Skeletal muscle insulin resistance: roles of fatty acid metabolism and exercise
Open accessAbstract
The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability of insulin to properly cause glucose uptake into skeletal muscle. Insulin resistance is associated with high levels of stored lipids in skeletal muscle cells. Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells. Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle. Additionally, a single session of aerobic exercise increases glucose uptake by muscle during exercise, increases the ability of insulin to promote glucose uptake, and increases glycogen accumulation after exercise, all of which are important to blood glucose control. There also is some indication that resistance exercise may be effective in preventing insulin resistance. The information provided is intended to help clinicians understand and explain the roles of exercise in reducing insulin resistance.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Exercise upregulates proteins and enzymes that participate in fatty acid oxidation and increases insulin sensitivity and glucose uptake in skeletal muscle.
“exercise is known to upregulate proteins and enzymes that participate in fatty acid oxidation and to increase insulin sensitivity and glucose uptake in SkM [21]”
Contractile activity improves insulin sensitivity for as long as 24 hours after exercise.
“Muscle contraction is known to stimulate translocation of the Glut4 glucose transporter via an insulin-independent mechanism (reviewed elsewhere [79]), but the insulin sensitizing properties of contractile activity are evident up to 24 h post-exercise, indicating that additional mechanisms come into play [84].”
From Intramuscular triacylglycerol and insulin resistance: guilty as charged or wrongly accused? (2010) · cites this paper as [84]
One acute exercise session can fully or almost fully restore insulin-stimulated glucose uptake in muscle of obese humans and rodents.
“Indeed, it is well recognized that even an acute bout of exercise can lead to complete or near-complete reversal of impaired insulin-stimulated glucose uptake into skeletal muscle of obese humans and rodents [84].”
From Intramuscular triacylglycerol and insulin resistance: guilty as charged or wrongly accused? (2010) · cites this paper as [84]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 190 · Cited by 209
Research works printed but not linked: 1
- 52 Turcotte LP, Richter EA, Kiens B. Lipid metabolism in exercise. In: Hargreaves M, ed. Exercise Metabolism . Champaign, IL: Human Kinetics; 1995:99-130.
- Authors
- Turcotte, L. P., & Fisher, J. S.
- Affiliations
- University of Southern California (US)
- Saint Louis University (US)
- Venue
- Physical Therapy
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-11-01
- Volume
- 88
- Issue
- 11
- Pages
- 1279-1296
- ISSN
- 0031-9023 (ISSN-L)
- 1538-6724
- PMC
- PMC2579902
- OpenAlex
- W2127302695
- Cited by
- 209
- References
- 190
- Citations by year
- 2026: 4 · 2025: 13 · 2024: 20 · 2023: 19 · 2022: 13 · 2021: 7 · 2020: 13 · 2019: 9 · 2018: 13 · 2017: 16 · 2016: 11 · 2015: 13 · 2014: 7 · 2013: 9 · 2012: 8
- FWCI
- 0.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Physical Therapy (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r29ar045168-04)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR 45168)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- skeletal muscle insulin resistance, fatty acid metabolism, aerobic exercise training, resistance training, glucose uptake, lipid oxidation, intramyocellular lipid, glycogen accumulation, glycemic control, insulin sensitivity
- MeSH terms
- Diabetes Mellitus, Fatty Acids, Glucose, Humans, Insulin, Insulin Resistance, Lipid Peroxidation, Exercise, Muscle, Skeletal, CD36 Antigens
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review