An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle
An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle
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DOI：
10.1152/ajpregu.00538.2010
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发表时间：
2011-06-01
影响因子：
2.8
通讯作者：
Gibala, Martin J.
中科院分区：
文献类型：
--
作者：
Little, Jonathan P.;Safdar, Adeel;Gibala, Martin J.
低容量，高强度的间歇训练（HIT）增加骨骼肌线粒体的能力，但很少有人知道有关促进这种适应性反应的潜在机制。我们的目的是研究在人骨骼肌线粒体生物合成的分子过程中，在一个急性发作的HIT。8名健康男性进行了4 x 30-s的最大强度的自行车运动，中间穿插4分钟的休息。肌肉活检样品（股外侧肌）之前和之后立即运动，并在3和24小时的恢复。在休息时，大多数过氧化物酶体增殖物激活受体γ共激活因子（PGC）-1 α，线粒体生物发生的主调节剂，在胞质组分中检测到。运动激活胞浆中p38 MAPK和AMPK。核PGC-1 α蛋白增加3小时从运动中恢复，一个时间点，正好与线粒体基因的mRNA表达增加。其次是线粒体蛋白质含量和酶活性的增加后，24小时的恢复。这些发现支持了这样的假设，即急性低容量HIT通过涉及PGC-1 α核丰度增加的机制激活线粒体生物合成。
Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 x 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor gamma coactivator (PGC)-1 alpha, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1 alpha protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1 alpha.