Exercice, entraînement et âge érythrocytaire

Abstract

Cette étude explore l'effet de l'exercice sur l'âge moyen des érythrocytes. Nous avons évalué l'âge des érythrocytes circulants par la mesure de deux sondes reconnues pour varier avec l'âge érythrocytaire, soit la densité des érythrocytes et le rapport des sous-unités de la protéine 4.1. Aucune variation statistiquement significative de ces deux paramètres n'a été constatée en réponse à un exercice physique intense ou à un entraînement physique régulier. La mesure du rapport de la bande 4.1. pourrait donc être intégrée à un panel de sondes du vieillissement érythrocytaire permettant d'évaluer l'âge d'une population de globules rouges. It has long been recognized that an increase in plasma haemoglobin can originate from intravascular haemolysis. Haemolysis could be indicative of erythrocyte (RBC) destruction associated with several pathologies as well as with different sport activities. Indeed, with severe physical exercise, haemolysis could be derived from mechanical disruption of RBCs against blood-vessel walls. Such a mechanical disruption-induced haemolysis triggers erythropoiesis, and foresees and increase in young RBC population with intense physical activity. Several authors have already reported changes in some exercise-associated haematological parameters, changes indicative of an increase in young RBCs. These observations, although supporting the hypothesis of an increased bone marrow stimulation with exercise, are not based on solid probes for assessment of RBC age, and represent a poor image of bone marrow stimulation. In 1979, Sauberman et al described an irreversible aging-induced change in the ratio of 2 RBC cytoskeletal proteins, phosphoproteins 4.1a and 4.1b. These changes were later reported to occur in different pathological conditions (transient erythroblastopenia and haemolytic anemia), with 4.1b prevailing in young RBCs and 4.1a in old RBCs. Using the irreversible change in 4.1a/4.1 total ratio as a probe for RBC age determination, the authors intended to establish standards for 4.1 protein ratio and to assess the exercise-induced variations of that same ratio. A group of healthy male volunteers ( N = 20, age: 20 to 40 yr) were classified according to their training status: a sedentary group ( N = 10; V ˙ O 2 max < 50 ml·min −1 ·kg −1 ), and a trained group ( N = 10; V ˙ O 2 max > 50 ml·min −1 ·kg −1 ). Blood samples were collected on heparin from an antecubital vein before and after a 1 h duration rectangular exercise at 75% of V ˙ O 2 max. Lysed and washed RBC membranes were then submitted to electrophoretic separation, and the 4.1a/4.1 total ratio measured by densitometry after coloration. Density of RBC population was measured on a phtalate ester gradient. The expected dehydration-induced haemoconcentration was confirmed by an increase in leucocytes and platelets counts, while RBC counts remained unchanged. In these conditions, an absence of variation in haematocrit values is indicative of the loss of RBCs. However, encountered RBC losses do not support the previous hypothesis of a preferential elimination of aged RBCs neither of a precocious aging of RBCs induced by exercise and training: no significant change was observed for the mean RBC density and the cytoskeletal 4.1a/4.1 total RBC protein ratio before and after exercise and with training. There is little doubt that physical exercise induces the destruction of a certain number of RBCs against vessel walls. Using the above-described probes, such mechanical destruction appears to be independent of RBC age and is apparently without effect on erythropoietic activity. In an ergogenic perspective, the apparent absence of significant effect of exercise and training on both probes could eventually be of great interest in detecting massive supplementation in in vitro aged RBCs, ie autologous blood doping.