Camila Oliveira de Souza

Brazilian Jiu-Jitsu Simulated Competition Part II: Physical Performance, Time-Motion, Technical-Tactical Analyses, and Perceptual Responses.

Abstract Andreato, LV, Julio, UF, Gonçalves Panissa, VL, Del Conti Esteves, JV, Hardt, F, Franzói de Moraes, SM, Oliveira de Souza, C, and Franchini, E. Brazilian jiu-jitsu simulated competition part II: Physical performance, time-motion, technical-tactical analyses, and perceptual responses. J Strength Cond Res 29(7): 2015–2025, 2015—The aim of this study was to analyze performance, time structure, technical actions, and perceptual responses in Brazilian jiu-jitsu athletes during a simulated competition. For this purpose, 10 athletes were analyzed in a simulated competition (4 matches of 10 minutes). Physical tests and scales of the perception of effort and recovery were applied. The matches were recorded for the purpose of technical-tactical analysis and to determine the time structure. The main results show that in the simulated competition, reaction time (F 2.5,17.6 = 2.7; p = 0.087; &eegr; 2 = 0.28) and flexibility (F 7,63 = 1.5; p = 0.172; &eegr; 2 = 0.15) were unchanged across the matches. An analysis of variance showed a significant difference for grip endurance using the kimono (F 2.0,15.9 = 8.1; p = 0.004; &eegr; 2 = 0.50), which was not confirmed by the Bonferroni test. Jump height indicated postactivation potentiation after match 2 (F 7,63 = 3.5; p = 0.003; &eegr; 2 = 0.28). The maximal isometric handgrip strength in the dominant hand (F 3.2,28.6 = 2.9; p = 0.049; &eegr; 2 = 0.24) and in the nondominant hand (F 7,63 = 3.8; p = 0.002; &eegr; 2 = 0.30) showed a decline after matches 3 and 4. Although these data indicate the onset of fatigue, the effort/pause ratio of the matches was not altered (F 3,12 = 0.6; p = 0.624; &eegr; 2 = 0.13). The perceptions of effort (F 3,27 = 0.9; p = 0.469; &eegr; 2 = 0.09) and recovery (F 1.9,17.0 = 2.4; p = 0.125; &eegr; 2 = 0.21) and the degree of fatigue reported (F 1.5,13.8 = 0.5; p = 0.588; &eegr; 2 = 0.05) did not change during the simulated competition. Thus, it may be concluded that the execution of successive matches causes a decline in maximal isometric handgrip strength. No changes in the time structure of the matches or in the perceptual responses were observed.

Palmitoleic Acid (N-7) Attenuates the Immunometabolic Disturbances Caused by a High-Fat Diet Independently of PPARα

Palmitoleic acid (PMA) has anti-inflammatory and antidiabetic activities. Here we tested whether these effects of PMA on glucose homeostasis and liver inflammation, in mice fed with high-fat diet (HFD), are PPAR-α dependent. C57BL6 wild-type (WT) and PPAR-α-knockout (KO) mice fed with a standard diet (SD) or HFD for 12 weeks were treated after the 10th week with oleic acid (OLA, 300 mg/kg of b.w.) or PMA 300 mg/kg of b.w. Steatosis induced by HFD was associated with liver inflammation only in the KO mice, as shown by the increased hepatic levels of IL1-beta, IL-12, and TNF-α; however, the HFD increased the expression of TLR4 and decreased the expression of IL1-Ra in both genotypes. Treatment with palmitoleate markedly attenuated the insulin resistance induced by the HFD, increased glucose uptake and incorporation into muscle in vitro, reduced the serum levels of AST in WT mice, decreased the hepatic levels of IL1-beta and IL-12 in KO mice, reduced the expression of TLR-4 and increased the expression of IL-1Ra in WT mice, and reduced the phosphorylation of NF 𝜅B (p65) in the livers of KO mice. We conclude that palmitoleate attenuates diet-induced insulin resistance, liver inflammation, and damage through mechanisms that do not depend on PPAR-α.

Brazilian Jiu-Jitsu Simulated Competition Part I: Metabolic, Hormonal, Cellular Damage, and Heart Rate Responses

Abstract Andreato, LV, Julio, UF, Panissa, VLG, Esteves, JVDC, Hardt, F, de Moraes, SMF, de Souza, CO, and Franchini, E. Brazilian jiu-jitsu simulated competition part I: Metabolic, hormonal, cellular damage, and heart rate responses. J Strength Cond Res 29(9): 2538–2549, 2015—The aim of this study was to analyze physiological responses in Brazilian jiu-jitsu athletes during simulated competition. To this end, 10 athletes (age: 28 ± 4 years, body mass: 81.8 ± 7.4 kg, body fat: 13.0 ± 4.8%, systematic practice: 11 ± 4 years) were analyzed in simulated competition (4 matches of 10 minutes). Blood samples were taken to assess energy demand, hormonal responses, and cell damage. Additionally, the heart rate variability (HRV) response was analyzed. The main results show that in simulated competition, during the last matches, athletes had lower lactate (p < 0.001), epinephrine (p < 0.001), norepinephrine (p < 0.001), and insulin (p = 0.002) concentrations. Increases observed in creatine kinase (p < 0.001), aspartate aminotransferase (p < 0.001), alanine aminotransferase (p = 0.007), and creatinine (p < 0.001) seen, especially, in the last matches are indicative of possible cell damage. The HRV reflected a decrease in the RR medium (average of the normal R-R intervals) (p = 0.001) during the competition. Thus, it is concluded that successive matches from competition generate a gradual decrease of adrenergic and glycolytic activities, which is accompanied by a gradual increase in cell damage markers and decrease in the RR medium of the HRV.

Effect of infliximab on metabolic disorders induced by Walker-256 tumor in rats

BACKGROUND The purpose of this study was to investigate the effect of infliximab, an anti-tumor necrosis factor α (TNFα) monoclonal antibody, on the progression of cachexia and several metabolic parameters affected by the Walker-256 tumor in rats. METHODS Infliximab (0.5 mg/kg) was ip administered, twice a day, beginning at the day in which the Walker-256 tumor cells were inoculated. After 12 days of treatment, the tumor growth, some parameters of cachexia/anorexia, the blood levels of triacylglycerol, glucose, lactate and urea, the peripheral response to insulin and the hepatic glycolysis and gluconeogenesis were investigated. The peripheral response to insulin was evaluated by the insulin tolerance test and the glycolysis and gluconeogenesis in isolated perfused liver. RESULTS The treatment with infliximab did not alter the growth of the Walker-256 tumor, but attenuated (p < 0.05) the reduction of body weight and prevented (p < 0.05) the loss of retroperitoneal adipose tissue induced by the tumor. Moreover, treatment with infliximab tended to minimize the loss of gastrocnemius muscle, the reduction in food intake, the peripheral response to insulin and the liver gluconeogenesis from alanine, as well as the increased blood triacylglycerol, caused by the tumor. In contrast, treatment with infliximab did not attenuate the reduction in hepatic glycolysis and glycemia, nor did it minimize the rise in blood levels of lactate and urea induced by the tumor. CONCLUSION The treatment with infliximab ameliorated some changes associated with cachexia, such as the reduction of adipose tissue and body weight, suggesting that TNFα plays a significant role in mediating these changes induced by the tumor. In addition, infliximab tended to improve or had no effect on other metabolic parameters affected by the Walker-256 tumor, suggesting that other mediators or tumor-related events are involved in these disorders.

Palmitoleic Acid Improves Metabolic Functions in Fatty Liver by PPARα-Dependent AMPK Activation.

Background: Palmitoleic acid, since described as lipokine, increases glucose uptake by modulation of 5′AMP‐activated protein kinase (AMPK), as well as increasing lipolysis by activation of peroxisome proliferator‐activated receptor‐α (PPARα), in adipose tissue. However, in liver, the effects of palmitoleic acid on glucose metabolism and the role of PPARα remain unknown. Objective: To investigate whether palmitoleic acid improved the hepatic insulin sensitivity of obese mice. Methods: C57BL6 and PPARα knockout (KO) mice were fed for 12 weeks with a standard diet (SD) or high‐fat diet (HF), and in the last 2 weeks were treated with oleic or palmitoleic acid. Results: Palmitoleic acid promoted a faster uptake of glucose in the body, associated with higher insulin concentration; however, even when stimulated with insulin, palmitoleic acid did not modulate the insulin pathway (AKT, IRS). Palmitoleic acid increased the phosphorylation of AMPK, upregulated glucokinase and downregulated SREBP‐1. Regarding AMPK downstream, palmitoleic acid increased the production of FGF‐21 and stimulated the expression of PPARα. Palmitoleic acid treatment did not increase AMPK phosphorylation, modulate glucokinase or increase FGF‐21 in liver of PPARα KO mice. Conclusions: In mice fed with a high‐fat diet, palmitoleic acid supplementation stimulated the uptake of glucose in liver through activation of AMPK and FGF‐21, dependent on PPARα. J. Cell. Physiol. 232: 2168–2177, 2017.

Impact of Doxorubicin Treatment on the Physiological Functions of White Adipose Tissue

White adipose tissue (WAT) plays a fundamental role in maintaining energy balance and important endocrine functions. The loss of WAT modifies adipokine secretion and disrupts homeostasis, potentially leading to severe metabolic effects and a reduced quality of life. Doxorubicin is a chemotherapeutic agent used clinically because of its good effectiveness against various types of cancer. However, doxorubicin has deleterious effects in many healthy tissues, including WAT, liver, and skeletal and cardiac muscles. Our objective was to investigate the effects of doxorubicin on white adipocytes through in vivo and in vitro experiments. Doxorubicin reduced the uptake of glucose by retroperitoneal adipocytes and 3T3-L1 cells via the inhibition of AMP-activated protein kinase Thr172 phosphorylation and glucose transporter 4 content. Doxorubicin also reduced the serum level of adiponectin and, to a greater extent, the expression of genes encoding lipogenic (Fas and Acc) and adipogenic factors (Pparg, C/ebpa, and Srebp1c) in retroperitoneal adipose tissue. In addition, doxorubicin inhibited both lipogenesis and lipolysis and reduced the hormone-sensitive lipase and adipose tissue triacylglycerol lipase protein levels. Therefore, our results demonstrate the impact of doxorubicin on WAT. These results are important to understand some side effects observed in patients receiving chemotherapy and should encourage new adjuvant treatments that aim to inhibit these side effects.

Tumor necrosis factor alpha abolished the suppressive effect of insulin on hepatic glucose production and glycogenolysis stimulated by cAMP

BACKGROUND Tumor necrosis factor alpha (TNFα) is implicated in the development of insulin resistance in obesity, type 2 diabetes and cancer. However, its ability to modulate the action of insulin on glycogen catabolism in the liver is controversial. The aim of the present study was to investigate whether TNFα acutely affects the suppression by insulin of hepatic glucose production (HGP) and glycogenolysis stimulated by cyclic adenosine monophosphate (cAMP). METHODS TNFα (10 μg/kg) was injected intravenously to rats and, 1 or 6h later, their livers were subjected to in situ perfusion with cAMP (3 μM), in the presence or absence of physiological (20 μU/mL) or supraphysiological (500 μU/mL) concentrations of insulin. RESULTS The injection of TNFα, 1 or 6h before liver perfusion, had no direct effect on the action of cAMP in stimulating HGP and glycogenolysis. However, when TNFα was injected 1h, but not 6h, before liver perfusion it completely abolished (p<0.05) the suppressive effect of 20 μU/mL insulin on HGP and glycogenolysis stimulated by cAMP. Furthermore, the injection of TNFα 1h or 6h before liver perfusion did not influence the suppression of cAMP-stimulated HGP and glycogenolysis by 500 μU/mL insulin. CONCLUSION TNFα acutely abolished the suppressive effect of physiological, but not supraphysiological, levels of insulin on HGP and glycogenolysis stimulated by cAMP, suggesting an important role of this mechanism to the increased HGP in several pathological states.

Is Palmitoleic Acid a Plausible Nonpharmacological Strategy to Prevent or Control Chronic Metabolic and Inflammatory Disorders

Although dietary fatty acids can modulate metabolic and immune responses, the effects of palmitoleic acid (16:1n-7) remain unclear. Since this monounsaturated fatty acid is described as a lipokine, studies with cell culture and rodent models have suggested it enhances whole body insulin sensitivity, stimulates insulin secretion by β cells, increases hepatic fatty acid oxidation, improves the blood lipid profile, and alters macrophage differentiation. However, human studies report elevated blood levels of palmitoleic acid in people with obesity and metabolic syndrome. These findings might be reflection of the level or activity of stearoyl-CoA desaturase-1, which synthesizes palmitoleate and is enhanced in liver and adipose tissue of obese patients. The aim of this review is to describe the immune-metabolic effects of palmitoleic acid observed in cell culture, animal models, and humans to answer the question of whether palmitoleic acid is a plausible nonpharmacological strategy to prevent, control, or ameliorate chronic metabolic and inflammatory disorders. Despite the beneficial effects observed in cell culture and in animal studies, there are insufficient human intervention studies to fully understand the physiological effects of palmitoleic acid. Therefore, more human-based research is needed to identify whether palmitoleic acid meets the promising therapeutic potential suggested by the preclinical research.

Association between aerobic exercise and rosiglitazone avoided the NAFLD and liver inflammation exacerbated in PPAR-α knockout mice.

Nonalcoholic fatty liver disease (NAFLD) is one of the main liver diseases today, and may progress to steatohepatitis, cirrhosis, and hepatocellular carcinoma. Some studies have shown the beneficial effects of aerobic exercise on reversing NAFLD. To verify whether chronic aerobic exercise improves the insulin resistance, liver inflammation, and steatohepatitis caused by a high fat diet (HF) and whether PPARα is involved in these actions. C57BL6 wild type (WT) and PPAR‐α knockout (KO) mice were fed with a standard diet (SD) or HF during 12 weeks; the HF mice were trained on a treadmill during the last 8 weeks. Serum glucose and insulin tolerances, serum levels of aspartate aminotransferase, hepatic content of triacylglycerol, cytokines, gene expression, and protein expression were evaluated in all animals. Chronic exposure to HF diet increased triacylglycerol accumulation in the liver, leading to NAFLD, increased aminotransferase in the serum, increased peripheral insulin resistance, and higher adiposity index. Exercise reduced all these parameters in both animal genotypes. The liver lipid accumulation was not associated with inflammation; trained KO mice, however, presented a huge inflammatory response that was probably caused by a decrease in PPAR‐γ expression. We conclude that exercise improved the damage caused by a HF independently of PPARα, apparently by a peripheral fatty acid oxidation in the skeletal muscle. We also found that the absence of PPARα together with exercise leads to a decrease in PPAR‐γ and a huge inflammatory response. J. Cell. Physiol. 232: 1008–1019, 2017.

Palmitoleic acid reduces the inflammation in LPS-stimulated macrophages by inhibition of NFκB, independently of PPARs

Palmitoleic acid (PM, 16:1n‐7) has anti‐inflammatory properties that could be linked to higher expression of PPARα, an inhibitor of NFκB. Macrophages play a major role in the pathogenesis of chronic inflammation, however, the effects of PM on macrophages are underexplored. Thus, we aimed to investigate the effects of PM in activated macrophages as well the role of PPARα. Primary macrophages were isolated from C57BL/6 wild type (WT) and PPARα knockout (KO) mice, cultured under standard conditions and exposed to lipopolysaccharides LPS (2.5 μg/ml) and PM 600 μmol/L conjugated with albumin for 24 hours. The stimulation with LPS increased the production of interleukin (IL)‐6 and IL‐1β while PM decreased the production of IL‐6 in WT macrophages. In KO macrophages, LPS increased the production of tumour necrosis factor (TNF)‐α and IL‐6 and PM decreased the production of TNFα. The expression of inflammatory markers such NFκB and IL1β were increased by LPS and decreased by PM in both WT and KO macrophages. PM reduced the expression of MyD88 and caspase‐1 in KO macrophages, and the expression of TLR4 and HIF‐1α in both WT and KO macrophages, although LPS had no effect. CD86, an inflammatory macrophage marker, was reduced by PM independently of genotype. PM increased PPARγ and reduced PPARβ gene expression in macrophages of both genotypes, and increased ACOX‐1 expression in KO macrophages. In conclusion, PM promotes anti‐inflammatory effects in macrophages exposed to LPS through inhibition of inflammasome pathway, which was independent of PPARα, PPARϒ and AMPK, thus the molecular mechanisms of anti‐inflammatory response caused by PM is still unclear.