We examined the effects of exposure to 10-12 days intermittent hypercapnia [IHC: 5:5-min hypercapnia (FICO₂, 0.05)-to-normoxia for 90 min (n=10)]; intermittent hypoxia [IH: 5:5-min hypoxia-to-normoxia for 90 min (n=11)] or 12 days of continuous hypoxia [CH: 1560m (n=7)], or both IH followed by CH, on cardiorespiratory and cerebrovascular function during steady-state cycling exercise with and without hypoxia (FIO₂, 0.14). Cerebrovascular reactivity to CO₂ was also monitored. During all procedures, ventilation, end-tidal gases, blood pressure (BP), muscle and cerebral oxygenation (near infrared spectroscopy) and middle cerebral artery blood flow velocity (MCAv) were measured continuously. Dynamic cerebral autoregulation (CA) was assessed using transfer-function analysis. Hypoxic exercise resulted in increases in ventilation, hypocapnia, heart rate and cardiac output when compared with normoxic exercise (P<0.05); these responses were unchanged following IHC, but were elevated following the IH and CH exposure (P<0.05) with no between-intervention differences. Following IH and/or CH exposure, the greater hypocapnia during hypoxic exercise provoked a decrease in MCAv (P<0.05 vs. pre-exposure), which was related to lowered cerebral oxygenation (r= 0.54; P<0.05). Following any intervention, during hypoxic exercise, the apparent impairment in CA, reflected in lowered low-frequency phase between MCAv and BP, and MCAv-CO₂ reactivity were unaltered. Conversely, during hypoxic exercise following both IH and/or CH there was less of a decrease in muscle oxygenation (P<0.05; vs. pre-exposure). Thus, IH or CH induces some adaptation at the muscle level and lowers MCAv and cerebral oxygenation during hypoxic exercise, potentially mediated by the greater hypocapnia, rather than a compromise in CA or MCAv-reactivity.