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Metabolic bases of excess post-exercise oxygen consumption: a review
Abstract
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 O2 consumption in excess of resting that occurs after exercise. The O2 debt 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 initial, fast ("alactacid"), and second, slow ("lactacid"), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2 consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2 debt 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 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 O2 consumption. 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 "O2 debt" 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.
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“however, numerous studies have demonstrated a dissociation between them [36].”
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“Lactate may explain, together with an increase in body temperature and the triacylglycerol cycle, only the short term component of EPOC [10,45].”
From High-Intensity Interval Resistance Training (HIRT) influences resting energy expenditure and respiratory ratio in non-dieting individuals (2012) · cites this paper as [10]
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Trindade, C. D. Z., Schneider, C. D., Zacca, R., Monteiro, S. B., Fernandes, R. J., & Castro, F. A. D. S. (2026) · Physiologia · doi:10.3390/physiologia6020024
“EPOC is influenced by several mechanisms, including phos-phocreatine resynthesis, the thermogenic effect of elevated body temperature, increased circulating catecholamines and lactate clearance, highlighting its multifactorial metabolic origin [1].”
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“It should be noted that the term “oxygen debt” implies a causal mechanism underlying the increase in metabolic rate post-exercise; “EPOC” avoids such confusion (Gaesser and Brooks, 1984).”
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Metadata
- Authors
- GAESSER, G. A., & BROOKS, G. A.
- Affiliations
- University of California, Los Angeles (US)
- Venue
- Medicine & Science in Sports & Exercise
- Published
- 1984-01
- Volume
- 16
- Issue
- 1
- Pages
- 29???43
- ISSN
- 0195-9131 (ISSN-L)
- OpenAlex
- W1976154872
- Cited by
- 529
- References
- 0
- Citations by year
- 2026: 14 · 2025: 14 · 2024: 24 · 2023: 19 · 2022: 12 · 2021: 16 · 2020: 16 · 2019: 19 · 2018: 16 · 2017: 13 · 2016: 24 · 2015: 17 · 2014: 14 · 2013: 21 · 2012: 22
- FWCI
- 14.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Medicine & Science in Sports & Exercise (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- excess post-exercise oxygen consumption, oxygen debt, lactate oxidation, mitochondrial oxygen consumption, post-exercise recovery, catecholamines, thyroxine, glucocorticoids, fatty acids, calcium, body temperature, energy metabolism
- MeSH terms
- Amphibians, Anaerobiosis, Animals, Carbon, Physical Exertion, Glycogen, Humans, Lactates, Metabolism, Mitochondria, Oxygen Consumption, Lactic Acid
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