Dyslipidemia (high concentrations of LDL-c and low concentrations of HDL-c) is a major cause of cardiovascular events, which are the leading cause of death in the world. On the other hand, nutrition and regular exercise can be an interesting strategy to modulate lipid profile, acting as prevention or treatment, inhibiting the risk of diseases due to its anti-inflammatory and anti-atherogenic characteristics. Additionally, the possibility of controlling different training variables, such as type, intensity and recovery interval, can be used to maximize the benefits of exercise in promoting cardiovascular health. However, the mechanisms by which exercise and nutrients act in the regulation of cholesterol and its fractions, such as reverse cholesterol transport, receptors and transcription factors involved, such as PPARs and their role related to exercise, deserve further discussion. Therefore, the objective of this review is to debate about non-medical approaches to increase HDL-c, such as nutritional and training strategies, and to discuss the central mechanisms involved in the modulation of lipid profile during exercise, as well as that can be controlled by physical trainers or sports specialists in attempt to maximize the benefits promoted by exercise. The search for papers was performed in the databases: Medline (Pubmed), Science Direct, Scopus, Sport Discus, Web of Science, Scielo and Lilacs until February 2016.

Macrophages are cells of the innate immune response that trigger inflammation resolution. The phenotype of "classically activated macrophages" (M1) has anti-tumoricidal and anti-bactericidal activities. On the other hand, "alternatively activated macrophages" (M2) are involved in tissue remodeling and immunomodulatory functions. The change in the polarization of macrophages varies according to the diversity of cytokines present in the microenvironment or by the stimuli of an antigen. It involves such factors as interferon-regulatory factors, peroxisome proliferator-activated receptors (PPARs), hypoxia-inducible factors (HIFs), and signal transducers and activators of transcription (STATs). Switching the phenotype of macrophages can help attenuate the development of an inflammatory disease. Exercise can promote alterations in the number of innate immune cells and stimulates phagocytic function. Chronic exercise seems to inhibit macrophage infiltration into adipose tissue by attenuating the expression of F4/80 mRNA. Furthermore, exercise may also increase the expression of M2 markers and reduce TNF-α and TLR4 mRNA expression, which activates the inflammatory pathway of NF-κB. Chronic exercise reduces β2-adrenergic receptors in monocytes and macrophages by modulating TLR4 signaling as well as suppressing IL-12 production, a stimulator of interferon Y. In this review, we discuss macrophage polarization in metabolic diseases and how exercise can modulate macrophage plasticity.

The prevalence of obesity in pediatric population is increasing at an accelerated rate in many countries, and has become a major public health concern. Physical activity, particularly exercise training, remains to be a cornerstone of pediatric obesity interventions. The purpose of our current randomized intervention trial was to compare the effects of two types of training matched for training volume, aerobic and concurrent, on body composition and metabolic profile in obese adolescents. Thus the aim of the study was compare the effects of two types of training matched for training volume, aerobic and concurrent, on body composition and metabolic profile in obese adolescents. 32 obese adolescents participated in two randomized training groups, concurrent or aerobic, for 20 weeks (50 mins x 3 per week, supervised), and were compared to a 16-subject control group. We measured the percentage body fat (%BF, primary outcome), fat-free mass, percentage of android fat by dual energy x-ray absorptiometry, and others metabolic profiles at baseline and after interventions, and compared them between groups using the Intent-to-treat design. In 20 weeks, both exercise training groups significantly reduced %BF by 2.9-3.6 % as compare to no change in the control group (p = 0.042). There were also positive changes in lipid levels in exercise groups. No noticeable changes were found between aerobic and concurrent training groups. The benefits of exercise in reducing body fat and metabolic risk profiles can be achieved by performing either type of training in obese adolescents. Registration number: RBR-4HN597 .

Obesity is a risk factor able to trigger several inflammatory alterations and the imbalance between pro- and anti-inflammatory cytokine productions. Physical exercise is an important strategy for reduction of inflammatory established process. The aim of this study was to evaluate the effect of 16 weeks of three exercise training programs in the inflammatory profile and insulin resistance in overweight/obesity. Thirty two men and women (46.4±10.1 years; 162.0±9.1 cm; 82.0±13.6 kg) were divided into three groups for training on a treadmill: continuous at 70% maximum heart rate (HRmax) 5 times a week (CONT); 1×4 min (1-bout) and 4×4 min (high intensity interval training, HIIT) at 90% HRmax 3 times a week. Interleukin (IL) 6 and IL-10, tumor necrosis factor-alpha (TNF-α), insulin and adiponectin levels were analyzed by enzyme-linked immunosorbent assay, and homeostasis model assessment insulin resistance was calculated. After 16 weeks of training blood concentrations of IL-6 decreased in the HIIT group (P=0.035), TNF-α decreased in the CONT (P=0.037) and increased in HIIT (P=0.001) and adiponectin decreased in the three training models. There was a trend towards decreased body weight and body mass index (BMI) after HIIT only (P=0.059 and P=0.060, respectively). Despite the decrease of adiponectin and the increase of TNF-α in HIIT group, insulin sensitivity showed a trend for improvement (P=0.08). HIIT program decreased IL-6 at rest and although not significant was the only who tended to decrease total body weight and BMI. Taken together, our data suggest that both HIIT as well as CONT exercises training program promotes changes in inflammatory profile in overweight/obesity, but dissimilar response is seen in TNF-α levels.

BDNF is associated with brain health and positively modulated by exercise; however, the influence of physical fitness status on BDNF is incipient. This study investigated the BDNF response after acute‐exercise sessions performed at low, moderate, and high intensities and the relationship between physical fitness status and BDNF response. Twenty‐eight men, divided according to physical fitness status (50th percentile for VO_2max), performed three randomised acute exercise sessions at low (90% of VT1), moderate (midpoint between VT1‐VT2), and high (midpoint between VT2‐W_max) intensities until exhaustion or for up to 60 min. Lactate and BDNF were determined pre and post‐exercises. For BDNF, there were main effects of time (p = 0.003) and interaction (p < 0.001), showing an increase post high‐intensity exercise (p < 0.001). Changes in BDNF presented differences between conditions (p < 0.001) with greater increase in high‐intensity compared with the others (p = 0.003). For lactate, there were main effects of time (p < 0.001), condition (p < 0.001), and interaction (p < 0.001) with greater concentration in high‐intensity. High‐intensity exercise exhibited inverse correlation between the changes in BDNF and lactate (r=−0.38, p = 0.044). There was significant correlation between BDNF and VO_2max for moderate (r = −0.57, p = 0.002) and a trend for high‐intensity condition (r = −0.37, p = 0.050) and when evaluating BDNF according to physical fitness level, it was observed that subjects with lower physical fitness levels had greater increases in BDNF in short‐time high‐intensity exercise (p = 0.041). In conclusion, short‐time high‐intensity exercise seems to be more efficient in increasing BDNF concentration, and physical fitness level influences this response, as healthy individuals with lower physical fitness levels were more responsive.

Previous studies have shown an association between adiposity, especially intra-abdominal adipose tissue, and hemodynamic/metabolic comorbidities in adults, however it is not clear in pediatric population. The aim of the study was to analyze the relationship between non-alcoholic fatty liver disease (NAFLD) and components of metabolic syndrome (MS) with values of intra-abdominal (IAAT) and subcutaneous (SCAT) adipose tissue in obese children and adolescents.