Junior, IF. Combined training (aerobic plus strength) potentiates a reduction in body fat but demonstrates no difference on the lipid profile in postmenopausal women when compared with aerobic training with a similar training load. J Strength Cond Res 30(1): 226-234, 2016-The aim of this study was to verify the effects of aerobic and combined training on the body composition and lipid profile of obese postmenopausal women and to analyze which of these models is more effective after equalizing the training load. Sixty-five postmenopausal women (age = 61.0 6 6.3 years) were divided into 3 groups: aerobic training (AT, n = 15), combined training (CT [strength + aerobic], n = 32), and control group (CG, n = 18). Their body composition upper body fat (TF), fat mass (FM), percentage of FM, and fat-free mass (FFM) were estimated by dual-energy x-ray absorptiometry. The lipid profile, total cholesterol, highdensity lipoprotein (HDL) cholesterol, and low-density lipoprotein cholesterol were assessed. There was a statistically significant difference in the TF (AT = 24.4%, CT = 24.4%, and CG = 1.0%, p = 0.001) and FFM (AT = 1.7%, CT = 2.6%, and CG = 21.4%, p = 0.0001) between the experimental and the control groups. Regarding the percentage of body fat, there was a statistically significant difference only between the CT and CG groups (AT = 22.8%, CT = 23.9%, and CG = 0.31%; p = 0.004). When training loads were equalized, the aerobic and combined training decreased core fat and increased FFM, but only the combined training potentiated a reduction in percentage of body fat in obese postmenopausal women after the training program. High-density lipoprotein-c levels increased in the combined group, and the chol/HDL ratio (atherogenic index) decreased in the aerobic group; however, there were no significant differences between the intervention programs. Taken together, both the exercise training programs were effective for improving body composition and inducing an antiatherogenic status.

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.

Background: Elevated screen time has been associated with addictive behaviors, such as alcohol and sugar intake and smoking. Considering the substantial increase in screen time caused by social isolation policies, this study aimed to analyze the association of increased screen time in different devices during the COVID-19 pandemic with consumption and increased desire of alcohol, smoking, and sweetened foods in adults.Methods: A sample of 1,897 adults with a mean age of 37.9 (13.3) years was assessed by an online survey, being composed by 58% of women. Participants were asked whether screen time in television, cell phone, and computer increased during the pandemic, as well as how much time is spent in each device. Closed questions assessed the frequency of alcohol and sweetened food consumption, smoking, and an increased desire to drink and smoke during the pandemic. Educational level, age, sex, feeling of stress, anxiety, depression, and use of a screen device for physical activity were covariates. Binary logistic regression models considered adjustment for covariates and for mutual habits.Results: Increased television time was associated with increased desire to drink (OR = 1.46, 95% CI: 1.12; 1.89) and increased sweetened food consumption (OR = 1.53, 95% CI: 1.18; 1.99), while an increase in computer use was negatively associated with consumption of alcohol (OR = 0.68, 95% CI: 0.53; 0.86) and sweetened foods (OR = 0.78, 95% CI: 0.62; 0.98). Increased cell phone time was associated with increased sweetened food consumption during the pandemic (OR = 1.78, 95% CI: 1.18; 2.67). Participants with increased time in the three devices were less likely to consume sweetened foods for ≥5 days per week (OR = 0.63, 95% CI: 0.39; 0.99) but were twice as likely to have sweetened food consumption increased during pandemic (OR = 2.04, 95% CI: 1.07; 3.88).Conclusion: Increased screen time was differently associated with consumption and desire for alcohol and sweets according to screen devices. Increased time in television and cell phones need to be considered for further investigations of behavioral impairments caused by the pandemic.

BackgroundThe outbreak of novel coronavirus disease 2019 (COVID-19) has caused a global panic and public concern due to its mortality ratio and lack of treatments/vaccines. Reduced levels of physical activity have been reported during the outbreak, affecting the normal daily pattern.ObjectiveTo investigate (i) the relationship of physical activity level with sleep quality and (ii) the effects of reduction physical activity levels on sleep quality.MethodsA Google form was used to address personal information, COVID-19 personal care, physical activity, and mental health of 1,907 adult volunteers. Binary logistic regression was used to verify the association of physical activity parameters and sleep quality.ResultsInsufficient physical activity levels were a risk factor to have disturbed sleep pattern [OR: 1.28, 95% CI (1.01–1.62)]; however, when the BMI was added to the analysis, there was no more statistical difference [OR: 1.23, 95% CI (0.96–1.57)]. On the other hand, we found that the reduction of physical activity levels was associated with negative changes in sleep quality [OR: 1.73, 95% CI (1.37–2.18)], regardless all the confounders [OR: 1.30, 95% CI (1.01–1.68)], unless when feeling of depression was added in Model 6 [OR: 1.28, 95% CI (0.99–1.66)].ConclusionDisruption in daily physical activity routine, rather than physical activity level, negatively influences sleep quality during the COVID-19 quarantine.

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Postmenopausal women with a combination of hypertriacylglycerolaemia, a high level of abdominal fat and a sedentary lifestyle are more likely to have metabolic disturbances.

The pathogenesis of muscle atrophy plays a central role in cancer cachexia, and chemotherapy contributes to this condition. Therefore, the present study aimed to evaluate the effects of endurance exercise on time-dependent muscle atrophy caused by doxorubicin. For this, C57 BL/6 mice were subcutaneously inoculated with Lewis lung carcinoma cells (LLC group). One week after the tumor establishment, a group of these animals initiated the doxorubicin chemotherapy alone (LLC + DOX group) or combined with endurance exercise (LLC + DOX + EXER group). One group of animals was euthanized after the chemotherapy cycle, whereas the remaining animals were euthanized one week after the last administration of doxorubicin. The practice of exercise combined with chemotherapy showed beneficial effects such as a decrease in tumor growth rate after chemotherapy interruption and amelioration of premature death due to doxorubicin toxicity. Moreover, the protein degradation levels in mice undergoing exercise returned to basal levels after chemotherapy; in contrast, the mice treated with doxorubicin alone experienced an increase in the mRNA expression levels of the proteolytic pathways in gastrocnemius muscle (Trim63, Fbxo32, Myostatin, FoxO). Collectively, our results suggest that endurance exercise could be utilized during and after chemotherapy for mitigating muscle atrophy promoted by doxorubicin and avoid the resumption of tumor growth.

Palmitoleic acid (POA, 16:1n-7) is a lipokine that has potential nutraceutical use to treat non-alcoholic fatty liver disease. We tested the effects of POA supplementation (daily oral gavage, 300 mg/Kg, 15 days) on murine liver inflammation induced by a high fat diet (HFD, 59% fat, 12 weeks). In HFD-fed mice, POA supplementation reduced serum insulin and improved insulin tolerance compared with oleic acid (OA, 300 mg/Kg). The livers of POA-treated mice exhibited less steatosis and inflammation than those of OA-treated mice with lower inflammatory cytokine levels and reduced toll-like receptor 4 protein content. The anti-inflammatory effects of POA in the liver were accompanied by a reduction in liver macrophages (LM, CD11c + ; F4/80 + ; CD86 + ), an effect that could be triggered by peroxisome proliferator activated receptor (PPAR)-γ, a lipogenic transcription factor upregulated in livers of POA-treated mice. We also used HFD-fed mice with selective deletion of PPAR-γ in myeloid cells (PPAR-γ KO LyzCre+ ) to test whether the beneficial anti-inflammatory effects of POA are dependent on macrophages PPAR-γ. POA-mediated improvement of insulin tolerance was tightly dependent on myeloid PPAR-γ, while POA anti-inflammatory actions including the reduction in liver inflammatory cytokines were preserved in mice bearing myeloid cells deficient in PPAR-γ. This overlapped with increased CD206 + (M2a) cells and downregulation of CD86 + and CD11c + liver macrophages. Moreover, POA supplementation increased hepatic AMPK activity and decreased expression of the fatty acid binding scavenger receptor, CD36. We conclude that POA controls liver inflammation triggered by fat accumulation through induction of M2a macrophages independently of myeloid cell PPAR-γ.