Local heating of the skin produces a well established bi-phasic (initial peak, IP; plateau phase, PP) response in skin blood flow that has been suggested to achieve maximal values (BFskmax) when temperatures up to 44°C are used (Cracowski et al. 2006). It is reported that sensory nerve fibres and endothelial derived nitric oxide predominantly mediate IP and PP respectively (Minson, 2010). Therefore, thermal hyperemia provides a tool to examine the mechanisms of vascular reactivity under different experimental conditions. Hypoxemia is known to increase cutaneous blood flow (Simmons et al. 2007), however, its effect on the phases of thermal hyperemia are unknown. With local ethical approval and written informed consent, 12 subjects (9 males and 4 females) were exposed to normoxia (NO, 21% O2) and hypoxia (HY, 12% O2) for 9 hours in a temperature controlled environmental chamber. Skin blood flow (BFsk), oxygen saturation (SpO2), heart rate (HR) and mean arterial blood pressure (MAP) were obtained at 1 and 9 hours during both exposures. To obtain an index of BFsk, a laser Doppler probe was attached to the volar aspect of the forearm while subjects were supine. Subsequent to obtaining baseline BFsk (clamped at 33°C), thermal hyperemia was induced by increasing skin temperature (Tsk) via a heating unit at a rate of 0.5°C every 5 seconds up to 42°C and held constant for 30 minutes. Thereafter, Tsk was increased to 44°C for 10 minutes to achieve BFskmax. BFsk is presented as perfusion units (PU), cutaneous vascular conductance (CVC; calculated as BFsk/MAP) and also normalised to maximal skin blood flow (%CVCmax). Values are means (SD) compared by paired t-test and fully repeated measures 2 (1h vs 9h) x 2 (normoxia vs hypoxia) ANOVA. By design, hypoxia decreased SpO2 (NO, 99(1) vs HY, 87(4)%; P=0.00), which resulted in increased HR (NO, 58(8) vs HY, 81(11)beats/min; P=0.00) and MAP (NO, 88(10) vs HY, 92(13)mmHg; P=0.038). No differences in baseline BFsk were detected between NO and HY (NO, 15(7) vs HY, 13(7)PU; P=0.65). In contrast IP (NO, 121(33) vs HY, 153(39)PU; P=0.00), PP (NO, 166(39) vs HY, 204(39)PU; P=0.00) and BFskmax (NO, 198(49) vs HY, 229(43)PU; P=0.05) all were elevated during HY (see figure 1). However, when expressed as CVC, IP (NO, 1.5(0.5) vs HY, 1.9(0.4)CVC; P=0.01), and PP phase (NO, 2.1(0.6) vs HY, 2.4(0.6)CVC; P=0.01) remained elevated whilst CVCmax (NO, 2.5(0.7) vs HY, 2.7(0.6)CVC; P=0.31) was not. In contrast, when expressed as %CVCmax, IP remained increased (NO, 61(9) vs HY, 70(9)%CVCmax; P=0.02) but the PP was unaltered (NO, 78(8) vs HY, 80(9)%CVCmax; P=0.43). These data indicate that acute hypoxemia alters thermal hyperemia. Therefore, thermoregulation and exercise capacity may be effected during periods of exposure to hot and hypoxic environments.