We investigated the effects of vagal reductions in O₂ delivery on oxygen consumption (O₂) in the anesthetized freshwater turtle Trachemys scripta. Specifically, these experiments tested the hypothesis that reductions in arterial oxygen partial pressure (PO₂) and/or systemic oxygen transport (SOT) trigger a metabolic downregulation. During electric stimulation of the efferent branch of the sectioned right vagus nerve (RVEF), systemic cardiac output decreased 60-70%, systemic PO₂ fell by ~30%, and SOT decreased by 60-70%. During RVEF simulation, O₂ dropped ~35%. During control conditions, injection of the metabolic uncoupler 2,4-dinitrophenol (DNP) more than doubled O₂, reflecting an increase in ATP turnover. RVEF stimulation after DNP injection produced similar cardiovascular and blood gas changes as before DNP, but O₂ was higher than the O₂ measured in untreated control animals, indicating that oxygen availability during RVEF stimulation is still sufficient to support O₂ rates that are even higher than resting rates. We conclude that vagal stimulation triggers metabolic downregulation, primarily through the effects on oxygen transport, although the factor(s) that trigger the hypometabolism remain unknown. The PO₂ may still be an important messenger in metabolic control, but our results suggest that changes in SOT to the metabolically active tissues, rather than changes in PO₂ per se, play an important role in triggering hypometabolism in the freshwater turtle.