| A transcriptional map of the impact of endurance exercise training on skeletal muscle phenotype. | |
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MedLine Citation:
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PMID: 20930125 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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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:
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Title: Journal of applied physiology (Bethesda, Md. : 1985) Volume: 110 ISSN: 1522-1601 ISO Abbreviation: J. Appl. Physiol. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-01-13 Completed Date: 2011-08-02 Revised Date: 2012-01-10 |
Medline Journal Info:
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Nlm Unique ID: 8502536 Medline TA: J Appl Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 46-59 Citation Subset: IM |
Affiliation:
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Translational Biomedicine, Heriot-Watt University, Edinburgh, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological
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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:
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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 RR017718-10/RR/NCRR NIH HHS; RR-17718/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Transcription Factors |
| Comments/Corrections | |
Comment In:
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J Appl Physiol. 2011 Jan;110(1):13-4
[PMID:
21071585
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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