Modelling of Blood Lactate Time-Courses During Exercise and/or the Subsequent Recovery: Limitations and Few Perspectives.

Because lactate is an important metabolic intermediate and a signalling molecule between/within cells/organs, it appears essential to be able to describe the kinetics of this central molecule, during and/or after physical exercise. The present study aimed to confront three models and their approaches [Freund and co-workers (F&co), Beneke and co-workers (B&co), and Quittmann and co-workers (Q&co)] to investigate the lactate exchange (γ1) and removal (γ2) abilities (min-1) during and/or after exercise. Nine healthy male subjects performed 3- and 6-min easy, moderate, and heavy exercise. Blood lactate concentration (BLC) was measured every 5 s over the entire period of exercise and recovery. Approaches differ depending on the domain in which the model is applied: considering exercise and part of the recovery (B&co and Q&co) or the entire period of recovery (F&co). The different approaches result in differing γ1 and γ2 values. Model fitting is closer to the experimental values following the method (model and approach) of F&co. Complementary analyses show that consideration of (i) exercise drastically impairs the quality of model fitting and therefore the γ1 and γ2 values and (ii) the entire period of recovery considerably improves the quality of fits and therefore of the γ1 and γ2 values. We conclude that (i) it is neither realistic nor reliable to take into account exercise and recovery in the same model and (ii) the longer the period of recovery studied, the better the quality of the γ1 and γ2 values.

Preventive measures for the critical postexercise period in sickle cell trait and disease.

The immediate postexercise/physical activity period is critical for sickle cell trait (SCT) carriers and disease (SCD) patients. Exercise-related blood acidosis is known to trigger the cascade of HbS deoxygenation and polymerization, leading to red blood cell sickling and subsequent complications. Unfortunately, two facts worsen exercise-related blood acidosis during the initial postexercise period: First, blood lactate and H+ concentrations continue to increase for several minutes after exercise completion, exacerbating blood acidosis. Second, blood lactate concentration remains elevated and pH altered for 20-45 min during inactivity after intense exercise, keeping acid/base balance disturbed for a long period after exercise. Therefore, the risk of complications (including vasoocclusive crises and even sudden death) persists and even worsens several minutes after intense exercise completion in SCT carriers or SCD patients. Light physical activity following intense exercise (namely, active recovery) may, by accelerating lactate removal and acid/base balance restoration, reduce the risk of complications. Scientific evidence suggests that light exercise at or below the first lactate threshold is an appropriate strategy.

Lactate recovery kinetics in response to high-intensity exercises.

PURPOSE: The aim of this study was to investigate lactate recovery kinetics after high-intensity exercises. METHODS: Six competitive middle-distance runners performed 500-, 1000-, and 1500-m trials at 90 % of their current maximal speed over 1500 m. Each event was followed by a passive recovery to obtain blood lactate recovery curves (BLRC). BLRC were fitted by the bi-exponential time function: La(t) = La(0) + A 1(1-e (-γ1t) ) + A 2(1-e (-γ2t) ), where La(0) is the blood lactate concentration at exercise completion, and γ 1 and γ 2 enlighten the lactate exchange ability between the previously active muscles and the blood and the overall lactate removal ability, respectively. Applications of the model provided parameters related to lactate release, removal and accumulation rates at exercise completion, and net amount of lactate released during recovery. RESULTS: The increase of running distance was accompanied by (1) a continuous decrease in γ 1 (p < 0.05), (2) a primary decrease (p < 0.05) and then a stabilization of γ 2, and (3) a constant increase in blood concentrations (p < 0.05) and whole body accumulation of lactate (p < 0.05). Estimated net lactate release, removal and accumulation rates at exercise completion, as well as the net amount of lactate released during recovery were not significantly altered by distance. CONCLUSION: Alterations of lactate exchange and removal abilities have presumably been compensated by an increase in muscle-to-blood lactate gradient and blood lactate concentrations, respectively, so that estimated lactate release, removal and accumulation rates remained almost stable as distance increased.

Muscle MCT4 Content Is Correlated with the Lactate Removal Ability during Recovery Following All-Out Supramaximal Exercise in Highly-Trained Rowers.

The purpose of this study was to test if the lactate exchange (γ1) and removal (γ2) abilities during recovery following short all-out supramaximal exercise correlate with the muscle content of MCT1 and MCT4, the two isoforms of the monocarboxylate transporters family involved in lactate and H(+) co-transport in skeletal muscle. Eighteen lightweight rowers completed a 3-min all-out exercise on rowing ergometer. Blood lactate samples were collected during the subsequent passive recovery to assess an individual blood lactate curve (IBLC). IBLC were fitted to the bi-exponential time function: La(t) = [La](0) + A1(1 - [Formula: see text]) + A2(1 - [Formula: see text]) where [La](0) is the blood lactate concentration at exercise completion and the velocity constants γ1 and γ2 denote the lactate exchange and removal abilities, respectively. An application of the bi-compartmental model of lactate distribution space allowed estimation of the lactate removal rate at exercise completion [LRR(0)]. Biopsy of the right vastus lateralis was taken at rest to measure muscle MCT1 and MCT4 content. Fiber type distribution, activity of key enzymes and capillary density (CD) were also assessed. γ1 was correlated with [La](0) (r = -0.54, P < 0.05) but not with MCT1, MCT4 or CD. γ2 and LRR(0) were correlated with MCT4 (r = 0.63, P < 0.01 and r = 0.73, P < 0.001, respectively) but not with MCT1 or cytochrome c oxidase activity. These findings suggest that the lactate exchange ability is highly dependent on the milieu so that the importance of the muscle MCT1 and MCT4 content in γ1 was hidden in the present study. Our results also suggest that during recovery following all-out supramaximal exercise in well-trained rowers, MCT4 might play a significant role in the distribution and delivery of lactate for its subsequent removal.