| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Departments of
1 Geriatrics
2 Physiology & Biophysics
7 Orthopaedic Surgery, University of Arkansas for Medical Sciences, 4301 West Markham, Little Rock, AR 72205, USA
3
Department of Pediatrics, Arkansas Children's Hospital Research Institute, Little Rock, AR 72202, USA
4
Division of Genomic Medicine, University of Sheffield, Royal Hallamshire Hospital, Sheffield S10 2JF, UK
5
Central Arkansas Veteran's Healthcare System, Little Rock, AR 72205, USA
6
Interleukin Genetics, Inc., Waltham, MA 02459, USA
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-1ß, IL-6 and tumor necrosis factor-
(TNF-)) 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-1ß 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.
(Received 7 May 2004;
accepted after revision 21 August 2004;
first published online 26 August 2004)
Corresponding author C. A. Peterson: University of Arkansas for Medical Sciences, 4301 West Markham, 807, Little Rock, AR 72205, USA. Email: petersoncharlottea{at}uams.edu
This article has been cited by other articles:
|
|
 |
|
  R. A. Dennis, B. Przybyla, C. Gurley, P. M. Kortebein, P. Simpson, D. H. Sullivan, and C. A. Peterson Aging alters gene expression of growth and remodeling factors in human skeletal muscle both at rest and in response to acute resistance exercise Physiol Genomics, February 19, 2008; 32(3): 393 - 400. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-S. Wang, H.-Y. Lin, M.-L. Cheng, and M.-K. Wong Chronic intermittent hypoxia modulates eosinophil- and neutrophil-platelet aggregation and inflammatory cytokine secretion caused by strenuous exercise in men J Appl Physiol, July 1, 2007; 103(1): 305 - 314. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Cauci, M. Di Santolo, G. Casabellata, K. Ryckman, S. M. Williams, and S. Guaschino Association of interleukin-1{beta} and interleukin-1 receptor antagonist polymorphisms with bacterial vaginosis in non-pregnant Italian women Mol. Hum. Reprod., April 1, 2007; 13(4): 243 - 250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. W Duff Evidence for genetic variation as a factor in maintaining health Am. J. Clinical Nutrition, February 1, 2006; 83(2): 431S - 435S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. S Kornman Interleukin 1 genetics, inflammatory mechanisms, and nutrigenetic opportunities to modulate diseases of aging Am. J. Clinical Nutrition, February 1, 2006; 83(2): 475S - 483S. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
