Document Detail


Exercise training reverses impaired skeletal muscle metabolism induced by artificial selection for low aerobic capacity.
MedLine Citation:
PMID:  21048074     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have used a novel model of genetically imparted endurance exercise capacity and metabolic health to study the genetic and environmental contributions to skeletal muscle glucose and lipid metabolism. We hypothesized that metabolic abnormalities associated with low intrinsic running capacity would be ameliorated by exercise training. Selective breeding for 22 generations resulted in rat models with a fivefold difference in intrinsic aerobic capacity. Low (LCR)- and high (HCR)-capacity runners remained sedentary (SED) or underwent 6 wk of exercise training (EXT). Insulin-stimulated glucose transport, insulin signal transduction, and rates of palmitate oxidation were lower in LCR SED vs. HCR SED (P < 0.05). Decreases in glucose and lipid metabolism were associated with decreased β₂-adrenergic receptor (β₂-AR), and reduced expression of Nur77 target proteins that are critical regulators of muscle glucose and lipid metabolism [uncoupling protein-3 (UCP3), fatty acid transporter (FAT)/CD36; P < 0.01 and P < 0.05, respectively]. EXT reversed the impairments to glucose and lipid metabolism observed in the skeletal muscle of LCR, while increasing the expression of β₂-AR, Nur77, GLUT4, UCP3, and FAT/CD36 (P < 0.05) in this tissue. However, no metabolic improvements were observed following exercise training in HCR. Our results demonstrate that metabolic impairments resulting from genetic factors (low intrinsic aerobic capacity) can be overcome by an environmental intervention (exercise training). Furthermore, we identify Nur77 as a potential mechanism for improved skeletal muscle metabolism in response to EXT.
Authors:
Sarah J Lessard; Donato A Rivas; Erin J Stephenson; Ben B Yaspelkis; Lauren G Koch; Steven L Britton; John A Hawley
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-11-03
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  300     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-24     Completed Date:  2011-01-20     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R175-82     Citation Subset:  IM    
Affiliation:
Royal Melbourne Institute of Technology, Bundoora, Victoria, Australia.
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MeSH Terms
Descriptor/Qualifier:
Animals
Carbohydrate Metabolism / genetics,  physiology
Lipid Metabolism / genetics,  physiology
Models, Animal
Muscle, Skeletal / metabolism*
Nuclear Receptor Subfamily 4, Group A, Member 1 / physiology
Physical Conditioning, Animal / physiology*
Physical Endurance / genetics*,  physiology*
Rats
Rats, Inbred Strains
Receptors, Adrenergic, beta / physiology
Signal Transduction / physiology
Grant Support
ID/Acronym/Agency:
R24 RR017718-10/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Nr4a1 protein, rat; 0/Nuclear Receptor Subfamily 4, Group A, Member 1; 0/Receptors, Adrenergic, beta
Comments/Corrections

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