Document Detail


Interleukin-1 polymorphisms are associated with the inflammatory response in human muscle to acute resistance exercise.
MedLine Citation:
PMID:  15331687     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Inflammation appears to play an important role in the repair and regeneration of skeletal muscle after damage. We tested the hypothesis that the severity of the inflammatory response in muscle after an acute bout of resistance exercise is associated with single nucleotide polymorphisms (SNPs) previously shown to alter interleukin-1 (IL-1) activity. Using a double-blind prospective design, sedentary young men were screened (n = 100) for enrolment (n = 24) based upon having 1 of 4 haplotype patterns composed of five polymorphic sites in the IL-1 gene cluster: IL-1A (+4845), IL-1B (+3954), IL-1B (-511), IL-1B (-3737) and IL-1RN (+2018). Subjects performed a standard bout of resistance leg exercise and vastus lateralis biopsies were obtained pre-, and at 24, and 72 h post-exercise. Inflammatory marker mRNAs (IL-1beta, IL-6 and tumor necrosis factor-alpha (TNF-alpha)) and the number of CD68(+) macrophages were quantified. Considerable variation was observed in the expression of these gene products between subjects. At 72 h post-exercise, IL-1beta had increased in a number of subjects (n = 10) and decreased (n = 4) or did not change (n = 10) in others. Inflammatory responses were significantly associated with specific haplotype patterns and were also influenced by individual SNPs. Subjects with genotypes 1.1 at IL-1B (+3954) or 2.2 at IL-1B (-3737) had approximately a 2-fold higher median induction of several markers, but no increase in macrophages, suggesting that cytokine gene expression is elevated per macrophage. The IL-1RN (+2018) SNP maximized the response specifically within these groups and was associated with increased macrophage recruitment. This is the first report that IL-1 genotype is associated with the inflammation of skeletal muscle following acute resistance exercise that may potentially affect the adaptations to chronic resistance exercise.
Authors:
Richard A Dennis; Todd A Trappe; Pippa Simpson; Chad Carroll; B Emma Huang; Radhakrishnan Nagarajan; Edward Bearden; Cathy Gurley; Gordon W Duff; William J Evans; Kenneth Kornman; Charlotte A Peterson
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2004-08-26
Journal Detail:
Title:  The Journal of physiology     Volume:  560     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2004 Nov 
Date Detail:
Created Date:  2004-11-08     Completed Date:  2005-04-13     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  617-26     Citation Subset:  IM    
Affiliation:
Department of Geriatrics, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, AR 72205, USA.
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MeSH Terms
Descriptor/Qualifier:
Adult
Double-Blind Method
Humans
Inflammation
Interleukin-1 / biosynthesis,  genetics*
Male
Muscle, Skeletal / metabolism,  pathology*
Physical Exertion / physiology*
Polymorphism, Single Nucleotide / genetics*
Prospective Studies
RNA, Messenger / biosynthesis,  genetics
Grant Support
ID/Acronym/Agency:
AG00831/AG/NIA NIH HHS; AG012411/AG/NIA NIH HHS; M01-RR14288/RR/NCRR NIH HHS; P20 RR-16460/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Interleukin-1; 0/RNA, Messenger
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