Abstract

Diabetic peripheral neuropathy (DPN) is a typical complication of diabetes. No definitive treatment and prevention of DPN has been established, and very few data on the role of exercise training on DPN have been reported. The protective and therapeutic effects of aerobic physical activity on the development of DPN in Type 1 were investigated. Rats were assigned to 5 groups: C (control), E (exercise), D (diabetic), DEx (exercise after diabetic), ExD (diabetic after exercise); C containing 10 animals and E, D, DEx, ExD containing 15 animals. Diabetes was induced with streptozotocin (STZ) (45 mg/kg, ip). Development of diabetes was confirmed by measuring blood glucose levels 2 days after STZ treatment. Body weights of all the animals were evaluated weekly throughout the experiment. Motor dysfunction defined by a significant increase in compound muscle action potential (CMAP) latency was recorded. The amplitude of CMAP which mainly reflects axonal dysfunction was also measured using standard techniques. Sciatic nerve morphometry and blood glucose levels were analyzed in all the groups. Blood glucose level significantly increased 2 days after STZ injection. All diabetic rats showed decreased body weight compared to control rats. An increase in motor latency of CMAP and a decrease in amplitude of CMAP, indicative of neuropathy, were seen in STZ rats. On the completion of the study (the 56th day post-STZ), histological examination revealed significant myelin loss (thinner myelin) in sciatic nerves of STZ rats. Treatment with swimming exercise had no effect on glycemic control but restored body weight, CMAP amplitude, CMAP latency or motor dysfunction in the diabetic animals. This study suggests that swimming exercise training has protective and therapeutic effects on DPN of STZ-induced diabetic rats.

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