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Postexercise red cell aggregation is negatively correlated with blood lactate rate of disappearance.

In three separate studies, we have observed that the rise in blood lactate during exercise is correlated to blood viscosity and red cell aggregation. Whether these results were related to an effect of blood rheology on lactate production by muscles or on lactate disappearance remains unknown. The modelling of postexercise lactate kinetics allows a fair evaluation of lactate production by muscles (gamma1) and lactate disappearance (gamma2), the latter being easily measurable with simplified protocols. We thus investigated the relationships between pre- and postexercise blood rheology and gamma2. Ten subjects (2 female and 8 males; age 16-45 yr, weight 62-106.5 kg) exhibiting a wide range of gamma2 (from 2 to 7.7x10(-2) min(-1)) underwent a maximal exercise-test with postexercise calculation of gamma2 with the simplified formula gamma2=0.0724+0.755(Lac8-Lac20)/(Lac8.Deltat)-0.00684Lac20 where Lac8 and Lac20 are lactate concentrations 8 and 10 min after exercise stop at the level of VO2max, as previously reported. During exercise whole blood viscosity eta(b) increased (+15%, p<0.01) due to a rise in hematocrit (p<0.05) and plasma viscosity (+0.08+/-0.03 mPa.s, p<0.05), while red cell rigidity was unchanged. Red cell aggregation (Myrenne M1) increased by 11% (p<0.05). Postexercise M1 (measured at VO2max) was the only hemorheologic parameter correlated to gamma2 (r=-0.697, p=0.037). We find once again a statistical relationship between lactate at exercise and red cell aggregation. Microcirculatory adaptations influenced by red cell aggregation may influence lactate disposal (as reflected by gamma2), adding its effect to that of the balance between carbohydrates and fat oxidation which is the major determinant of blood lactate concentrations at exercise in physiological conditions.