短暂的高强度间歇运动激活AMPKp38 MAPK信号,并增加人类骨骼肌中PGC-1的表达

Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1 in human skeletal muscle

 

 

然后,受试者在空气制动测功器(Repco)上进行4次拼尽全力的30-s的自行车赛,每次比赛之间休息4分钟。在第一次和最后一次练习之后,纱布很快被取下,通过一次切口获得活检样本(练习结束后10秒内)

 

考虑到间歇性训练能够刺激导致线粒体生物合成的信号通路,而不是那些负责肌肉生长的信号通路,看来这种训练可能更接近于耐力型训练,即通过激活信号通路进行抗性训练

 

综上所述,本研究表明,430-s拼尽全力的自行车赛会增加AMPK 1AMPK 2p38 MAPK的磷酸化水平和恢复3hPGC-1mRNA表达水平。因此,通过AMPKp38 MAPKPGC-1的特定信号可以部分解释间歇性运动训练导致的代谢重塑,包括线粒体生物合成和葡萄糖和脂肪酸氧化能力的增强。

 

Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1 in human skeletal muscle

 

Subjects then performed four 30-s all out cycling bouts on the air-braked ergometer (Repco) with 4 min of rest between bouts. Immediately following the first and last exercise bout, the gauze was quickly removed and a biopsy sample was obtained through one of the incisions (within 10 s following the completion of the exercise bout)

given the potency of interval training to stimulate the signaling pathways that lead to mitochondrial biogenesis, but not those responsible for muscle growth, it appears that such training may be closer to endurance type training that resistance training in terms of activation of signaling pathways

 

In summary, the present study showed that four 30-s bouts of all out cycling increased phosphorylation of AMPK1, AMPK2, and p38 MAPK immediately following exercise and the mRNA expression of PGC-1 after 3 h of recovery. Specific signaling through AMPK and p38 MAPK to PGC-1 may therefore explain in part the metabolic remodeling induced by intense interval exercise training, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.

 

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