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1 Center for the Study of Health Effects of Exercise in Childrene, University of California, Irvine, Irvine, CA, USA; Department of Pediatrics, University of California, Irvine, Irvine, CA, USA
2 Department of Orthopaedics, University of California, Irvine, Irvine, CA, USA; Department of Physiloogy and Biophysics, College of Medicine, University of California, Irvine, Irvine, CA, USA
3 Department of Microbiology and Molecular Genetics, University of California, Irvine, Irvine, CA, USA; Institute for Genomics and Bioinformatics, University of California, Irvine, Irvine, CA, USA
4 Department of Biological Chemistry, University of California, Irvine, Irvine, CA, USA
5 Institute for Genomics and Bioinformatics, University of California, Irvine, Irvine, CA, USA; Institute for Genomics and Bioinformatics, University of California, Irvine, Irvine, CA, USA
* To whom correspondence should be addressed. E-mail: dcooper{at}uci.edu.
Exercise leads to increases in circulating levels of peripheral blood mononuclear cells (PBMCs) and to a simultaneous, seemingly paradoxical increase in both pro- and anti-inflammatory mediators. Whether this is paralleled by changes in gene expression within the circulating population of PBMCs is not fully understood. Fifteen healthy men (18-30 years-old) performed 30 min of constant work rate cycle ergometry (~80% peak VO2). Blood samples were obtained pre-exercise (PRE), end-exercise (END-EX), and 60 min into recovery (RECOVERY), and gene expression was measured using microarray analysis (Affymetrix GeneChips). Significant differential gene expression was defined using a posterior probability of differential expression of 0.99 and a Bayesian p-value of 0.005. Significant changes were observed from PRE to END-EX in 311 genes, from END-EX to RECOVERY in 552 genes, and from PRE to RECOVERY in 293 genes. PRE to END-EX up-regulation of PBMC genes related to stress and inflammation [e.g., heat shock protein (Hsp) 70 (3.70-fold) and dual specificity phosphatase-1 (4.45-fold)] was followed by a return of these genes to baseline by RECOVERY. The gene for interleukin-1 receptor antagonist (an anti-inflammatory mediator) increased between END-EX and RECOVERY (1.52-fold). Chemokine genes associated with inflammatory diseases--MIP-1
(1.84-fold), MIP-1
(2.88-fold), and RANTES (1.34-fold) were up-regulated but returned to baseline by RECOVERY. Exercise also up-regulated growth and repair genes such as epiregulin (3.50-fold), platelet-derived growth factor (1.55-fold), and hypoxia-inducible factor-I (2.40-fold). A single bout of heavy exercise substantially alters PBMC gene expression characterized in many cases by a brisk activation and deactivation of genes associated with stress, inflammation, and tissue repair.
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