Physical training prevents body weight gain but does not modify adipose tissue gene expression

The relationship of body weight (BW) with white adipose tissue (WAT) mass and WAT gene expression pattern was investigated in mice submitted to physical training (PT). Adult male C57BL/6 mice were submitted to two 1.5-h daily swimming sessions (T, N = 18), 5 days/week for 4 weeks or maintained sedentary (S, N = 15). Citrate synthase activity increased significantly in the T group (P < 0.05). S mice had a substantial weight gain compared to T mice (4.06 ± 0.43 vs 0.38 ± 0.28 g, P < 0.01). WAT mass, adipocyte size, and the weights of gastrocnemius and soleus muscles, lung, kidney, and adrenal gland were not different. Liver and heart were larger and the spleen was smaller in T compared to S mice (P < 0.05). Food intake was higher in T than S mice (4.7 ± 0.2 vs 4.0 ± 0.3 g/animal, P < 0.05) but oxygen consumption at rest did not differ between groups. T animals showed higher serum leptin concentration compared to S animals (6.37 ± 0.5 vs 3.11 ± 0.12 ng/mL). WAT gene expression pattern obtained by transcription factor adipocyte determination and differentiation-dependent factor 1, fatty acid synthase, malic enzyme, hormone-sensitive lipase, adipocyte lipid binding protein, leptin, and adiponectin did not differ significantly between groups. Collectively, our results showed that PT prevents BW gain and maintains WAT mass due to an increase in food intake and unchanged resting metabolic rate. These responses are closely related to unchanged WAT gene expression patterns

Potential of physical training for the prevention of metabolic disorders induced by hypercaloric diet

O aumento do consumo de alimentos ricos em gorduras e carboidratos associado à reduzida prática de exercícios físicos pode ter como consequência o desenvolvimento da obesidade e de distúrbios metabólicos, tais como intolerância à glicose, resistência à insulina, diabetes tipo 2 e dislipidemias. O músculo esquelético contribui diretamente para o desenvolvimento e progressão dos distúrbios metabólicos, especialmente em decorrência da disfunção mitocondrial. Uma das ferramentas amplamente utilizada para o tratamento de distúrbios metabólicos é o treinamento físico, pois promove adaptações metabólicas no sentido oposto aos prejuízos metabólicos induzidos por dietas hipercalóricas. O presente estudo teve por objetivo avaliar se o treinamento físico aeróbio seria capaz de prevenir o desenvolvimento de distúrbios metabólicos induzidos por dieta hipercalórica composta por ração de cafeteria mais frutose e sacarose diluídas em água de beber em camundongos, e se essa resposta seria mediada por adaptações no músculo esquelético. Os resultados obtidos revelaram que o treinamento físico aeróbio preveniu os distúrbios metabólicos induzidos por dieta hipercalórica, tais como deposição de gordura, hiperfagia, hiperglicemia e aumento de pressão arterial, bem como melhorou a capacidade aeróbia. Essas respostas foram associadas apenas ao aumento na capilarização do músculo esquelético, já que a capacidade oxidativa determinada pela citrato sintase e a expressão da proteína PGC-1? não modificaramThe increased consumption of foods rich in fats and carbohydrates associated with reduced physical exercise may result in the development of obesity and metabolic disorders such as glucose intolerance, insulin resistance, type 2 diabetes and dyslipidemia. Skeletal muscle contributes directly to the development and progression of metabolic disorders, especially as a result of mitochondrial dysfunction. One of the tools widely used for the treatment of metabolic disorders is physical training, which promotes metabolic adaptations in the opposite direction to metabolic damage induced by hypercaloric diets. The present study aimed to evaluate whether physical training could prevent the development of metabolic disorders induced by hypercaloric diet consisting of cafeteria diet plus fructose and sucrose diluted in drinking water in mice, and if this response was mediated by adaptations in skeletal muscle. The results showed that physical training prevented metabolic disorders induced by hypercaloric diet, such as fat deposition, hyperphagia, hyperglycemia, increased blood pressure, and improved aerobic capacity. These responses were associated only with the increase in skeletal muscle capillarity, because oxidative capacity citrate synthase and protein expression of PGC-1? did not chang