Despite the known metabolic benefits of exercise, an integrated metabolic understanding of exercise is lacking. Here, we use in vivo steady-state isotope-labeled infusions to quantify fuel flux and oxidation during exercise in fasted, fed, and exhausted female mice, revealing several novel findings. Exercise strongly promoted glucose fluxes from liver glycogen, lactate, and glycerol, distinct from humans. Several organs spared glucose, a process that broke down in exhausted mice despite concomitant hypoglycemia. Proteolysis increased markedly, also divergent from humans. Fatty acid oxidation dominated during fasted exercise. Ketone production and oxidation rose rapidly, seemingly driven by a hepatic bottleneck caused by gluconeogenesis-induced cataplerotic stress. Altered fuel consumption was observed in organs not directly involved in muscle contraction, including the pancreas and brown fat. Several futile cycles surprisingly persisted during exercise, despite their energy cost. In sum, we provide a comprehensive, integrated, holistic, and quantitative accounting of metabolism during exercise in an intact organism.

中文翻译：

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小鼠急性运动期间营养通量的定量


尽管运动的代谢益处已知，但缺乏对运动的综合代谢理解。在这里，我们使用 体内稳态同位素标记的输注来量化禁食、进食和疲惫的雌性小鼠运动过程中的燃料通量和氧化，揭示了几个新发现。运动强烈促进了来自肝糖原、乳酸和甘油的葡萄糖通量，这与人类不同。几个器官保留了葡萄糖，尽管伴有低血糖，但这一过程在疲惫的小鼠中崩溃了。蛋白水解显著增加，也与人类不同。在禁食运动期间，脂肪酸氧化占主导地位。酮体的产生和氧化迅速增加，似乎是由糖异生诱导的猝退应激引起的肝脏瓶颈驱动的。在不直接参与肌肉收缩的器官中观察到燃料消耗量改变，包括胰腺和棕色脂肪。尽管它们需要消耗能量，但令人惊讶的是，在运动过程中仍然存在几个徒劳的循环。总之，我们对完整生物体运动过程中的新陈代谢进行了全面、综合、整体和定量的核算。