• Santos Diogo Francisco da Silva Dos DFDSD Laboratory of Studies of Pain and Inflammation, School of Applied Sciences, State University of Campinas, Pedro Zaccaria 1300, L, Melo Aquino Bruna de B Laboratory of Studies of Pain and Inflammation, School of Applied Sciences, State University of Campinas, Pedro Zaccaria 1300, Limeira, Sao Paulo, , Carolina Ocanha Jorge, Azambuja Graciana de G Laboratory of Studies of Pain and Inflammation, School of Applied Sciences, State University of Campinas, Pedro Zaccaria 1300, Limeira, Sao Paulo, , Jalile Garcia Schiavuzzo, Suzy Krimon, Neves Juliana Dos Santos JDS Department of Morphology, Piracicaba Dental School, State University of Campinas, Limeira 901, Piracicaba, Sao Paulo, Brazil., Carlos Amilcar Parada, and Maria Claudia Gonçalves Oliveira-Fusaro.
• Laboratory of Studies of Pain and Inflammation, School of Applied Sciences, State University of Campinas, Pedro Zaccaria 1300, Limeira, Sao Paulo, Brazil.
• Neuroscience. 2017 Sep 1; 358: 58-69.

AbstractMuscle pain is an important health issue and frequently related to static force exertion. The aim of this study is to evaluate whether peripheral inflammatory mechanisms are involved with static contraction-induced muscle pain in rats. To this end, we developed a model of muscle pain induced by static contraction performed by applying electrical pulses through electrodes inserted into muscle. We also evaluated the involvement of neutrophil migration, bradykinin, sympathetic amines and prostanoids. A single session of sustained static contraction of gastrocnemius muscle induced acute mechanical muscle hyperalgesia without affecting locomotor activity and with no evidence of structural damage in muscle tissue. Static contraction increased levels of creatine kinase but not lactate dehydrogenase, and induced neutrophil migration. Dexamethasone (glucocorticoid anti-inflammatory agent), DALBK (bradykinin B1 antagonist), Atenolol (β1 adrenoceptor antagonist), ICI 118,551 (β2 adrenoceptor antagonist), indomethacin (cyclooxygenase inhibitor), and fucoidan (non-specific selectin inhibitor) all reduced static contraction-induced muscle hyperalgesia; however, the bradykinin B2 antagonist, bradyzide, did not have an effect on static contraction-induced muscle hyperalgesia. Furthermore, an increased hyperalgesic response was observed when the selective bradykinin B1 agonist des-Arg9-bradykinin was injected into the previously stimulated muscle. Together, these findings demonstrate that static contraction induced mechanical muscle hyperalgesia in gastrocnemius muscle of rats is modulated through peripheral inflammatory mechanisms that are dependent on neutrophil migration, bradykinin, sympathetic amines and prostanoids. Considering the clinical relevance of muscle pain, we propose the present model of static contraction-induced mechanical muscle hyperalgesia as a useful tool for the study of mechanisms underlying static contraction-induced muscle pain.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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