Cerebrovascular responses to incremental exercise during hypobaric hypoxia: effect of oxygenation on maximal performance

Abstract

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, inspired Po2(PiO2) 86 Torr]; and 3) chronic hypoxia [CH; 4,300 m, PiO286 Torr]. At maximal work rate (Ẇmax), fraction of inspired oxygen (FiO2) was surreptitiously increased to 0.60, while subjects were encouraged to continue pedaling. Changes in cerebral (frontal lobe) (COX) and muscle (vastus lateralis) oxygenation (MOX) (near infrared spectroscopy), middle cerebral artery blood flow velocity (MCA Vmean; transcranial Doppler), and end-tidal Pco2(PetCO2) were analyzed across %Ẇmax(significance at P < 0.05). At SL, PetCO2, MCA Vmean, and COXfell as work rate rose from 75 to 100% Ẇmax. During AH, PetCO2and MCA Vmeandeclined from 50 to 100% Ẇmax, while COXfell from rest. With CH, PetCO2and COXdropped throughout exercise, while MCA Vmeanfell only from 75 to 100% Ẇmax. MOXfell from rest to 75% Ẇmaxat SL and AH and throughout exercise in CH. The magnitude of fall in COX, but not MOX, was different between conditions (CH > AH > SL). FiO20.60 at Ẇmaxdid not prolong exercise at SL, yet allowed subjects to continue for 96 ± 61 s in AH and 162 ± 90 s in CH. During FiO20.60, COXrose and MOXremained constant as work rate increased. Thus cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia (PiO286 Torr), since its reversal was associated with improved performance.