercise (LRE) in athletes. Methods: Eighteen male team-sport athletes (20.44 ± 1.25 years) participated in the study. In a randomized crossover design, participants were exposed to five fractions of inspired oxygen (FiO2: 21.0%, 17.2%, 16.2%, 14.8%, 13.6%) under resting (HP) and exercise (HE) conditions, with a 3-day washout period. The exercise protocol involved knee extensions performed at 50% of the one-repetition maximum (50% 1RM). Key physiological metrics, including SmO₂, SpO2, heart rate (HR), and total hemoglobin (tHb), were continuously monitored. Results: During exercise, SmO₂ declined progressively as FiO₂ decreased, with significant reductions observed across all hypoxic levels compared to normoxia (p < 0.05). SpO₂ decreased significantly at FiO₂ levels of 16.2%, 14.8%, and 13.6% (all p < 0.05), with the most pronounced drop at 13.6%. A strong positive correlation between muscle and peripheral oxygen saturation changes was found during exercise (r = 0.974, p = 0.005), but not at rest (r = 0.763, p = 0.133). Interestingly, during exercise, the percentage changes in HE SmO₂ and HE SpO₂ across sequential hypoxic level transitions (Δlevel 1 to Δlevel 5), the reduction in HE SmO₂ was significantly greater than that in HE SpO₂ (paired t-tests: all P ≤ 0.010). Discussion: This discrepancy is likely driven by localized physiological mechanisms, such as contraction-induced mechanical occlusion impeding regional blood flow and the slower temporal response of pulse oximetry. While SpO2 provides a proxy for systemic oxygen delivery, the localized metabolic demand and vascular autoregulation within the active skeletal muscle dictate intramuscular oxygen availability, thereby decoupling local deoxygenation from systemic trends. Conclusions: SpO₂ reductions are neither equivalent to nor proportional to SmO₂ during exercise. Systemic oxygenation alone fails to accurately reflect the severity of localized muscle deoxygenation under hypoxic conditions. Therefore, optimizing hypoxic training requires monitoring both systemic and local oxygenation to ensure accurate assessment of muscular hypoxic stress.