PERIPHERAL AND CENTRAL SENSITIZATION AFTER ECCENTRIC MUSCLE EXERCISE

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。疼痛调查使用诱发疼痛的方案和/或具有自然发生疼痛的样本参与者。检查实验引起的疼痛的研究在其对自然发生的疼痛的适用性方面是有限的，因为实验引起的疼痛更可预测和可控，而没有相同的含义和情感后果。纤维肌痛综合征(FMS)患者表现出紧张性伤害性冲动输入，这至少是他们痛觉过敏/超敏和中枢敏化的部分原因。我们假设，间歇性炎性疼痛有助于触发信号级联反应，从而增加这些患者的外周和中枢敏化。这些可能的炎症性发作之一与活动或劳累造成的肌肉损伤有关。我们提出的解决炎症在FMS疼痛中的作用的方法是研究炎症介质和/或急性时相反应物。我们将研究延迟性肌肉酸痛(DOMS)中的这些炎症标志物。偏心性肌肉收缩可以可靠地引起在DOMS方案执行后发生的暂时性肌肉酸痛和疼痛。此外，有令人信服的证据表明，偏心性肌肉收缩的强度和随后的肌肉酸痛之间存在剂量-反应关系。我们计划在诱发DOMS之前和之后检查中枢/外周对热/机械刺激的敏化或脱敏。此外，我们还将检测已知参与疼痛信号传递的炎症标志物，包括急性时相反应物(ESR、CRP、新喋呤)、细胞因子和其他炎症介质，如血浆和尿液中的MARCKS(肉豆蔻醇丙氨酸富含蛋白激酶C底物)，以探讨它们与FMS中枢敏化的密切关系。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Investigations of pain use protocols that induce pain and/or sample participants with naturally occurring pain. Research examining experimentally induced pain is limited in its applicability to naturally occurring pain because experimentally induced pain is more predictable and controllable without the same meaning and emotional consequences. Patients with fibromyalgia syndrome (FMS) show evidence of tonic nociceptive impulse input, which is at least partially responsible for their hyperalgesia/allodynia and central sensitization. We hypothesize that intermittent bouts of inflammatory pain are instrumental in triggering signal cascades that increase peripheral and central sensitization in these patients. One of these possible inflammatory bouts is related to muscle injury from activity or exertion. Our proposed method of addressing the role of inflammation for pain in FMS is to study inflammatory mediators and/or acute phase reactants. We will study these inflammatory markers in delayed-onset muscle soreness (DOMS). Eccentric muscle contractions can reliably induce temporary muscle soreness and pain that occur after the performance of the DOMS protocol. In addition, there is convincing evidence of a dose-response relationship between the intensity of the eccentric muscle contractions and subsequent muscle soreness. We plan to examine central/peripheral sensitization or desensitization to thermal/mechanical stimuli before and after DOMS has been induced. In addition, we will test well validated markers of inflammation, that are also known to be involved in pain signaling, including acute phase reactants (ESR, CRP, neopterin), cytokines, and other inflammatory mediators like MARCKS (myristolated alanine rich protein kinase C substrate) in plasma and urine to investigate their close relationship with central sensitization in FMS.