muscle damage

Hiroshige Y1,2, Watanabe D3, Wada M21International 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, JapanBackground: 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 functionFunding acknowledgements: None.Topic: Electrophysical & isothermal agents; Musculoskeletal; Sport & sports injuriesEthics approval required: YesInstitution: Hiroshima UniversityEthics committee: The Animal Care CommitteeEthics number: C14-11All authors, affiliations and abstracts have been published as submitted.

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Intense or unaccustomed exercise can induce muscle damage and systemic inflammation, as reflected by increases in interleukin-6 (IL-6) and creatine kinase (CK). Selenium, an essential trace element with antioxidant and immunomodulatory properties, may attenuate these responses, yet evidence in recreationally active populations is limited. This study investigated whether 14 days of selenium supplementation (200 µg/day L-selenomethionine) could mitigate post-exercise IL-6 and CK elevations in recreationally active male university students. A randomized, double-blind, placebo-controlled trial was conducted with 64 healthy males aged 18–21 years, who were randomly assigned to the selenium (SEL, n = 32) or placebo (PLA, n = 32) groups. After supplementation, participants performed a standardized eccentric plyometric protocol, and blood samples were collected pre-exercise and at 24 and 48 hours post-exercise for IL-6 and CK assessment. Both markers increased significantly after exercise in all participants (p < 0.001), but the rises were attenuated in the selenium group, which also showed faster recovery compared with placebo. Significant group × time interactions were observed for both IL-6 and CK (p < 0.001), indicating a differential response over time. These findings suggest that short-term selenium supplementation provides dual protective effects by reducing inflammation and preserving muscle integrity, highlighting its potential as a nutritional strategy to enhance recovery in recreationally active individuals. Further research with larger and more diverse populations is warranted.

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