Exercise training attenuates neuropathic pain and cytokine expression after chronic constriction injury of rat sciatic nerve.

Background: The underlying mechanism of exercise on neuropathic pain is not well understood. We investigated whether physical exercise regulates the functional recovery and heat shock protein 72 (Hsp72), tumor necrosis factor-α (TNF-α), and interlukin-1β (IL-1β) expression after chronic constriction injury (CCI) of the sciatic nerve.

Methods: Male Sprague-Dawley rats were divided into 7 groups: control, sham operated (SO), SO with swimming or treadmill exercise (SOSE or SOTE), CCI, CCI with swimming or treadmill exercise (CCISE or CCITE). We recorded body weight, thermal withdrawal latency, and mechanical withdrawal threshold as well as Hsp72, TNF-α, and IL-1β expression in sciatic nerve.

Results: The body weights in the control and SO groups were heavier than those in the SOSE, SOTE, CCI, CCISE, and CCITE groups. CCI rats with swimming or treadmill exercise showed significant increase in thermal withdrawal latency and mechanical withdrawal threshold when compared with CCI rats without exercise on day 21 after CCI. Both CCISE and CCITE groups demonstrated greater Hsp72 expression and lower TNF-α or IL-1β level than did the CCI group in sciatic nerve on day 21 after CCI.

Conclusions: These results suggest that progressive exercise training decreases peripheral neuropathic pain as well as TNF-α and IL-1β overproduction and increases HSP72 expression after CCI of the sciatic nerve.