abstract
- Many small mammals thermoregulate through shivering in muscle and/or non-shivering thermogenesis (NST) via brown adipose tissue (BAT) by the actions of mitochondrial uncoupling proteins (UCPs). An up-regulation of these mechanisms would be advantageous in a cold environment but not in conditions of low oxygen as it leads to needless increases in energy expenditure. We examined the chronic effect of 4 weeks of exposure to hypobaric hypoxia (H, 480 mm Hg), cold (C, 5 degrees C) and the combination of the two stressors (HC) compared to normoxic thermoneutral controls (N, 28 degrees C) in male CD-1 mice. We found that hypoxic/cold acclimated mice had significantly lower body temperatures (T(b)) after acclimation along with complete abolishment of diurnal T(b) fluctuations. Capacity for NST was assessed by changes in intrascapular BAT mass, mitochondrial content and UCP1 content per milligram mitochondria. Acclimation caused distinct remodeling of BAT that was reflected in differences in NE-induced increases in oxygen consumption (VO(2)) used to assess NST capacity. Reduction of T(b) in HC acclimated mice was not due to a decreased heat-generating capacity of BAT. VO(2) during an acute temperature challenge (32 to 4 degrees C) in normoxia was similar in all treatment groups compared to controls but thermal conductance was greater in C acclimated mice and T(b) higher in HC acclimated mice. We propose that an overriding inhibition by hypoxia on neural feedback pathways persists even after weeks of acclimation when combined with chronic cold.