Moderate-intensity endurance exercise prevents short-term starvation-induced intramyocellular lipid accumulation but not insulin resistance
Metabolism, ISSN: 0026-0495, Vol: 60, Issue: 8, Page: 1051-1057
2011
- 10Citations
- 45Captures
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Metrics Details
- Citations10
- Citation Indexes10
- CrossRef10
- 10
- Captures45
- Readers45
- 45
Article Description
Exercise has the potential to alleviate the resistance to insulin-mediated glucose uptake precipitated by elevated circulating free fatty acids (FFAs) in conditions such as obesity, lipid infusion, and starvation. In this study, 6 lean healthy men underwent two 3-day periods of starvation with either no exercise or daily endurance exercise (80 min d −1 at 50% maximal rate of oxygen consumption) and a 3-day mixed diet without exercise. Insulin sensitivity was determined by intravenous glucose tolerance test, and intramyocellular lipid (IMCL) concentration was measured by 1 H magnetic resonance spectroscopy. In both starvation conditions, fasting plasma FFAs were significantly elevated, whereas plasma glucose and whole-body insulin sensitivity were significantly reduced. Vastus lateralis IMCL to water ratio was significantly elevated after starvation without exercise compared with that after starvation with exercise or that after mixed diet. Intramyocellular lipid to water ratio was not different between starvation with exercise and mixed diet. In healthy lean men, exercise during starvation prevents the accumulation of IMCL yet does not affect the starvation-induced changes in FFAs and insulin sensitivity. Unlike during lipid infusion or obesity-induced insulin resistance, exercise cannot overcome the reduction in insulin action caused by starvation. We propose that carbohydrate availability is a key modulator of the combined effects of exercise and circulating FFAs on insulin sensitivity.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0026049511000059; http://dx.doi.org/10.1016/j.metabol.2011.01.003; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=79960561561&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/21353260; https://linkinghub.elsevier.com/retrieve/pii/S0026049511000059; https://dx.doi.org/10.1016/j.metabol.2011.01.003
Elsevier BV
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