Abstract
PURPOSE: This study evaluates the effect of hyperoxia on cerebral oxygenation and neuromuscular fatigue mechanisms of the elbow flexor muscles following ergometer rowing. METHODS: In 11 competitive male rowers (age, 30 ± 4 years), we measured near-infrared spectroscopy determined frontal lobe oxygenation (ScO(2)) and transcranial Doppler ultrasound determined middle cerebral artery mean flow velocity (MCA V (mean)) combined with maximal voluntary force (MVC), peak resting twitch force (P (tw)) and cortical voluntary activation (VA(TMS)) of the elbow flexor muscles using electrical motor point and magnetic motor cortex stimulation, respectively, before, during, and immediately after 2,000 m all-out effort on rowing ergometer with normoxia and hyperoxia (30% O(2)). RESULTS: Arterial hemoglobin O(2) saturation was reduced to 92.5 ± 0.2% during exercise with normoxia but maintained at 98.9 ± 0.2% with hyperoxia. The MCA V (mean) increased by 38% (p < 0.05) with hyperoxia, while only marginally increased with normoxia. Similarly, ScO(2) was not affected with hyperoxia but decreased by 7.0 ± 4.8% from rest (p = 0.04) with normoxia. The MVC and P (tw) were reduced (7 ± 3% and 31 ± 9%, respectively, p = 0.014), while VA(TMS) was not affected by the rowing effort in normoxia. With hyperoxia, the deficit in MVC and P (tw) was attenuated, while VA(TMS) was unchanged. CONCLUSION: These data indicate that even though hyperoxia restores frontal lobe oxygenation the resultant attenuation of arm muscle fatigue following maximal rowing is peripherally rather than centrally mediated.