High-intensity swimming alleviates nociception and neuroinflammation in a mouse model of chronic post-ischemia pain by activating the resolvin E1-chemerin receptor 23 axis in the spinal cord

This study explores how high-intensity swimming can reduce chronic pain and inflammation in a mouse model that mimics complex regional pain syndrome type-I (CRPS-1). The researchers found that only high-intensity swimming, not low-intensity, reduced chronic pain in mice. The study revealed that high-intensity swimming restored the expression of resolvin E1 and chemerin receptor 23, which were previously downregulated in the spinal cords of mice experiencing chronic pain. Resolvin E1 promotes pain relief by binding to chemerin receptor 23 in the nervous system. Silencing chemerin receptor 23 reversed the pain-reducing effects of high-intensity swimming, indicating that this pathway is crucial for exercise-induced pain relief. This suggests that high-intensity swimming helps alleviate chronic pain by activating the resolvin E1-chemerin receptor 23 axis in the spinal cord.

• 1
  High-intensity swimming (HIS), but not low-intensity swimming (LIS), significantly alleviated mechanical and thermal hyperalgesia in CPIP mice.
• 2
  HIS upregulated the expression of the RvE1-ChemR23 axis in the spinal cords of CPIP mice, increasing RvE1 levels in the spinal cord and CSF.
• 3
  The analgesic effect of HIS was inhibited by silencing ChemR23 in the spinal cord, indicating the involvement of the RvE1-ChemR23 axis in HIS-induced analgesia.