Effects Of CGRP On Exercise-Induced Fatigue Of Rats

Objective To study the effects of CGRP on the exercise-induced fatigue of rats.Methods Healthy adult male Sprague-Dawley rats were randomly divided into five groups according to the different pretreatment:the blank control group, the PBS pretreatment group, the CGRP pretreatment group, the CAP pretreatment group, the CAP pretreatment+CGRP pretreatment group. The rats were sacrificed at the resting state, the exercise to 80 min and the exercise to exhaustion, Then the immunohistochemistry and radioimmunoassay was used to detecting the expression of CGRP at the condition of the different pretreatment, the HE staining was used to detecting the change of morphous formation of skeletal muscle at the condition of the different pretreatment, the chemistry colorimetric method was used to detecting the change of superoxide dismutase, glutathione peroxidase, catalase, and malondialdehyde at the conditions of the different pretreatment.Resultsâ‘ the time of the treadmill exercise to exhaustion was significantly decurtated after CGRP pretreatment(P<0.05), and the time of the treadmill exercise to exhaustion was significantly prolonged after CAP pretreatment(P<0.05).â‘¡Immunohistochemistry and radioimmunoassay showed that CGRP immunopositive products were elliptical or rod-shape at longitudinal section of muscle fiber. The expression of CGRP was significantly increased after the CGRP pretreatment(P<0.05), and the expression of CGRP was significantly decreased after the CAP pretreatment(P<0.05).â‘¢HE staining showed that there were no obvious differences in morphous constitution of skeletal muscle in all groups at the resting state. There were also no obvious changes in morphous constitution of skeletal muscle at the other groups at the exercise to 80 min than at the resting state, excluding cell nucleus of skeletal muscle were significantly increased and augmented at the CGRP pretreatment group, Cell nucleus of skeletal muscle were significantly increased and augmented in all other groups, while there were no obvious changes in morphous constitution of skeletal muscle at the CAP pretreatment group at exercise to exhaustion than at the resting state.â‘£The chemistry colorimetric showed that the content of MDA was significantly increased(P<0.05), and the activity of SOD, GSH-PX, CAT was significantly decreased after the CGRP pretreatment(P<0.05), While the content of MDA was significantly decreased(P<0.05), and the activity of SOD, GSH-PX, CAT was significantly increased after the CAP pretreatment(P<0.05). Conclusion The CGRP intensified the generation of exercise-induced fatigue Objective To explore the effects of CGRP on the AChE at exercise-induced fatigued rat neuromuscular junctions.Methods The animals and the experimental methods were the same as in the primary part. The immunohistochemistry and histochemistry was used to detecting the changes of the expression and activity of AChE. Then the expression and activity of AChE were also detected by enzyme linked immunoadsorbent assay and chemistry colorimetric method. Then linear correlation and linear regression were tested between the CGRP concentration and the expression or activity of AChE.Resultsâ‘ Immunohistochemistry, enzyme linked immunoadsorbent assay, histochemistry and chemistry colorimetric method showed that the expression and activity of AChE at the gastrocnemius neuromuscular junction of rat was significantly decreased after CGRP pretreatment(P<0.05), and the expression and activity of AChE of the gastrocnemius neuromuscular junction of rat was significantly increased after the CAP pretreatment(P<0.05).â‘¡The linear correlation and regression analysis showed there was negativity correlation between the CGRP concentration and the expression AChE or and activity of AChE (resting state r=0.78; exercise to 80 min r=0.92; exercise to exhaustion r=0.88 respectively).Conclusion Our study suggests that CGRP promoted the production of exercise-induced fatigue through the regulation the expression of AChE at the gastrocnemius neuromuscular junction of rat.