Low-intensity exercise induces acute shifts in liver and skeletal muscle substrate metabolism but not chronic adaptations in tissue oxidative capacity
Low-intensity exercise induces acute shifts in liver and skeletal muscle substrate metabolism but not chronic adaptations in tissue oxidative capacity
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DOI：
10.1152/japplphysiol.00820.2018
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发表时间：
2019-07-01
影响因子：
3.3
通讯作者：
Noland, Robert C.
中科院分区：
文献类型：
--
作者：
Fuller, Scott E.;Huang, Tai-Yu;Noland, Robert C.
在健康雄性C57 BL/6 J小鼠中测试了急性和慢性（6周; 5天/周; 1小时/天）低强度跑步机运动后肝脏和骨骼肌底物代谢的适应性。低强度运动使脂质利用最大化;因此，我们假设参与脂质代谢的途径将受到最强烈的影响。急性运动几乎耗尽肝糖原立即运动后（0小时），而肝脏甘油三酯（TAG）存储增加运动后的早期阶段（0-3小时）。此外，肝脏过氧化物酶体增殖物激活受体-γ共激活因子-1 α（PGC-1 α）基因表达和脂肪氧化（线粒体和过氧化物酶体）在运动后立即增加（0 h），而肝脏中的碳水化合物和氨基酸氧化在24-48 h后达到峰值。或者，骨骼肌对急性运动的反应不太强烈，因为储存的底物（糖原和TAG）保持不变，PGC-1 α基因表达的诱导延迟（3小时），线粒体底物氧化途径（碳水化合物，氨基酸和脂质）基本不变。过氧化物酶体脂质氧化在急性运动后骨骼肌底物代谢中表现出最动态的变化;然而，这种反应也被延迟（运动后3-24 h达到峰值），过氧化物酶体基因的表达不受影响。有趣的是，6周的训练在一个类似的强度限制体重增加，增加肌糖原，并减少TAG的积累在肝脏和肌肉;然而，底物氧化途径保持不变，在这两个组织。总的来说，这些结果表明，健康小鼠急性低强度运动引起的底物代谢变化在肝脏中比骨骼肌中更快和更强;但是，在此情况下，以类似强度训练6周不足以诱导任一组织中底物代谢途径的重塑。在健康小鼠肝脏和骨骼肌中测试强度运动对底物代谢途径的影响。这是第一个研究描述运动诱导的过氧化物酶体脂质代谢的适应，也报告了线粒体底物代谢途径（碳水化合物，脂质和氨基酸）的全面适应。急性低强度运动诱导两种组织中线粒体和过氧化物酶体代谢的变化，但这种强度的训练并没有诱导健康小鼠代谢途径的适应性重塑。
Adaptations in hepatic and skeletal muscle substrate metabolism following acute and chronic (6 wk; 5 days/wk; 1 h/day) low-intensity treadmill exercise were tested in healthy male C57BL/6J mice. Low-intensity exercise maximizes lipid utilization; therefore, we hypothesized pathways involved in lipid metabolism would be most robustly affected. Acute exercise nearly depleted liver glycogen immediately postexercise (0 h), whereas hepatic triglyceride (TAG) stores increased in the early stages after exercise (0-3 h). Also, hepatic peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha) gene expression and fat oxidation (mitochondrial and peroxisomal) increased immediately postexercise (0 h), whereas carbohydrate and amino acid oxidation in liver peaked 24-48 h later. Alternatively, skeletal muscle exhibited a less robust response to acute exercise as stored substrates (glycogen and TAG) remained unchanged, induction of PGC-1 alpha gene expression was delayed (up at 3 h), and mitochondrial substrate oxidation pathways (carbohydrate, amino acid, and lipid) were largely unaltered. Peroxisomal lipid oxidation exhibited the most dynamic changes in skeletal muscle substrate metabolism after acute exercise; however, this response was also delayed (peaked 3-24 h postexercise), and expression of peroxisomal genes remained unaffected. Interestingly, 6 wk of training at a similar intensity limited weight gain, increased muscle glycogen, and reduced TAG accrual in liver and muscle; however, substrate oxidation pathways remained unaltered in both tissues. Collectively, these results suggest changes in substrate metabolism induced by an acute low-intensity exercise bout in healthy mice are more rapid and robust in liver than in skeletal muscle; however, training at a similar intensity for 6 wk is insufficient to induce remodeling of substrate metabolism pathways in either tissue.NEW & NOTEWORTHY Effects of low-intensity exercise on substrate metabolism pathways were tested in liver and skeletal muscle of healthy mice. This is the first study to describe exercise-induced adaptations in peroxisomal lipid metabolism and also reports comprehensive adaptations in mitochondrial substrate metabolism pathways (carbohydrate, lipid, and amino acid). Acute low-intensity exercise induced shifts in mitochondrial and peroxisomal metabolism in both tissues, but training at this intensity did not induce adaptive remodeling of metabolic pathways in healthy mice.