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首页> 外文期刊>The European Journal of Neuroscience >Eccentric exercise induces chronic alterations in musculoskeletal nociception in the rat
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Eccentric exercise induces chronic alterations in musculoskeletal nociception in the rat

机译：离心运动诱发大鼠骨骼肌肉痛觉的慢性改变

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Eccentric muscle exercise is a common cause of acute and chronic (lasting days to weeks) musculoskeletal pain. To evaluate the mechanisms involved, we have employed a model in the rat, in which eccentric hind limb exercise produces both acute mechanical hyperalgesia as well as long-term changes characterized by enhanced hyperalgesia to subsequent exposure to an inflammatory mediator. Eccentric exercise of the hind limb produced mechanical hyperalgesia, measured in the gastrocnemius muscle, which returned to baseline at 120 h post-exercise. When nociceptive thresholds had returned to baseline, intramuscular injection of prostaglandin E_2 (PGE_2) induced hyperalgesia that was unattenuated 240 h later, much longer than PGE_2-induced hyperalgesia in unexercised rats (4 h). This marked prolongation of PGE_2 hyperalgesia induced by eccentric exercise was prevented by the spinal intrathecal injection of oligodeoxynucleotide antisense to protein kinase C epdilon, a second messenger in nociceptors implicated in the induction of chronic pain. Exercise-induced hyperalgesia and prolongation of PGE_2 hyperalgesia were inhibited by the spinal intrathecal administration of antisense for the interleukin-6 but not the tumor necrosis factor alpha type 1 receptor. These findings provide further insight into the mechanism underlying exercise-induced chronic muscle pain, and suggest novel approaches for the prevention and treatment of exercise- or work-related chronic musculoskeletal pain syndromes.
机译：偏心肌肉运动是急性和慢性（持续数天至数周）肌肉骨骼疼痛的常见原因。为了评估所涉及的机制，我们在大鼠中采用了一种模型，在该模型中，偏心的后肢运动会产生急性机械性痛觉过敏以及以继发于炎性介质后增强的痛觉过敏为特征的长期变化。后肢的离心运动在腓肠肌中产生了机械性痛觉过敏，运动后120 h恢复到基线。当伤害阈值恢复到基线时，肌注前列腺素E_2（PGE_2）引起的痛觉过敏在240小时后未减弱，比未接受运动的大鼠（4 h）的PGE_2诱导的痛觉过敏长得多。脊髓鞘内注射寡脱氧核苷酸对蛋白激酶C epdilon的反义可防止这种由离心运动引起的PGE_2痛觉过敏的明显延长，蛋白激酶C epdilon是伤害性感受器的第二个信使，与慢性疼痛的诱发有关。运动诱导的痛觉过敏和PGE_2痛觉过敏的延长受到了鞘内注射白细胞介素6的反义作用，但没有抑制肿瘤坏死因子α1型受体。这些发现进一步揭示了运动诱发的慢性肌肉疼痛的潜在机制，并提出了预防和治疗与运动或工作有关的慢性肌肉骨骼疼痛综合征的新方法。

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