Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, ON, Canada N1G 2W1.
Section for Cell Biology and Physiology, Department of Biology, University of Copenhagen, Copenhagen, Denmark.
J Physiol. 2018 Sep;596(18):4375-4391. doi: 10.1113/JP276228. Epub 2018 Aug 14.
Mammals defend against cold-induced reductions in body temperature through both shivering and non-shivering thermogenesis. The activation of non-shivering thermogenesis is primarily driven by uncoupling protein-1 in brown adipose tissue and to a lesser degree by the browning of white adipose tissue. Endurance exercise has also been shown to increase markers of white adipose tissue browning. This study aimed to determine whether prior exercise training would alter the response to a cold challenge and if this would be associated with differences in indices of non-shivering thermogenesis. It is shown that exercise training protects against cold-induced weight loss by increasing food intake. Exercise-trained mice were better able to maintain their core temperature, independent of differences in markers of non-shivering thermogenesis.
Shivering is one of the first defences against cold, and as skeletal muscle fatigues there is an increased reliance on non-shivering thermogenesis. Brown and beige adipose tissues are the primary thermogenic tissues regulating this process. Exercise has also been shown to increase the thermogenic capacity of subcutaneous white adipose tissue. Whether exercise has an effect on the adaptations to cold stress within adipose tissue and skeletal muscle remains to be shown. Male C57BL/6 mice were either subjected to voluntary wheel running or remained sedentary for 12 days. Exercise led to decreased body weight and increased glucose tolerance. Mice were then divided into groups kept at 25°C room temperature or a cold challenge of 4°C for 48 h. Exercised mice were protected against cold-induced reductions in weight and in parallel with increased food intake. Providing exercised mice with the same amount of food as sedentary mice eliminated the protection against cold-induced weight loss. Cold exposure led to greater reductions in rectal temperature in sedentary compared to exercised mice. This protective effect was not explained by differences in the browning of white adipose tissue or brown adipose tissue mass. Similarly, the ability of the β -adrenergic agonist CL 316,243 to increase energy expenditure was attenuated in previously exercised mice, suggesting that the activation of uncoupling protein-1 in brown and/or beige adipocytes is not the source of protective effects. We speculate that the protection against cold-induced reductions in rectal temperature could potentially be linked to exercise-induced alterations in skeletal muscle.
哺乳动物通过颤抖和非颤抖产热来抵抗低温引起的体温降低。非颤抖产热的激活主要由棕色脂肪组织中的解偶联蛋白 1 驱动，在较小程度上由白色脂肪组织的褐变驱动。耐力运动也已被证明能增加白色脂肪组织褐变的标志物。本研究旨在确定先前的运动训练是否会改变对冷挑战的反应，如果会，这是否与非颤抖产热的指标差异有关。研究表明，运动训练通过增加食物摄入来防止冷诱导的体重减轻。经过训练的小鼠能够更好地维持核心体温，而与非颤抖产热的标志物差异无关。
颤抖是抵御寒冷的第一道防线之一，随着骨骼肌疲劳，对非颤抖产热的依赖增加。棕色和米色脂肪组织是调节这一过程的主要产热组织。运动也已被证明能增加皮下白色脂肪组织的产热能力。运动对脂肪组织和骨骼肌对冷应激适应的影响仍有待证明。雄性 C57BL/6 小鼠要么进行自愿轮跑，要么保持 12 天的静止状态。运动导致体重减轻和葡萄糖耐量增加。然后，将小鼠分为两组，一组保持在 25°C 的室温下，一组暴露在 4°C 的寒冷环境中 48 小时。运动小鼠免受冷诱导的体重减轻的影响，同时伴随着食物摄入量的增加。给予运动小鼠与静止小鼠相同数量的食物，消除了对冷诱导体重减轻的保护作用。与运动小鼠相比，寒冷暴露导致静止小鼠直肠温度下降更大。这种保护作用不能用白色脂肪组织或棕色脂肪组织质量的褐变差异来解释。同样，β-肾上腺素能激动剂 CL316243 增加能量消耗的能力在之前运动的小鼠中减弱，表明棕色和/或米色脂肪细胞中解偶联蛋白 1 的激活不是保护作用的来源。我们推测，对冷诱导的直肠温度降低的保护作用可能与运动引起的骨骼肌变化有关。
