In the amphibian Bufo marinus, progressive hypoxia below a critical PO
2 elicits a transient 50% increase in O-2, consumption that coincides
with the onset of lactate formation. The present study was designed to
test the hypothesis that lactate causes the observed rise in metaboli
c rate. Arterial bolus infusions of pH-neutral sodium lactate solution
s (4 mmol/kg body wt) in toads maintained under hypoxia actually elici
t a similar increase in metabolic rate. The application of adrenergic
antagonists (bretylium tosylate, phentolamine, propranolol, and reserp
ine) inhibits this response, suggesting that catecholamines are involv
ed. Moreover, animals injected with lactate move to a cooler environme
nt (behavioral hypothermia), a behavioral response that is beneficial
during hypoxia. We hypothesize that, in accordance with Cannon's conce
pt of an emergency response, lactate may function as an alarm signal d
uring hypoxia. However, the signal function of lactate is observed in
animals both under hypoxia and under normoxia and should thus be consi
dered in future studies whenever elevated lactate levels are present,
e.g., during and after exercise.