Low intensity exercise following peripheral nerve injury promotes nerve regeneration, whereas high intensity exercise has a negative effect. Our study aimed to assess the influence of low intensity exercise on the expression of proteins related to cell death regulation and axonal regrowth.

The sciatic nerves of 10-week-old male Wistar rats were crushed, using iced clips. The animals were randomized into 3 groups: injured rats not subjected to exercise (SC group) to assess spontaneous recovery; injured rats subjected to exercise by disturbance stimulator (SCex group); non-injured rats (Sham group). The animals were sacrificed at 2 or 4 weeks after injury. Immunofluorescence against BDNF, NGF, GAP 43, and Caspase-3 was performed and the expression levels of each marker were calculated per unit area. Two-way Anova for multiple comparisons with Tukey's test was used.

BDNF expression was significantly increased in the SC group compared to the Sham group (P<0.05). NGF did not show any significant difference among the group in terms of treatment and time. GAP 43 expression was significantly decreased in the SC and SCex groups as compared to the Sham group (P<0.05), and 4 weeks was significantly increased (P<0.05). Caspase-3 expression showed an increasing trend in the SC group and increased significantly at 4 weeks (P<0.05).

The up-regulation of BDNF following NGF during nerve regeneration suggests that cell death is observed after nerve injury, but can be reduced by exercise. At later stages after injury, trophic factors protecting cells from death are down-regulated, possibly resulting in the increased cell death. GAP43 expression increased over time in the injured rats, indicating elongation of regenerating axons. In this study, we show that low intensity exercise reduces cell death in the injured nerve and promotes elongation of regenerating axons. Our future goal is to examine the potential effect of exercise on neural plasticity.