Metabolic bases of excess post-exercise oxygen consumption: A review

The classical “oxygen debt” hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O₂consumption in excess of resting that occurs after exercise. The O₂debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between intial, fast (“alactacid“), and second, slow (“lactacid”), O₂-debt curve components. They hypothesized that the fast phase of the post-exercise O₂consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O₂debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO₂The 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 VO₂may be understood in terms of those factors which directly or indirectly influence mitochondrial O₂consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term “O₂debt” be used to describe a set of phenomena during recovery from exercise. The terms “alactacid debt” and “lactacid debt,” which suggest a mechanism, are inappropriate. 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.