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骨骼肌收缩功能障碍对肥胖患者生物力学改变的潜在影响。

Potential contributions of skeletal muscle contractile dysfunction to altered biomechanics in obesity.

作者信息

Bollinger Lance M

机构信息

Department of Kinesiology and Health Promotion, University of Kentucky, Lexington, KY, United States.

出版信息

Gait Posture. 2017 Jul;56:100-107. doi: 10.1016/j.gaitpost.2017.05.003. Epub 2017 May 13.

DOI:10.1016/j.gaitpost.2017.05.003
PMID:28528004
Abstract

Obesity alters whole body kinematics and joint kinetics during activities of daily living which are thought to contribute to increased risk of musculoskeletal injury, development of lower extremity joint osteoarthritis (OA), and physical disability. To date, it has widely been accepted that excess adipose tissue mass is the major driver of biomechanical alterations in obesity. However, it is well established that obesity is a systemic disease affecting numerous, if not all, organ systems of the body. Indeed, obesity elicits numerous adaptations within skeletal muscle, including alterations in muscle structure (ex. myofiber size, architecture, lipid accumulation, and fiber type), recruitment patterns, and contractile function (ex. force production, power production, and fatigue) which may influence kinematics and joint kinetics. This review discusses the specific adaptations of skeletal muscle to obesity, potential mechanisms underlying these adaptations, and how these adaptations may affect biomechanics.

摘要

肥胖会改变日常生活活动中的全身运动学和关节动力学,这些变化被认为会增加肌肉骨骼损伤风险、下肢关节骨关节炎(OA)的发生几率以及身体残疾的可能性。迄今为止,人们普遍认为过多的脂肪组织是肥胖导致生物力学改变的主要驱动因素。然而,肥胖是一种影响身体众多(即便不是所有)器官系统的全身性疾病,这一点已得到充分证实。事实上,肥胖会引发骨骼肌内的多种适应性变化,包括肌肉结构的改变(如肌纤维大小、结构、脂质蓄积和纤维类型)、募集模式以及收缩功能(如力量产生、功率产生和疲劳),而这些变化可能会影响运动学和关节动力学。本综述讨论了骨骼肌对肥胖的具体适应性变化、这些适应性变化背后的潜在机制,以及这些适应性变化如何影响生物力学。

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