Seeking the optimal hematocrit: May hemorheological modelling provide a solution?

Jean-Frédéric Brun1, Emmanuelle Varlet-Marie2,3, Marlène Richou1

  • 1U1046 INSERM, UMR 9214 CNRS «Physiopathologie and Médecine Expérimentale du Cœur et des Muscles - PHYMEDEXP», Unité d'Explorations Métaboliques (CERAMM), Université de Montpellier, Département de Physiologie Clinique, Hôpital Lapeyronie CHRU Montpellier, France.

Hematocrit increases during exercise and is usually decreased after regular training. However the interpretation of these facts is ambiguous since hematocrit is both a determinant of oxygen supply and the major determinant of blood viscosity. Classically hematocrit was assumed to impair blood flow, but it has been evidenced to exert a biphasic effect on it. In order to cope with these two apparently opposite effects of hematocrit, hemorheologists have proposed the concept hematocrit/viscosity ratio (h/η). This h/η ratio is related to tissue oxygenation in vascular diseases (eg, POAD) but not in healthy subjects. h/η displays a bell-shaped curve as a function of hematocrit and the hematocrit value corresponding to the maximal h/η can be assumed to be a theoretically optimal hematocrit. We propose to analyse exercise-related alterations in hematocrit according to this theoretical approach, viscosity at high shear rate being reconstructed with Quemada's equation from actual plasma viscosity and red cell rigidity at various hematocrit levels. While theoretical and actual h/η are fairly correlated in athletes both before and after exercise, actual hematocrit is lower at rest and higher after exercise compared to the theoretical one. The main statistic correlate of these discrepancies between actual and predicted hematocrit is red cell rigidity. Submaximal exercise acutely decreases the h/η ratio (despite increasing both hematocrit and viscosity). This change is well predicted by the model and there is a strong correlation between predicted and actual h/η ratio. Endurance training tends to increase h/η and to reduce the discrepancy between predicted and actual hematocrit. Accordingly trained athletes have a higher h/η (both model-predicted and actual) than sedentary subjects, and a lower hematocrit, this lowering being rather correlated to training volume than to fitness improvement. On the whole, this approach suggests that homeostatic "viscoregulation" in athletes results in a fine tuning of h/η which seems to be a closely regulated parameter. Hematocrit alterations in this context are an adaptation involved in this regulation.

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