Analysis reveals varied O2 transport mechanics in hypoxia and hyperoxia during exercise, suggesting endurance limitations.
We utilized non‐invasive methods and novel computational approaches to examine the effects of acutely varying fractional inspired O 2 (FIO 2 ) on convective and diffusive steps of O 2 transport and muscle tissue (de)oxygenation during incremental cycling to exhaustion in 10 Tier 3 and 4 endurance athletes breathing either 0.152, 0.209, or 0.298 FIO 2 . At submaximal work rates (100–275 W) in hypoxia, higher cardiac output compensated for lower arterial O 2 content. At maximal work rate, convective O 2 transport was lower in hypoxia (mean [95%CI]: 5.37 [5.14–5.59] L/min, q < 0.0001) and higher in hyperoxia (6.84 [6.50–7.18] L/min, q = 0.043) compared to normoxia (6.56 [6.16–6.95] L/min), whereas O 2 diffusive conductance did not differ between conditions (94 [82–106], 98 [83–112], 98[87–109] mL/min/mmHg for hypoxia, normoxia and hyperoxia, respectively, p = 0.490). Consequently, maximal O 2 uptake (V̇O 2max ) was lower in hypoxia (4.06 [3.85–4.27] L/min, q < 0.0001) and higher in hyperoxia (5.02 [4.85–5.19] L/min, q = 0.003) compared to normoxia (4.83 [4.63–5.02] L/min). In hypoxia, muscle tissue saturation index was 1%–4%‐units lower compared to normoxia and hyperoxia during submaximal cycling but similar at maximal work rate. In summary, central and peripheral compensatory mechanisms maintained O 2 uptake despite altered FIO 2 at submaximal work rates. At maximal work rate the effects of hypoxia and hyperoxia on V̇O 2max were mediated through convective O 2 transport.
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Lehtonen et al. (2025) studied this question.
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