Effects of acclimatization to cold baths on men's responses to whole-body cooling in air.

The purpose of this study was to investigate the thermoregulatory mechanisms underlying artificial acclimatization to cold and to compare them with those of naturally acclimatized men. Six white men were cooled, nude, in air at 10 degrees C for 2 h before and after they had been acclimatized by ten daily cold (15 degrees C) baths of 30-60 min followed by rapid rewarming in hot (38-42 degrees C) water, and again 4 months later after acclimatization had decayed. Six control subjects also underwent the same tests, providing an opportunity to discriminate between changes caused by the immersions and those caused by extraneous influences. Acclimatization significantly reduced heat production and heat loss (P < 0.05) but did not change heat debt. The reduced heat production was accompanied by reductions in shivering (P < 0.10) and in cold-induced muscle tenseness; no evidence of nonshivering thermogenesis or active brown fat was found. These findings are attributed to increased tissue insulation, mediated by an enhanced vascular response to cold that did not involve the cutaneous circulation and was probably located in skeletal muscle. Thermal sensation and discomfort did not change, although perceived strain tended to increase (P = 0.08). Acclimatization was accompanied by, but was unrelated to, slower cooling of the finger and toe. The main conclusions, and many specific findings, agree with those of two previous studies made by the same techniques in naturally acclimatized men wintering in Antarctica. Other significant findings included changes--in particular reduced thermoneutral rectal temperature and a delayed onset of shivering--that are commonly regarded as evidence of acclimatization but were in fact unrelated to it as they also occurred in the control group. They are attributed to extraneous influences, in particular the relaxation of heightened arousal ('first-time effects') found in the baseline tests.

Cardiovascular and metabolic responses to noradrenaline in men acclimatized to cold baths.

The purpose of this study was to see whether artificial acclimatization to cold would reduce the pressor response to noradrenaline (NA) as natural acclimatization has been shown to do, and whether it would induce nonshivering thermogenesis. Three white men were infused with NA at four dosage levels between 0.038 and 0.300 microgram.kg-1.min-1 (2-23 micrograms.min-1), before and after artificial acclimatization to cold and again 4 months later when acclimatization had decayed. Acclimatization was induced by ten daily cold (15 degrees C) baths of 30-60 min followed by rapid rewarming in hot (38-42 degrees C) water, and was confirmed by tests of the subjects' responses to whole-body cooling in air. Three control subjects also underwent the first and third tests. Acclimatization substantially reduced the pressor response to NA at 0.150 and 0.300 micrograms.kg-1.min-1, confirming earlier findings by the same technique in naturally acclimatized men, and its decay increased this response to beyond its initial levels (P < 0.05 for both changes). Acclimatization did not change the response to NA of heart rate, subjective impressions, skin temperature of finger and toe, pulmonary ventilation, or plasma free fatty acids and ketone bodies. At no time did NA increase oxygen consumption, or increase skin temperature or heat flow over reported sites of brown fat. These findings would seem to show that acclimatization to cold reduces sensitivity to the pressor effect of NA but does not induce nonshivering thermogenesis, and that the reduced sensitivity is replaced by a hypersensitivity to NA when acclimatization decays.

Fire fighters' exposure to carbon monoxide during Australian bushfires.

Fatal entrapments of Australian bushfire fighters have led to suggestions that carbon monoxide (CO) poisoning could have contributed to these accidents by impairing the fire fighters' judgement. Carboxyhemoglobin saturation (COHb%) levels were assessed from alveolar CO levels in 24 fire fighters working with handtools and in 12 accompanying scientific observers, before and after fire fighting (duration 37-187 min) on 15 experimental bushfires. Carboxyhemoglobin levels increased on average by 0.7% per hour in the fire fighters and by 0.3% per hour in the observers. Nonsmoking fire fighters had lower COHb% after fires than the smokers had before fires. Estimates of environmental CO concentrations (including cigarette smoke) during the fires averaged 31 parts per million (ppm) for the smokers, 17 ppm for the nonsmoking crew members, and 11 ppm for the observers, none of whom smoked. The highest estimates of environmental CO arising solely from bushfire smoke were 40 to 50 ppm. Smokers were exposed to as much CO from their cigarettes as from bushfire smoke. Carboxyhemoglobin levels at the end of 8-hr fire fighting shifts, predicted from these levels of environmental CO, averaged about 5% (maximum 11%) in smokers and about 3% (maximum 7%) in nonsmokers. Acute levels of COHb% of this degree are not considered to have significant effects on health or performance. These results indicate that bushfire fighters are generally unlikely to experience hazardous levels of CO exposure.