This study examined the effects of different pressure threshold inspiratory loads on lactate clearance and plasma acid–base balance during recovery from maximal exercise.
Eight moderately trained males (V˙O2peak = 4.29 ± 0.46 L·min−1) performed, on different days, four maximal incremental cycling tests (power started at 0 W and increased by 20 W·min−1) of identical duration (exercise time during the first trial was 16.32 ± 1.12 min). During 20-min recovery, subjects either rested passively or breathed through a constant pressure threshold inspiratory load of 10 (ITL10), 15 (ITL15), or 20 (ITL20) cm H2O. Plasma lactate concentration ([La−]) was measured, and acid–base balance was quantified using the physicochemical approach, which describes the dependency of [H+] on the three independent variables: strong ion difference ([Na+] + [K+] − [Cl−] + [La−]), the total concentration of weak acids, and the partial pressure of carbon dioxide.
Peak exercise responses were not significantly different between trials. During recovery, the area under the plasma [La−] curve was not different between trials (pooled mean = 261 ± 60 mEq) and the [La−] measured at the end of the 20-min recovery was also similar (passive recovery = 9.2 ± 3.1 mEq·L−1, ITL10 = 9.3 ± 3.1 mEq·L−1, ITL15 = 8.7 ± 2.8 mEq·L−1, ITL20 = 8.7 ± 3.2 mEq·L−1). Similarly, changes in other strong ions contributing to strong ion difference and total concentration of weak acids, partial pressure of carbon dioxide, and, therefore, [H+] were not different between trials.
These data suggest that, in individuals of moderate endurance training status, inspiratory loading at the intensities used in the present study does not accelerate lactate clearance or modify plasma acid–base balance during recovery from maximal exercise.
1Sport, Health and Performance Enhancement Research Group, School of Science and Technology, Nottingham Trent University, Clifton, Nottingham, UNITED KINGDOM; 2Division of Nutritional Sciences, School of Biosciences, Sutton Bonington Campus, The University of Nottingham, Leicestershire, UNITED KINGDOM; 3Department of Gene Therapy, National Heart and Lung Institute, Imperial College London, London, UNITED KINGDOM; and 4School of Life Sciences, Northumbria University, Newcastle upon Tyne, UNITED KINGDOM
Address for correspondence: Michael A. Johnson, Ph.D., Sport, Health and Performance Enhancement Research Group, School of Science and Technology, Nottingham Trent University, Clifton Lane, Clifton, Nottingham NG11 8NS, United Kingdom; E-mail: Michael.firstname.lastname@example.org.
Submitted for publication July 2011.
Accepted for publication November 2011.