Effects of Endurance and Resistance Training on Calcitonin Gene-Related Peptide and Acetylcholine Receptor at Slow and Fast Twitch Skeletal Muscles and Sciatic Nerve in Male Wistar Rats
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. 1. Introduction Calcitonin gene-related peptide (CGRP), generated from the calcitonin gene [1–3], is distributed in the peripheral and central nervous systems of vertebrate and invertebrate species [4, 5]. CGRP’s target organs are numerous, and its range of biological actions is extensive; for instance, CGRP is a very potent vasodilator [4–7], possesses positive chronotropic and inotropic effects [8], modulates neurotransmission in central [9] and peripheral [9] synapses, and modulates systemic circulation [4, 10]. In the peripheral nervous system, CGRP coexists with ACh in motoneurons [3], and studies have shown that enhances the expression of the acetylcholine receptor subunit mRNA in skeletal muscles [11], and prolongs the mean open time of AChR channels [12]. Other studies also have indicated that motoneuron but not is upregulated by axotomy or blockade of neuronal activity, suggesting that this particular peptide plays a role in motoneuron regeneration [13, 14]. These results, therefore, suggest that acts as an anterograde “trophic” agent that controls the synthesis and function of muscle AChRs via cAMP-mediated pathways at the neuromuscular junction (NMJ) [9, 15]. Its proposed effects at the NMJ include prolonged mean open time of AChR channels [13] and increased desensitization of AChR via a phosphorylation mechanism in the short term [16–19] and increased synthesis of AChR via a cAMP-associated
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