Efeitos agudos do exercício de força muscular sobre a memória, respostas inflamatórias e neuronais em ratos resistentes à insulina

Abstract

Type 2 Diabetes Mellitus (T2DM) has the highest prevalence among all cases of diabetes in the world (90 to 95% of cases) and its increase is related to a sedentary lifestyle, inadequate diet, and obesity. The main characteristic of T2DM is insulin resistance (IR) in peripheral tissues, which leads to the development of a hyperglycemic condition. Furthermore, chronically, IR can lead to an increase in inflammatory cytokines and a reduction in muscle mass and strength. Furthermore, this condition can harm the central nervous system, what may cause an increased pro-inflammatory status in the brain, a reduced brain-derived neurotrophic factor (BDNF) concentration, and a consequent decrease in memory. To better understand the physiological consequences of T2DM and IR, studies have used experimental models of rodents, with those with greater ecological validity those that induce T2DM and IR through hypercaloric diets. Previously, a study carried out by our research group (LAFISE) standardized a hyperlipidic diet (48% of fat) associated with the ingestion of a fructose solution (30%) to induce IR. However, it is still unknown whether IR induced by this diet can promote memory damage. Physical exercise (PE) is strongly recommended as a non-pharmacological tool for the management of the complications of T2DM and IR. It is already known that both aerobic exercise (AE) and resistance exercise (RE) produce metabolic and cognitive improvements in individuals with IR. However, previous studies focused mainly on investigating the acute and chronic effects of AE. rats. Thus, the present study aimed to investigate the acute effects of RE on memory, neurotrophic and inflammatory responses in insulin-resistant rats. Initially we investigated whether IR induction with the high-fat diet and fructose promotes the worsening of strength and memory, alters muscle and hippocampal inflammatory profiles, and reduces BDNF concentration in the hippocampus. It was observed that insulin-resistant rats showed muscle inflammation, worsening of long-term memory (LTM) and reduced concentration of BDNF in the hippocampus. After we investigated if an acute bout of RE could alter these responses in the insulin-resistant rats. The results showed that acute bout of RE prevented the worsening of LTM caused by IR induction, increased the concentration of BDNF in the hippocampus, and increased muscle pro-inflammatory status. Thus, it is possible to conclude that an acute bout of RE may mitigate the adverse effects of IR on memory, neurotrophic and inflammatory factors in the rats.