Affiliations: Laboratoire de Pharmacocinétique Clinique, Faculté de Pharmacie, Université Montpellier I, France | Service Central de Physiologie Clinique, Centre d'Exploration et de Réadaptation des Anomalies du Métabolisme Musculaire (CERAMM), CHU Lapeyronie, Montpellier, France
Note: [] Corresponding author: Dr J.F. Brun, MD, PhD, Service Central de Physiologie Clinique, Centre d'Exploration et de Réadaptation des Anomalies du Métabolisme Musculaire (CERAMM), CHU Lapeyronie, 34295 Montpellier‐cédex 5, France. Tel.: +33 04 67 33 82 84; Fax: +33 04 67 33 89 86; Telex: CHR MONTP 480 766 F; E‐mail: [email protected].
Abstract: Blood lactate increases during exercise. Although this increase was classically interpreted as a “Pasteur‐like effect” resulting from anaerobiosis, it is now clear that it mostly results from a shift in the balance of oxidation of substrates in the muscle, with carbohydrate becoming the predominant fuel. However, we have repeatedly observed that the rise in blood lactate during exercise is correlated to blood viscosity and red cell aggregation. More recently we investigated this issue with the modelling of postexercise lactate kinetics, that allows a fair evaluation of lactate production by muscles (γ1) and lactate disappearance (γ2). Postexercise red cell aggregation (Myrenne M1) appears to be correlated to γ2. Thus microcirculatory adaptations influenced by red cell aggregation may influence lactate disposal, adding its effect to that of the balance between carbohydrates and fat. On the other hand, the rise in blood lactate seems to induce some alterations in erythrocyte rheology at exercise. Correlations between its concentrations during exercise and erythrocyte rigidity support the concept that lactate, at least when it rises above the 4 mmol.l−1 threshold impairs red cell deformability. Moreover, it seems that endurance training influences erythrocyte response to lactate. While lactate did not in vitro affect erythrocyte aggregation, it impaired (as expected) erythrocyte deformability in sedentary subjects but it (unexpectedly) improved it in trained subjects. This difference may be due to training‐induced adaptations in erythrocyte metabolism, including transmembrane transfer via monocarboxylate transporters which show marked alterations in this context. This specific training‐induced pattern of response to lactate may provide an alternative explanation to the exercise‐induced arterial hypoxemia that occurs in such athletes.
