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本文引用的文献

1
Skeletal muscle protein anabolic response to resistance exercise and essential amino acids is delayed with aging.随着年龄增长，骨骼肌蛋白质对阻力运动和必需氨基酸的合成代谢反应会延迟。
J Appl Physiol (1985). 2008 May;104(5):1452-61. doi: 10.1152/japplphysiol.00021.2008. Epub 2008 Mar 6.
2
AMPK activation attenuates S6K1, 4E-BP1, and eEF2 signaling responses to high-frequency electrically stimulated skeletal muscle contractions.AMPK激活减弱了S6K1、4E-BP1和eEF2对高频电刺激骨骼肌收缩的信号反应。
J Appl Physiol (1985). 2008 Mar;104(3):625-32. doi: 10.1152/japplphysiol.00915.2007. Epub 2008 Jan 10.
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Proteolytic gene expression differs at rest and after resistance exercise between young and old women.年轻女性和老年女性在静息状态及抗阻运动后，蛋白水解基因表达存在差异。
J Gerontol A Biol Sci Med Sci. 2007 Dec;62(12):1407-12. doi: 10.1093/gerona/62.12.1407.
4
Time course of proteolytic, cytokine, and myostatin gene expression after acute exercise in human skeletal muscle.急性运动后人体骨骼肌中蛋白水解、细胞因子及肌生长抑制素基因表达的时间进程。
J Appl Physiol (1985). 2007 Nov;103(5):1744-51. doi: 10.1152/japplphysiol.00679.2007. Epub 2007 Sep 6.
5
AMPK activation stimulates myofibrillar protein degradation and expression of atrophy-related ubiquitin ligases by increasing FOXO transcription factors in C2C12 myotubes.在C2C12肌管中，AMPK激活通过增加FOXO转录因子来刺激肌原纤维蛋白降解和萎缩相关泛素连接酶的表达。
Biosci Biotechnol Biochem. 2007 Jul;71(7):1650-6. doi: 10.1271/bbb.70057. Epub 2007 Jul 7.
6
S6 kinase deletion suppresses muscle growth adaptations to nutrient availability by activating AMP kinase.S6激酶缺失通过激活AMP激酶来抑制肌肉生长对营养可利用性的适应性变化。
Cell Metab. 2007 Jun;5(6):476-87. doi: 10.1016/j.cmet.2007.05.006.
7
Accumulation of mitochondrial DNA deletion mutations in aged muscle fibers: evidence for a causal role in muscle fiber loss.老年肌纤维中线粒体DNA缺失突变的积累：对肌纤维丢失起因果作用的证据。
J Gerontol A Biol Sci Med Sci. 2007 Mar;62(3):235-45. doi: 10.1093/gerona/62.3.235.
8
Aging-associated reductions in AMP-activated protein kinase activity and mitochondrial biogenesis.与衰老相关的AMP激活蛋白激酶活性降低和线粒体生物合成减少。
Cell Metab. 2007 Feb;5(2):151-6. doi: 10.1016/j.cmet.2007.01.008.
9
AMP-activated protein kinase agonists increase mRNA content of the muscle-specific ubiquitin ligases MAFbx and MuRF1 in C2C12 cells.AMP激活的蛋白激酶激动剂可增加C2C12细胞中肌肉特异性泛素连接酶MAFbx和MuRF1的mRNA含量。
Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1555-67. doi: 10.1152/ajpendo.00622.2006. Epub 2007 Jan 30.
10
Resistance exercise, muscle loading/unloading and the control of muscle mass.抗阻运动、肌肉负荷/卸载与肌肉质量的控制
Essays Biochem. 2006;42:61-74. doi: 10.1042/bse0420061.

AMP 激活的蛋白激酶是否对衰老的快肌骨骼肌质量起负向调节作用？

Does AMP-activated protein kinase negatively mediate aged fast-twitch skeletal muscle mass?

作者信息

Gordon Scott E, Lake Jordan A, Westerkamp Christopher M, Thomson David M

机构信息

Human Performance Laboratory, 363 Ward Sports Medicine Building, East Carolina University, Greenville, NC 27858, USA.

出版信息

Exerc Sport Sci Rev. 2008 Oct;36(4):179-86. doi: 10.1097/JES.0b013e3181877e13.

DOI:10.1097/JES.0b013e3181877e13
PMID:18815486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2659413/
Abstract

The activity of 5'-adenosine monophosphate (AMP)-activated protein kinase (AMPK), a negative regulator of cell size, is up-regulated with age in resting and overloaded fast-twitch skeletal muscle but not slow-twitch muscle. Here, we provide evidence to support the hypothesis that elevated AMPK activity plays a potentially important integrative role in the age-related atrophy and diminished capacity for growth specific to fast-twitch skeletal muscle.

摘要

5'-单磷酸腺苷（AMP）激活的蛋白激酶（AMPK）是细胞大小的负调节因子，其活性在静息和超负荷的快肌骨骼肌中随年龄增长而上调，但在慢肌中并非如此。在此，我们提供证据支持以下假说：AMPK活性升高在与年龄相关的快肌骨骼肌萎缩以及特定的生长能力下降中发挥潜在的重要整合作用。