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The Efficacy of Microcurrent Therapy on Eccentric Contraction-Induced Muscle Damage in Rat Fast-Twitch Skeletal Muscle

The Efficacy of Microcurrent Therapy on Eccentric Contraction-Induced Muscle Damage in Rat Fast-Twitch Skeletal Muscle

作     者:Yosuke Hiroshige Daiki Watanabe Chihiro Aibara Keita Kanzaki Satoshi Matsunaga Masanobu Wada 

作者机构:Department of Physical Education Faculty of Physical Education International Pacific University Okayama-shi Japan Graduate School of Integrated Arts and Sciences Hiroshima University Higashihiroshima-shi Japan Research Fellow of Japan Society for the Promotion of Science Department of Clinical Nutrition Faculty of Health Science and Technology Kawasaki University of Medical Welfare Kurashiki-shi Japan Faculty of Education University of Miyazaki Miyazaki-shi Japan 

出 版 物:《Open Journal of Applied Sciences》 (应用科学(英文))

年 卷 期:2018年第8卷第3期

页      面:89-102页

学科分类:1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主  题:Ryanodine Receptor Sarcoplasmic Reticulum SERCA Myosin ATPase 

摘      要:Microcurrent (MC) therapy, in which a very small electric current is applied to the body, has widely been used to promote tissue healing and relieve symptoms. The aim of this study was to examine the effect of MC treatment on eccentric contraction (ECC)-induced muscle damage in rat fast-twitch skeletal muscles. Tibialis anterior muscles underwent 200 repeated ECCs in situ and were then stimulated (25 μA, 0.3 Hz) for 20 min (MC treatment). MC treatment was performed immediately after ECC and during a recovery period of 3 days (a total of 4 times). Three days after ECC, the muscles were excised and used for measure of force output and for biochemical analyses. In MC-treated muscles, tetanic forces at 20 Hz and 100 Hz were partially and fully restored, respectively, whereas in non-treated muscles, both forces remained depressed. Biochemical analyses revealed that MC treatment partially or completely inhibited ECC-induced reductions: in 1) the Ca2+-release function of sarcoplasmic reticulum (SR), 2) proteolysis of ryanodine receptor, a Ca2+ release channel of SR, and 3) myosin ATPase activity. On the other hand, MC treatment was unable to lessen increases in the activity of calpain, a cytosolic, Ca2+-activated neutral protease. These results indicate that MC treatment results in beneficial effects, such as restoration of muscle performance following ECC, although the precise mechanisms are still unknown at this time.

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