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EXERCISE AND RESPIRATORY PHYSIOLOGY

Effects of high-intensity training on muscle lactate transporters and postexercise recovery of muscle lactate and hydrogen ions in women

¹School of Human Movement and Exercise Science, The University of Western Australia, Crawley, Western Australia, Australia; ²Facoltà di Scienze Motorie, Università degli Studi di Verona, Verona, Italy; ³Institute of Food, Nutrition, and Human Health, Massey University, Palmerston North, New Zealand; ⁴EA 701, Unité de Formation et de Recherche Médecine, Université Montpellier 1, ⁶Institut National de la Santé et de la Recherche Médicale, ERI 25, Montpellier; and ⁵Université Evry Val d'Essonne, Unité de Formation et de Recherche Sciences Fondamentales et Appliquées, Evry, France

Submitted 3 December 2007 ; accepted in final form 29 September 2008

The purpose of this study was to investigate the effects of high-intensity interval training (3 days/wk for 5 wk), provoking large changes in muscle lactate and pH, on changes in intracellular buffer capacity (βm_{in vitro}), monocarboxylate transporters (MCTs), and the decrease in muscle lactate and hydrogen ions (H⁺) after exercise in women. Before and after training, biopsies of the vastus lateralis were obtained at rest and immediately after and 60 s after 45 s of exercise at 190% of maximal O₂ uptake. Muscle samples were analyzed for ATP, phosphocreatine (PCr), lactate, and H⁺; MCT1 and MCT4 relative abundance and βm_{in vitro} were also determined in resting muscle only. Training provoked a large decrease in postexercise muscle pH (pH 6.81). After training, there was a significant decrease in βm_{in vitro} (–11%) and no significant change in relative abundance of MCT1 (96 ± 12%) or MCT4 (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 βm_{in vitro} and MCT relative abundance are not linked to the degree of muscle lactate and H⁺ accumulation during training. Furthermore, training that is very intense may actually lead to decreases in βm_{in vitro}. The smaller postexercise decrease in muscle H⁺ after 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⁺ during the recovery from supramaximal exercise.

buffer capacity; monocarboxylate transporter 1; monocarboxylate transporter 4; phosphocreatine resynthesis; females