The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index.
Lipid metabolism during endurance exercise
Open accessAbstract
Endogenous triacylglycerols represent an important source of fuel for endurance exercise. Triacylglycerol oxidation increases progressively during exercise; the specific rate is determined by energy requirements of working muscles, fatty acid delivery to muscle mitochondria, and the oxidation of other substrates. The catecholamine response to exercise increases lipolysis of adipose tissue triacylglycerols and, presumably, intramuscular triacylglycerols. In addition, increases in adipose tissue and muscle blood flow decrease fatty acid reesterification and facilitate the delivery of released fatty acids to skeletal muscle. Alterations in fatty acid mobilization and the relative use of adipose and intramuscular triacylglycerols during exercise depend, in large part, on degree of fitness and exercise intensity. Compared with untrained persons exercising at the same absolute intensity, persons who have undergone endurance training have greater fat oxidation during exercise without increased lipolysis. Available evidence suggests that the training-induced increase in fat oxidation is due primarily to increased oxidation of non-plasma-derived fatty acids, perhaps from intramuscular triacylglycerol stores. Fat oxidation is lower in high-intensity exercise than in moderate-intensity exercise, in part because of decreased fatty acid delivery to exercising muscles. Parenteral lipid supplementation during high-intensity exercise increases fat oxidation, but the effect of ingesting long-chain or medium-chain triacylglycerols on substrate metabolism during exercise is less clear. This review discusses the relation between fatty acid mobilization and oxidation during exercise and the effect of endurance training, exercise intensity, and lipid supplementation on these responses.
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“Interestingly, due to poor circulation in peripheral adipose tissue and an increased ratio of FA:albumin after exercise, the albumin binding capacity may be surpassed and high levels of unbound serum free fatty acids can create a harmful condition [15].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Once FAs leave the adipocyte they first bind to albumin, which can bind as many as 12 FA molecules [15].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“While FAox fluctuates continuously, the endocrine system is principally responsible for the regulation of lipid oxidation at rest and during exercise [15].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“At exercise intensities <65% VO2max muscle glycogen and IMTG oxidation increase considerably to as much as 50% of energy expenditure, depending on exercise duration [15, 48].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [15]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Lipolytic activity within adipose tissue and intramuscular fat is highly active during moderate-intensity endurance exercise by the action of catecholamines, leading to elevated circulating glycerol levels [134,188].”
From Regulation of Energy Substrate Metabolism in Endurance Exercise (2021) · cites this paper as [134]
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“The exercise-induced catecholamine release stimulates lipolysis, liberating FAs from the glycerol molecule [8, 15].”
From Understanding the factors that effect maximal fat oxidation. (2018) · cites this paper as [15]
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“fat is the most abundant endogenous energy depot that is >60 times the amount stored as glycogen (<3000 kcal) in humans, although this is heavily dependent on adiposity [134]”
From Regulation of Energy Substrate Metabolism in Endurance Exercise (2021) · cites this paper as [134]
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“sustained endurance capacity and the attenuation of glycogen depletion are largely mediated by the metabolism of fat by providing fatty acids (FA) for β-oxidation in the mitochondria [132,133,134].”
From Regulation of Energy Substrate Metabolism in Endurance Exercise (2021) · cites this paper as [134]
In the citing paper
“Exercise training increases mitochondrial content, an adaptation that supports greater ATP production but is paralleled by greater capacity for lipid oxidation (39, 40).”
In the citing paper
“During exercise, skeletal muscle also uses lipid as fuel, which originates from the triglycerides stored in muscle and free fatty acids (FFAs) released from WAT29.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [29]
In the citing paper
“Exerkines are not merely cytokines, however, as hormones, neurotransmitters or metabolites associated with exercise, such as catecholamines40, lactate41 or FFAs29, can also serve as exerkines with endocrine signalling potential42.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [29]
In the citing paper
“Exercise facilitates WAT lipolysis to provide FFA for utilization as fuel29.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [29]
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Metadata
- Authors
- Horowitz, J. F., & Klein, S.
- Affiliations
- Washington University in St. Louis (US)
- Venue
- The American Journal of Clinical Nutrition
- Publisher
- Elsevier BV
- Published
- 2000-08
- Volume
- 72
- Issue
- 2
- Pages
- 558S-563S
- ISSN
- 0002-9165 (ISSN-L)
- OpenAlex
- W2170377446
- Cited by
- 397
- References
- 76
- Citations by year
- 2026: 11 · 2025: 18 · 2024: 17 · 2023: 18 · 2022: 22 · 2021: 24 · 2020: 28 · 2019: 16 · 2018: 18 · 2017: 14 · 2016: 23 · 2015: 22 · 2014: 20 · 2013: 11 · 2012: 14
- FWCI
- 0.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal of Clinical Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p41rr000954-34)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK37948, R01DK037948)
- National Center for Research Resources (RR 00954, RR0036)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- lipid metabolism, endurance exercise, triacylglycerol oxidation, fat oxidation, lipolysis, fatty acid mobilization, adipose tissue, catecholamines, endurance training, exercise intensity, lipid supplementation, medium-chain triglycerides, long-chain triglycerides, skeletal muscle
- MeSH terms
- Adipose Tissue, Exercise Test, Fatty Acids, Humans, Lipolysis, Mitochondria, Physical Endurance, Physical Fitness, Triglycerides, Exercise, Muscle, Skeletal, Dietary Supplements
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