Adrenergic control of post‐exercise metabolism
Abstract
After strenuous exercise there is a sustained increase in resting O 2 consumption. The magnitude and duration of the excess post‐exercise O 2 consumption (EPOC) is a function of exercise intensity and exercise duration. Some of the mechanisms underlying the rapid EPOC component (<1 h) are well defined, while the mechanisms causing the prolonged EPOC component (>1 h) are not fully understood. It has been suggested that β‐adrenergic stimulation is of importance for the prolonged component. There is an increased level of plasma adrenaline and noradrenaline during exercise, and it is shown that catecholamines stimulate energy expenditure through β‐adrenoceptors. After exercise an increased fat oxidation and an increased rate of triglyceride fatty acid (TG–FA) cycling may account for a significant part of the prolonged EPOC component. These processes may be stimulated by catecholamines. However, the return of plasma concentration of catecholamines to resting levels after exercise is more rapid than the return of O 2 uptake. But plasma concentration of catecholamines may be an insensitive indicator of sympathetic activity, since the clearance rate of catecholamines is high. Also, the sensitivity to catecholamines may be increased after exercise. A decreased post‐exercise O 2 uptake has been shown when β‐blockade is administered in dogs before the exercise bout. In a pilot study in humans, administration of β‐antagonist after exercise did not seem to change EPOC.
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The delayed component of EPOC is related to elevated lipid metabolism during the recovery period, and the sympathetic nervous system (SNS) and catecholamine act as key regulators.
“The delayed component of EPOC is related to elevated lipid metabolism during the recovery period, and the sympathetic nervous system (SNS) and catecholamine act as key regulators [7].”
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- Authors
- BØRSHEIM, E., KNARDAHL, S., HØSTMARK, A. T., & BAHR, R.
- Affiliations
- National Institute of Occupational Health (NO)
- University of Oslo (NO)
- Corresponding author
- BØRSHEIM, E.
- Venue
- Acta Physiologica Scandinavica
- Publisher
- Wiley
- Published
- 1998-02
- Volume
- 162
- Issue
- 3
- Pages
- 313-323
- ISSN
- 0001-6772 (ISSN-L)
- 1365-201X
- OpenAlex
- W2000225993
- Cited by
- 49
- References
- 78
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 1
- FWCI
- 0.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Acta Physiologica Scandinavica (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, beta-adrenergic stimulation, catecholamines, epinephrine, norepinephrine, fat oxidation, energy expenditure, sympathetic activity, beta-adrenergic blockade, post-exercise metabolism
- MeSH terms
- Animals, Energy Metabolism, Physical Exertion, Humans, Receptors, Adrenergic, Sympathetic Nervous System, Muscle, Skeletal
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