We sought to describe cerebrovascular responses to incremental exercise and test the hypothesis that changes in cerebral oxygenation influence maximal performance. Eleven men cycled in three conditions: 1) sea level (SL); 2) acute hypoxia (AH: hypobaric chamber, P_IO₂ 86mmHg); and 3) chronic hypoxia (CH: 4,300m, P_IO₂ 86mmHg). At maximal work rate (Wmax), F_IO₂ was surreptitiously increased to 0.60 while subjects were encouraged to continue pedaling. Changes in cerebral (frontal lobe) and muscle (vastus lateralis) oxygenation (C_OX, M_OX; near infrared spectroscopy), middle cerebral artery blood flow velocity (MCA-Vmean; transcranial Doppler) and end-tidal CO₂ (P_ETCO₂) were analyzed across %Wmax (significance at P<0.05). At SL, P_ETCO₂, MCA-Vmean and C_OX fell as work rate rose from 75 to 100% Wmax. During AH, P_ETCO₂ and MCA-Vmean declined from 50 to 100% Wmax while C_OX fell from rest. With CH, P_ETCO₂ and C_OX dropped throughout exercise, while MCA-Vmean fell only from 75 to 100% Wmax. M_OX fell from rest to 75% Wmax at SL and AH, and throughout exercise in CH. The magnitude of fall in C_OX, but not M_OX, was different between conditions (CH>AH>SL). F_IO₂ 0.60 at Wmax did not prolong exercise at SL, yet allowed subjects to continue for 96±61s in AH and 162±90s in CH. During F_IO₂ 0.60, C_OX rose and M_OX remained constant as work rate increased. Thus, cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia (P_IO₂ 86mmHg) since its reversal was associated with improved performance.