Regular physical exercise has been described as a good strategy for prevention or reduction of musculoskeletal pain. The Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) has been investigated as a promising target for the control of inflammatory pain. Therefore, the aim of this study was to evaluate whether activation of PPARγ receptors is involved in the reduction of acute muscle pain by chronic exercise and, in this case, whether this process is modulated by inflammatory cytokines. To this end, Wistar rats were submitted to swimming physical training for a period of 10 weeks, 5 days per week, 40 min/day, in an intensity of 4% of the body mass. Muscle hyperalgesia was measured by Randall Selitto test and pro-inflammatory cytokines were quantified by ELISA. The results showed that swimming physical training prevented the onset of acute mechanical muscle hyperalgesia and the increase in muscle levels of Cytokine-induced neutrophil chemoattractant 1 (CINC-1) induced by carrageenan into gastrocnemius muscle. In addition, local pre-treatment with the selective PPARγ receptors antagonist GW9662 reversed the mechanical muscle hypoalgesia and the modulation of CINC-1 levels induced by swimming physical training. These data suggest that swimming physical training prevented the onset of acute mechanical muscle hyperalgesia by a mechanism dependent of PPARγ receptors, which seems to contribute to this process by modulation of the pro-inflammatory cytokine CINC-1, and highlight the potential of PPARγ receptors as a target to control musculoskeletal pain and to potentiate the reduction of musculoskeletal pain induced by exercise.

中文翻译：

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游泳体育锻炼通过依赖于PPARγ受体和CINC-1的机制防止了急性肌肉疼痛的发作。

定期进行体育锻炼被描述为预防或减轻肌肉骨骼疼痛的好方法。已研究过氧化物酶体增殖物激活受体γ（PPARγ）作为控制炎症性疼痛的有希望的靶标。因此，本研究的目的是评估PPARγ受体的激活是否与慢性运动减轻急性肌肉疼痛有关，在这种情况下，该过程是否受到炎性细胞因子的调节。为此，以体重的4％的强度，将Wistar大鼠进行游泳运动训练，持续10周，每周5天，40分钟/天。通过Randall Selitto测试测量肌肉痛觉过敏，并通过ELISA定量测定促炎细胞因子。结果表明，游泳体育锻炼阻止了急性机械性肌肉痛觉过敏的发作以及角叉菜胶诱导的腓肠肌向腓肠肌诱导的细胞因子诱导的中性粒细胞趋化因子1（CINC-1）肌肉水平的增加。此外，用选择性PPARγ受体拮抗剂GW9662进行的局部预处理可以逆转机械肌肉的痛觉过敏和游泳体育锻炼诱导的CINC-1水平的调节。这些数据表明，游泳体育锻炼通过依赖于PPARγ受体的机制阻止了急性机械性肌肉痛觉过敏的发作，该机制似乎通过调节促炎性细胞因子CINC-1来促进这一过程，