A hypometabolic response during acute exposure to hypoxia has been measured
in both endothermic and ectothermic vertebrates. In the turtle, we determi
ned the metabolic response to normocapnic hypoxia and hypercapnic hypoxia.
In addition, we tested the hypothesis that hypoxic hypometabolism was a reg
ulated response that did not depend on O-2 availability. Metabolic, cardiov
ascular, and blood gas measurements were collected in anesthetized turtles
under two conditions: during normocapnic hypoxia [fractional inspired O-2 F
IO2 = 0.1 and 0.05] and during hypercapnic hypoxia [FIO2 = 0.1 and 0.05 plu
s fractional inspired CO2 (FICO2) = 0.05]. During normoxia, rate of O-2 con
sumption ((V) over dot (O2)) was 0.82 ml.min(-1). kg(-1) and was reduced by
nearly 30% at the lowest FIO2. Normocapnic hypoxia of FIO2 = 0.1 had no si
gnificant effect on (V) over dot (O2). The addition of 5% CO2 to the inspir
ed air did not enhance the effects of hypoxia. Injections of 2,4-dinitrophe
nol increased (V) over dot (O2) during hypercapnic hypoxia in some animals
to levels greater than those measured during normoxia. We conclude that hyp
oxia produces a hypometabolic state in anesthetized turtles, and the pharma
cological stimulation of (V) over dot (O2) counteracts the effects of hypox
ia on metabolism. The hypoxic hypometabolism in turtles most likely represe
nts a regulated response and does not reflect limited O-2 availability at t
he cellular level. Finally, we hypothesize that hypoxemia induced by the ri
ght-to-left cardiac shunt often associated with diving may trigger the deve
lopment of a hypometabolic state and therefore contribute to the prolongati
on of aerobic dive times.