Role of TNF-α/TNFR1 in intense acute swimming-induced delayed onset muscle soreness in mice
Autor: | Sergio M. Borghi, Thiago M. Cunha, Waldiceu A. Verri, Roberto I. Tatakihara, Marli Cardoso Martins-Pinge, Sergio H. Ferreira, Fernando Q. Cunha, Renato D. R. Cardoso, Ana C. Zarpelon, Rubia Casagrande, Felipe A. Pinho-Ribeiro |
---|---|
Rok vydání: | 2014 |
Předmět: |
Blood Glucose
Male medicine.medical_specialty Hydrocortisone Physical Exertion DOMS Muscle pain Experimental and Cognitive Psychology Endogeny medicine.disease_cause Receptors Tumor Necrosis Factor Etanercept NATAÇÃO (FISIOLOGIA) Mice Behavioral Neuroscience Gastrocnemius muscle chemistry.chemical_compound Internal medicine Delayed onset muscle soreness Leukocytes Animals Medicine Muscle Skeletal Swimming Peroxidase Soleus muscle Dose-Response Relationship Drug Tumor Necrosis Factor-alpha business.industry Anti-Inflammatory Agents Non-Steroidal Myalgia Glutathione Spinal cord Surgery Mice Inbred C57BL Endocrinology medicine.anatomical_structure Spinal Cord chemistry Receptors Tumor Necrosis Factor Type I Hyperalgesia Oxidative stress Immunoglobulin G TNF-α medicine.symptom business |
Zdroj: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
ISSN: | 0031-9384 |
DOI: | 10.1016/j.physbeh.2014.01.023 |
Popis: | The injection of cytokines such as TNF-α induces muscle pain. Herein, it was addressed the role of endogenous TNF-α/TNFR1 signaling in intense acute swimming-induced muscle mechanical hyperalgesia in mice. Mice were exposed to water during 30s (sham) or to a single session of 30–120min of swimming. Intense acute swimming induced a dose-dependent (time of exercise-dependent) muscle mechanical hyperalgesia, which peaked after 24h presenting characteristics of delayed onset muscle soreness (DOMS). The intense acute swimming (120min)-induced muscle mechanical hyperalgesia was reduced in etanercept (soluble TNF receptor) treated and TNFR1 deficient (−/−) mice. TNF-α levels increased 2 and 4h after intense acute swimming in soleus muscle (but not in gastrocnemius), and spinal cord, respectively. Exercise induced an increase of myeloperoxidase activity and decrease in reduced glutathione levels in an etanercept-sensitive and TNFR1-dependent manners in the soleus muscle, but not in the gastrocnemius muscle. Concluding, TNF-α/TNFR1 signaling mediates intense acute swimming-induced DOMS by an initial role in the soleus muscle followed by spinal cord, inducing muscle inflammatory hyperalgesia and oxidative stress. The knowledge of these mechanisms might contribute to improve the training of athletes, individuals with physical impairment and intense training such as military settings. |
Databáze: | OpenAIRE |
Externí odkaz: |