Submitted on May 26, 2006
Accepted on October 29, 2006
High-intensity exercise acutely decreases the membrane content of MCT1 and MCT4 and buffer capacity in human skeletal muscle
David J Bishop1*, Johann Edge2, Claire THOMAS3, and Jacques Mercier4
1 Human Movement and Exercise Science, University of Western Australia, CRAWLEY, Western Australia, Australia
2 Institute of Food, Nutrition and Human Health, Massey University, Palmerston North, New Zealand
3 Institut de Biologie, Laboratoire de Physiologie EA701, Montpellier, France
4 Service D'exploration De La Respiratoire, Hopital Arnaud De Villeneuve, Montpellier, Italy
* To whom correspondence should be addressed. E-mail: bishop{at}motorie.univr.it.
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 (
min 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 min vitro humans. Six active females volunteered for this study. Biopsies of the vastus lateralis were obtained at rest and immediately after 45 s of exercise at 200% of VO2max. min vitro was determined by titration and MCT relative abundance determined by Western blots. High-intensity exercise was associated with a significant decrease in both MCT1 (-24%) and MCT4 (-26%) and a decrease in min vitro (-11%; 135.4 ± 3.4 to 119.2 ± 1.6 µmol H+.g dm-1.H-1; P<0.05). These
changes were consistently observed in all subjects. In conclusion, a single bout of highintensity exercise decreased both MCT relative abundance and min vitro, suggesting that muscle pH regulation may be impaired by high-intensity exercise. These findings also
indicate the need for careful study design when examining training-induced changes in lactate uptake, MCT expression and min vitro.
