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The purpose of this study is to investigate the effects of alpha-lipoic acid supplementation on redox status, physiological and biochemical parameters in G6PD deficient individuals after acute exercise.
In a randomized double-blind, crossover design, 12 adult volunteers with G6PD deficiency of both sexes will be supplemented with either 600 mg of alpha-lipoic acid (experimental condition - EC) or placebo (control condition - CC) every day for 4 weeks. Before intervention, all participants will be informed about the study protocol, fill a medical history questionnaire and sign an informed consent form. Moreover, measurements of anthropometric characteristics and physiological parameters, as well as a VO2max test will be performed.
Participants will perform 4 trials of exercise (70% VO2max for 45min and 90% till exhaustion) before and after each condition. Blood samples will be collected before, immediately after and 1 hour after exercise. Moreover, measurements of anthropometric characteristics and physiological parameters will be performed before and after each condition. There will be a washout period of at 4 weeks between conditions.
Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Crossover Assignment, Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor), Primary Purpose: Treatment
Alpha-lipoic acid, Placebo
Department of Physical Education & Sport Science of the University of Thessaly
Not yet recruiting
University of Thessaly
Published on BioPortfolio: 2016-10-19T02:38:21-0400
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A nutritional condition produced by a deficiency of FOLIC ACID in the diet. Many plant and animal tissues contain folic acid, abundant in green leafy vegetables, yeast, liver, and mushrooms but destroyed by long-term cooking. Alcohol interferes with its intermediate metabolism and absorption. Folic acid deficiency may develop in long-term anticonvulsant therapy or with use of oral contraceptives. This deficiency causes anemia, macrocytic anemia, and megaloblastic anemia. It is indistinguishable from vitamin B 12 deficiency in peripheral blood and bone marrow findings, but the neurologic lesions seen in B 12 deficiency do not occur. (Merck Manual, 16th ed)
Enzymes that catalyze the exohydrolysis of 1,4-alpha-glucosidic linkages with release of alpha-glucose. Deficiency of alpha-1,4-glucosidase may cause GLYCOGEN STORAGE DISEASE TYPE II.
A 20-carbon branched chain fatty acid. In phytanic acid storage disease (REFSUM DISEASE) this lipid may comprise as much as 30% of the total fatty acids of the plasma. This is due to a phytanic acid alpha-hydroxylase deficiency.
Deficiency of the protease inhibitor ALPHA 1-ANTITRYPSIN, leading primarily to degradation of elastin of the alveolar walls, as well as other structural proteins of a variety of tissues. (From Scriver, Beaudet, Sly, & Valle, The Metabolic and Molecular Bases of Inherited Disease, 7th ed, p4125)