Adaptations in Mitochondrial Enzymatic Activity Occurs Independent of Genomic Dosage in Response to Aerobic Exercise Training and Deconditioning in Human Skeletal Muscle
Adaptations in Mitochondrial Enzymatic Activity Occurs Independent of Genomic Dosage in Response to Aerobic Exercise Training and Deconditioning in Human Skeletal Muscle
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DOI：
10.3390/cells8030237
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发表时间：
2019-03-01
期刊：
影响因子：
6
通讯作者：
Jeppesen, Tina D.
中科院分区：
文献类型：
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作者：
Fritzen, Andreas M.;Thogersen, Frank B.;Jeppesen, Tina D.
线粒体 DNA (mtDNA) 复制被认为是运动训练诱导的线粒体适应的一个组成部分。因此，线粒体DNA水平经常被用作训练研究中线粒体适应的指标。我们研究了耐力运动训练引起的线粒体酶变化与基因组剂量无关的假设，方法是研究 10 名健康、未经训练的男性志愿者在进行六周的膝伸肌运动训练，然后进行四个星期的单腿去适应后骨骼肌中的线粒体 DNA 含量，并将结果与对侧未经训练的腿的结果进行比较。研究结果与柠檬酸合酶活性、线粒体复合物活性和线粒体膜标记物（孔蛋白和心磷脂）的含量进行了比较。单腿伸膝运动可将耐力表现提高 120%，同时功率输出和峰值摄氧量分别增加 49% 和 33% (p < 0.01)。在训练过的腿中，柠檬酸合酶和线粒体呼吸链复合物 I-IV 活性分别增加了 51% 和 46-61% (p < 0.001)。尽管训练诱导线粒体 TCA 和 ETC 酶活性显着增加，但线粒体 DNA 和线粒体内膜和外膜标记物（即心磷脂和孔蛋白）没有变化。相反，去适应使耐力能力降低了 41%，肌肉柠檬酸合酶活性降低了 32%，线粒体复合物 I-IV 活性降低了 29-36% (p < 0.05)，而先前训练的腿中 mtDNA、孔蛋白和心磷脂含量没有任何变化。研究结果表明，有氧耐力运动训练后线粒体酶活性的适应以及去适应的相反影响与线粒体基因组数量的变化无关，并且可能与线粒体DNA转录率的变化有关。
Mitochondrial DNA (mtDNA) replication is thought to be an integral part of exercise-training-induced mitochondrial adaptations. Thus, mtDNA level is often used as an index of mitochondrial adaptations in training studies. We investigated the hypothesis that endurance exercise training-induced mitochondrial enzymatic changes are independent of genomic dosage by studying mtDNA content in skeletal muscle in response to six weeks of knee-extensor exercise training followed by four weeks of deconditioning in one leg, comparing results to the contralateral untrained leg, in 10 healthy, untrained male volunteers. Findings were compared to citrate synthase activity, mitochondrial complex activities, and content of mitochondrial membrane markers (porin and cardiolipin). One-legged knee-extensor exercise increased endurance performance by 120%, which was accompanied by increases in power output and peak oxygen uptake of 49% and 33%, respectively (p < 0.01). Citrate synthase and mitochondrial respiratory chain complex I-IV activities were increased by 51% and 46-61%, respectively, in the trained leg (p < 0.001). Despite a substantial training-induced increase in mitochondrial activity of TCA and ETC enzymes, there was no change in mtDNA and mitochondrial inner and outer membrane markers (i.e., cardiolipin and porin). Conversely, deconditioning reduced endurance capacity by 41%, muscle citrate synthase activity by 32%, and mitochondrial complex I-IV activities by 29-36% (p < 0.05), without any change in mtDNA and porin and cardiolipin content in the previously trained leg. The findings demonstrate that the adaptations in mitochondrial enzymatic activity after aerobic endurance exercise training and the opposite effects of deconditioning are independent of changes in the number of mitochondrial genomes, and likely relate to changes in the rate of transcription of mtDNA.