PERIPHERAL AND CENTRAL SENSITIZATION AFTER ECCENTRIC MUSCLE EXERCISE

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 疼痛调查使用诱发疼痛的方案和/或自然发生疼痛的样本参与者。研究实验诱发疼痛的研究在其对自然发生的疼痛的适用性方面受到限制，因为实验诱发疼痛更可预测和可控，而没有相同的意义和情感后果。 纤维肌痛综合征（FMS）患者表现出强直性伤害性冲动输入的证据，这至少是部分负责他们的痛觉过敏/异常性疼痛和中枢敏化。我们假设，间歇性发作的炎性疼痛是在触发信号级联，增加外周和中枢敏化这些患者的工具。其中一种可能的炎症发作与活动或用力引起的肌肉损伤有关。 我们提出的方法，解决炎症的作用，疼痛FMS是研究炎症介质和/或急性期反应物。 我们将研究这些炎症标志物在延迟性肌肉酸痛（DOMS）。 偏心肌肉收缩可以可靠地诱发在执行DOMS协议之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与随后的肌肉酸痛之间存在剂量反应关系。 我们计划检查中央/外周敏化或脱敏热/机械刺激之前和之后DOMS已诱导。此外，我们还将检测经过充分验证的炎症标志物，这些标志物也已知参与疼痛信号传导，包括血浆和尿液中的急性期反应物（ESR、CRP、新蝶呤）、细胞因子和其他炎症介质，如MARCKS（富含肉豆蔻酸的蛋白激酶C底物），以研究它们与FMS中枢致敏的密切关系。

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.