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Interactions Between Monocarboxylate Transporter MCT1 Gene Variants and the Kinetics of Blood Lactate Production and Removal After High-Intensity Efforts: A Cross-Sectional Study

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Author
Maculewicz, Ewelina
Mastalerz, Andrzej
Mroz, Anna
Johne, Monika
Krawczak-Wojcik, Katarzyna
Pabin, Agata
Garbacz, Aleksandra
Komar, Katarzyna
Massidda, Myosotis
Šťastný, PetrORCiD Profile - 0000-0003-2841-374XWoS Profile - S-3467-2016Scopus Profile - 57060625300
Bojarczuk, Aleksandra

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Publication date
2025
Published in
Genes
Publisher / Publication place
Multidisciplinary Digital Publishing Institute (MDPI)
Volume / Issue
16 (10)
ISBN / ISSN
ISSN: 2073-4425
ISBN / ISSN
eISSN: 2073-4425
Funding Information
UK//COOP
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  • Faculty of Physical Education and Sport

This publication has a published version with DOI 10.3390/genes16101160

Abstract
Background/Objectives: Lactate (LA) is a key metabolite in exercise metabolism, transported across cell membranes by monocarboxylate transporters (MCTs). Although genetic variation in MCT genes has been linked to LA kinetics, evidence in athletic populations remains limited. This study investigated nine MCT1 polymorphisms (rs4301628, rs12028967, rs10857983, rs3789592, rs10776763, rs1049434, rs6537765, rs7556664, rs7169) in relation to LA metabolism. Methods: 337 Polish and Czech males (elite athletes, sub-elite competitors, physically active controls) performed two maximal Wingate tests. Buccal swabs were collected for DNA extraction and single nucleotide polymorphism (SNP) genotyping. LA was assessed before and after the tests. Results: Five variants (rs3789592, rs7556664, rs7169, rs1049434, rs6537765) remained significantly associated with LA measured 30 min after the second Wingate (LA30 ') and delta clearance capacity (DCC) in elites (codominant and recessive models: p = 0.01-0.03; false discovery rate (FDR)-adjusted p = 0.02-0.04). Rs10776763 showed the broadest associations, surviving FDR for LA30 ' in all models (p = 0.003-0.03; FDR-adjusted p = 0.01-0.03) and for LA accumulation capacity (ACC) in the recessive model (p = 0.01; FDR-adjusted p = 0.03). Rs12028967 also supported a clearance role, with LA30 ' significant in elites (p = 0.004; FDR-adjusted p = 0.01) and DCC in the overall cohort (p = 0.02; FDR-adjusted p = 0.03). In contrast, rs4301628 and rs10857983 demonstrated isolated LA30 ' effects in elites (p = 0.004-0.01; FDR-adjusted p = 0.01), and no production-phase endpoint other than rs10776763 survived FDR; ACC remained significant in the recessive model (p = 0.01; FDR-adjusted p = 0.03). Conclusions: The results suggest that MCT1 polymorphisms contribute to differences in LA metabolism and warrant replication in larger, more diverse cohorts.
Keywords
MCT1, genotype, lactate kinetics, polymorphisms, Wingate,
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https://hdl.handle.net/20.500.14178/3301
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WOS:001601539800001
SCOPUS:2-s2.0-105020032808
PUBMED:41153377
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