Exercise-induced metabolic fluctuations influence AMPK, p38-MAPK and CaMKII phosphorylation in human skeletal muscle.
Exercise-induced metabolic fluctuations influence AMPK, p38-MAPK and CaMKII phosphorylation in human skeletal muscle.
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DOI：
10.14814/phy2.12462
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发表时间：
2015-09
影响因子：
2.5
通讯作者：
Daussin FN
中科院分区：
文献类型：
--
作者：
Combes A;Dekerle J;Webborn N;Watt P;Bougault V;Daussin FN
在从休息到运动的过渡过程中，代谢反应速率大幅增加，以维持细胞内ATP的使用。这些代谢需求激活了几个启动信号转导通路的激酶，这些信号转导通路调节线粒体生物发生的转录调节。本研究的目的是确定代谢波动本身是否影响已知的调节过氧化物酶体增殖物激活受体γ辅活化子-1α(PGC-1α)的信号级联。在两种不同的情况下，9名男性进行了连续(30分钟)和间歇性(30分钟×1分钟间隔，间隔1分钟的恢复)70%的锻炼。每次运动后分别于安静、+0h和+3h取股外侧肌骨骼肌活检标本。通过分析VO2反应来确定与运动引起的代谢率变化相对应的代谢波动。在间歇运动期间，代谢波动是2.8倍，尽管持续运动的总作业量相同(间歇运动和持续运动后分别为317±2.41 kJ和312±5.56 kJ)。AMPK(˜2.9倍，P<0.0 1)、钙/钙调蛋白依赖的蛋白激酶II(˜2.7倍，P<0.0 1)和p38丝裂原激活的蛋白激酶(˜4.2倍，P<0.0 1)的磷酸化在两种运动中都立即增加，并且在间歇运动(条件x时间相互作用，P<0.0 5)后增加。与单次匹配的工作和强度的连续运动相比，单次间歇性运动可以诱导这些调节前列腺素C-1α的信号通路更大的激活。运动对线粒体生物发生的慢性适应还有待研究。
During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). On two separate occasions, nine men performed a continuous (30-min) and an intermittent exercise (30 × 1-min intervals separated by 1-min of recovery) at 70% of . Skeletal muscle biopsies from the vastus lateralis were taken at rest and at +0 h and +3 h after each exercise. Metabolic fluctuations that correspond to exercise-induced variation in metabolic rates were determined by analysis of VO2 responses. During intermittent exercise metabolic fluctuations were 2.8-fold higher despite identical total work done to continuous exercise (317 ± 41 vs. 312 ± 56 kJ after intermittent and continuous exercise, respectively). Increased phosphorylation of AMP-activated protein kinase (AMPK) (˜2.9-fold, P < 0.01), calcium/calmodulin-dependent protein kinase II (CaMKII) (˜2.7-fold, P < 0.01) and p38-mitogen-activated protein kinase (MAPK) (˜4.2-fold, P < 0.01) occurred immediately in both exercises and to a greater extent after the intermittent exercise (condition x time interaction, P < 0.05). A single bout of intermittent exercise induces a greater activation of these signaling pathways regulating PGC-1α when compared to a single bout of continuous exercise of matched work and intensity. Chronic adaptations to exercise on mitochondria biogenesis are yet to be investigated.