Etel Rocha-Vieira

The Effect of Adding Whole-Body Vibration to Squat Training on the Functional Performance and Self-Report of Disease Status in Elderly Patients with Knee Osteoarthritis: A Randomized, Controlled Clinical Study

OBJECTIVES The study objectives were to evaluate the effects of adding whole-body vibration to squat training on functional performance and self-report of disease in elderly individuals with knee osteoarthritis (OA). DESIGN This was a prospective, randomized trial in which selected variables were evaluated at three periods: 3 weeks prior to the training, immediately prior, and after the end of the training. SUBJECTS Twenty-three (23) elderly subjects were evaluated using four functional performance tests: Berg Balance Scale (BBS), Timed Get Up and Go Test (TGUG), Chair Stand Test (CST), and 6-Minute Walk Test (6MWT), and a self-report of the status of disease (WOMAC). INTERVENTIONS The intervention lasted for 12 weeks, 3 times per week. The participants were randomized into two groups: (1) squat training with whole-body vibration, and (2) squat training without vibration. RESULTS Although there was no statistical difference in functional performance and self-report of disease status between the groups, performance in all the functional tests and in all the domains of WOMAC improved in the vibration group compared to their initial status. In the exercise group, performance improved only two tests (BBS and 6MWT), and there was a reduction in self-reported pain (WOMAC) compared to their initial status. CONCLUSIONS Although the addition of whole-body vibration to squat training failed to result in a significant improvement in functional performance and self-reported status of knee osteoarthritis in the elderly, the intragroup results suggest that whole-body vibration may represent a feasible and effective way of improving the functionality and self-perception of disease status in older adults with knee OA.

The Effect of Different Water Immersion Temperatures on Post-Exercise Parasympathetic Reactivation

Purpose We evaluated the effect of different water immersion (WI) temperatures on post-exercise cardiac parasympathetic reactivation. Methods Eight young, physically active men participated in four experimental conditions composed of resting (REST), exercise session (resistance and endurance exercises), post-exercise recovery strategies, including 15 min of WI at 15°C (CWI), 28°C (TWI), 38°C (HWI) or control (CTRL, seated at room temperature), followed by passive resting. The following indices were assessed before and during WI, 30 min post-WI and 4 hours post-exercise: mean R-R (mR-R), the natural logarithm (ln) of the square root of the mean of the sum of the squares of differences between adjacent normal R–R (ln rMSSD) and the ln of instantaneous beat-to-beat variability (ln SD1). Results The results showed that during WI mRR was reduced for CTRL, TWI and HWI versus REST, and ln rMSSD and ln SD1 were reduced for TWI and HWI versus REST. During post-WI, mRR, ln rMSSD and ln SD1 were reduced for HWI versus REST, and mRR values for CWI were higher versus CTRL. Four hours post exercise, mRR was reduced for HWI versus REST, although no difference was observed among conditions. Conclusions We conclude that CWI accelerates, while HWI blunts post-exercise parasympathetic reactivation, but these recovery strategies are short-lasting and not evident 4 hours after the exercise session.

Severe Calorie Restriction Reduces Cardiometabolic Risk Factors and Protects Rat Hearts from Ischemia/Reperfusion Injury

Background and Aims: Recent studies have proposed that if a severe caloric restriction (SCR) is initiated at the earliest period of postnatal life, it can lead to beneficial cardiac adaptations later on. We investigated the effects of SCR in Wistar rats from birth to adult age on risk factors for cardiac diseases (CD), as well as cardiac function, redox status, and HSP72 content in response to ischemia/reperfusion (I/R) injury. Methods and Results: From birth to the age of 3 months, CR50 rats were fed 50% of the food that the ad libitum group (AL) was fed. Food intake was assessed daily and body weight were assessed weekly. In the last week of the SCR protocol, systolic blood pressure and heart rate were measured and the double product index was calculated. Also, oral glucose and intraperitoneal insulin tolerance tests were performed. Thereafter, rats were decapitated, visceral fat was weighed, and blood and hearts were harvested for biochemical, functional, tissue redox status, and western blot analyzes. Compared to AL, CR50 rats had reduced the main risk factors for CD. Moreover, the FR50 rats showed increased cardiac function both at baseline conditions (45% > AL rats) and during the post-ischemic period (60% > AL rats) which may be explained by a decreased cardiac oxidative stress and increased HSP72 content. Conclusion: SCR from birth to adult age reduced risk factors for CD, increased basal cardiac function and protected hearts from the I/R, possibly by a mechanism involving ROS.

The effect of insulin resistance and exercise on the percentage of CD16+ monocyte subset in obese individuals

Obesity is a low‐grade chronic inflammation condition, and macrophages, and possibly monocytes, are involved in the pathological outcomes of obesity. Physical exercise is a low‐cost strategy to prevent and treat obesity, probably because of its anti‐inflammatory action. We evaluated the percentage of CD16− and CD16+ monocyte subsets in obese insulin‐resistant individuals and the effect of an exercise bout on the percentage of these cells. Twenty‐seven volunteers were divided into three experimental groups: lean insulin sensitive, obese insulin sensitive and obese insulin resistant. Venous blood samples collected before and 1 h after an aerobic exercise session on a cycle ergometer were used for determination of monocyte subsets by flow cytometry. Insulin‐resistant obese individuals have a higher percentage of CD16+ monocytes (14.8 ± 2.4%) than the lean group (10.0 ± 1.3%). A positive correlation of the percentage of CD16+ monocytes with body mass index and fasting plasma insulin levels was found. One bout of moderate exercise reduced the percentage of CD16+ monocytes by 10% in all the groups evaluated. Also, the absolute monocyte count, as well as all other leukocyte populations, in lean and obese individuals, increased after exercise. This fact may partially account for the observed reduction in the percentage of CD16+ cells in response to exercise. Insulin‐resistant, but not insulin‐sensitive obese individuals, have an increased percentage of CD16+ monocytes that can be slightly modulated by a single bout of moderate aerobic exercise. These findings may be clinically relevant to the population studied, considering the involvement of CD16+ monocytes in the pathophysiology of obesity. Copyright

High intensity interval training modulates hippocampal oxidative stress, BDNF and inflammatory mediators in rats

Although High Intensity Interval Training (HIIT) are being associated to increase cardiovascular and metabolic adaptation, there is controversy and limited information about the effects of HIIT on hippocampal oxidative stress, pro- and anti-inflammatory cytokines balance and neurotrophic status. Thus, this study evaluated the effects of six weeks of HIIT on hippocampal redox state (oxidative damage and enzymatic and non-enzymatic antioxidant defenses), neuroimmune mediators (TNFα, IL-6, IL-1β and IL-10) and brain-derived neurotrophic (BDNF) levels. After six weeks of HIIT young adults male Wistar rats presented reduced oxidative damage and increased enzymatic (superoxide dismutase) and non-enzymatic activity in hippocampus. Moreover HIIT induced a decrease in cytokine content (TNFα, IL-6, IL-1β and IL-10) and enhanced hippocampal BDNF levels. In conclusion, the present study showed for the first time a positive effect of six weeks of HIIT on reducing hippocampal oxidative stress by decreasing lipoperoxidation and inflammatory markers, as well enhancing antioxidant defenses and BDNF content.

Increased Migratory and Activation Cell Markers of Peripheral Blood Lymphocytes in an Experimental Model of Nephrotic Syndrome

The present study aimed to evaluate the expression of CD80 and CD18 in subpopulations of peripheral blood leukocytes and oxidative kidney damage in rats with nephrotic syndrome (NS) induced by doxorubicin (Dox) in comparison to control animals at different time points. Male adult Wistar rats were submitted to 24-hour urine and blood collection for biochemical and immunological analysis at 7, 14, 21, and 28 days after Dox injection. After euthanasia, the kidneys were removed for histological analysis and the evaluation of oxidative stress. The phenotypic characterization of leukocytes was performed using flow cytometry. Dox-injected animals exhibited increased CD18 expression in cytotoxic T lymphocytes, NK cells, and monocytes and high CD80 expression in monocytes. Kidney oxidative damage was positively correlated with CD80 expression in monocytes and serum levels of creatinine. These results suggest that phagocytic and cytotoxic cells are preferentially recruited to the tissue injury site, which may contribute to kidney dysfunction in this animal model of NS. The blockade of integrin and costimulatory molecules may provide new therapeutic opportunities for NS.

Divergent cytokine response following maximum progressive swimming in hot water

Exercise promotes transitory alterations in cytokine secretion, and these changes are affected by exercise duration and intensity. Considering that exercise responses also are affected by environmental factors, the goal of the present study was to investigate the effect of water temperature on the cytokine response to maximum swimming. Swiss mice performed a maximum progressive swimming exercise at 31 or 38 °C, and plasma cytokine levels were evaluated immediately or 1, 6 or 24 h after exercise. The cytokine profile after swimming at 31 °C was characterized by increased interleukin (IL)‐6 and monocyte chemotactic protein‐1 (MCP‐1) levels, which peaked 1 h after exercise, suggesting an adequate inflammatory milieu to induce muscle regeneration. Transitory reductions in IL‐10 and IL‐12 levels also were observed after swimming at 31 °C. The cytokine response to swimming was modified when the water temperature was increased to 38 °C. Although exercise at 38 °C also led to IL‐6 secretion, the peak in IL‐6 production occurred 6 h after exercise, and IL‐6 levels were significantly lower than those observed after maximum swimming at 31 °C (p = 0·030). Furthermore, MCP‐1 levels were lower and tumour necrosis factor‐α levels were higher immediately after swimming at 38 °C, suggesting a dysregulated pro‐inflammatory milieu. These alterations in the cytokine profile can be attributed in part to reduced exercise total work because exhaustion occurred sooner in mice swimming at 38 °C than in those swimming at 31 °C. Copyright

Lymphocyte Redox Imbalance and Reduced Proliferation after a Single Session of High Intensity Interval Exercise.

This study investigated whether an acute session of high-intensity interval training (HIIT) is sufficient to alter lymphocyte function and redox status. Sixteen young healthy men underwent a HIIT session on a cycloergometer, consisting of eight bouts of 1 min at 90–100% of peak power, with 75 seconds of active recovery at 30 W between bouts. Venous blood was collected before, immediately after, and 30 minutes after the HIIT session. In response to Staphylococcus aureus superantigen B (SEB) stimulation, lymphocyte proliferation decreased and the IL-2 concentration increased after the HIIT session. However, the HIIT session had no effect on lymphocyte proliferation or IL-2 response to phytohemagglutinin stimulation. The HIIT session also induced lymphocyte redox imbalance, characterized by an increase in the concentration of thiobarbituric acid reactive substances and a decrease in the activity of the antioxidant enzyme catalase. Lymphocyte viability was not affected by the HIIT session. The frequencies of CD25+ and CD69+ T helper and B lymphocytes in response to superantigen stimulation were lower after exercise, suggesting that superantigen-induced lymphocyte activation was reduced by HIIT. However, HIIT also led to a reduction in the frequency of CD4+ and CD19+ cells, so the frequencies of CD25+ and CD69+ cells within the CD4 and CD19 cell populations were not affected by HIIT. These data indicate that the reduced lymphocyte proliferation observed after HIIT is not due to reduced early lymphocyte activation by superantigen. Our findings show that an acute HIIT session promotes lymphocyte redox imbalance and reduces lymphocyte proliferation in response to superantigenic, but not to mitogenic stimulation. This observation cannot be explained by alteration of the early lymphocyte activation response to superantigen. The manner in which lymphocyte function modulation by an acute HIIT session can affect individual immunity and susceptibility to infection is important and requires further investigation.

Neuroendocrine Inflammatory Responses in Overweight/Obese Infants.

Childhood obesity is related to a cascade of neuroendocrine inflammatory changes. However, there remains a gap in the current literature regarding the possible occurrence of these changes in overweight/obese infants. The objective of this study was to evaluate adipokines, cortisol, brain-derived neurotrophic factor (BDNF) and redox status in overweight/obese infants versus normal-weight peers. A cross-sectional study was conducted with 50 infants (25 in the overweight/obese group and 25 in the normal-weight group) between 6 and 24 months. Plasma levels of leptin, adiponectin, resistin, soluble tumor necrosis factor (TNF) receptors, chemokines, BDNF, serum cortisol and redox status were measured. Unpaired Students t-test was used to analyze the results and a probability of p<0.05 was acceptable for rejection of the null hypothesis. The Pearson correlation was used to verify the association between the biomarkers analyzed in each group. Plasma levels of leptin (p = 0.0001), adiponectin (p = 0.0007) and BDNF (p = 0.003), and serum cortisol (p = 0.048) were significantly higher in overweight/obese infants than normal-weight infants. In contrast, the concentration of thiobarbituric acid reactive substances (TBARS) (p = 0.004), and catalase (p = 0.045) and superoxide dismutase activity (p = 0.02) were lower in overweight/obese infants than normal-weight peers. All the results together indicate neuroendocrine inflammatory response changes in overweight/obese infants between 6 and 24 months. Although there is already an environment that predisposes for a subsequent pro-inflammatory response, neuroendocrine secretion changes that permit the control of the inflammatory process in this age interval can be observed.

The in vitro exposure to cypermethrin does not inhibit the proliferative response of peripheral blood mononuclear cells

Abstract This study evaluated the effect of in vitro exposure to cypermethrin on peripheral blood mononuclear cells proliferative response, considering reduced peripheral blood mononuclear cells proliferative response observed in individuals occupationally exposed to pyrethroids. Peripheral blood mononuclear cells were obtained from 21 healthy subjects (28.0 ± 9.0 years old). The effect of cypermethrin (at 0.5, 1.0 and 5.0 mg/ml) on cell viability was evaluated by flow cytometry using an apoptosis detection kit. Cell proliferation (PI) was evaluated by 5-(and 6)-carboxyfluorescein diacetate succinimidyl ester (CFSE) fluorescence decay using flow cytometry. Cells labeled with CFSE were exposed, in vitro, to cypermethrin (0.5, 1.0, 2.0, 2.5 and 4 μg/ml) and stimulated with phytohemagglutinin (PHA 1.0 or 5.0 μg/ml) for 5 d (37 °C, 5% CO2). The in vitro treatment of peripheral blood mononuclear cells with cypermethrin did not induce apoptosis or necrosis after 5 d in culture. Stimulation by PHA induced cell proliferation (PI = 1.29 ± 1.09 and 2.01 ± 0.62, PHA at 1.0 and 5.0 μg/ml, respectively, mean ± SD) and in vitro exposure to cypermethrin did not alter cellular proliferative response to PHA (PI = 1.80 ± 0.50, 2.60 ± 0.05 and 2.10 ± 1.20 for cypermethrin at 1.0, 2.0 and 4.0 μg/ml, respectively, and PHA at 5.0 μg/ml). In vitro treatment of peripheral blood mononuclear cells with cypermethrin, at the doses tested, does not affect cell viability or proliferation. These findings suggest that the reduction of proliferation observed on lymphocytes derived from individuals occupationally exposed to pesticides may be related to other mechanisms than direct action of cypermethrin on lymphocytes.