An increased blood lactate concentration is common during physiological (exercise) and pathophysiological stress (stress hyperlactataemia). In disease states, there is overwhelming evidence that stress hyperlactataemia is a strong independent predictor of mortality. However, the source, biochemistry, and physiology of exercise-induced and disease-associated stress hyperlactataemia are controversial. The dominant paradigm suggests that an increased lactate concentration is secondary to anaerobic glycolysis induced by tissue hypoperfusion, hypoxia, or both. However, in the past two decades, much evidence has shown that stress hyperlactataemia is actually due to increased aerobic lactate production, with or without decreased lactate clearance. Moreover, this lactate production is associated with and is probably secondary to adrenergic stimulation. Increased lactate production seems to be an evolutionarily preserved protective mechanism, which facilitates bioenergetic efficiency in muscle and other organs and provides necessary substrate for gluconeogenesis. Finally, lactate appears to act like a hormone that modifies the expression of various proteins, which themselves increase the efficiency of energy utilisation and metabolism. Clinicians need to be aware of these advances in our understanding of stress hyperlactataemia to approach patient management according to logical principles. We discuss the new insights and controversies about stress hyperlactataemia.
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