Gaesser, G. A., & Brooks, G. A. (1984). Metabolic bases of excess post-exercise oxygen consumption: A review. Medicine and Science in Sports and exercise, 16, 29-43.

The classical oxygen debt hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with oxygen consumption in excess of resting that occurs after exercise. The oxygen debt was supposed to represent the oxidation of a minor fraction (20%) of the lactate formed during exercise and the provision of energy to reconvert the remaining 80% of the lactate to glycogen during recovery. Margaria (1933) modified this concept by distinguishing between the initial fast (alactacid) and second slow (lactacid) oxygen debt curve components. The fast phase was the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2-debt was too simplistic. There is a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2. The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a reservoir of carbon, which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2 may be understood in terms of those factors which directly or indirectly influence mitochondrial oxygen consumption. Included among those factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Elevated temperature is perhaps the most important of these.

Implication. As no complete explanation of the post-exercise metabolism exists, the term oxygen debt should be used to describe a set of phenomena during recovery from exercise. Alactacid and lactacid debts should not be used as they suggest mechanisms. Use of alternative terms (e.g., excess post-exercise oxygen consumption - EPOC) and recovery O2 will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.

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