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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Numerous studies have demonstrated a dissociation between EPOC and lactate metabolism during recovery.
“however, numerous studies have demonstrated a dissociation between them [36].”
Lactate may explain, together with an increase in body temperature and the triacylglycerol cycle, only the short-term component of EPOC.
“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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“Exhaustive anaerobic exercise results in a depletion of energy and oxygen stores, the disruption of ionic, osmotic and biochemical balances, hypoxemia and acidosis (Gaesser and Brooks, 1984; Wood, 1991; Scarabello et al., 1992; Gale et al., 2011).”
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Scott, C. B., Leighton, B. H., Ahearn, K. J., et al. (2010) · The Journal of Strength and Conditioning Research · doi:10.1519/jsc.0b013e3181c6a128 · Cited by 59 · see citing works
“It is therefore apparent that EPOC after a single bout of resistance training is not dependent on lactate concentrations as aerobic studies have previously concluded (5).”
Misconceptions about Aerobic and Anaerobic Energy Expenditure
Scott, C. B. (2005) · Journal of the International Society of Sports Nutrition · doi:10.1186/1550-2783-2-2-32 · Cited by 59 · see citing works
Metabolic Mechanisms of Vocal Fatigue
Nanjundeswaran, C., VanSwearingen, J. M., & Abbott, K. V. (2016) · Journal of Voice · doi:10.1016/j.jvoice.2016.09.014 · Cited by 59 · see citing works
Body mass, body composition and sleeping metabolic rate before, during and after endurance training
Westerterp, K. R., Meijer, G. A. L., Schoffelen, P. F. M., & Janssen, E. M. E. (1994) · European Journal of Applied Physiology · doi:10.1007/bf01094789 · Cited by 58 · see citing works
Billat, V. L., Mille-Hamard, L., Demarle, A., & Koralsztein, J. P. (2002) · European Journal of Applied Physiology · doi:10.1007/s00421-002-0648-7 · Cited by 58 · see citing works
“…the lactate to glycogen conversion (Gaesser and Brooks 1984), to other phenomena, such as lactate and H+ removal (Sahlin 1992), elevated body temperature, elevated cost of respiration and cardiac work (Gaesser and Brooks 1984), and an increase of catecholamine concentrations (Gladden et al. 1982).”
BackgroundInfluentialExercise and Regulation of Lipid Metabolism
Noland, R. C. (2015) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2015.06.017 · Cited by 59 · see citing works
Burt, D., Lamb, K., Nicholas, C., & Twist, C. (2013) · European Journal of Sport Science · doi:10.1080/17461391.2013.783628 · Cited by 57 · see citing works
“Other mechanisms that contribute to the EPOC include the replenishment of myoglobin and haemoglobin and the resynthesis of adenosine tri-phosphate (ATP) and creatine phosphate (Bahr, 1992; Gaesser & Brooks, 1984).”
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Paoli, A., Moro, T., & Bianco, A. (2015) · Clinical Physiology and Functional Imaging · doi:10.1111/cpf.12136 · Cited by 59 · see citing works
“However, lactate may explain, together with an increase in body temperature (Gaesser & Brooks, 1984), only the short-term component of EPOC; © 2014 Scandinavian Society of Clinical Physiology and Nuclear Medicine.”
BackgroundEffects of menstrual phase on performance and recovery in intense intermittent activity
Middleton, L. E., & Wenger, H. A. (2005) · European Journal of Applied Physiology · doi:10.1007/s00421-005-0073-9 · Cited by 55 · see citing works
“Another portion will reflect the removal of lactate and H+ (Gaesser and Brooks 1984; Sahlin 1992).”
BackgroundInfluentialSmall actions, big costs: the behavioural energetics of a commercially important invertebrate
Robson, A. A., Laurent Chauvaud, A., Wilson, R. P., & Halsey, L. G. (2012) · Journal of The Royal Society Interface · doi:10.1098/rsif.2011.0713 · Cited by 55 · see citing works
Factors influencing excess postexercise oxygen consumption in trained and untrained women
Frey, G. C., Byrnes, W. C., & Mazzeo, R. S. (1993) · Metabolism · doi:10.1016/0026-0495(93)90053-q · Cited by 55 · see citing works
The effects of intensity on the energetics of brief locomotor activity
Baker, E. J., & Gleeson, T. T. (1999) · Journal of Experimental Biology · doi:10.1242/jeb.202.22.3081 · Cited by 54 · see citing works
- 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 › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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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