Abstract

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.

Highlights

  • Eccentric contractions (ECCs), in which skeletal muscles are stretched while contracting, are a part of normal activities such as walking downstairs or lowing a heavy weight, and frequently cause an immediate and protracted loss of skeletal muscle force [1] [2]

  • 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, the precise mechanisms are still unknown at this time

  • This study focused on alterations in two proteins of sarcoplasmic reticulum (SR), i.e., SR Ca2+-ATPase (SERCA) and ryanodine receptor (RyR), and myosin ATPase, because the function of these three proteins is vital for skeletal muscle contraction [15] [16] [17]

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Summary

Introduction

Eccentric contractions (ECCs), in which skeletal muscles are stretched while contracting, are a part of normal activities such as walking downstairs or lowing a heavy weight, and frequently cause an immediate and protracted loss of skeletal muscle force [1] [2]. The loss of muscle force is primarily ascribable to muscle damage, including increased membrane permeability [3], ultrastructural disruption [4], inflammation [5] and proteolysis [6]. Ca2+-activated neutral proteases and skeletal muscles contain the ubiquitous calpains (calpain-1 and calpain-2) and the muscle-specific calpain (calpain-3) [8]. A ubiquitin-related proteasome, another cytosolic protease, is activated in skeletal muscles subjected to ECC [1], it is unclear to what extent muscle proteins are degraded by activated proteasome. It seems quite plausible that these changes account for prolonged force deficit

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