Vasomotor responses to hypoxia and cold air

At altitude, hypoxia coexists with other environmental stressors, in particular cold. Cold injury (CI) remains a frequent pathological consequence of exposure to altitude (>2800 m) [1]. A number of studies [2,3] have examined extremity vasomotor responses during local cold stress in controlled laboratory conditions at high altitude and have suggested that systemic arterial hypoxia exaggerates cold-induced cutaneous vasoconstriction and impairs any cold-induced vasodilatation (CIVD) response. Recently, Keramides et al. [4] reported that hypoxic exposure impairs the local rewarming response of the hands. In this way, hypoxia increases the risk of CI for a given temperature, but this hypothesis has not been tested in a dynamic air environment or during whole body exposure to the thermal stimulus, similar to that when at altitude. It is this dynamic response which determines the 'dose' of cold experienced by the extremities and thereby the risk of CI. It was hypothesized that vasoconstriction and vasodilatation would occur at warmer skin temperatures when breathing a hypoxic compared to normoxic gas mixture.