The present study tested the hypothesis that exposure to an oxygen-depleted thermoneutral environment causes significant changes in skin vasomotion and therefore in skin temperature. Five healthy male volunteers (mean ± S.D.; age 32.2 ± 10.8 years; height 1.82 ± 0.07 m; weight 83.2 ± 12.2 kg) participated in two trials separated by a minimum of 24 h. Throughout each trial they lay supine in a room maintained at 28.6 ± 0.4°C and inspired the breathing gas mixture via a mouthpiece. Each trial comprised a 10 min control period, followed by a 15 min exposure to either air or a hypoxic gas mixture (P_I,O2 = 0.08 ATA), and finally a 5 min recovery period. During the control and recovery periods subjects inspired room air. The protocol of the study was approved by the National Ethics Committee of Slovenia.

Local vascular responses to hypoxia were observed indirectly by recording the skin temperature at seven sites (fingertip, forearm, forehead, chest, thigh, calf, toe) using thermistors, supplemented by infrared thermography. Tympanic temperature (T_ty) was noted at regular intervals. Haemoglobin saturation (S_a,O2) was monitored with a pulse oximeter attached to the toe. Heart rate (HR), systolic (SAP) and diastolic (DAP) arterial pressure, minute inspiratory volume (V_I) and end-tidal CO₂ level (F_ET,CO2) were recorded continuously. Analysis of variance (ANOVA) for repeated measures was used to assess the differences in the recorded variables between the two experimental conditions. HR (P < 0.001), SAP (P < 0.001), DAP (P < 0.001) and V_I (P < 0.001) were significantly elevated during the hypoxic exposure. The hypoxia-induced increase in V_I resulted in a subsequent significant drop in F_ET,CO2 (P < 0.001). S_a,O2 decreased significantly (P < 0.001) from 97 ± 1.5 % in the control period to a minimum of 71 ± 15.7 % during the hypoxic exposure. There was no change in T_ty in either experimental condition, and mean skin temperature did not differ significantly during or between conditions. However, finger and toe temperatures fell significantly (P < 0.001) from 34.1 ± 0.8 and 30.8 ± 1.5 °C in the control period to a minimum value of 33.4 ± 1.1 and 30.4 ± 1.7 °C, respectively, during hypoxia, indicating peripheral vasoconstriction. In contrast, there was a gradual increase in forearm, chest, thigh and calf temperatures (P < 0.001). No statistically significant difference between the two conditions was observed in forehead temperature. Equivalent changes in skin temperature were observed with the infrared thermography. The response times of the hypoxia-induced changes in finger and toe temperatures suggest that they are attributable to the reduced S_a,O2, rather than to the reduced F_ET,CO2. Namely, the observed changes in S_a,O2 and finger temperature occurred within 2 min of the hypoxic exposure (4 min for toe temperature), whereas F_ET,CO2 remained unchanged during this initial period of hypoxic exposure.

It is concluded that exposure to an oxygen-depleted environment can affect skin blood flow in humans. The evoked vascular responses are regionally dependent and differ qualitatively. Hypoxia-induced reduction of skin blood flow in distal extremities could predispose individuals to cold injury at altitude.

This work was supported, in part, by the Ministry of Education, Science and Sport (Republic of Slovenia).