Hematocrit in oxygen transport and swimming in rainbow trout (Oncorhynchus mykiss)

The optimal hematocrit (Hct(opt)) hypothesis was tested by altering Hct (and arterial blood oxygen content, Ca-O2) between extreme states of anemia and polycythemia (Hct = 8-55%) in the rainbow trout. Since blood viscosity (eta) effects on cardiac output (Q) and O-2 transport (T-O2) are likely to be greatest when O-2 demand and Q are maximal, we challenged fish to swim to their critical swimming velocity (U-crit) in a swim-tunnel respirometer at 13 degrees C and measured maximal oxygen uptake (V-O2max), maximum Q(Q(max)), and other cardiovascular variables. In addition, experimental temperature was lowered to 5 degrees C to increase eta. Consistent with the Hct(opt) hypothesis, the decreased Ca-O2 in anemic(Hct < 22%) fish caused significant reductions in U-crit and V-O2max. In contradiction to the Hct(opt) hypothesis, and despite an exponential relationship between eta and Hct, maximal T-O2 (T-O2max) and U-crit increased with polycythemia up to Hct 55%. Although there was a peak for V-O2max, it occurred at an Hct (42%) well above the normocythemic range (23-33%). These results clearly demonstrate that eta is not significant in setting normocythemia in rainbow trout. The novel finding of an Hct-dependent relationship for exercise-induced arterial hypoxemia may be indicative of a diffusion limitation to normocythemia. We suggest that factors involved in setting normocythemia in vertebrates should include diffusion limitations to oxygen transfer in addition to blood viscosity and oxygen transport constraints.