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Swimming Training Reduces Neuroma Pain by Regulating Neurotrophins

Jinge Tian; Xin, Zhang; Tingting, Yu; Yongming, Xu; Shaofeng, Pu; Yingying, Lv; Dongping, Du
Medicine & Science in Sports & Exercise: Post Acceptance: August 25, 2017
doi: 10.1249/MSS.0000000000001411
Original Investigation: PDF Only

AbstractIntroductionNeuroma formation after peripheral nerve transection leads to severe neuropathic pain in amputees. Previous studies suggested physical exercise could bring beneficial effect on alleviating neuropathic pain. Yet the effect of exercise on neuroma pain still remained unclear. In addition, long-term exercise can affect the expression of neurotrophins (NTs), such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), which play key roles in nociceptor sensitization and nerve sprouting following nerve injury. Here, we investigated whether long-term swimming exercise could relieve neuroma pain by modulating NTs expression.MethodsWe used a tibial neuroma transposition (TNT) rat model to mimic neuroma pain. Following TNT surgery, rats were performed swimming exercise for 5 weeks. Neuroma pain and tactile sensitivities were detected using von Frey filaments. Immunofluorescence was applied to analyze neuroma formation. NGF and BDNF expression in peripheral neuroma, dorsal root ganglion (DRG) and spinal cord were measured using ELISA and western blotting.ResultsTNT led to neuroma formation, induced neuroma pain and mechanical allodynia in hind paw. 5-week swimming exercise inhibited neuroma formation, relieved mechanical allodynia in the hind paw and neuroma pain in the lateral ankle. The analgesic effect lasted for at least one week, even the exercise ceased. TNT elevated the expressions of BDNF and NGF in peripheral neuroma, DRG and spinal cord to different extents. Swimming also decreased the elevation of NTs expression.ConclusionsSwimming exercise not only inhibits neuroma formation induced by nerve transection, but also relieves pain behavior. These effects might be associated with the modulation of NTs.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

Introduction

Neuroma formation after peripheral nerve transection leads to severe neuropathic pain in amputees. Previous studies suggested physical exercise could bring beneficial effect on alleviating neuropathic pain. Yet the effect of exercise on neuroma pain still remained unclear. In addition, long-term exercise can affect the expression of neurotrophins (NTs), such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), which play key roles in nociceptor sensitization and nerve sprouting following nerve injury. Here, we investigated whether long-term swimming exercise could relieve neuroma pain by modulating NTs expression.

Methods

We used a tibial neuroma transposition (TNT) rat model to mimic neuroma pain. Following TNT surgery, rats were performed swimming exercise for 5 weeks. Neuroma pain and tactile sensitivities were detected using von Frey filaments. Immunofluorescence was applied to analyze neuroma formation. NGF and BDNF expression in peripheral neuroma, dorsal root ganglion (DRG) and spinal cord were measured using ELISA and western blotting.

Results

TNT led to neuroma formation, induced neuroma pain and mechanical allodynia in hind paw. 5-week swimming exercise inhibited neuroma formation, relieved mechanical allodynia in the hind paw and neuroma pain in the lateral ankle. The analgesic effect lasted for at least one week, even the exercise ceased. TNT elevated the expressions of BDNF and NGF in peripheral neuroma, DRG and spinal cord to different extents. Swimming also decreased the elevation of NTs expression.

Conclusions

Swimming exercise not only inhibits neuroma formation induced by nerve transection, but also relieves pain behavior. These effects might be associated with the modulation of NTs.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

Author for correspondence: Dongping Du, E-mail: dudp@sjtu.edu.cn, Address: No. 600, Yishan Road, Shanghai, China. Fax: +86-21-24058330. Tel:+86-21-24058896

* These authors contributed equally to this work.

The work was supported by grants from Natural Science Foundation of China (8167237 and 81370093, to Dongping Du; 81400803, to Xin Zhang). The authors declare no conflicts of interest. The results of the present study do not constitute endorsement by the American College of Sports Medicine. The results of the study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation.

Accepted for Publication: 15 August 2017

© 2017 American College of Sports Medicine