Cerebral desaturation during exercise reversed by O2 supplementation.

The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation ([Formula: see text]) were determined using near-infrared spectroscopy. Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row. The study was randomized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design. During exercise with an inspired O2 fraction of 0.21, the arterial CO2 pressure (35 ± 1 mmHg; mean ± SE) and O2 pressure (77 ± 2 mmHg) as well as the hemoglobin saturation (91.9 ± 0.7%) were reduced ( P < 0.05).[Formula: see text] was reduced from 80 ± 2 to 63 ± 2% ( P < 0.05), and the near-infrared spectroscopy-determined concentration changes in deoxy- (ΔHb) and oxyhemoglobin (ΔHbO2) of the vastus lateralis muscle increased 22 ± 3 μM and decreased 14 ± 3 μM, respectively ( P < 0.05). Increasing the inspired O2fraction to 0.30 did not affect ventilation (174 ± 4 l/min), but arterial CO2 pressure (37 ± 2 mmHg), O2 pressure (165 ± 5 mmHg), and hemoglobin O2saturation (99 ± 0.1%) increased ( P < 0.05).[Formula: see text] remained close to the resting level during exercise (79 ± 2 vs. 81 ± 2%), and although the muscle ΔHb (18 ± 2 μM) and ΔHbO2 (-12 ± 3 μM) were similar to those established without O2 supplementation, work capacity increased from 389 ± 11 to 413 ± 10 W ( P < 0.05). These results indicate that an elevated inspiratory O2fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles.