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1 Denver Health Sciences Center and Colorado Springs Campuses, University of Colorado Altitude Research Center, Aurora, Colorado, United States
2 Thermal and Mountain Medicine Division, USARIEM, Natick, Massachusetts, United States
* To whom correspondence should be addressed. E-mail: asubudhi{at}uccs.edu.
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, PIO2 86mmHg); and 3) chronic hypoxia (CH: 4,300m, PIO2 86mmHg). At maximal work rate (Wmax), FIO2 was surreptitiously increased to 0.60 while subjects were encouraged to continue pedaling. Changes in cerebral (frontal lobe) and muscle (vastus lateralis) oxygenation (COX, MOX; near infrared spectroscopy), middle cerebral artery blood flow velocity (MCA-Vmean; transcranial Doppler) and end-tidal CO2 (PETCO2) were analyzed across %Wmax (significance at P<0.05). At SL, PETCO2, MCA-Vmean and COX fell as work rate rose from 75 to 100% Wmax. During AH, PETCO2 and MCA-Vmean declined from 50 to 100% Wmax while COX fell from rest. With CH, PETCO2 and COX dropped throughout exercise, while MCA-Vmean fell only from 75 to 100% Wmax. MOX fell from rest to 75% Wmax at SL and AH, and throughout exercise in CH. The magnitude of fall in COX, but not MOX, was different between conditions (CH>AH>SL). FIO2 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 FIO2 0.60, COX rose and MOX remained constant as work rate increased. Thus, cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia (PIO2 86mmHg) since its reversal was associated with improved performance.
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