Regulation and limitations to fatty acid oxidation during exercise
Open accessAbstract
Abstract Fatty acids (FAs) as fuel for energy utilization during exercise originate from different sources: FAs transported in the circulation either bound to albumin or as triacylglycerol (TG) carried by very low density lipoproteins and FAs from lipolysis of muscle TG stores. Despite a high rate of energy expenditure during high intensity exercise the total FA oxidation is suppressed to below that observed during moderate intensity exercise. Although this has been known for many years, the mechanisms behind this phenomenon are still not fully elucidated. A failure of adipose tissue to deliver sufficient FAs to exercising muscle has been proposed, but evidence is emerging that factors within the muscle might be of more importance. The high rate of glycolysis during high intensity exercise might be the ‘driving force’ via the increased production of acetyl‐CoA, which in turn is trapped by carnitine. This will lead to decreased availability of free carnitine for long chain FA transport into mitochondria. This review summarizes our present view on how FA metabolism is regulated during exercise with a special focus on the limitations in FA oxidation in the transition from moderate to high intensity exercise in humans.
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FA transport across the muscle cell membrane occurs via transport proteins, mainly CD36.
“Fatty acid transport across the muscle cell membrane occurs via transport proteins, mainly CD36 [24, 25].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Limitations to the rate of FAox appear to be mediated by cellular transport rather than systematic transport of serum FAs from adipose tissue.
“Despite the positive circulatory effects of endurance training, limitations to the rate of FAox appear to be mediated by cellular transport rather than systematic transport of serum FAs from adipose tissue [24].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
FAox is directly influenced by HAD activity in addition to the transport of FAs across the cellular and mitochondrial membranes.
“Fatty acid oxidation is directly influenced by HAD activity [1, 18] in addition to the transport of FAs across the cellular and mitochondrial membranes [24, 37, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
As exercise intensity increases beyond moderate intensity, carnitine can be a limitation of FA substrate utilization due to the buffering of glycolytic acetyl-carnitine during high intensity exercise.
“Therefore, as exercise intensity increases beyond moderate intensity, carnitine can be a limitation of FA substrate utilization due to the buffering of glycolytic acetyl-carnitine during high intensity exercise [24, 37, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
CPT-1 can be a FA transport limitation, ultimately reducing FAox at higher exercise intensities.
“At exercise intensities >75% VO2max, muscle free carnitine concentrations decrease progressively [24] and therefore CPT-1 can be a FA transport limitation, ultimately reducing FAox at higher exercise intensities [24, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
At exercise intensities >75% VO2max, muscle free carnitine concentrations decrease progressively.
“At exercise intensities >75% VO2max, muscle free carnitine concentrations decrease progressively [24] and therefore CPT-1 can be a FA transport limitation, ultimately reducing FAox at higher exercise intensities [24, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
During high intensity exercise, large quantities of acetyl-CoA are produced via fast glycolysis which enter the mitochondrial matrix and supersede TCA cycle utilization.
“During high intensity exercise however, large quantities of acetyl-CoA are also produced via fast glycolysis which enter the mitochondrial matrix and supersede TCA cycle utilization [24, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
CPT-1 concentration, located within the mitochondrial membrane during exercise, appears to be regulated in part by exercise intensity.
“CPT-1 concentration, located within the mitochondrial membrane during exercise appears to be regulated in part by exercise intensity [24, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
FA cellular transport proteins (CD36 and CPT-1) and mitochondrial density (HAD) are likely the limitation of FAox during high intensity exercise.
“Therefore, FA cellular transport proteins (CD36 and CPT-1) [24, 25] and mitochondrial density (HAD) are likely the limitation of FAox during high intensity exercise [42].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Free carnitine is used to buffer excess glycolytic derived acetyl-CoA by forming acetyl-carnitine, and therefore the limited concentration of free carnitine is a rate limiting step in FA transport/oxidation.
“Thus, free carnitine is used to buffer excess glycolytic derived acetyl-CoA by forming acetyl-carnitine [24, 35, 38], and therefore the limited concentration of free carnitine is a rate limiting step in FA transport/oxidation (Fig. 1).”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Exercising at 60% VO2max has been shown to increase CPT-1 concentrations.
“However, exercising at 60% VO2max has been shown to increase CPT-1 concentrations.”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
The abundant fast glycolysis derived acetyl-carnitine concentrations at high exercise intensities directly limits FA-acetyl transport into the mitochondria, limiting FAox potential.
“The result of the abundant fast glycolysis derived acetyl-carnitine concentrations at high exercise intensities directly limits FA-acetyl transport into the mitochondria, limiting FAox potential [24, 37, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
No significant changes in CPT-1 concentrations were observed in subjects exercising at lower exercise intensities (50% VO2max) compared to rest.
“No significant changes in CPT-1 concentrations were observed in subjects exercising at lower exercise intensities (50% VO2max) compared to rest [24].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
The limitations of FAox at higher intensities are due to the vast amount of acetyl-CoA produced by fast glycolysis.
“The limitations of FAox at higher intensities is due to the vast amount of acetyl-CoA produced by fast glycolysis [24, 38].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Carnitine concentrations are a direct limitation of FAox at higher exercise intensities (>65% VO2max) to both IMTG and serum FAox, regardless of mitochondrial enzymatic activity in untrained and moderately trained subjects.
“Additionally, it has also been shown that carnitine concentrations are a direct limitation of FAox (Fig. 1) at higher exercise intensities (>65% VO2max) to both IMTG [24] and serum FAox [38], regardless of mitochondrial enzymatic activity in untrained and moderately trained subjects.”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Efforts to mitigate the limitations of free carnitine on MFO at high exercise intensities have been unsuccessful.
“Interestingly, efforts to mitigate the limitations of free carnitine on MFO at high exercise intensities have been unsuccessful [24].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Exercise intensity has the most profound effect on MFO based on a combination of events including FA transport changes and hormone fluctuation, which can increase lipolytic rate.
“Exercise intensity has the most profound effect on MFO based on a combination of events which include FA transport changes [24, 25] and hormone fluctuation, which can increase lipolytic rate [7].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Although FAox was not measured, increases in muscle carnitine were able to buffer excess acetyl CoA by forming acetylcarnitine and thus increase PDH activity (38%) at 80% VO2max.
“While FAox was not measured, increases in muscle carnitine were able to buffer excess acetyl CoA by forming acetylcarnitine and thus increase pyruvate dehydrogenase (PDH) activity (38%) at 80% VO2max [24].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Exogenous carnitine supplementation increased muscle carnitine by 21% after 4 weeks, but no differences in performance were observed.
“While exogenous carnitine supplementation increased muscle carnitine by 21% after 4 weeks of supplementation, no differences in performance were observed.”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
Increased expression of FAox transport and oxidative cell proteins (CD36, CPT-1, HAD, etc.) that results in increased FAox is a result of exercise intensity.
“The increased expression of FAox transport and oxidative cell proteins (CD36, CPT-1, HAD, etc.) that results in an increase FAox are a result of exercise intensity [24, 49].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
High intensity exercise (>75% VO2max) eclipses the FAox oxidative potential, relying on fast glycolysis, or more specifically PDH, to produce CHO-derived acetyl-CoA for ATP re-synthesis.
“High intensity exercise (>75% VO2max) eclipses the FAox oxidative potential relying on fast glycolysis, or more specifically PDH to produce CHO-derived acetyl-CoA [24] for ATP re-synthesis [35, 67].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [24]
During exercise, the contribution from circulating plasma TG is minimal.
“During exercise, the contribution from circulating plasma TG is minimal [142].”
From Regulation of Energy Substrate Metabolism in Endurance Exercise (2021) · cites this paper as [142]
The oxidation of long chain FA (i.e., FA with >12 carbon atoms) have to be converted to their acylcarnitine form to enter the mitochondria for β-oxidation by a reaction catalysed by carnitine palmitoyltransferase 1 (CPT-1).
“The oxidation of long chain FA (i.e., FA with >12 carbon atoms) have to be converted to their acylcarnitine form to enter the mitochondria for β-oxidation by a reaction catalysed by carnitine palmitoyltransferase 1 (CPT-1) [142].”
From Regulation of Energy Substrate Metabolism in Endurance Exercise (2021) · cites this paper as [142]
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“At exercise intensities >75% VO2max, muscle free carnitine concentrations decrease progressively [24] and therefore CPT-1 can be a FA transport limitation, ultimately reducing FAox at higher exercise intensities [24, 38].”
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Bâcle, A., & Ferreira, T. (2018) · Elsevier eBooks · doi:10.1016/b978-0-12-811297-7.00027-5 · Cited by 2 · see citing works
- Authors
- Jeppesen, J., & Kiens, B.
- Affiliations
- University of Copenhagen (DK)
- ORCID
- Kiens, Bente
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2012-03
- Volume
- 590
- Issue
- 5
- Pages
- 1059-1068
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC3381814
- OpenAlex
- W2130411423
- Cited by
- 151
- References
- 60
- Citations by year
- 2026: 10 · 2025: 8 · 2024: 7 · 2023: 10 · 2022: 6 · 2021: 8 · 2020: 14 · 2019: 16 · 2018: 15 · 2017: 7 · 2016: 11 · 2015: 10 · 2014: 16 · 2013: 11 · 2012: 2
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- fatty acid oxidation, physical activity, high-intensity exercise, moderate-intensity exercise, energy metabolism, triacylglycerol lipolysis, VLDL, L-carnitine, acetyl-CoA, glycolysis
- MeSH terms
- Animals, Fatty Acids, Humans, Mitochondria, Oxidation-Reduction, Exercise, Muscle, Skeletal
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