Matched work high-intensity interval and continuous running induce similar increases in PGC-1α mRNA, AMPK, p38, and p53 phosphorylation in human skeletal muscle
Matched work high-intensity interval and continuous running induce similar increases in PGC-1α mRNA, AMPK, p38, and p53 phosphorylation in human skeletal muscle
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DOI：
10.1152/japplphysiol.01040.2011
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发表时间：
2012-04-01
影响因子：
3.3
通讯作者：
Morton, James P.
中科院分区：
文献类型：
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作者：
Bartlett, Jonathan D.;Joo, Chang Hwa;Morton, James P.
Bartlett JD，Hwa Joo C，Jeong TS，Louhelainen J，Cochran AJ，Gibala MJ，Gregson W，Close GL，Drust B，Morton JP。匹配的高强度间歇运动和连续跑可引起人骨骼肌中PGC-1αmRNA、AMPK、p38和P53磷酸化的类似增加。应用生理学杂志112：1135-1143,2012。2012年1月29日首次发布；doi：10.1152/japplPhysiol.01040.2011。-本研究的目的是验证以下假设：与与所做工作匹配的中等强度连续(CONT)跑相比，急性高强度间歇跑(HIT)可诱导与线粒体生物发生相关的信号通路更大的激活。在重复测量设计中，10名积极运动的男性执行两种跑步方案，包括HIT[在点O-2max上90%最大耗氧量((V)时6x3min)，其间穿插着在点O-2max上以50%(V)的3分钟恢复期，在点O-2max上有7分钟的热身和降温期[在点O-2max上以70%(V)的速度连续跑50min]或CONT(在点O-2max上以70%(V)的速度连续跑50min)。因此，在平均强度、持续时间和距离跑方面，两种方案都是匹配的。分别于运动前、运动后和运动后3h取股外侧肌组织标本。肌糖原下降(P<；0.05)，HIT组和CONT组相似(分别为116+/-11和111+/-17 mmol/kg干重)。P38MAPK(Thr180/Tyr182)(1.9<；0.1倍vs.1.5+/-0.2倍)和AMPK(Thr172(1.5+/-0.3倍vs.1.5+/-0.1倍)的磷酸化(P-)分别在运动后即刻增加(P<；0.05)，并在运动后3h恢复至基础水平。P-P53(Ser15)(HIT，2.7+/-0.8倍；CONT，2.1+/-0.8倍)、PGC-1αmRNA(HIT，4.2+/-1.7倍；CONT，4.5+/-0.9倍)和HSP72 mRNA(HIT，4.4+/-2倍；CONT，3.5+/-1倍)均在运动后3h增加(P<；0.05)，但两项参数均未见增加(P>；0.05)。在上述信号或基因表达反应方面，试验之间没有任何差异(P>；0.05)。我们提供了新的数据，证明了急性击打和连续跑步(当平均强度、持续时间和完成的功相匹配时)诱导了与线粒体生物发生调控相关的分子信号通路的相似激活。此外，这是首次报道收缩诱导人类骨骼肌中P53的磷酸化，从而突出了运动可能启动线粒体生物发生的另一条途径。
Bartlett JD, Hwa Joo C, Jeong TS, Louhelainen J, Cochran AJ, Gibala MJ, Gregson W, Close GL, Drust B, Morton JP. Matched work high-intensity interval and continuous running induce similar increases in PGC-1 alpha mRNA, AMPK, p38, and p53 phosphorylation in human skeletal muscle. J Appl Physiol 112: 1135-1143, 2012. First published January 29, 2012; doi:10.1152/japplphysiol.01040.2011.-The aim of the present study was to test the hypothesis that acute high-intensity interval (HIT) running induces greater activation of signaling pathways associated with mitochondrial biogenesis compared with moderate-intensity continuous (CONT) running matched for work done. In a repeated-measures design, 10 active men performed two running protocols consisting of HIT [6 x 3-min at 90% maximal oxygen consumption ((V) over dot O-2max) interspersed with 3-min recovery periods at 50% (V) over dot O-2max with a 7-min warm-up and cool-down period at 70% (V) over dot O-2max] or CONT (50-min continuous running at 70% (V) over dot O-2max). Both protocols were matched, therefore, for average intensity, duration, and distance run. Muscle biopsies (vastus lateralis) were obtained preexercise, postexercise, and 3 h postexercise. Muscle glycogen decreased (P < 0.05) similarly in HIT and CONT (116 +/- 11 vs. 111 +/- 17 mmol/kg dry wt, respectively). Phosphorylation (P-) of p38MAPK(Thr180/Tyr182) (1.9 < 0.1- vs. 1.5 +/- 0.2-fold) and AMPK(Thr172) (1.5 +/- 0.3- vs. 1.5 +/- 0.1-fold) increased immediately postexercise (P < 0.05) in HIT and CONT, respectively, and returned to basal levels at 3 h postexercise. P-p53(Ser15) (HIT, 2.7 +/- 0.8-fold; CONT, 2.1 +/- 0.8-fold), PGC-1 alpha mRNA (HIT, 4.2 +/- 1.7-fold; CONT, 4.5 +/- 0.9-fold) and HSP72 mRNA (HIT, 4.4 +/- 2-fold; CONT, 3.5 +/- 1-fold) all increased 3 h postexercise (P < 0.05) although neither parameter increased (P > 0.05) immediately postexercise. There was no difference between trials for any of the above signaling or gene expression responses (P > 0.05). We provide novel data by demonstrating that acute HIT and CONT running (when matched for average intensity, duration, and work done) induces similar activation of molecular signaling pathways associated with regulation of mitochondrial biogenesis. Furthermore, this is the first report of contraction-induced p53 phosphorylation in human skeletal muscle, thus highlighting an additional pathway by which exercise may initiate mitochondrial biogenesis.