The influence of severe passive heat stress and hypohydration (HYPO) on cardiorespiratory and cerebrovascular function is unknown. We hypothesized that: 1) heating-induced hypocapnia and peripheral redistribution of cardiac output (Q ) would compromise blood flow velocity in the middle cerebral artery (MCAv) and cerebral oxygenation; 2) HYPO would exacerbate the hyperthermic-induced hypocapnia, further decreasing MCAv; and 3) heating would reduce MCAv-CO₂ reactivity, thereby altering ventilation. Ten males, resting supine in a water-perfused suit, underwent progressive hyperthermia [0.5°C increments in core (oesophageal) temperature (T_C) to +2°C] whilst euhydrated (EUH) or HYPO by 1.5% body mass (attained previous evening). Time-control (i.e. non-heat stressed) data were obtained on 6 of these subjects. Cerebral oxygenation (near-infrared spectroscopy), MCAv, end-tidal PCO2 (P_ETCO₂) and arterial blood pressure, Q (Finometer) and brachial and carotid blood flows (CCA) were measured continuously each 0.5°C change in T_C. At each level, hypercapnia was achieved through 3-min administrations of 5% CO₂ and hypocapnia was achieved with controlled hyperventilation. At baseline in HYPO, HR, MCAv and CCA were elevated (P<0.05 vs. EUH). MCAv-CO₂ reactivity was unchanged in both groups at all T_C levels. Independent of hydration, hyperthermic-induced hyperventilation caused a severe drop in P_ETCO₂ [-8 ± 1 mm Hg °C^-1], which was related to lower MCAv [-15 ± 3% °C^-1; R² = 0.98; P<0.001]. Elevations in Q were related to increases in brachial blood flow (R²=0.65; P<0.01) and reductions in MCAv (R²=0.70; P<0.01), reflecting peripheral distribution of Q. Cerebral oxygenation was maintained, presumably via enhanced O₂-extraction or regional differences in cerebral perfusion.