Abstract

The aim of this study was to investigate effects of endurance and resistance training (ET and RT) on CGRP and AChRs at slow and fast twitch muscles and sciatic nerve in rats. Twenty-five male rats were randomly assigned into three groups including sedentary (SED), endurance training (ET), and resistance training (RT). Animals of ET exercised for 12 weeks, five times/week, and 60 min/day at 30 m/min. Animals of RT were housed in metal cage with 2 m high wire-mesh tower, with water bottles set at the top. 48 h after the last session of training protocol, animals were anaesthetized. The right sciatic nerves were removed; then, Soleus (SOL) and Tibialis anterior (TA) muscles were excised and immediately snap frozen in liquid nitrogen. All frozen tissues were stored at −80°C. Results showed that, after both ET and RT, CGRP content as well as AChR content of SOL and TA muscles significantly increased. But there was no significant difference among groups at sciatic nerve' CGRP content. In conclusion, data demonstrate that ET and RT lead to changes of CGRP and AChR content of ST and FT muscles. The changes indicate to the importance of neuromuscular activity.

Highlights

  • Calcitonin gene-related peptide (CGRP), generated from the calcitonin gene [1,2,3], is distributed in the peripheral and central nervous systems of vertebrate and invertebrate species [4, 5]

  • No significant difference was observed between endurance training (ET) and resistance training (RT) at SOL muscle CGRP (P = 0.212), and there was no significant difference between ET and RT regarding AT muscle CGRP content (P = 0.283)

  • There is a trend at sciatic nerve CGRP content to increase following ET

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Summary

Introduction

Calcitonin gene-related peptide (CGRP), generated from the calcitonin gene [1,2,3], is distributed in the peripheral and central nervous systems of vertebrate and invertebrate species [4, 5]. Its proposed effects at the NMJ include prolonged mean open time of AChR channels [13] and increased desensitization of AChR via International Journal of Peptides a phosphorylation mechanism in the short term [16,17,18,19] and increased synthesis of AChR via a cAMP-associated pathway in the longer term [20, 21]. These observations support the idea that the peptide may participate in the control of G4 acetylcholinesterase (G4 AChE) at the NMJ [16]. Fernandez and Hodges-Savola have indicated that motoneuron-derived CGRPα plays a key role in the trophic control of AChE molecular forms in adult NMJs [22]

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