High force reaching task induces widespread inflammation, increased spinal cord neurochemicals and neuropathic pain.
Repetitive strain injuries (RSI), which include several musculoskeletal disorders and nerve compression injuries, are associated with performance of repetitive and forceful tasks. In this study, we examined in young, adult Sprague-Dawley rats, the effects of performing a voluntary, moderate repetition, high force (MRHF; nine reaches/min; 60% maximum pulling force) task for 12 weeks on motor behavior and nerve function, inflammatory responses in forearm musculoskeletal and nerve tissues and serum, and neurochemical immunoexpression in cervical spinal cord dorsal horns. We observed no change in reach rate, but reduced voluntary participation and grip strength in week 12, and increased cutaneous sensitivity in weeks 6 and 12, the latter indicative of mechanical allodynia. Nerve conduction velocity (NCV) decreased 15% in the median nerve in week 12, indicative of low-grade nerve compression. ED-1 cells increased in distal radius and ulna in week 12, and in the median nerve and forearm muscles and tendons in weeks 6 and 12. Cytokines IL-1alpha, IL-1beta, TNF-alpha, and IL-10 increased in distal forearm bones in week 12, while IL-6 increased in tendon in week 12. However, serum analysis revealed only increased TNF-alpha in week 6 and macrophage inflammatory protein 3a (MIP3a) in weeks 6 and 12. Lastly, Substance P and neurokinin-1 were both increased in weeks 6 and 12 in the dorsal horns of cervical spinal cord segments. These results show that a high force, but moderate repetition task, induced declines in motor and nerve function as well as peripheral and systemic inflammatory responses (albeit the latter was mild). The peripheral inflammatory responses were associated with signs of central sensitization (mechanical allodynia and increased neurochemicals in spinal cord dorsal horns).
Elliott
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MB
Department of Physical Therapy, Temple University, 3307 North Broad Street, Philadelphia, PA 19140, USA. melanie.elliott@jefferson.edu
Barr
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Clark
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Amin
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Amin
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Barbe
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D000704:Analysis of Variance; D000818:Animals; D001842:Bone and Bones / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D053331:Ectodysplasins / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007249:Inflammation / Q000473:pathology* / Q000503:physiopathology*; D008264:Macrophages / Q000378:metabolism; D009068:Movement / Q000502:physiology*; D009141:Musculoskeletal System / Q000378:metabolism; D009431:Neural Conduction / Q000502:physiology; D009437:Neuralgia / Q000473:pathology* / Q000503:physiopathology*; D015288:Neurokinin A / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012684:Sensory Thresholds / Q000502:physiology; D012867:Skin / Q000294:innervation; D013116:Spinal Cord / Q000378:metabolism*; D013373:Substance P / Q000378:metabolism; D013997:Time Factors; D034941:Upper Extremity / Q000294:innervation
D016207:Cytokines; D053331:Ectodysplasins; D013373:Substance P; D015288:Neurokinin A