The influence of cyclic concentric and eccentric submaximal muscle loading on cell viability in the rabbit knee joint

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• 作者：Monika Horisberger^a ; ^b ; Rafael Fortuna^a ; Timothy R. Leonard^a ; Victor Valderrabano^b ; Walter Herzog^a ; ^{Walter@kin.ucalgary.ca}
• 关键词：Osteoarthritis ; Joint degeneration ; Chondrocyte death ; Muscle loading ; Eccentric ; Concentric ; Cell viability ; Knee joint ; Animal model ; Confocal microscopy ; Rehabilitation
• 刊名：Clinical Biomechanics
• 出版年：2012
• 期刊代码：56_02680033
• 类别：med
• 出版时间：March, 2012
• 卷：27
• 期：3
• 页码：292-298
• 文件大小：1246 K

摘要

Background

Cartilage loading is associated with the onset and progression of osteoarthritis and cell death may play an important role in these processes. Although much is known about cell death in joint impact loading, there is no information on joints loaded by muscular contractions. The aim of this study was to evaluate the influence of muscle generated eccentric and concentric submaximal joint loading on chondrocyte viability. We hypothesised that eccentric muscle activation leads to increased cell death rates compared to concentric loading and to controls.

Methods

16 rabbits received either 50 min of uni-lateral, cyclic eccentric (n = 8) or concentric (n = 8) knee loading. Muscle activation for these dynamic conditions was equivalent to an activation level that produced 20%of maximum isometric force. Contralateral joints served as unloaded controls. Cell viability was assessed using confocal microscopy.

Findings

Eccentric contractions produced greater knee loading than concentric contractions. Sub-maximal contractions caused a significant increase in cell death in the loaded knees compared to the unloaded controls, and eccentric loading caused significantly more cell death than concentric loading.

Interpretation

Cyclic sub-maximal muscle loading of the knee caused increased chondrocyte death in rabbits. These findings suggest that low levels of joint loading for prolonged periods, as occurs in endurance exercise or physical labour, may cause chondrocyte death, thereby predisposing joints to degeneration.