Gabriel R de Freitas1, Caroline C do Espírito Santo2, Nicolas A M M de Machado-Pereira3, Franciane Bobinski4, Adair R S Dos Santos5, Jocemar Ilha6. 1. Núcleo de Pesquisa em Lesão Medular (Core of Spinal Cord Injury Research) (NULEME), Programa de Pós-Graduação em Fisioterapia (PPGFt), Departamento de Fisioterapia, Centro de Ciências da Saúde e do Esporte (CEFID), Universidade do Estado de Santa Catarina (UDESC), Florianópolis, Santa Catarina, Brazil. 2. Núcleo de Pesquisa em Lesão Medular (NULEME), Laboratório Neurobiologia da Dor e Inflamação (Neurobiology Laboratory of Pain and Inflammation) (LANDI), Departamento de Ciências Fisiológicas, Universidade Federal de Santa Catarina (UFSC), Florianópolis, Santa Catarina, Brazil. 3. Núcleo de Pesquisa em Lesão Medular (NULEME), Departamento de Fisioterapia, Centro de Ciências da Saúde e do Esporte (CEFID), Universidade do Estado de Santa Catarina (UDESC). 4. Núcleo de Pesquisa em Lesão Medular (NULEME), Programa de Pós-Graduação em Fisioterapia (PPGFt), Departamento de Fisioterapia, Centro de Ciências da Saúde e do Esporte (CEFID), Universidade do Estado de Santa Catarina (UDESC), and Programa de Pós-Graduação em Ciências da Saúde, Universidade do Sul de Santa Catarina (UNISUL), Palhoça, Santa Catarina, Brazil. 5. Laboratório Neurobiologia da Dor e Inflamação (LANDI), Departamento de Ciências Fisiológicas, Universidade Federal de Santa Catarina (UFSC). 6. Núcleo de Pesquisa em Lesão Medular (NULEME), Programa de Pós-Graduação em Fisioterapia (PPGFt), Departamento de Fisioterapia, Centro de Ciências da Saúde e do Esporte (CEFID), Universidade do Estado de Santa Catarina (UDESC), Rua Pascoal Simone, 358-Coqueiros, Florianópolis, Santa Catarina, CEP 88080-350, Brazil.
Abstract
Background: Electrical stimulation is often used to treat weakness in people with spinal cord injury (SCI); however its efficacy for increasing strength and trophism is weak, and the mechanisms underlying the therapeutic benefits are unknown. Objective: The purpose of this study was to analyze the effects of neuromuscular electrical stimulation (NMES) on muscle function, trophism, and the Akt pathway signaling involved in muscular plasticity after incomplete SCI in rats. Design: This was an experimental study. Methods: Twenty-one adult female Wistar rats were divided into sham, SCI, and SCI plus NMES groups. In injured animals, SCI hemisection was induced by a surgical procedure at the C5-C7 level. The 5-week NMES protocol consisted of biceps brachii muscle stimulation 5 times per week, initiated 48 h after injury. Forepaw function and strength, biceps muscle trophism, and the expression of phosphorylated Akt, p70S6K, and GSK-3ß cellular anabolic pathway markers in stimulated muscle tissue were assessed. Results: There was an increase in bicep muscle strength in the NMES group compared with the untreated SCI group, from postoperative day 21 until the end of the evaluation period. Also, there was an increase in muscle trophism in the NMES group compared with the SCI group. Forelimb function gradually recovered in both the SCI group and the NMES group, with no differences between them. Regarding muscle protein expression, the NMES group had higher values for phospho-Akt, phospho-p70S6K, and phospho-GSK-3ß than did the SCI group. Limitations: The experimental findings were limited to an animal model of incomplete SCI and may not be fully generalizable to humans. Conclusions: Early cyclical NMES therapy was shown to increase muscle strength and induce hypertrophy after incomplete SCI in a rat model, probably by increasing phospho-Akt, phospho-p70S6K, and phospho-GSK-3ß signaling protein synthesis.
Background: Electrical stimulation is often used to treat weakness in people with spinal cord injury (SCI); however its efficacy for increasing strength and trophism is weak, and the mechanisms underlying the therapeutic benefits are unknown. Objective: The purpose of this study was to analyze the effects of neuromuscular electrical stimulation (NMES) on muscle function, trophism, and the Akt pathway signaling involved in muscular plasticity after incomplete SCI in rats. Design: This was an experimental study. Methods: Twenty-one adult female Wistar rats were divided into sham, SCI, and SCI plus NMES groups. In injured animals, SCI hemisection was induced by a surgical procedure at the C5-C7 level. The 5-week NMES protocol consisted of biceps brachii muscle stimulation 5 times per week, initiated 48 h after injury. Forepaw function and strength, biceps muscle trophism, and the expression of phosphorylated Akt, p70S6K, and GSK-3ß cellular anabolic pathway markers in stimulated muscle tissue were assessed. Results: There was an increase in bicep muscle strength in the NMES group compared with the untreated SCI group, from postoperative day 21 until the end of the evaluation period. Also, there was an increase in muscle trophism in the NMES group compared with the SCI group. Forelimb function gradually recovered in both the SCI group and the NMES group, with no differences between them. Regarding muscle protein expression, the NMES group had higher values for phospho-Akt, phospho-p70S6K, and phospho-GSK-3ß than did the SCI group. Limitations: The experimental findings were limited to an animal model of incomplete SCI and may not be fully generalizable to humans. Conclusions: Early cyclical NMES therapy was shown to increase muscle strength and induce hypertrophy after incomplete SCI in a rat model, probably by increasing phospho-Akt, phospho-p70S6K, and phospho-GSK-3ß signaling protein synthesis.