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Background. Due to the deleterious effects of obesity on muscle tissue and the search for tools to reverse these losses, it is important to understand the effect of physical exercises on the muscle structure of obese individuals. This study aimed to analyze the effect of wholebody vibration (WBV) on the histomorphological parameters of the anterior tibial muscle using the monosodium l-glutamate (MSG) obesity model. Methods. MSG-obese rats that were exposed to WBV on a vibrating platform with a frequency of 60 Hz, the amplitude of 2 mm, three times/week, 10 min/day, for eight weeks (from postnatal day (PN) 80 to PN136). The histomorphology of the anterior tibial muscle was evaluated. Results. When performing a WBV exercise, the animals showed altered structural responses in the MSG animals, such as reduced muscle mass, increased connective tissue, and nuclear activity. The WBV reduced the extracellular matrix and the nuclear activity in the MSG animals, showing efficiency in the protocol. Conclusions. Even with the aggressive character of the MSG model, the WBV exercise was able to induce repair to the muscle tissue of these animals, thus being a safe protocol for use in similar conditions.

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The model of obesity induced by monosodium glutamate cytotoxicity on the hypothalamic nuclei is widely used in the literature. However, MSG promotes persistent muscle changes and there is a significant lack of studies that seek to elucidate the mechanisms by which damage refractory to reversal is established. This study aimed to investigate the early and chronic effects of MSG induction of obesity upon systemic and muscular parameters of Wistar rats. The animals were exposed to MSG subcutaneously (4 mg·g−1 b.w.) or saline (1.25 mg·g−1 b.w.) daily from PND01 to PND05 (n = 24). Afterwards, in PND15, 12 animals were euthanized to determine the plasma and inflammatory profile and to assess muscle damage. In PND142, the remaining animals were euthanized, and samples for histological and biochemical analyses were obtained. Our results suggest that early exposure to MSG reduced growth, increased adiposity, and inducted hyperinsulinemia and a pro-inflammatory scenario. In adulthood, the following were observed: peripheral insulin resistance, increased fibrosis, oxidative distress, and a reduction in muscle mass, oxidative capacity, and neuromuscular junctions, increased fibrosis, and oxidative distress. Thus, we can conclude that the condition found in adult life and the difficulty restoring in the muscle profile is related to the metabolic damage established early on.

The model of obesity induced by monosodium glutamate cytotoxicity on the hypothalamic nuclei is widely used in the literature. However, MSG promotes persistent muscle changes and there is a significant lack of studies that seek to elucidate the mechanisms by which damage refractory to reversal is established. This study aimed to investigate the early and chronic effects of MSG in-duction of obesity upon systemic and muscular parameters of Wistar rats. Animals were exposed to MSG subcutaneously (4 mg.g-1 b.w.) or saline (1.25 mg.g-1 b.w.) daily from PND01 to PND05 (n = 24). After, in PND15, 12 animals were euthanized to determine the plasma and inflammatory profile and to assess muscle damage. In PND142, the remaining animals were euthanized, and samples for histological and biochemical analyses were obtained. Our results suggest that early exposure to MSG reduced growth, and increased adiposity, induction hyperinsulinemia, and a pro-inflammatory scenario. In adulthood were found, peripheral insulin resistance, reduced muscle mass, oxidative capacity, neuromuscular junctions, increased fibrosis, and oxidative distress. Thus, we can conclude that the condition found in adult life and the difficulty in restoring the muscle profile are related to the metabolic damages established early.