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Pathophysiology of upper extremity muscle disorders

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Author: Visser, B. · Dieën, J.H. van
Institution: TNO Kwaliteit van Leven
Source:Journal of Electromyography and Kinesiology, 1, 16, 1-16
Identifier: 239121
doi: doi:10.1016/j.jelekin.2005.06.005
Keywords: Workplace · Veilig en Gezond Werken · Cumulative trauma disorders · Low-intensity contraction · Muscle pain · Myalgia · Repetitive strain injury · Calcium ion · Cytochrome c oxidase · Anaerobic metabolism · Calcium cell level · Clinical feature · Fascia · Feedback system · Heat shock · Human · Hypothesis · Mechanical stress · Morphology · motor unit · Muscle blood flow · Muscle blood vessel · Muscle cell · Muscle contraction · Muscle disease · Muscle force · Muscle injury · Muscle metabolism · Myalgia · nociception · Pathophysiology · Reperfusion injury · Review · Sensitization · Shear stress · Skeletal muscle · Biomechanics · Humans · Muscle, Skeletal · Muscular Diseases · Upper Extremity


A review of the literature on the pathophysiology of upper extremity muscle disorders (UEMDs) was performed. An overview is given of clinical findings and hypotheses on the pathogenesis of UEMDs. The literature indicates that disorders of muscle cells and limitations of the local circulation underlie UEMDs. However, these disorders identified do not necessarily lead to symptoms. The following mechanisms have been proposed in the literature: (1) selective recruitment and overloading of type I (Cinderella) motor units; (2) intra-cellular Ca2+ accumulation; (3) impaired blood flow; (3b) reperfusion injury; (3.3c) blood vessel-nociceptor interaction; (4a) myofascial force transmission; (4b) intramuscular shear forces; (5) trigger points; (6) impaired heat shock response. The results of the review indicate that there are multiple possible mechanisms, but none of the hypotheses forms a complete explanation and is sufficiently supported by empirical data. Overall, the literature indicates that: (1) sustained muscle activity, especially of type I motor units, may be a primary cause of UEMDs; (2) in UEMDs skeletal muscle may show changes in morphology, blood flow, and muscle activity; (3) accumulation of Ca2+ in the sarcoplasm may be the cause of muscle cell damage; (4) it seems plausible that suboptimal blood flow plays a role in pathogenesis of UEMDs; (5) since the presence of fiber disorders is not a sufficient condition for the development of UEMSDs additional mechanisms, such as sensitization, are assumed to play a role. © 2005 Elsevier Ltd. All rights reserved. Chemicals / CAS: calcium ion, 14127-61-8; cytochrome c oxidase, 72841-18-0, 9001-16-5