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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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“In addition, EE remains elevated over the early period following endurance exercise due to high metabolic demands, which can be evaluated by the excess post-exercise oxygen consumption (EPOC) (Gaesser and Brooks 1984).”
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“The recovery aspects noted by Kellmann and Kallus (Kell-mann et al., 1999) and the physiological regeneration processes (Drust et al., 2007; Gaesser et al., 1984) provide context for understanding the mood and performance changes observed in our study.”
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BackgroundModeling the Metabolic Energetics of Brief and Intermittent Locomotion in Lizards and Rodents
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BackgroundPopulation variability in thermal performance of pre-spawning adult Chinook salmon
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“Recovery data (%AAS, %MMR, hourly EPOC and cumulative EPOC) were non-independent across time and were analyzed using repeated measures ANOVA.”
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“In an attempt to quantify the amount of oxygen available to restore the homeostasis after WB1, the difference between the measured V̇O2 and the predicted V̇O2 for a given recovery PO was calculated and quantified as EPOC.”
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“It takes into account the individual’s cardiorespiratory fitness, the intensity and the duration of the work load and the duration and effectiveness of the recovery periods during intermittent work [17].”
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“Such elevated physiological variables during downhill riding could also be associated to prior work done during climbing (Macdermid & Stannard, 2012) and its subsequent metabolic effects (Gaesser & Brooks, 1983).”
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“EPOC occurs due to elevated respiratory rate, heart rate, ATP and CP restoration, lactate removal and temperature regulation [43].”
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??1-adrenoreceptors regulate resting metabolic rate
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“Energy from the phosphagen system (E PCR ) was calculated based on the fast component of the excess post-exercise oxygen consumption (EPOC) [27].”
MethodPhysiological and behavioral responses to social isolation and starvation in a social fish
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Relationships between VO2 and blood lactate responses after all-out running exercise
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“Some of the physiologicalmechanisms responsible for early EPOC are well defined, such as replenishments of body O2 stores, adenosine triphosphate (ATP), and creatine phosphate (PCr) utilized during exercise (Knuttgen and Saltin 1972; Gaesser and Brooks 1984).”
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Some aspects of metabolism following a 35 km road run
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Oxygen deficit is not affected by the rate of transition from rest to submaximal exercise
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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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