OBJECTIVE: We investigated the effects of electrical stimulation and low-intensity laser (LIL) energy on the mitochondrial function of cultured C2C12 myotubes in order to find a dosage that could be used to improve the function of mitochondria, and then rehabilitate exercise-induced damage and fatigue. BACKGROUND DATA: Many other studies in the past demonstrated that LIL had a cytoprotective effect, and a recent study also found that LIL could reduce muscular fatigue during tetanic contractions in rats. METHODS: Cultured C2C12 myotubes were subjected to electrical stimulation or/and LIL irradiation at various intensities. Reactive oxygen species (ROS) were detected with a fluorescent probe (DCFH-DA) and mitochondrial function was assessed with an MTT assay. RESULTS: The results showed that electrical stimulation at 20 ms, 5 Hz, and 45 V for 75 min can induce mitochondrial dysfunction in cultured C2C12 myotubes. Electrical stimulation-induced mitochondrial dysfunction was improved, but degeneration occurred with LIL at doses of 0.33-8.22 and 11.22-14.16 J/cm2, respectively, and these changes were markedly increased with LIL at 0.33 and 1.34 J/cm2, respectively. CONCLUSIONS: We conclude that treatment of myotubes with the proper dosage of LIL irradiation significantly diminished production of ROS and restored mitochondrial function, and this may provide a foundation for the use of photobiomodulation to treat exercise-induced mitochondrial dysfunction or skeletal muscular fatigue.
OBJECTIVE: We investigated the effects of electrical stimulation and low-intensity laser (LIL) energy on the mitochondrial function of cultured C2C12 myotubes in order to find a dosage that could be used to improve the function of mitochondria, and then rehabilitate exercise-induced damage and fatigue. BACKGROUND DATA: Many other studies in the past demonstrated that LIL had a cytoprotective effect, and a recent study also found that LIL could reduce muscular fatigue during tetanic contractions in rats. METHODS: Cultured C2C12 myotubes were subjected to electrical stimulation or/and LIL irradiation at various intensities. Reactive oxygen species (ROS) were detected with a fluorescent probe (DCFH-DA) and mitochondrial function was assessed with an MTT assay. RESULTS: The results showed that electrical stimulation at 20 ms, 5 Hz, and 45 V for 75 min can induce mitochondrial dysfunction in cultured C2C12 myotubes. Electrical stimulation-induced mitochondrial dysfunction was improved, but degeneration occurred with LIL at doses of 0.33-8.22 and 11.22-14.16 J/cm2, respectively, and these changes were markedly increased with LIL at 0.33 and 1.34 J/cm2, respectively. CONCLUSIONS: We conclude that treatment of myotubes with the proper dosage of LIL irradiation significantly diminished production of ROS and restored mitochondrial function, and this may provide a foundation for the use of photobiomodulation to treat exercise-induced mitochondrial dysfunction or skeletal muscular fatigue.
Authors: Larissa Aline Santos; Rodrigo Labat Marcos; Shaiane Silva Tomazoni; Adriane Aver Vanin; Fernanda Colella Antonialli; Vanessa dos Santos Grandinetti; Gianna Móes Albuquerque-Pontes; Paulo Roberto Vicente de Paiva; Rodrigo Álvaro Brandão Lopes-Martins; Paulo de Tarso Camillo de Carvalho; Jan Magnus Bjordal; Ernesto Cesar Pinto Leal-Junior Journal: Lasers Med Sci Date: 2014-03-21 Impact factor: 3.161
Authors: Fernanda Colella Antonialli; Thiago De Marchi; Shaiane Silva Tomazoni; Adriane Aver Vanin; Vanessa dos Santos Grandinetti; Paulo Roberto Vicente de Paiva; Henrique Dantas Pinto; Eduardo Foschini Miranda; Paulo de Tarso Camillo de Carvalho; Ernesto Cesar Pinto Leal-Junior Journal: Lasers Med Sci Date: 2014-06-19 Impact factor: 3.161
Authors: Paulo V Mezzaroba; Dalton M Pessôa Filho; Alessandro M Zagatto; Fabiana Andrade Machado Journal: Lasers Med Sci Date: 2018-03-15 Impact factor: 3.161