Abstract

The optimal hematocrit (Hct opt) hypothesis was tested by altering Hct (and arterial blood oxygen content, Ca O 2 ) between extreme states of anemia and polycythemia (Hct = 8–55%) in the rainbow trout. Since blood viscosity (η) effects on cardiac output (Q̇) and O 2 transport (Ṫ O 2 ) are likely to be greatest when O 2 demand and Q̇ are maximal, we challenged fish to swim to their critical swimming velocity (U crit) in a swim-tunnel respirometer at 13°C and measured maximal oxygen uptake (V̇ O 2max ), maximum Q̇(Q̇ max), and other cardiovascular variables. In addition, experimental temperature was lowered to 5°C to increase η. Consistent with the Hct opt hypothesis, the decreased Ca O 2 in anemic (Hct < 22%) fish caused significant reductions in U crit and V̇ O 2max . In contradiction to the Hct opt hypothesis, and despite an exponential relationship between η and Hct, maximal Ṫ O 2 (Ṫ O 2max ) and U crit increased with polycythemia up to Hct 55%. Although there was a peak for V̇ O 2max , it occurred at an Hct (42%) well above the normocythemic range (23–33%). These results clearly demonstrate that η 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.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call