Submitted on December 3, 2007
Accepted on September 29, 2008
Effects of high-intensity training on muscle lactate transporters and post-exercise recovery of muscle lactate and hydrogen ions in women
David J. Bishop1*, Johann Edge2, Claire THOMAS3, and Jacques Mercier4
1 Facolta di Scienze Motorie, Universita di Verona, via Casorati 43, VERONA, I-37131, Italy; School of 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; School of Human Movement and Exercise Science, University of Western Australia, Crawley, Western Australia, Australia
3 UFR Medicine, EA701, Universite Montpellier 1, Montpellier, France; Universite Evry Val d'Essonne, UFR Sciences Fondamentales et Appliquees, Evry, France
4 UFR Medicine, EA701, Universite Montpellier 1, Montpellier, France; INSERM, ERI 25, Montpellier, France
* To whom correspondence should be addressed. E-mail: David.Bishop{at}univr.it.
The purpose of this study was to investigate the effects of high-intensity interval training (3 d/wk for 5 wk), provoking large changes in muscle lactate and pH, on changes in intracellular buffer capacity (
min-vitro), monocarboxylate transporters (MCTs), and the decrease in muscle lactate and hydrogen ions (H+), after-exercise, in women. Pre and post training, biopsies of the vastus lateralis were obtained at rest, immediately after, and 60 s following 45 s of exercise at 190% of VO2max. Muscle samples were analysed for ATP, PCr, lactate and H+; MCT1 and MCT4 relative abundance and min-vitro were also determined in resting muscle only. Training provoked a large decrease in after-exercise muscle pH (pH=6.81). Following training, there was a significant decrease in min-vitro (-11%) and no significant change in either MCT1 (96 ± 12 %) or MCT4 relative abundance (120 ± 21%). During the 60-s recovery after exercise, training was associated with no change in the decrease in muscle lactate, a significantly smaller decrease in muscle H+ and increased PCr resynthesis. These results suggest that increases in Bmin-vitro and MCT relative abundance are not linked to the degree of muscle lactate and H+ accumulation during training. Furthermore, training that is too intense may actually lead to decreases in min-vitro. The smaller post-exercise decrease in muscle H+ folowing training is a further novel finding and suggests that training that results in a decrease in H+ accumulation and an increase in PCr resynthesis can actually reduce the decrease in muscle H+ following supra-maximal exercise.
