Hiroshige Y1,2, Watanabe D3, Wada M2
1International Pacific University, Physical Education, Okayama, Japan, 2Hiroshima University, Graduate School of Integrated Arts and Sciences, Higashihiroshima, Japan, 3University of Electro-Communications, Department of Engineering Science, Chofu, Japan
Background: Eccentric contractions (ECC), in which skeletal muscles are stretched while contracting, are a part of activity of daily living and frequently cause an immediate and protracted loss of skeletal muscle force. The loss of muscle force is primarily ascribable to muscle damage, including increased membrane permeability, ultrastructural disruption, inflammation and proteolysis. It is well known that ECC is also responsible for delayed onset of muscle soreness (DOMS) that occurs secondarily to inflammation of muscle membranes. 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. There is very little information on whether MC therapy also has a beneficial effect on ECC-related muscle damage. With the consideration that MC treatment has the potential to alleviate tissue damage, it might be expected that MC treatment would inhibit ECC-related proteolysis. However, no studies have examined this point to date.
Purpose: The aim of this study was to examine the effect of MC treatment on ECC-induced muscle damage in rat fast-twitch skeletal muscles, with focus on key proteins involved in excitation-contraction coupling.
Methods: The experiments were performed on 9- to 10-week-old male Wistar rats (n = 16). Tibialis anterior muscles underwent 200 repeated ECCs in situ. After ECC, the animals were randomly divided into a MC-treated and a non-treated group (n = 8 for each group). Tibialis anterior muscles from MC-treated rats were stimulated (25 µA, 0.3 Hz) for 20 min (MC treatment), using electric stimulator. 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.
Results: 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 inhibited ECC-induced changes, i.e., 1) impaired Ca2+-release function of sarcoplasmic reticulum (SR), 2) proteolysis of ryanodine receptor, a Ca2+ release channel of SR, and 3) decreased 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.
Conclusion(s): MC treatment can facilitate restoration of force production after ECC, possibly by attenuating dysfunction of SR and myosin.
Implications: Muscle damage and resultant depressions in muscle performance are universal symptoms familiar to most athletes, because muscle contractions during many of sport activities and training include a substantial eccentric component. To date, various treatment strategies have been done to attenuate the extent of the depression in muscle function and to facilitate recovery. Little scientific evidence, however, exists to support the effectiveness of any of these interventions. This study provides evidence that MC therapy results in beneficial effects, such as restoration of muscle performance following ECC.
Keywords: microcurrent therapy, muscle damage, muscle function
Funding acknowledgements: None.
Purpose: The aim of this study was to examine the effect of MC treatment on ECC-induced muscle damage in rat fast-twitch skeletal muscles, with focus on key proteins involved in excitation-contraction coupling.
Methods: The experiments were performed on 9- to 10-week-old male Wistar rats (n = 16). Tibialis anterior muscles underwent 200 repeated ECCs in situ. After ECC, the animals were randomly divided into a MC-treated and a non-treated group (n = 8 for each group). Tibialis anterior muscles from MC-treated rats were stimulated (25 µA, 0.3 Hz) for 20 min (MC treatment), using electric stimulator. 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.
Results: 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 inhibited ECC-induced changes, i.e., 1) impaired Ca2+-release function of sarcoplasmic reticulum (SR), 2) proteolysis of ryanodine receptor, a Ca2+ release channel of SR, and 3) decreased 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.
Conclusion(s): MC treatment can facilitate restoration of force production after ECC, possibly by attenuating dysfunction of SR and myosin.
Implications: Muscle damage and resultant depressions in muscle performance are universal symptoms familiar to most athletes, because muscle contractions during many of sport activities and training include a substantial eccentric component. To date, various treatment strategies have been done to attenuate the extent of the depression in muscle function and to facilitate recovery. Little scientific evidence, however, exists to support the effectiveness of any of these interventions. This study provides evidence that MC therapy results in beneficial effects, such as restoration of muscle performance following ECC.
Keywords: microcurrent therapy, muscle damage, muscle function
Funding acknowledgements: None.
Topic: Electrophysical & isothermal agents; Musculoskeletal; Sport & sports injuries
Ethics approval required: Yes
Institution: Hiroshima University
Ethics committee: The Animal Care Committee
Ethics number: C14-11
All authors, affiliations and abstracts have been published as submitted.
