A study of lactate metabolism without tracer during passive and active postexercise recovery in humans

Abstract

Tracers have been used extensively to study lactate metabolism in humans during rest and exercise. Nevertheless, quantification of in vivo lactate kinetics as measured by lactate tracers remains controversial and new data are necessary to clarify the issue. The present study has developed a simple kinetic model which does not require labelled molecules and which yields proportional and quantitative information on lactate metabolism in humans during postexercise recovery performed at different levels of intensity. Five subjects took part in six experiments each of which began with the same strenuous exercise (StrEx; 1 min, 385 W, 110 rpm). The StrEx of each session was followed by a different intensity of recovery: passive recovery (PR) and active recoveries (AR) with power outputs of 60, 90, 120, 150 and 180 W, respectively. Blood lactate concentration was measured prior to and immediately after StrEX and regularly during the 1st h of recovery. Oxygen uptake ($\dot VO_2$) was measured every 30 s during the whole session. The results showed that the disappearance rate constant (k_e) increases abruptly from PR [0.080 (SEM 0.004) min⁻¹] to moderate AR [60W: 0.189 (SEM 0.039) min⁻¹] and decreases slowly during more intense AR [180 W: 0.125 (SEM 0.027) min⁻¹]. The lactate apparent clearance (Cl·F⁻¹) was calculated from the area under the lactate concentration-time curve. The Cls·F⁻¹ increased 1.81 (SEM 0.17) fold from PR to moderate AR (60 W) and only 1.31 (SEM 0.14) from PR to the most intense AR (180 W). Using the model, the apparent lactate production (F″K₀) was also calculated. The F″K₀ increased regularly following a slightly curvilinear function of$\dot VO_2$ and was 2.61 (SEM 0.53) fold greater during the most intense AR (180 W) than during PR. Because of the lack of data concerning the size of apparent lactate distribution volume (V _d), the apparent turnover rate (R_bl) has been presented here related toV _d. The R_bl·V ⁻¹_d increased also following a slightly curvilinear function of$\dot VO_2$. The R_bl·V ⁻¹_d was 85.90 (SEM 14.42) μmol·min⁻¹·l⁻¹ during PR and reached 314.09 (SEM 153.95) μmol·min⁻¹·l⁻¹ during the most intense AR (180 W). In conclusion the model presented here does not require labelled molecules and firstly makes it possible to follow the proportional change of apparent lactate clearance and apparent lactate production during active postexercise recovery in comparison with passive recovery conditions and secondly to estimate the blood lactate turnover.