The importance of exercise has been widely accepted by the public, professional organizations and the medical community, and the number of people around the world who practice day-to-day regular physical activity has recently increased. Physical activity is a primary requirement for the maintenance and promotion of health. However, intense exercise induces an increase in substrate utilization by the working muscles, resulting in an increased use of oxygen. This rise in oxygen consumption combined with the activation of specific metabolic pathways during or after exercise results in the generation of Reactive Oxygen Species (ROS). These substances are produced naturally by oxidative metabolic processes and are highly reactive. ROS can be useful in some situations; for example, macrophages use hydrogen peroxide to destroy bacteria. ROS increases during high-intensity exercise and its production is related to a large number of diseases, such as emphysema, inflammatory diseases, atherosclerosis, cancer and aging. During evolution, living organs developed an endogenous mechanism to minimize the damage caused by ROS, termed the antioxidant defense system. The imbalance between the production of ROS and the removal of these compounds by the antioxidant defense system causes a condition known as oxidative stress. This interesting paradox is exemplified by the hypothesis that physical exercises known to promote appropriate standards of health are also related to increased ROS production, which in turn closely correlate with various diseases. Recent publications have shown that ROS produced by exercise in adequate amounts may be linked to exercise benefits, both for health and for athletic performance. Thus, the aim of this article is to examine the close association between physical exercise and the production of ROS through an extensive literature review.

Acute exercise increases the amount of circulating inflammatory cells and cytokines to maintain physiological homeostasis. However, it remains unclear how physical training regulates exercise-induced inflammation and performance. Here, we demonstrate that acute high intensity exercise promotes an inflammatory profile characterized by increased blood IL-6 levels, neutrophil migratory capacity, and leukocyte recruitment to skeletal muscle vessels. Moreover, we found that physical training amplified leukocyte–endothelial cell interaction induced by acute exercise in skeletal muscle vessels and diminished exercise-induced inflammation in skeletal muscle tissue. Furthermore, we verified that disruption of the gp-91 subunit of NADPH-oxidase inhibited exercise-induced leukocyte recruitment on skeletal muscle after training with enhanced exercise time until fatigue. In conclusion, the training was related to physical improvement and immune adaptations. Moreover, reactive oxygen species (ROS) could be related to mechanisms to limit aerobic performance and its absence decreases the inflammatory response elicited by exercise after training.

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Obesity is associated with an energy imbalance that results from excessive energy intake, low diet quality and a sedentary lifestyle. In this regard, the increased consumption of a high‐refined carbohydrate diet (HC) is strongly related to higher adiposity and low‐grade inflammation. Aerobic training is a well‐known non‐pharmacological intervention to treat obesity and metabolic disturbances. However, the mechanisms through which aerobic training ameliorates the low‐grade inflammation induced by the HC diet need to be further investigated. Herein, our hypothesis was that aerobic training would decrease the recruitment of leukocytes in the adipose tissue thereby reducing the levels of cytokines and improving metabolism in mice fed the HC diet. Male Balb/c were assigned to the following groups: control non‐trained (C‐NT), control trained (C‐T), HC‐NT and HC‐T. Mice were submitted to moderate‐intensity training sessions that consisted of running 60 min/day for 8 weeks. The intravital microscopy technique was performed in vivo in anesthetized mice to visualize the microvasculature of the adipose tissue. The HC diet induced obesity and increased the influx of immune cells into the adipose tissue. In contrast, HC‐T mice presented a lower adiposity and adipocyte area. Furthermore, HC‐T mice showed an increased resting energy expenditure, a decreased recruitment of immune cells in the adipose tissue, reduced cytokine levels, and ameliorated hyperglycemia and fatty liver deposition relative to HC‐NT mice. Collectively, our data enhance the understanding about the anti‐inflammatory effect of aerobic training and shed light on the adipose tissue‐mediated mechanisms by which training promotes a healthier metabolic profile.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Inflammation is an adaptive response that is triggered by the noxious stimuli in order to maintain the homeostasis. Previous studies have shown that higher lipolysis rate after fasting is associated with the influx of leukocytes and increased cytokine levels in the epididymal adipose tissue (EAT). Fat mobilization is also highly activated during and post‐exercise. In spite of substantial evidences having supported the link between inflammation and exercise, the association between EAT, cytokines and acute exercise is less explored. Herein, we characterized the EAT inflammation following exercise in lean and obese mice. We used in vivo confocal imaging from EAT vessel to display the higher recruitment of neutrophils 0 and 6 hours post‐exercise in lean mice. Additionally, we found that exercise enhanced the levels of IL‐6 and TNF‐alpha in the EAT which were correlated with increased serum free fatty acids in lean mice. Interestingly, obese mice subjected to exercise showed lower pro‐inflammatory level of cytokines in the EAT and lost the correlation between IL‐6, TNF‐alpha and free fatty acids. Furthermore, obese mice increased IL‐10 24h post‐exercise. Together, our data show that exercise induces inflammation in the EAT in lean mice. These responses may have a physiological purpose and be important to stimulate fat breakdown. Conversely, exercise in obese mice promoted a reduction in pro‐inflammatory mediators and elevated IL‐10. Despite of the low‐grade inflammation being associated with metabolic dysfunctions, at least in part, the inflammatory milieu in EAT may be also important to regulate fat remodeling induced by exercise.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.