Document Detail

Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome.
MedLine Citation:
PMID:  15347626     Owner:  NLM     Status:  MEDLINE    
Aerobic conditioned muscle shows increased oxidative metabolism or glucose relative to untrained muscle at a given absolute exercise intensity. The studies of a targeted risk reduction intervention through defined exercise (STRRIDE) study is an aerobic exercise intervention in men and women with features of metabolic syndrome (Kraus WE, Torgan CE, Duscha BD, Norris J, Brown SA, Cobb FR, Bales CW, Annex BH, Samsa GP, Houmard JA, and Slentz CA, Med Sci Sports Exerc 33: 1774-1784, 2001), with four muscle biopsies taken during training and detraining time points. Here, we expanded a previous study (Hittel DS, Kraus WE, and Hoffman EP, J Physiol 548: 401-410, 2003) and used mRNA profiling to investigate gene transcripts associated with energy and substrate metabolism in STRRIDE participants. We found coordinate regulation of key metabolic enzymes with aerobic training in metabolic syndrome (aspartate aminotransferase 1, lactate dehydrogenase B, and pyruvate dehydrogenase-alpha(1)). All were also quickly downregulated by detraining, although the induction was not an acute response to activity. Protein and enzymatic assays were used to validate mRNA induction with aerobic training and loss with detraining (96 h to 2 wk) in 10 male and 10 female STRRIDE subjects. We propose that training coordinately increases the levels of aspartate aminotransferase 1, lactate dehydrogenase B, and pyruvate dehydrogenase-alpha(1) subunit, increasing glucose metabolism in muscle by liberating pyruvate for oxidative metabolism and, therefore, limiting lactate efflux. Serial measurement of fasting plasma lactate from 62 subjects from the same exercise group demonstrated a significant decrease of circulating lactate with training. We also found evidence for sex-specific molecular remodeling of muscle with ubiquinol-cytochrome c reductase core protein II, a component of mitochondrial respiratory complex III, which showed an increase after training that was specific to women. These biochemical adaptations complement existing molecular models for improved glucose tolerance with exercise intervention in prediabetic individuals.
Dustin S Hittel; William E Kraus; Chuck J Tanner; Joseph A Houmard; Eric P Hoffman
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Publication Detail:
Type:  Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-09-03
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  98     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2005 Jan 
Date Detail:
Created Date:  2004-12-13     Completed Date:  2005-05-11     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  168-79     Citation Subset:  IM    
Research Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Avenue NW, Washington, DC 20010, USA.
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MeSH Terms
Blood Glucose / analysis*
Gene Expression Regulation
Lactic Acid / blood*
Metabolic Syndrome X / genetics,  physiopathology*
Middle Aged
Muscle Proteins / genetics,  metabolism*
Muscle, Skeletal / physiopathology*
Obesity / genetics,  physiopathology*
Oxidoreductases / genetics,  metabolism*
Sex Factors
Grant Support
Reg. No./Substance:
0/Blood Glucose; 0/Muscle Proteins; 50-21-5/Lactic Acid; EC 1.-/Oxidoreductases

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