HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 295/6/R1991    most recent 00863.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Bishop, D. Articles by Mercier, J. Search for Related Content PubMed PubMed Citation Articles by Bishop, D. Articles by Mercier, J.

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