Fish Oil - Omega-3 Exerts Protective Effect in Oxidative Stress and Liver Dysfunctions Resulting from Experimental Sepsis.

Background: Sepsis is a severe global health problem, with high morbidity and mortality. In sepsis, one of the main affected organs is the liver. Hepatic alterations characterize a negative prognostic. Omega-3 fatty acids (ω3), eicosapentaenoic acid, and docosahexaenoic acid, are part of the main families of polyunsaturated fatty acids. ω3 has been used in studies as sepsis treatment and as a treatment for non-alcoholic liver disease. Aim: We aimed to evaluate the effects of treatment with fish oil (FO) rich in ω3 on liver changes and damage resulting from experimental sepsis. Methodology: A model of severe sepsis in Wistar rats was used. Oxidative stress in the liver tissue was evaluated by means of tests of thiobarbituric acid reactive substances, 2,7-dihydrodichlorofluorescein diacetate , catalase, and glutathione peroxidase, in the serum TBARS, DCF, thiols and, to assess liver dysfunction, alanine aminotransferase and aspartate aminotransferase. Hepatic tissue damage was evaluated using H&E histology. Results: In assessments of oxidative stress in liver tissue, a protective effect was observed in the tests of TBARS, DCF, CAT, and GPx, when compared the sepsis versus sepsis+ω3 groups. Regarding the oxidative stress in serum, a protective effect of treatment with ω3 was observed in the TBARS, DCF, and thiols assays, in the comparison between the sepsis and sepsis+ω3 groups. ω3 had also a beneficial effect on biochemical parameters in serum in the analysis of ALT, creatinine, urea, and lactate, observed in the comparison between the sepsis and sepsis+ω3 groups. Conclusion: The results suggest ω3 as a liver protector during sepsis with an antioxidant effect, alleviating injuries and dysfunctions.

O3 concentration and duration of exposure are factors influencing the environmental health risk of exercising in Rio Grande, Brazil.

Ozone (O3) represents a great threat to human health, contributing to respiratory diseases and premature mortality. This pollutant is often considered a critical pollutant in regions of southern Brazil. Exposure to this pollutant during vigorous physical activity should be the subject of thorough investigations due to the increased ventilation rate and altered breathing pattern present during vigorous physical activity that result in greater inhalation of O3. Thus, this study aimed to evaluate the health risk of exposure to low, mean, and high concentrations of O3 during different durations of exercise in the city of Rio Grande (southern Brazil). Healthy young men (n = 45) performed cardiopulmonary exercise testing, and ventilation rate data were collected to predict total ventilation and pollutant inhalation during a 5 km running session. The O3 concentration in the city of Rio Grande was obtained from data reported by the Copernicus Atmosphere Monitoring Service (CAMS). The environmental health risk was calculated based on the potential intake dose. The lowest, mean, and highest concentrations of O3 detected during the monitoring period were 32.5, 64.9, and 115.2 µg/m3, respectively. In all evaluated scenarios, there was a toxicological risk (RQ > 1), except when exercising when the O3 concentration was lowest for the shortest length of time (p < 0.001). As the concentration of O3 and the duration of the exposure increase, the health risk is increased. Therefore, O3 concentration and duration of exposure are factors influencing the health risk of exercising. These findings are extremely relevant in cities that have high levels of O3, such as the city of Rio Grande.

Air pollution inhalation during acute exercise is dependent of the body mass index and ventilation of young men.

Obesity and physical inactivity threaten human health, and both could be solved with exercise. However, a higher amount of pollutants is inhaled during exercise. Exposure to air pollution increases the incidence and progression of diseases. Therefore, the aim of the study was to investigate the rate of pollution inhalation of lean, overweight, and obese individuals in a low and high-intensity hypothetical exercise session. Healthy sedentary men (n = 135) classified as lean, overweight, or obese were enrolled in our study. All participants performed a cardiopulmonary exercise testing (CPX) to collect ventilation rate (VE) data, which was used to predict total ventilation and pollutant inhalation of a 5-km running session. Air pollutant concentration of São Paulo City, Brazil was evaluated and the toxicological risk was estimated based on the potential intake dose. The concentrations of PM2.5 were 29.57 µg/m3 and 51.71 µg/m3, PM10 were 45.85 µg/m3 and 74 µg/m3, NO2 were 63.71 µg/m3 and 66.65 µg/m3, and O3 were 69 µg/m3 and 37 µg/m3, respectively in the summer and winter. In the hypothetical exercise session, total VE and time in both the first and second threshold were increased in the obese group (p < 0.001) (p < 0.001). The inhalation of PM2.5, PM10, NO2, and O3, during the hypothetical session, was increased in obese individuals (p < 0.001). Obese individuals should be considered a susceptible population, once they are more exposed to air pollution during exercise.

Blood flow restriction impairs the inflammatory adaptations of strength training in overweight men: a clinical randomized trial.

The aim of this study was to evaluate the impact of high-intensity strength training (ST) or low-intensity strength training with blood flow restriction (ST-BFR) on monocyte subsets, the expression of C-C chemokine receptor 5 (CCR5), and CD16 on monocytes, and tumor necrosis factor alpha (TNF-α) production of overweight men. Thirty overweight men were randomly assigned to conventional ST or ST-BFR. Both groups performed exercises of knee extension and biceps curl with equal volume (3 sessions/week) over 8 weeks, and the peripheral frequency of monocytes (CD14+CD16-, classical monocytes; CD14+CD16+, intermediate monocytes; CD14-CD16+, nonclassical monocytes), the mean fluorescence intensity (MFI) of CCR5 and CD16 on CD14+ monocytes; and the production of TNF-α by lipopolysaccharide (LPS)-stimulated cells were quantified. Eight weeks of ST increased the frequency of CD14+CD16- monocytes (p = 0.04) and reduced the percentage of CD14-CD16+ (p = 0.02) and the production of TNF-α by LPS-stimulated cells (p = 0.03). The MFI of CD16 on CD14+ monocytes decreased after the ST intervention (p = 0.02). No difference in monocyte subsets, CCR5 or CD16 expression, and TNF-α production were identified after ST-BFR intervention (p > 0.05). The adoption of ST promotes anti-inflammatory effects on monocyte subsets of overweight men, but this effect was lost when BFR was adopted. Novelty High-intensity strength training reduces the production of TNF-α and the peripheral frequency of CD16+ monocytes in overweight men. Blood flow restriction method blunts the strength training adaptations on monocyte subsets and pro-inflammatory TNF-α production in overweight men.