Document Detail


A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype.
MedLine Citation:
PMID:  20930125     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The molecular pathways that are activated and contribute to physiological remodeling of skeletal muscle in response to endurance exercise have not been fully characterized. We previously reported that ∼800 gene transcripts are regulated following 6 wk of supervised endurance training in young sedentary males, referred to as the training-responsive transcriptome (TRT) (Timmons JA et al. J Appl Physiol 108: 1487-1496, 2010). Here we utilized this database together with data on biological variation in muscle adaptation to aerobic endurance training in both humans and a novel out-bred rodent model to study the potential regulatory molecules that coordinate this complex network of genes. We identified three DNA sequences representing RUNX1, SOX9, and PAX3 transcription factor binding sites as overrepresented in the TRT. In turn, miRNA profiling indicated that several miRNAs targeting RUNX1, SOX9, and PAX3 were downregulated by endurance training. The TRT was then examined by contrasting subjects who demonstrated the least vs. the greatest improvement in aerobic capacity (low vs. high responders), and at least 100 of the 800 TRT genes were differentially regulated, thus suggesting regulation of these genes may be important for improving aerobic capacity. In high responders, proangiogenic and tissue developmental networks emerged as key candidates for coordinating tissue aerobic adaptation. Beyond RNA-level validation there were several DNA variants that associated with maximal aerobic capacity (Vo(₂max)) trainability in the HERITAGE Family Study but these did not pass conservative Bonferroni adjustment. In addition, in a rat model selected across 10 generations for high aerobic training responsiveness, we found that both the TRT and a homologous subset of the human high responder genes were regulated to a greater degree in high responder rodent skeletal muscle. This analysis provides a comprehensive map of the transcriptomic features important for aerobic exercise-induced improvements in maximal oxygen consumption.
Authors:
Pernille Keller; Niels B J Vollaard; Thomas Gustafsson; Iain J Gallagher; Carl Johan Sundberg; Tuomo Rankinen; Steven L Britton; Claude Bouchard; Lauren G Koch; James A Timmons
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2010-10-07
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  110     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-13     Completed Date:  2011-08-02     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  46-59     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / physiology*
Animals
Humans
Male
Muscle Contraction / physiology*
Muscle, Skeletal / physiology*
Oxygen Consumption / physiology*
Phenotype
Physical Exertion / physiology*
Physical Fitness / physiology
Rats
Running / physiology*
Task Performance and Analysis
Transcription Factors / physiology*
Grant Support
ID/Acronym/Agency:
5P60-DK-20572/DK/NIDDK NIH HHS; HL-45670/HL/NHLBI NIH HHS; HL-47317/HL/NHLBI NIH HHS; HL-47321/HL/NHLBI NIH HHS; HL-47323/HL/NHLBI NIH HHS; HL-47327/HL/NHLBI NIH HHS; R24 RR017718/RR/NCRR NIH HHS; R24 RR017718-10/RR/NCRR NIH HHS; RR-17718/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Transcription Factors
Comments/Corrections
Comment In:
J Appl Physiol (1985). 2011 Jan;110(1):13-4   [PMID:  21071585 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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