Exercício de força protege do fenótipo do tipo ansioso/depressivo em camundongos submetidos a um modelo de estresse

Abstract

The anxiety/depression dyad has been a recurrent disease in the world population in recent years, being a disabling factor and aggravated by the fact that two central pathologies are associated. Resistance physical exercise has been studied in addition to its effects at the peripheral level, aiming at the improvement of depressive patients, but less studied compared to other sports modalities, such as aerobic exercise. Thus, the objective of this work was to evaluate the protective effect of resistance physical exercise against the anxiety/depression dyad in male mice exposed to stress and the involvement of neuroinflammation and hippocampal neurogenesis. This work was approved by the Ethics Committee on the use of animals under the number #1535120320. Male Swiss mice (35 days old), divided into two groups (sedentary and exercised) started the resistance exercise protocol, going through a week of adaptation and in the following four weeks, there was an increase in loads when climbing the stairs each week. Three days after the end of the exercise protocol the animals were divided and two groups were exposed to stress, undergoing behavioral tests seven and eight days after prolonged single emotional stress (Esps). The results showed a protective effect of resistance exercise against changes caused by exposure to stress in predictive tests of anxiety and depression. This effect of exercise is somehow related to its ability to modulate central proteins involved in neuroinflammation, which was shown to be exacerbated in sedentary animals exposed to stress. Likewise, exercise has been shown to modulate the protein kinase B (Akt)/mechanistic target of rapamycin (mTOR) pathway in the hippocampus, a central structure associated with neurogenesis processes and target of studies on the pathophysiology of the anxiety/depression-like dyad, in addition to preventing decrease of the tropomyosin kinase B (TRκB) receptor in this structure. Both exposure to strenght exercise and exposure to stress led to an increase in glucocorticoid receptor (GR) levels, demonstrating that the effects of exercise are directly independent of GR. Stress exposure led to increases in circulating corticosterone levels only in sedentary animals. Both strenght exercise and stress did not cause locomotor damage in the animals. Taken together, the results presented here demonstrate a protective role of resistance exercise in male mice subjected to stress, by modulating hippocampal neuroinflammation, in addition to modulating the Akt/mTOR pathway and neurogenesis.