EFFECT OF HEMATOCRIT ON SYSTEMIC O-2 TRANSPORT IN HYPOXIC AND NORMOXIC EXERCISE IN RATS

The effect of hematocrit (Hct) on O-2 transport in hypoxic [inspired Po-2 (PIO2) similar to 70 Torr] and normoxic (PIO2 similar to 145 Torr) exercise was studied in rats acclimatized to 3 wk of PIO2 at similar to 70 Torr (A rats) and in nonacclimatized littermates (NA rats). Isovolumic exchange transfusion of plasma or red blood cells was used to lower Hct in A rats from similar to 60 to 45% and to raise Hct of NA rats from 45 to 60%. Controls were A and NA rats exchange transfused with whole blood at constant Hct. Lowering Hct of A rats lowered the arterial O-2 concentration (Ca-O2) and the arterial-mixed venous O-2 difference and increased the maximal cardiac output (Qmax) without changes in maximal O-2 uptake (Vo(2max)) or in the product of Qmax X Ca-O2, circulatory O-2 convection at maximal exercise (TO2max). Raising Hct in NA rats produced the opposite changes in Ca-O2, arterial-mixed venous O-2 difference, and Qmax, but VO2max and TO2max increased significantly, both in hypoxia and normoxia, because of relatively small changes in Qmax. In NA rats, a steeper slope of the line relating VO2max to calculated mean capillary PO2 at high Hct suggested a higher tissue O-2 diffusing capacity with high Hct. For a given Hct and Qmax, systemic arterial pressure was higher in A rats. The data suggest that 1) the effect of Hct on systemic hemodynamics is different in A and NA rats, resulting in different effects on VO2max, 2) factors in addition to Hct contribute to the high systemic vascular resistance of A rats; and 3) increased diffusive conductance for O-2, as well as increased TO2max, could be responsible for the effect of Hct on VO2max of NA rats.