Efeitos hepáticos dos ciclos de treino e destreino, do treinamento intervalado de alta intensidade, em modelo experimental induzido por dieta hiperlipídica

Abstract

Obesity is a risk factor for the development of non-alcoholic fatty liver disease (NAFLD), considered one of the main causes of liver functional impairment. Practicing physical exercise associated with eating a balanced diet is the first line of NAFLD treatment, but sustaining this new lifestyle in the long term is a challenge and regaining body weight is a recurring issue. Body weight regain can lead to potentially harmful metabolic changes, some of which remain unclear. Among exercise modalities, high-intensity interval training (HIIT) has gained notoriety for being made up of brief sessions, which eases the issue of lack of time to dedicate to frequent practice. With the aim of studying the hepatic effects after weight loss and recovery, resulting from training, detraining and retraining cycles obtained via HIIT, in an experimental mouse model with obesity, 80 C57Bl/6 mice (3 months old) were fed with a control diet (C, 10% lipids, n=40) or a diet rich in saturated fat (HF, 50% lipids, n=40) for 12 weeks. After this period, the animals were redivided into 8 groups, in which they did not train during the entire experiment (NT); trained throughout the experiment (T); trained, untrained and retrained (TNT) and those who trained and detrained (NTN); through high-intensity interval training without changes to their diets. The following analyzes were carried out: weekly monitoring of body mass (BM) and systolic blood pressure (SBP), biochemical tests, oral glucose tolerance test, liver stereology and RT-qPCR for genes related to lipogenesis (Srebp1c, Cherbp, Fas and Fat-cd36), β-oxidation (Pparα and Cpt1a) and endoplasmic reticulum stress (Atf4, Chop and Gadd45). At the end of the period of induction of metabolic changes, a significant increase in MC in the HF-NT group (+10%, p=0.003), SBP, glucose and lipid profile was observed, in addition to an increase of +104% (p <0.001) of hepatic steatosis, in relation to the C-NT group. These parameters were significantly reduced during training cycles, as well as the expression of lipogenic genes and endoplasmic reticulum stress, linked to increased oxidation of hepatic fatty acids. During the detraining cycles, a preservation of the reduction in the animals' body mass was observed, which reflected in the maintenance of other improvements, with emphasis on the groups that trained for two cycles (C-TNT and HF-TNT), which presented parameters similar to their analogues who trained during the 3 cycles (C-T and HF-T). Our results indicate that the reduction in hepatic steatosis and other metabolic improvements, arising from HIIT training cycles, continued during detraining cycles, even though the mice continued to ingest a high-fat diet.