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Muscle Glucose Metabolism following Exercise in the Rat
Open accessAbstract
Muscle glycogen stores are depleted during exercise and are rapidly repleted during the recovery period. To investigate the mechanism for this phenomenon, untrained male rats were run for 45 min on a motor-driven treadmill and the ability of their muscles to utilize glucose was then assessed during perfusion of their isolated hindquarters. Glucose utilization by the hindquarter was the same in exercised and control rats perfused in the absence of added insulin; however, when insulin (30-40,000 muU/ml) was added to the perfusate, glucose utilization was greater after exercise. Prior exercise lowered both, the concentration of insulin that half-maximally stimulated glucose utilization (exercise, 150 muU/ml; control, 480 muU/ml) and modestly increased its maximum effect. The increase in insulin sensitivity persisted for 4 h following exercise, but was not present after 24 h. The rate-limiting step in glucose utilization enhanced by prior exercise appeared to be glucose transport across the cell membrane, as in neither control nor exercised rats did free glucose accumulate in the muscle cell. Following exercise, the ability of insulin to stimulate the release of lactate into the perfusate was unaltered; however its ability to stimulate the incorporation of [(14)C]glucose into glycogen in certain muscles was enhanced. Thus at a concentration of 75 muU/ml insulin stimulated glycogen synthesis eightfold more in the fast-twitch red fibers of the red gastrocnemius than it did in the same muscle of nonexercised rats. In contrast, insulin only minimally increased glycogen synthesis in the fast-twitch white fibers of the gastrocnemius, which were not glycogen-depleted. The uptake of 2-deoxyglucose by these muscles followed a similar pattern suggesting that glucose transport was also differentially enhanced. Prior exercise did not enhance the ability of insulin to convert glycogen synthase from its glucose-6-phosphate-dependent (D) to its glucose-6-phosphate-independent (1) form. On the other hand, following exercise, insulin prevented a marked decrease in muscle glucose-6-phosphate, which could have diminished synthase activity in situ. The possibility that exercise enhanced the ability of insulin to convert glycogen synthase D to an intermediate form of the enzyme, more sensitive to glucose-6-phosphate, remains to be explored. These results suggest that following exercise, glucose transport and glycogen synthesis in skeletal muscle are enhanced due at least in part to an increase in insulin sensitivity. They also suggest that this increase in insulin sensitivity occurs predominantly in muscle fibers that are deglycogenated during exercise.
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“This was first described in studies showing that treadmill running caused a 2-fold increase in insulin-stimulated glucose uptake when assessed during the post-exercise period using a rat hindlimb perfusion model [76], and then later reproduced in human studies of one-legged exercise [77] and animals models of electrically stimulated muscle contraction [22].”
From Intramuscular triacylglycerol and insulin resistance: guilty as charged or wrongly accused? (2010) · cites this paper as [76]
In the citing paper
“A single bout of muscle contraction increases insulin sensitivity in perfused hindquarters of healthy animals (242, 255, 434) and in the whole body of healthy humans (230, 343).”
From Lack of Exercise Is a Major Cause of Chronic Diseases (2012) · cites this paper as [434]
In the citing paper
“In fact, even a single bout of exercise can enhance insulin-stimulated glucose uptake in whole muscle tissue 103-105 and individual muscle fibers.106, 107”
From Hormonal and Metabolic Changes of Aging and the Influence of Lifestyle Modifications (2021) · cites this paper as [103]
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Self-citation
Metadata
- Authors
- Richter, E. A., Garetto, L. P., Goodman, M. N., & Ruderman, N. B.
- Affiliations
- Boston University (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1982-04-01
- Volume
- 69
- Issue
- 4
- Pages
- 785-793
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC370132
- OpenAlex
- W2101474138
- Cited by
- 510
- References
- 36
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 8 · 2023: 10 · 2022: 10 · 2021: 13 · 2020: 20 · 2019: 15 · 2018: 15 · 2017: 16 · 2016: 20 · 2015: 12 · 2014: 12 · 2013: 7 · 2012: 17
- FWCI
- 6.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Keywords
- muscle glucose metabolism, physical activity, insulin sensitivity, glycogen synthesis, glucose transport, skeletal muscle, glycogen synthase, fast-twitch muscle, hindquarter perfusion, lactate release, glucose-6-phosphate, muscle glycogen depletion, gastrocnemius, treadmill running, 2-deoxyglucose uptake, post-exercise recovery
- MeSH terms
- Animals, Physical Exertion, Glucose, Glycogen, Glycogen Synthase, Insulin, Lactates, Male, Muscles, Perfusion, Rats, Inbred Strains, Time Factors, Rats
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