Post-exercise whole-body heat stress additively enhances endurance training-induced mitochondrial adaptations in mouse skeletal muscle
Post-exercise whole-body heat stress additively enhances endurance training-induced mitochondrial adaptations in mouse skeletal muscle
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运动后全身热应激进一步增强耐力训练诱导的小鼠骨骼肌线粒体适应
DOI：
10.1152/ajpregu.00525.2013
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发表时间：
2014
期刊：
影响因子：
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通讯作者：
Hideo Hatta.
中科院分区：
文献类型：
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作者：
Yuki Tamura;Yutaka Matsunaga;Hiroyuki Masuda;Yumiko Takahashi;Yuki Takahashi;Shin Terada;Daisuke Hoshino;Hideo Hatta.
最近的一项研究表明，热应激诱导C2 C12肌管中的线粒体生物发生，从而暗示热应激可能是一种有效的治疗方法，以增强耐力训练诱导的骨骼肌线粒体适应。然而，热应激是否真的诱导体内骨骼肌线粒体适应尚不清楚。在本研究中，我们报告了新的发现，1）ICR小鼠暴露于热环境中产生全身热应激，（40°C，30分钟/天，5天/周，3 wk）诱导线粒体适应，如线粒体酶活性增加（柠檬酸合酶和3-羟酰辅酶A脱氢酶）和呼吸链蛋白含量（2）运动后全身热应激可增加耐力训练诱导的线粒体适应（跑台运动，25 m/min，30 min/d，5 d/wk，3 wk）。此外，为了确定线粒体适应的候选机制，我们研究了运动后全身热应激对随后诱导线粒体基因转录的细胞信号级联的磷酸化状态的急性影响。我们发现，全身热应激增强了耐力运动诱导的p38 MAPK磷酸化，增加了p70 S6 K的磷酸化状态，p70 S6 K是哺乳动物雷帕霉素复合物1活性靶点的生物标志物，并且出乎意料地使骨骼肌中的AMP活化蛋白激酶及其下游靶点乙酰辅酶A羧化酶去磷酸化。我们目前的观察表明，热应激可以作为一种有效的运动后治疗。热应激治疗似乎对那些难以参加足够运动训练的人（如老年人，受伤的运动员和患者）有临床益处。
A recent study demonstrated that heat stress induces mitochondrial biogenesis in C2C12 myotubes, thereby implying that heat stress may be an effective treatment to enhance endurance training-induced mitochondrial adaptations in skeletal muscle. However, whether heat stress actually induces mitochondrial adaptations in skeletal muscle in vivo is unclear. In the present study, we report the novel findings that1) whole body heat stress produced by exposure of ICR mice to a hot environment (40°C, 30 min/day, 5 days/wk, 3 wk) induced mitochondrial adaptations such as increased mitochondrial enzyme activity (citrate synthase and 3-hydroxyacyl CoA dehydrogenase) and respiratory chain protein content (complexes I–V) in skeletal muscle in vivo and2) postexercise whole body heat stress additively enhanced endurance training-induced mitochondrial adaptations (treadmill running, 25 m/min, 30 min/day, 5 days/wk, 3 wk). Moreover, to determine the candidate mechanisms underlying mitochondrial adaptations, we investigated the acute effects of postexercise whole body heat stress on the phosphorylation status of cellular signaling cascades that subsequently induce mitochondrial gene transcription. We found that whole body heat stress boosted the endurance exercise-induced phosphorylation of p38 MAPK, increased the phosphorylation status of p70S6K, a biomarker of mammalian target of rapamycin complex 1 activity, and unexpectedly dephosphorylated AMP-activated protein kinase and its downstream target acetyl-CoA carboxylase in skeletal muscle. Our present observations suggest that heat stress can act as an effective postexercise treatment. Heat stress treatment appeared to be clinically beneficial for people who have difficulty participating in sufficient exercise training, such as the elderly, injured athletes, and patients.