Abstract 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, 9887–109 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.
Lehtonen et al. (Wed,) studied this question.
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