Variants of the Solute Carrier SLC16A1 Gene (MCT1) Associated With Metabolic Responses During a Long-Graded Test in Road Cyclists

• Autores: Carlos González Haro, María Soledad Soria Aznar, Jorge Vicente Romero, Ana Julia Fanlo, Blanca Sinués Porta, Jesús Fernando Escanero Marcén
• Localización: Journal of strength and conditioning research: the research journal of the NSCA, ISSN 1064-8011, Vol. 29, Nº. 12, 2015, págs. 3494-3505
• Idioma: inglés
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• Resumen

  • Variants of the solute carrier SLC16A1 gene have been associated with alterations in MCT1 expression, because of a lactate (La-) transport deficiency across the cell membrane and a blood La- accumulation. The aim of this study was to associate the allelic and genotypic frequencies of 1470T>A, 2917(1414) C>T, and IVS3-17A>C variants relative to the blood La- kinetics and metabolic responses to a progressive effort until exhaustion. Twenty-five well-trained road cyclists performed a long-graded laboratory test: 10 minutes at 2.0 W·kg-1, first step at 2.5 W·kg-1 with increments of 0.5 W·kg-1 every 10 minutes until exhaustion. Blood La-, nonesterified fatty acids (NEFAS), and glucose levels were measured; fat and carbohydrate oxidation rates were estimated through stoichiometric equations. Three variants of SLC16A1 gene were determined for each subject, which were divided in two groups: wt (wild type)/mt (mutated type) and mt/mt genotype group versus wt/wt genotype group. Metabolic responses were compared between both groups with an unpaired Student's t-test; Friedman and Wilcoxon tests were performed for nonparametric data. The statistical significance was set at p <= 0.05. For 1470TA polymorphism, no significant blood La- differences were found between groups. 2197(1414)C>T allele carriers and IVS3-17A>C carriers showed significantly higher blood La- levels, lower blood NEFAS, and glucose levels at submaximal intensities. These findings open a new perspective to investigate SLC16A1 variants (1470TA and IVS3-17A>C) on La- deficiency transport and its regulation/interaction with other metabolic pathways. Future studies would be needed to clarify whether 1470T>A, 2917(1414)C>T, and IVS3-17A>C allelic/genotypic distribution benefit performance in endurance athletes.