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Cited by 397Muscle metabolism and nutritionCardiovascular and exercise physiologyAdipose Tissue and Metabolism

Lipid metabolism during endurance exercise

Open access
Horowitz, Jeffrey F, Klein, Samuel·2000·The American Journal of Clinical Nutrition
DOI 10.1093/ajcn/72.2.558s
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Abstract

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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Crossref · 10.1093/ajcn/72.2.558s

Cites

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  • 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.

    “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]

    In “Lipid kinetics during rest and exercise” (pp. 1–3), the paper reports an increased fatty-acid-to-albumin ratio in blood leaving subcutaneous adipose tissue at the end of exercise. It says greater *local* fatty-acid concentrations could theoretically overwhelm albumin binding sites and cause harmful increases in unbound fatty acids. It does not establish high unbound levels in systemic serum after exercise, and it frames the harm as a theoretical possibility. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Once FAs leave the adipocyte they first bind to albumin, which can bind as many as 12 FA molecules.

    “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]

    The “Lipid kinetics during rest and exercise” section describes fatty acids released from adipose tissue and reports fatty-acid-to-albumin ratios in blood, supporting albumin binding. It does not say that albumin is the first binding partner or that one albumin molecule can bind as many as 12 fatty acids. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • The endocrine system is principally responsible for the regulation of lipid oxidation at rest and during exercise.

    “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]

    The “Lipid Kinetics During Rest and Exercise” section says hormones regulate adipose-tissue lipolysis at rest and that adrenergic stimulation increases it during exercise. But lipolysis is not the same as lipid oxidation: the Summary describes oxidation during exercise as an integration of neural, hormonal, circulatory, and muscular events. The paper does not establish that the endocrine system is principally responsible for regulating lipid oxidation. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • At exercise intensities <65% VO2max, muscle glycogen and IMTG oxidation increase considerably to as much as 50% of energy expenditure, depending on exercise duration.

    “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]

    The Exercise Intensity section says IMTG use increases with exercise intensity and can approach half of fat oxidized—not half of total energy expenditure. The Lipid Kinetics section says IMTG’s relative contribution to fat oxidation likely declines as exercise duration increases. The paper does not establish the claimed combined contribution of muscle glycogen and IMTG oxidation at intensities below 65% VO₂max. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • 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.

    “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]

    The Lipid Kinetics During Rest and Exercise section reports that adipose-tissue lipolysis rises two- to threefold during mild- or moderate-intensity exercise and is mediated by increased β-adrenergic stimulation. The paper describes catecholamine-driven intramuscular lipolysis as presumptive, not established. It measures glycerol appearance in plasma as an indicator of lipolysis but does not establish the claimed elevation in circulating glycerol concentration. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

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Cites

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Research works printed but not linked: 5

  1. [35]35. Holloszy JO. Effects of exercise on mitochondrial oxygen uptake and respiratory enzyme activity in skeletal muscle. J Biol Chem 1967;242:2278-82.
  2. [52]52. Romijn JA, Coyle EF, Zhang X-J, Sidossis LS, Wolfe RR. Fat oxi- dation is impaired somewhat during high-intensity exercise by lim- ited plasma FFA mobilization. J Appl Physiol 1995;79:1939-45.
  3. [58]58. Robinson IN, Zammit VA. Sensitivity of carnitine acyltransferase I to malonyl-CoA and related compounds with mitochondria from different rat tissues. Biochem J 1982;206:177-9.
  4. [66]66. Welch IM, Bruce C, Hill SE, Read NW. Duodenal and ileal lipid suppresses postprandial blood glucose and insulin responses in man. Clin Sci 1987;72:209-16.
  5. [71]71. Massicotte D, Peronnet F, Brisson GR, Hillaire-Marcel C. Oxida- tion of exogenous medium-chain fatty acids during prolonged exer- cise: comparison with glucose. J Appl Physiol 1992;73:1334-9.

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Related

Authors
Horowitz, J. F., & Klein, S.
Affiliations
Washington University in St. Louis (US)
ORCID
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)
DOI
10.1093/ajcn/72.2.558s
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
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
  • 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
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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