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衰老与运动对肌腱的影响。

Effect of aging and exercise on the tendon.

作者信息

Svensson Rene B, Heinemeier Katja Maria, Couppé Christian, Kjaer Michael, Magnusson S Peter

机构信息

Institute of Sports Medicine Copenhagen, Department of Orthopedic Surgery, Bispebjerg Hospital and Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark.

Department of Biomedical Sciences, Center for Healthy Aging, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark; and.

出版信息

J Appl Physiol (1985). 2016 Dec 1;121(6):1237-1246. doi: 10.1152/japplphysiol.00328.2016. Epub 2016 May 5.

Abstract

Here, we review the literature on how tendons respond and adapt to ageing and exercise. With respect to aging, there are considerable changes early in life, but this seems to be maturation rather than aging per se. In vitro data indicate that aging is associated with a decreased potential for cell proliferation and a reduction in the number of stem/progenitor-like cells. Further, there is persuasive evidence that turnover in the core of the tendon after maturity is very slow or absent. Tendon fibril diameter, collagen content, and whole tendon size appear to be largely unchanged with aging, while glycation-derived cross-links increase substantially. Mechanically, aging appears to be associated with a reduction in modulus and strength. With respect to exercise, tendon cells respond by producing growth factors, and there is some support for a loading-induced increase in tendon collagen synthesis in humans, which likely reflects synthesis at the very periphery of the tendon rather than the core. Average collagen fibril diameter is largely unaffected by exercise, while there can be some hypertrophy of the whole tendon. In addition, it seems that resistance training can yield increased stiffness and modulus of the tendon and may reduce the amount of glycation. Exercise thereby tends to counteract the effects of aging.

摘要

在此,我们回顾了关于肌腱如何对衰老和运动做出反应及适应的文献。关于衰老,生命早期会有相当大的变化,但这似乎是成熟而非衰老本身。体外数据表明,衰老与细胞增殖潜力降低以及干/祖细胞样细胞数量减少有关。此外,有确凿证据表明,成熟后肌腱核心的更新非常缓慢或不存在。肌腱纤维直径、胶原蛋白含量和整个肌腱大小在衰老过程中似乎基本不变,而糖基化衍生的交联显著增加。在力学方面,衰老似乎与模量和强度降低有关。关于运动,肌腱细胞通过产生生长因子做出反应,并且有一些证据支持运动负荷可诱导人体肌腱胶原蛋白合成增加,这可能反映了肌腱最外围而非核心部位的合成。平均胶原纤维直径在很大程度上不受运动影响,而整个肌腱可能会有一些肥大。此外,抗阻训练似乎可以增加肌腱的硬度和模量,并可能减少糖基化量。因此,运动往往会抵消衰老的影响。

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