Nc. Gonzalez et al., EFFECT OF HEMATOCRIT ON SYSTEMIC O-2 TRANSPORT IN HYPOXIC AND NORMOXIC EXERCISE IN RATS, Journal of applied physiology, 77(3), 1994, pp. 1341-1348
The effect of hematocrit (Hct) on O-2 transport in hypoxic [inspired P
o-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). Isov
olumic exchange transfusion of plasma or red blood cells was used to l
ower Hct in A rats from similar to 60 to 45% and to raise Hct of NA ra
ts from 45 to 60%. Controls were A and NA rats exchange transfused wit
h whole blood at constant Hct. Lowering Hct of A rats lowered the arte
rial O-2 concentration (Ca-O2) and the arterial-mixed venous O-2 diffe
rence 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, ci
rculatory 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 significantl
y, both in hypoxia and normoxia, because of relatively small changes i
n Qmax. In NA rats, a steeper slope of the line relating VO2max to cal
culated mean capillary PO2 at high Hct suggested a higher tissue O-2 d
iffusing capacity with high Hct. For a given Hct and Qmax, systemic ar
terial pressure was higher in A rats. The data suggest that 1) the eff
ect of Hct on systemic hemodynamics is different in A and NA rats, res
ulting in different effects on VO2max, 2) factors in addition to Hct c
ontribute to the high systemic vascular resistance of A rats; and 3) i
ncreased diffusive conductance for O-2, as well as increased TO2max, c
ould be responsible for the effect of Hct on VO2max of NA rats.