Resistance training affects the hemodynamic parameters of hypertensive and normotensive women differently, and regardless of performance improvement.

BACKGROUND: Although the positive effects of resistance training (RT) on strength and functional capacity have been well evidenced in the scientific literature, the effects of RT on blood pressure and the relationship of these responses with performance improvement are not yet well established. OBJECTIVE: This study aimed to analyze the effects of three and six months of RT on the hemodynamic parameters and functional capacity of hypertensive and normotensive women. METHOD: Sixteen hypertensive and 15 normotensive elderly women participated in a RT protocol designed to increase muscle strength and hypertrophy, lasting six months, twice a week. RESULTS: Systolic blood pressure (SBP) had a reduction at six months only in hypertensive patients, while diastolic blood pressure (DBP) decreased at six months of intervention in both groups (p < 0.05). SBP showed differences between the groups in the pretest (p < 0.05), but not at three and six months of intervention (p > 0.05). Heart rate (HR) was reduced at three months in hypertensive patients, and at six months in the normotensive (p < 0.05). The strength and functional mobility of both hypertensive and normotensive individuals significantly increased at three and six months of intervention (p < 0.05). Hypertensive women showed increased strength at all moments, while normotensive ones showed improvement only at six months. CONCLUSION: Moderate to high intensity RT improves the hemodynamic parameters of hypertensive and normotensive women differently, and independently of strength gain and functional capacity improvement.

Influence of the fish oil in the gut microbiota of wistar rats (Rattus norvegicus) treated with dexamethasone and amoxicillin.

The widespread use of antibiotics and anti-inflammatory has been more and more prominent. In spite of the proven pharmacological potential, its collateral effects are still being described. The fish oil is made of acids fatty polyunsaturated, as the omega 3. The aim of this paper is to check if there would be interference of this fish oil in the gut microbiota of rats when treated with dexamethasone and amoxicillin, joining with the parameter lipids and glycemic. This study was done with 42 Wistar rats, divided into 6 groups with 7 animals each: naive (CTL), amoxicillin (AMOX), dexamethasone (DEX), fish oil (OLP), associated amoxicillin and fish oil (AMOX + OLP) association dexamethasone and fish oil (DEX + OLP). The results show that the fish oil influenced in the concentration of blood glucose in the animals, keeping stable levels even after a pool of glucose. Differently, the fish oil increased the levels of LDL in the animals. The amoxicillin changed the mass of liver and spleen, changed the levels of triglyceride and changed the gut microbiota. The dexamethasone influenced the lipids parameters and mass of the spleen as well as it slightly increased the amount of cholesterol LDL. It is possible to conclude that fish oil increases the levels of LDL in the tested model and the dose tested, but is able to maintain glucose levels even after a pool of the same, and can be a preventive model with hyperglycemia.

Glucose homeostasis in rats treated with 4-vinylcyclohexene diepoxide is not worsened by dexamethasone treatment.

4-vinilcyclohexene diepoxide (4-VCD) causes premature ovarian failure and may result in estrogen deficiency, characterizing the transition to estropause in rodents (equivalent to menopause in women). Estropause/menopause is associated with metabolic derangements such as glucose intolerance and insulin resistance. Glucocorticoids (GCs) are known to exert diabetogenic effects. Thus, we aimed to investigate whether rats with premature ovarian failure are more prone to the diabetogenic effects of GC. For this, immature female rats received daily injections of 4-VCD [160mg/kg body weight (b.w.), intraperitoneally (i.p.)] for 15 consecutive days, whereas control rats received vehicle. After 168days of the completion of 4-VCD administration, rats were divided into 4 groups: CTL-received daily injections of saline (1mL/kg, b.w., i.p.) for 5days; DEX-received daily injections of dexamethasone (1mg/kg, b.w., i.p.) for 5days; VCD-treated as CTL group; VCD+DEX-treated as DEX group. Experiments and euthanasia occurred one day after the last dexamethasone injection. 4-VCD-treated rats exhibited ovary hypotrophy and reduced number of preantral follicles (p<0.05). Premature ovarian failure had no impact on the body weight gain or food intake, but both were reduced by the effects of dexamethasone. The increase in blood glucose, plasma insulin and triacylglycerol levels as well as the reduction in insulin sensitivity caused by dexamethasone treatment was not exacerbated in the VCD+DEX group of rats. Premature ovarian failure did change neither the hepatic content of glycogen and triacylglycerol nor the glycerol release from perigonadal adipose tissue. Glucose intolerance was observed in the VCD group after an ipGTT (p<0.05), but not after an oral glucose challenge. Glucose intolerance and compensatory pancreatic ß-cell mass caused by GC were not modified by ovarian failure in the VCD+DEX group. We conclude that reduced ovarian function has no major implications on the diabetogenic effects promoted by GC treatment, indicating that other factors related to aging may make rats more vulnerable to GC side effects on glucose metabolism.

Inflammatory cytokines in vitro production are associated with Ala16Val superoxide dismutase gene polymorphism of peripheral blood mononuclear cells.

Obesity is considered a chronic low-grade inflammatory state associated with a chronic oxidative stress caused by superoxide production (O(2)(-)). The superoxide dismutase manganese dependent (SOD2) catalyzes O(2)(-) in H(2)O(2) into mitochondria and is encoded by a single gene that presents a common polymorphism that results in the replacement of alanine (A) with a valine (V) in the 16 codon. This polymorphism has been implicated in a decreased efficiency of SOD2 transport into targeted mitochondria in V allele carriers. Previous studies described an association between VV genotype and metabolic diseases, including obesity and diabetes. However, the causal mechanisms to explain this association need to be more elucidated. We postulated that the polymorphism could influence the inflammatory response. To test our hypothesis, we evaluated the in vitro cytokines production by human peripheral blood mononuclear cells (PBMCs) carrier's different Ala16Val-SOD2 genotypes (IL-1, IL-6, IL-10, TNF-α, IFN-γ). Additionally, we evaluated if the culture medium glucose, enriched insulin, could influence the cytokine production. Higher levels of proinflammatory cytokines were observed in VV-PBMCs when compared to AA-PBMCs. However, the culture medium glucose and enriched insulin did not affect cytokine production. The results suggest that Ala16Val-SOD2 gene polymorphism could trigger the PBMCs proinflammatory cytokines level. However, discerning if a similar mechanism occurs in fat cells is an open question.