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长寿的 Snell 矮鼠()经抗阻训练后,对适应不良的阻抗增强,且 VCAM-1 上调增强。

Improved impedance to maladaptation and enhanced VCAM-1 upregulation with resistance-type training in the long-lived Snell dwarf () mouse.

机构信息

Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.

West Virginia School of Medicine, Division of Exercise Physiology, Morgantown, WV 26506, USA.

出版信息

Aging (Albany NY). 2022 Feb 3;14(3):1157-1185. doi: 10.18632/aging.203875.

DOI:10.18632/aging.203875
PMID:35113807
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8876912/
Abstract

Snell dwarf mice with the mutation are deficient in growth hormone, prolactin, and thyroid stimulating hormone and exhibit >40% lifespan extension. This longevity is accompanied by compromised muscular performance. However, research regarding young (3-month-old) Snell dwarf mice demonstrate exceptional responsivity to resistance-type training especially in terms of a shifted fiber type distribution and increased protein levels of vascular cell adhesion molecule-1 (VCAM-1), a possible mediator of such remodeling. In the present study, we investigated whether this responsiveness persists at 12 months of age. Unlike 12-month-old control mice, age-matched Snell dwarf mice remained resistant to training-induced maladaptive decreases in performance and muscle mass. This was accompanied by retainment of the remodeling capacity in muscles of Snell dwarf mice to increase VCAM-1 protein levels and a shift in myosin heavy chain (MHC) isoform distribution with training. Even decreasing training frequency for control mice, an alteration which protected muscles from maladaptation at 12 months of age, did not result in the overt remodeling observed for Snell dwarf mice. The results demonstrate a distinct remodeling response to resistance-type exercise operative in the context of the mutation of long-lived Snell dwarf mice.

摘要

Snell 矮小型小鼠由于突变而缺乏生长激素、催乳素和促甲状腺激素,表现出 >40%的寿命延长。这种长寿伴随着肌肉性能的受损。然而,关于年轻(3 个月大)Snell 矮小型小鼠的研究表明,它们对阻力型训练具有出色的反应能力,尤其是在纤维类型分布的改变和血管细胞黏附分子-1(VCAM-1)的蛋白水平增加方面,这可能是这种重塑的介导因素。在本研究中,我们研究了这种反应能力是否在 12 个月大时仍然存在。与 12 个月大的对照小鼠不同,同龄的 Snell 矮小型小鼠仍然能够抵抗训练引起的肌肉性能和肌肉质量的适应性下降。这伴随着 Snell 矮小型小鼠肌肉中 VCAM-1 蛋白水平的增加和肌球蛋白重链(MHC)同工型分布的改变,这种重塑能力得以保留。即使降低了对照小鼠的训练频率,这种改变可以保护肌肉免受 12 个月大时的适应性不良,但并没有导致如 Snell 矮小型小鼠那样明显的重塑。研究结果表明,在长寿的 Snell 矮小型小鼠的突变背景下,存在一种对阻力型运动的独特重塑反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/7c3b7218efd6/aging-14-203875-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/12cddb32c76d/aging-14-203875-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/8007a3c8a8e6/aging-14-203875-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/6e43c44a12df/aging-14-203875-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/7c3b7218efd6/aging-14-203875-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/12cddb32c76d/aging-14-203875-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/8007a3c8a8e6/aging-14-203875-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/6e43c44a12df/aging-14-203875-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f835/8876912/7c3b7218efd6/aging-14-203875-g004.jpg

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