Modulation effects of cordycepin on the skeletal muscle contraction of toad gastrocnemius muscle

蟾蜍 刺激 内科学 骨骼肌 虫草素 收缩(语法) 内分泌学 肌肉收缩 腓肠肌 肌肉疲劳 化学 解剖 生物 医学 肌电图 生物化学 神经科学
作者
Lihua Yao,Meng Wei,Rongfeng Song,Qiu-Ping Xiong,Wei Sun,Zhiqiang Luo,Wen-Wen Yan,Yuping Li,Xinping Liu,Haihang Li,Peng Xiao
出处
期刊:European Journal of Pharmacology [Elsevier]
卷期号:726: 9-15 被引量:9
标识
DOI:10.1016/j.ejphar.2014.01.016
摘要

Isolated toad gastrocnemius muscle is a typical skeletal muscle tissue that is frequently used to study the motor system because it is an important component of the motor system. This study investigates the effects of cordycepin on the skeletal muscle contractile function of isolated toad gastrocnemius muscles by electrical field stimulation. Results showed that cordycepin (20 mg/l to 100 mg/l) significantly decreased the contractile responses in a concentration-dependent manner. Cordycepin (50 mg/l) also produced a rightward shift of the contractile amplitude-stimulation intensity relationship, as indicated by the increases in the threshold stimulation intensity and the saturation stimulation intensity. However, the most notable result was that the maximum amplitude of the muscle contractile force was significantly increased under cordycepin application (122±3.4% of control). This result suggests that the skeletal muscle contractile function and muscle physical fitness to the external stimulation were improved by the decreased response sensitivity in the presence of cordycepin. Moreover, cordycepin also prevented the repetitive stimulation-induced decrease in muscle contractile force and increased the recovery amplitude and recovery ratio of muscle contraction. However, these anti-fatigue effects of cordycepin on muscle contraction during long-lasting muscle activity were absent in Ca2+-free medium or in the presence of all Ca2+ channels blocker (0.4 mM CdCl2). These results suggest that cordycepin can positively affect muscle performance and provide ergogenic and prophylactic benefits in decreasing skeletal muscle fatigue. The mechanisms involving excitation-coupled Ca2+ influxes are strongly recommended.
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