Résumé
Exercise‐induced arterial hypoxemia (EIAH), i.e., a significant drop of O2 arterial partial pressure during sea level exercise, has been shown in both aerobically trained athletes and athletic animal species. The mechanisms potentially involved include ventilation/perfusion inequality and/or pulmonary diffusing capacity limitation. In thoroughbred horses, EIAH is going with pulmonary haemorrhage (EIPH). Stress failure of pulmonary capillaries leading to diffusion limitation has been proposed. Indeed, during intense exercise, the increased cardiac output and blood viscosity combine to rise capillary wall stress. Blood rheology may participate to the increase of
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mismatch and capillary wall stress. High level of hematocrit (Hct) are known to alter blood flow distribution and rise shear stress in pulmonary capillaries. Any change in red blood cells (RBC) deformability may lead to aggregation at low shear rate, in post capillary veinules. There are contrasting data regarding the effects of blood rheology on EIPH in horses, however the large augmentation of hematocrit during exercise may cause vessel wall stress. In humans, greatest increase in hematocrit may participate to EIAH as well as RBC deformability. Today there is no consensus opinion and further studies of blood rheology in athletes is a field of interest.