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High-intensity exercise acutely decreases the membrane content of MCT1 and MCT4 and buffer capacity in human skeletal muscle

¹School of Human Movement and Exercise Science, The University of Western Australia, Crawley, Western Australia, Australia; ²EA 701 Muscles et Pathologies Chroniques, Département de Physiologie des Interactions, Faculté de Médecine, Institut de Biologie, Montpellier, France; and ³Laboratoire d'Etude de la Physiologie de l'Exercice, Departement Sciences et Techniques des Activités Physiques et Sportives, Unité de Formation et de Recherche des Sciences Fondamentales et Appliquées, Evry, France

Submitted 26 May 2006 ; accepted in final form 29 October 2006

The regulation of intracellular pH during intense muscle contractions occurs via a number of different transport systems [e.g., monocarboxylate transporters (MCTs)] and via intracellular buffering (m_{in vitro}). The aim of this study was to investigate the effects of an acute bout of high-intensity exercise on both MCT relative abundance and m_{in vitro} in humans. Six active women volunteered for this study. Biopsies of the vastus lateralis were obtained at rest and immediately after 45 s of exercise at 200% of maximum O₂ uptake. m_{in vitro} was determined by titration, and MCT relative abundance was determined in membrane preparations by Western blots. High-intensity exercise was associated with a significant decrease in both MCT1 (–24%) and MCT4 (–26%) and a decrease in m_{in vitro} (–11%; 135 ± 3 to 120 ± 2 µmol H⁺·g dry muscle^–1·pH^–1; P < 0.05). These changes were consistently observed in all subjects, and there was a significant correlation between changes in MCT1 and MCT4 relative abundance (R² = 0.92; P < 0.05). In conclusion, a single bout of high-intensity exercise decreased both MCT relative abundance in membrane preparations and m_{in vitro}. Until the time course of these changes has been established, researchers should consider the possibility that observed training-induced changes in MCT and m_{in vitro} may be influenced by the acute effects of the last exercise bout, if the biopsy is taken soon after the completion of the training program. The implications that these findings have for lactate (and H⁺) transport following acute, exhaustive exercise warrant further investigation.

buffer capacity; lactate transport; hydrogen ions