Most vertebrates utilize supplemental lactate production to support the energetic demands of vigorous, brief exercise. Despite similar patterns of accumulation, there appears to be a trichotomy with regards to lactate processing post-exercise. Most fish retain most of their lactate intramuscularly, using it for in situ glycogen replenishment. Recent evaluation of fish muscle concludes that pyruvate kinase reversal is a probable gluconeogenic pathway. Amphibians and reptiles also utilize lactate as a muscle glyconeogenic substrate, but lactate is not sequestered post-exercise. None of these groups utilize hepatic gluconeogenesis to any significant extent post-exercise, and muscle glucose uptake is limited. Lactate oxidation plays a major role post-exercise in mammals, with hepatic and muscular gluco- and glyconeogenesis contributing to a lesser extent. Glucocorticoids may regulate lactate release from fish muscle, although catecholamines may influence glyconeogenesis in reptile muscle. Insulin affects lactate metabolism indirectly through its effects on muscle glucose metabolism.