Acute Effects of L-Arginine Supplementation on Oxygen Consumption Kinetics and Muscle Oxyhemoglobin and Deoxyhemoglobin during Treadmill Running in Male Adults

International Journal of Exercise Science 12(2): 444-455, 2019. L-arginine is used as a nitric oxide related supplement intended to improve sports performance, and to enhance muscular recovery during exercise. However, the literature is inconclusive. The aim of this study was to determine the effects of acute oral L-arginine supplementation on O2 consumption kinetics and local muscle blood volume and oxygenation during treadmill running at two different intensities. Using a double-blind, crossover and placebo-controlled design, 11 young healthy male adults were randomly assigned to 6 g of L-arginine (ARG) or placebo (PLA) supplementation that was ingested 60 min before the exercise test. Tests consisted of treadmill run at two different intensities (5 min each; moderate, 90% of ventilatory threshold, VT; and heavy, 50% of the difference between VT and VO2peak) interspersed by 1-min walking. Respiratory gas exchange variables were measured continuously with an automated metabolic cart. Near infrared spectroscopy (NIRS) was used to continuously monitor muscle oxyhemoglobin and deoxyhemoglobin and total hemoglobin. Blood samples were collected before supplementation and 6 min after exercise. Two-way repeated measures ANOVA did not show differences in plasma nitrite concentrations between ARG or PLA conditions during the running tests. No significant differences were observed between ARG and PLA conditions for O2 kinetics as well as for NIRS variables. ARG supplementation does not improve physiological responses associated with oxygen cost and NIRS variables during running treadmill tests. Hence, our results do not support the use of L-arginine as an ergogenic aid for running performance in young healthy males

Effects of moderate and high intensity isocaloric aerobic training upon microvascular reactivity and myocardial oxidative stress in rats

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Weight loss enhances hepatic antioxidant status in a NAFLD model induced by high fat diet

Purpose. Nonalcoholic fatty liver disease (NAFLD) is a benign condition that can progress to more severe liver damage in a process mediated, in part, by disturbances in redox balance. Additionally, some argue that it is set to become the main cause of end-stage liver disease in the near future. Here, we investigated whether a diet-induced weight loss is able to reverse hepatic lipid accumulation and to reduce oxidative stress in liver from C57BL/6 mice fed a high-fat (HF) diet. Methods and results. Male C57BL/6 mice were divided into four groups: SC (standard chow, 10% energy from fat, 16 wk); HF (high fat diet, 50% energy from fat, 16 wk); SC-HF (SC 8 wk followed by HF 8 wk); and HF-SC (HF 8 wk followed by SC 8 wk). The HF diet during 8 (SC-HF) and 16 weeks (HF) downregulated mRNA levels and protein expression of Nrf2 and endogenous antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase) in the liver, caused liver steatosis, affected liver function markers, increased intra-abdominal and subcutaneous adipose tissue, and induced glucose intolerance and hypercholesterolemia compared to controls (SC). Diet-induced weight loss significantly reduced the intrahepatic lipid accumulation, improved glucose tolerance, and restored both gene and protein expression of the antioxidant enzymes. Conclusion. Our findings suggest that a dietary intervention aimed to induce weight loss may exert protective effects in NAFLD as it can reduce hepatic oxidative stress and intrahepatic lipid accumulation, which can hinder the progression of this condition to more severe states.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Exercise training in doxorubicin-induced heart failure: effects on the L-arginine-NO pathway and vascular reactivity

Heart failure (HF) is the end-stage of cardiovascular disease and is associated with a high incidence of thrombotic events. Nitric oxide (NO) mediates vasodilation and prevents platelet activation, providing an important antithrombotic effect. The aim of this study was to investigate the effects of aerobic training on survival, platelet L-arginine-NO pathway, and vasodilator properties in doxorubicin (DOX)-induced HF. Sprague Dawley rats were randomly assigned to saline/sedentary (SAL/SED), saline/exercise (SAL/EX), DOX/sedentary (DOX/SED), and DOX/exercise (DOX/EX) groups. Four weeks after intraperitoneal DOX injection (1mg/kg(-1)/d(-1); 10 days), shortening fraction in DOX/SED and DOX/EX was significantly reduced. Treadmill exercise was performed during 6 weeks, 5 days/week(-1), 30minutes/day(-1), 50% to 60% of maximum velocity. Survival was higher in DOX/EX (67%) than DOX/SED (33%). No differences were observed in intraplatelet L-arginine transport assessed by incubation with L- [(3)H]-arginine, nor in NOS activity measured by the conversion of L- [(3)H]-arginine into L- [(3)H]-citrulline among the groups. Vasodilation response to acetylcholine was impaired in DOX/SED and DOX/EX; in nitroglycerine, it was limited to DOX/SED. Aerobic training reduced mortality in DOX-induced HF animals and restored vascular smooth muscle relaxation properties. However, it did not ameliorate intraplatelet NO bioavailability and endothelial function during the period studied

1031-1034delTAAC (Leu125Stop): a novel familial <it>UBE3A</it> mutation causing Angelman syndrome in two siblings showing distinct phenotypes

<p>Abstract</p> <p>Background</p> <p>More than 50 mutations in the <it>UBE3A</it> gene (E6-AP ubiquitin protein ligase gene) have been found in Angelman syndrome patients with no deletion, no uniparental disomy, and no imprinting defect.</p> <p>Case Presentation</p> <p>We here describe a novel <it>UBE3A</it> frameshift mutation in two siblings who have inherited it from their asymptomatic mother. Despite carrying the same <it>UBE3A</it> mutation, the proband shows a more severe phenotype whereas his sister shows a milder phenotype presenting the typical AS features.</p> <p>Conclusions</p> <p>We hypothesized that the mutation Leu125Stop causes both severe and milder phenotypes. Potential mechanisms include: i) maybe the proband has an additional problem (genetic or environmental) besides the <it>UBE3A</it> mutation; ii) since the two siblings have different fathers, the <it>UBE3A</it> mutation is interacting with a different genetic variant in the proband that, by itself, does not cause problems but in combination with the <it>UBE3A</it> mutation causes the severe phenotype; iii) this <it>UBE3A</it> mutation alone can cause either typical AS or the severe clinical picture seen in the proband.</p