Abstract-The Palavras-chaves: ciclistas, mountain bike, RAST, testes de corridaResumen-"Validad del RAST para evaluar el rendimiento de potencia anaeróbica en comparación con el test de Wingate en los atletas de ciclismo." El objetivo fue investigar la validad del teste de RAST (Running-based Anaerobic Sprint Test) en evaluar el desempeño de la potencia anaeróbica través del uso del teste de Wingate en ciclistas trenados. Participaron del estudio 10 ciclistas masculinos (28,0±7,3 años) de la modalidad de Mountain bike. Después de la mensuración de las variables antropométricas, la potencia pico (PP), media (PM) y el índice de fatiga (IF) fueron determinados al acaso a partir de dos testes de Wingate y de dos testes de RAST. Fueron utilizados el test t independiente de Student, el análisis de correlación linear de Pearson (r) y el test de Bland-Altman. Los resultados demostraron, contrariamente al IF (33.8±4.6% vs. 37.8±7.9%; r=0.172), diferencias significativas entre el teste de Wingate y el RAST para PP y PM (W.kg-1 e W). Mismo que los valores de correlación de PP e PM (W) tengan sido fortes (0,831 e 0,714, respectivamente), la concordancia
Background: The metabolic syndrome (MetS) is an obesity-associated disorder of pandemic proportions and limited treatment options. Oxidative stress, low-grade inflammation and altered neural autonomic regulation, are important components and drivers of pathogenesis. Galantamine, an acetylcholinesterase inhibitor and a cholinergic drug that is clinically-approved (for Alzheimer's disease) has been implicated in neural cholinergic regulation of inflammation in several conditions characterized with immune and metabolic derangements. Here we examined the effects of galantamine on oxidative stress in parallel with inflammatory and cardio-metabolic parameters in subjects with MetS.Trial Design and Methods: The effects of galantamine treatment, 8 mg daily for 4 weeks or placebo, followed by 16 mg daily for 8 weeks or placebo were studied in randomly assigned subjects with MetS (n = 22 per group) of both genders. Oxidative stress, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase activities, lipid and protein peroxidation, and nitrite levels were analyzed before and at the end of the treatment. In addition, plasma cytokine and adipokine levels, insulin resistance (HOMA-IR) and other relevant cardio-metabolic indices were analyzed. Autonomic regulation was also examined by heart rate variability (HRV) before treatment, and at every 4 weeks of treatment.Results: Galantamine treatment significantly increased antioxidant enzyme activities, including SOD [+1.65 USOD/mg protein, [95% CI 0.39–2.92], P = 0.004] and CAT [+0.93 nmol/mg, [95% CI 0.34–1.51], P = 0.01], decreased lipid peroxidation [thiobarbituric acid reactive substances [log scale 0.72 pmol/mg, [95% CI 0.46–1.07], P = 0.05], and systemic nitrite levels [log scale 0.83 μmol/mg protein, [95% CI 0.57–1.20], P = 0.04] compared with placebo. In addition, galantamine significantly alleviated the inflammatory state and insulin resistance, and decreased the low frequency/high frequency ratio of HRV, following 8 and 12 weeks of drug treatment.Conclusion: Low-dose galantamine alleviates oxidative stress, alongside beneficial anti-inflammatory, and metabolic effects, and modulates neural autonomic regulation in subjects with MetS. These findings are of considerable interest for further studies with the cholinergic drug galantamine to ameliorate MetS.
Endothelial cells are thought to play a central role in the pathogenesis of antiphospholipid syndrome (APS). Omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation has been shown to improve endothelial function in a number of diseases; thus, it could be of high clinical relevance in APS. The aim of this study was to evaluate the efficacy of n-3 PUFA supplementation on endothelial function (primary outcome) of patients with primary APS (PAPS). A 16-week randomized clinical trial was conducted with 22 adult women with PAPS. Patients were randomly assigned (1:1) to receive placebo (PL, n = 11) or n-3 PUFA (ω-3, n = 11) supplementation. Before (pre) and after (post) 16 weeks of the intervention, patients were assessed for endothelial function (peripheral artery tonometry) (primary outcome). Patients were also assessed for systemic markers of endothelial cell activation, inflammatory markers, dietary intake, international normalized ratio (INR), and adverse effects. At post, ω-3 group presented significant increases in endothelial function estimates reactive hyperemia index (RHI) and logarithmic transformation of RHI (LnRHI) when compared with PL (+13 vs. −12%, p = 0.06, ES = 0.9; and +23 vs. −22%, p = 0.02, ES = 1.0). No changes were observed for e-selectin, vascular adhesion molecule-1, and fibrinogen levels (p > 0.05). In addition, ω-3 group showed decreased circulating levels of interleukin-10 (−4 vs. +45%, p = 0.04, ES = −0.9) and tumor necrosis factor (−13 vs. +0.3%, p = 0.04, ES = −0.95) and a tendency toward a lower intercellular adhesion molecule-1 response (+3 vs. +48%, p = 0.1, ES = −0.7) at post when compared with PL. No changes in dietary intake, INR, or self-reported adverse effects were observed. In conclusion, 16 weeks of n-3 PUFA supplementation improved endothelial function in patients with well-controlled PAPS. These results support a role of n-3 PUFA supplementation as an adjuvant therapy in APS. Registered at as NCT01956188.
Fundamento: A obesidade afeta a adolescência, podendo levar à síndrome metabólica (SM) e disfunção endotelial, um marcador precoce de risco cardiovascular. Apesar de a obesidade ser fortemente associada à síndrome da apneia obstrutiva do sono (SAOS), ainda não está claro o papel da SAOS na função endotelial em adolescentes obesos. Objetivo: Investigar se a obesidade durante a adolescência leva à SM e/ou SAOS e causa disfunção endotelial nesses indivíduos. Além disso, estudamos a possível associação dos fatores de risco para SM e do índice de apneia e hipopneia (IAH) com disfunção endotelial. Métodos: Estudamos 20 adolescentes obesos sedentários (AO; 14,2±1,6 anos, 100,9±20,3kg), e 10 adolescentes eutróficos (AE, 15,2±1,2 anos, 54,4±5,3kg) pareados por sexo. Avaliamos os fatores de risco para SM (critérios da Federação Internacional de Diabetes), função vascular (dilatação mediada pelo fluxo, DMF), capacidade funcional (VO 2 pico) e presença de SAOS (IAH > 1 evento/hora, pela polissonografia). Consideramos um p<0,05 como estatisticamente significativo. Resultados: AO apresentaram maior circunferência da cintura (CC), gordura corporal, triglicerídeos, pressão arterial sistólica (PAS) e diastólica (PAD), maiores níveis de LDL e menores HDL e VO 2 pico em comparação a AE. Não houve diferença no IAH entre os grupos. AO apresentaram menor DMF que AE (6,17±2,72 vs. 9,37±2,20%, p=0,005). Observou-se uma associação entre DMF e CC (R=-0,506, p=0,008) e entre DMF e PAS (R=-0,493, p=0,006). Conclusão: Em adolescentes, a obesidade associou-se à SM e causou disfunção endotelial. CC e PAS aumentadas poderiam estar envolvidas nessa alteração. SAOS foi detectada na maioria dos adolescentes independentemente de obesidade.
BackgroundThe increasing prevalence of obesity worldwide impacts childhood and adolescence, and this trend points to a significant growth rate of non‐transmissible chronic diseases in the near future. Endothelial dysfunction is an early marker of cardiovascular risk.ObjectiveTo determine a) whether obese adolescents have endothelial dysfunction and b) whether cardiovascular risk factors and obstructive sleep apnea (OSA) are associated with endothelial dysfunction.MethodsWe studied 20 obese adolescents (OA; median age 14 years, 100.9±20.3 kg), post pubescent, sedentary, not following any special diet or receiving any drug treatment, and compared them with 10 lean adolescents (LA, median age 15 years, 54.4±5.3 kg) paired for sex. Metabolic syndrome risk factors (MetS, International Diabetes Federation), vascular function (flow‐mediated dilation, FMD, and Reactive Hyperemia Index, RHI, by peripheral arterial tonometry, EndoPAT®), functional capacity and OSA using the apnea‐hypopnea index (AHI, polysomnography) were assessed.ResultsThe OA presented higher waist (WC) and cervical circumference, as well as higher proportion of body fat, triglycerides, SBP, DBP, LDL‐c and lower HDL‐c than the LA group. In the OA, 35% presented MetS, which was absent in the LA group. OSA was present in 86.6% of the OA and 50% of LA (AHI>1 event/hour). There was no difference between groups in the AHI, VO2 peak and RHI. The OA presented lower FMD than LA (6.17±2.72 vs. 9.37±2.20%, p=0.005). There was an association between FMD and WC (r=−0.506, p=0.008) and FMD and SBP (r=−0.493, p=0.006).ConclusionOSA was observed in most adolescents, regardless of obesity. OA presented MetS and endothelial dysfunction. Increased WC and SBP seem to be involved in this alteration.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The metabolic syndrome (MetS) is an obesity‐driven disorder with pandemic proportions and limited treatment options. Oxidative stress, low‐grade inflammation and altered autonomic regulation, are important components of MetS pathophysiology. We recently reported that galantamine, an acetylcholinesterase inhibitor and an FDA‐approved drug (for Alzheimer’s disease) alleviates the inflammatory state in MetS subjects. Here we examined the effects of galantamine on oxidative stress in parallel with inflammatory and cardio‐metabolic parameters in subjects with MetS. The effects of galantamine treatment, 8 mg daily for 4 weeks, followed by 16 mg daily for 8 weeks or placebo were studied in randomly assigned subjects with MetS (n=22 per group) of both genders. Oxidative stress, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase activities, lipid and protein peroxidation, and nitrite levels were analyzed before and at the end of the treatment. Plasma cytokine and adipokine levels, insulin resistance (HOMA‐IR) and other relevant cardio‐metabolic indices were also determined. Autonomic regulation was also examined by heart rate variability (HRV) before treatment, and at every 4 weeks of treatment. Galantamine treatment significantly increased antioxidant enzyme activities, including SOD (+1.65 USOD/mg protein, P=0.004) and CAT (+0.93 nmol/mg, P=0.011), decreased lipid peroxidation (thiobarbituric acid reactive substances, −5.45 pmol/mg, P=0.053) and systemic nitrite levels (−0.05 nit/mg protein, P=0.038) compared with placebo. In addition, galantamine significantly alleviated the inflammatory state and insulin resistance, and decreased the low frequency/high frequency ratio of HRV, following 8 and 12 weeks of drug treatment. In conclusion, a low‐dose galantamine treatment alleviates oxidative stress, alongside beneficial anti‐inflammatory, and metabolic effects, and modulates autonomic regulation in subjects with MetS. These findings are of considerable interest for further studies with galantamine to ameliorate MetS pathophysiology.
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