Given the basic assumption that ethnic groups residing in Arctic areas have more general and local cold exposure than ethnic groups who reside in

tropical areas, this may have resulted in genetic or functional adaptations over the course of their ancestry. Therefore, it is worthwhile to look at racial differences in local responses to cold. Many of the early studies on cold tolerance employed a cross-sectional approach comparing nonadapted controls with a population living or working in cold environments. Alternatively, if the control group could be drawn from individuals of similar ethnicity, it check details can be assumed that the primary difference is in environmental exposure rather than in genetic differences. In support of CIVD being a protective response, humans living in or native to a cold environment seems to have enhanced CIVD, marked by shortened onset times and higher amplitudes, compared with tropical or nonadapted

ICG-001 order individuals. For example, Arctic natives such as Inuit and Lapps generally have higher mean finger temperatures and CIVD responses compared with control populations from more temperate regions [12,45,56]. Negroid subjects are known to have lower finger skin temperatures during CIVD than Caucasians [54]. Leblanc et al. [47] observed no differences in skin thickness or cell size between skin biopsies of fishermen and controls; however, the fishing group had a greater number Fenbendazole of mast cells in the skin. Mast cells are present in several types of tissues, and contain many granules rich in histamine; H2 histamine receptors are located in smooth muscle cells, and cause a strong vasodilation when stimulated. Again, it is not known if these differences were inherited or acquired. Some ethnic groups continued to be exposed to local and whole body cold for centuries, like the Inuit, whereas other ethnic groups were mainly exposed to heat. Early population-based research demonstrated that Arctic residents have a better CIVD response than non-Arctic residents [12,45,56]. Even though the fingers

are relatively shorter and thicker for people living close to the poles [2,48], providing less biophysical [62] surface area for heat exchange, the fingers nevertheless seem to be able to lose more heat to the environment when exposed to severe cold. Locations where CIVD is observed coincide with the presence of AVAs in the human skin [7]. These AVAs contain alpha-2 receptors and are under powerful sympathetic control; when CIVD occurs, the strong muscle wall of the AVA suddenly relaxes. Hale and Burch [39] reported that AVAs form when there is a higher need for blood flow in the finger. However, the magnitude of this response is very small: 95% of the AVAs remain unchanged and the stimulus for AVA formation has to be severe, for instance, strong ischemia followed by hyperemia.