We tested the effect of hypoxia on cutaneous vascular regulation and defense of core temperature during cold exposure. Twelve subjects had two microdialysis fibres placed in the ventral forearm and were immersed to the sternum in a bathtub on parallel study days (normoxia and poikilocapnic hypoxia with an arterial O(2) saturation of 80%). One fibre served as the control (1 mM propranolol) and the other received 5 mM yohimbine (plus 1 mM propranolol) to block adrenergic receptors. Skin blood flow was assessed at each site (laser Doppler flowmetry), divided by mean arterial pressure to calculate cutaneous vascular conductance (CVC), and scaled to baseline. Cold exposure was first induced by a progressive reduction in water temperature from 36 to 23°C over 30 min to assess cutaneous vascular regulation, then by clamping the water temperature at 10°C for 45 min to test defense of core temperature. During normoxia, cold stress reduced CVC in control (-44 ± 4%) and yohimbine sites (-13 ± 7%; both P < 0.05 versus precooling). Hypoxia caused vasodilatation prior to cooling but resulted in greater reductions in CVC in control (-67 ± 7%) and yohimbine sites (-35 ± 11%) during cooling (both P < 0.05 versus precooling; both P < 0.05 versus normoxia). Core cooling rate during the second phase of cold exposure was unaffected by hypoxia (-1.81 ± 0.23°C h(-1) in normoxia versus -1.97 ± 0.33°C h(-1) in hypoxia; P > 0.05). We conclude that hypoxia increases cutaneous (non-noradrenergic) vasoconstriction during prolonged cold exposure, while core cooling rate is not consistently affected.

OBJECTIVE:As human thermoregulatory responses to maintain core body temperature (T) under multiple stressors such as cold, hypoxia, and dehydration (e.g., exposure to high-altitude) are varied, the combined effects of cold, hypoxia, and dehydration status on T in rats were investigated. The following environmental conditions were constructed: (1) thermoneutral (24 °C) or cold (10 °C), (2) normoxia (21% O) or hypoxia (12% O), and (3) euhydration or dehydration (48 h water deprivation), resulted in eight environmental conditions [2 ambient temperatures (T) × 2 oxygen levels × 2 hydration statuses)]. Each condition lasted for 24 h. RESULTS:Normoxic conditions irrespective of hypoxia or dehydration did not strongly decrease the area under the curve (AUC) in T during the 24 period, whereas, hypoxic conditions caused greater decreases in the AUC in T, which was accentuated with cold and dehydration (T × O × hydration, P = 0.040 by three-way ANOVA). In contrast, multiple stressors (T × O × hydration or T × O or O × hydration or T × hydration) did not affect locomotor activity counts (all P > 0.05), but a significant simple main effect for O and T was observed (P < 0.001). Heat loss index was not affected by all environmental conditions (all P > 0.05). In conclusion, decreases in T were most affected by multiple environmental stressors such as cold, hypoxia, and dehydration.

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg·min] completed 45 min of cycling, once in normoxia (NORM; [Formula: see text] = 0.21) and twice in hypoxia (HYP1/HYP2; [Formula: see text]= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit ) two distinctly different %V̇o [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (H) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and ) the same %V̇o [NORM: 45 (8)% and HYP2: 48 (5)%] with different H [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %V̇o, changes in rectal temperature (ΔT) and changes in esophageal temperature (ΔT) were greater at end-exercise in NORM [ΔT: 0.76 (0.19)°C; ΔT: 0.64 (0.22)°C] compared with HYP2 [ΔT: 0.56 (0.22)°C, < 0.01; ΔT: 0.42 (0.21)°C, < 0.01]. As a result of a greater H ( < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %V̇o compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all < 0.01) in NORM [1.10 (0.20) mg·cm·min] compared with HYP2 [0.71 (0.19) mg·cm·min]. However, at a fixed H, ΔT [0.75 (0.24)°C; = 0.77] and ΔT [0.63 (0.29)°C; = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm·min] was not different ( = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %V̇o, determines changes in core temperature and sweating during exercise. Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %V̇o) does not influence changes in thermoregulatory responses.

BACKGROUND:The thermoregulatory responses during simultaneous exposure to hypoxia and cold are not well understood owing to the opposite reactions of vasomotor tone in these two environments. Therefore, the purpose of this study was to investigate the influences of hypobaric hypoxia on various thermoregulatory responses, including skin blood flow (SkBF) during cold exposure. METHODS:Ten subjects participated in two experimental conditions: normobaric normoxia with cold (NC, barometric pressure (P) = 760 mmHg) and hypobaric hypoxia with cold (HC, P = 493 mmHg). The air temperature was maintained at 28 °C for 65 min and gradually decreased to 19 °C for both conditions. The total duration of the experiment was 135 min. RESULTS:The saturation of percutaneous oxygen (SpO) was maintained at 98-99% in NC condition, but decreased to around 84% in HC condition. The rectal and mean skin temperatures showed no significant differences between the conditions; however, the forehead temperature was higher in HC condition than in NC condition. The pulse rate increased in HC condition, and there was a strong negative relationship between SpO and pulse rate (r = - 0.860, p = 0.013). SkBF and blood pressure showed no significant differences between the two conditions. CONCLUSION:These results suggest that hypobaric hypoxia during cold exposure did not alter the overall thermoregulatory responses. However, hypobaric hypoxia did affect pulse rate regardless of cold exposure.

Anapyrexia is the regulated decrease in body temperature during acute exposure to hypoxia. This study examined resting rectal temperature (Trec) in adult humans during acute normobaric hypoxia (NH). Ten subjects breathed air consisting of 21% (NN), 14% (NH14), and 12% oxygen (NH12) for 30 min each in thermoneutral conditions while Trec and blood oxygen saturation (Spo2) were measured. Linear regression indicated that Spo2 was progressively lower in NH14 (p=0.0001) and NH12 (p=0.0001) compared to NN, and that Spo2 in NH14 was different than NH12 (p=0.00001). Trec was progressively lower during NH14 (p=0.014) and in NH12 (p=0.0001) compared to NN. The difference in Trec between NH14 and NH12 was also significant (p=0.0287). Spo2 was a significant predictor of Trec such that for every 1% decrease in Spo2, Trec decreased by 0.15°C (p=0.0001). The present study confirmed that, similar to many other species, human adults respond to acute hypoxia exposure by lowering rectal temperature.

KEY POINTS:For small mammals living in a cold, hypoxic environment, supplying enough O to sustain thermogenesis can be challenging. While heterothermic mammals are generally more tolerant of cold and hypoxia than homeothermic mammals, how they regulate O supply and demand during progressive cooling in hypoxia is largely unknown. We show that as ambient temperature is reduced in hypoxia, body temperature falls in both homeotherms and heterotherms. In the homeothermic rat, a decrease in O consumption rate and lung O extraction accompany this fall in body temperature, despite a relative hyperventilation. Paradoxically, in heterothermic mice, hamsters and ground squirrels, body temperature decreases more than in the homeothermic rat, even though they maintain ventilation, increase lung O extraction and maintain or elevate their O consumption rates. Variation in cold and hypoxia tolerance among homeotherms and heterotherms reflects divergent strategies in how O supply and demand are regulated under thermal and hypoxic challenges. ABSTRACT:Compared to homeothermic mammals, heterothermic mammals are reported to be exceptionally tolerant of cold and hypoxia. We hypothesised that this variation in tolerance stems from divergent strategies in how homeotherms and heterotherms regulate O supply versus O demand when exposed to hypoxia during progressive cooling. To test this hypothesis, we exposed adult rodents ranging in their degree of heterothermic expression (homeotherm: rats, facultative heterotherms: mice and hamsters, and obligate heterotherm: ground squirrels) to either normoxia (21% O ) or environmental hypoxia (7% O ), while reducing ambient temperature from 38 to 5°C. We found that when ambient temperature was reduced in normoxia, all species increased their O consumption rate and ventilation in parallel, maintaining a constant ventilatory equivalent and level of lung O extraction. Surprisingly, body temperature fell in all species, significantly so in the heterotherms. When ambient temperature was reduced in hypoxia, however, the homeothermic rat decreased their O consumption rate and lung O extraction despite an increase in their ventilatory equivalent, indicative of a relative hyperventilation. Heterotherms (mice, hamsters and ground squirrels), on the other hand, decreased their ventilatory equivalent, but increased lung O extraction and maintained or elevated their O consumption rates, yet their body temperature fell even more than in the rat. These results are consistent with the idea that homeotherms and heterotherms diverge in the strategies they use to match O supply and O demand, and that enhanced cold and hypoxia tolerance in heterotherms may stem from an improved ability to extract O from the inspired air.