title: Resistance exercise increases endothelial progenitor cells and angiogenic factors.
abstract: BACKGROUND
  Bone marrow-derived endothelial progenitor cells (EPC) are involved in vascular growth and repair. They increase in the circulation after a single bout of aerobic exercise, potentially related to muscle ischemia. Muscular endurance resistance exercise (MERE) bouts also have the potential to induce muscle ischemia if appropriately structured.
  
  
  OBJECTIVE
  The objective of this study is to determine the influence of a single bout of MERE on circulating EPC and related angiogenic factors.
  
  
  METHODS
  Thirteen trained men age 22.4 ± 0.5 yr (mean ± SEM) performed a bout of MERE consisting of three sets of six exercises at participants' 15-repetition maximum without resting between repetitions or exercises. The MERE bout duration was 12.1 ± 0.6 min. Blood lactate and HR were 11.9 ± 0.9 mmol·L and 142 ± 5 bpm, respectively, at the end of MERE. Blood was sampled preexercise and at 10 min, 2 h, and 24 h postexercise.
  
  
  RESULTS
  Circulating EPC and serum concentrations of vascular endothelial growth factors (VEGF-A, VEGF-C, and VEGF-D), granulocyte colony stimulating factor, soluble Tie-2, soluble fms-like tyrosine kinase-1, and matrix metalloproteinases (MMP-1, MMP-2, MMP-3, MMP-9, and MMP-9) were higher (P < 0.05) in the postexercise period. Circulating EPC levels were unchanged at 10 min postexercise but higher at 2 h postexercise (P < 0.05). The concentration of most angiogenic factors and metalloproteinases were higher at 10 min postexercise (VEGF-A, +38%; VEGF-C, +40%; VEGF-D, +9%; soluble Tie-2, +15%; soluble fms-like tyrosine kinase-1, +24%; MMP-1, +62%; MMP-2, +3%; MMP-3, +54%; and MMP-9, +45%; all P < 0.05). Soluble E-selectin was lower (P < 0.05) at 2 and 24 h postexercise, with endothelial microparticles and thrombomodulin unchanged.
  
  
  CONCLUSIONS
  Short intense bouts of MERE can trigger increases in circulating EPC and related angiogenic factors, potentially contributing to vascular adaptation and vasculoprotection.
authors.affiliation: 1Department of Health, Sport and Exercise Science, Waterford Institute of Technology, Waterford, IRELAND; and 2School of Life, Sport and Social Sciences, Edinburgh Napier University, Edinburgh, Scotland, UNITED KINGDOM.
authors.forename: Mark D
authors.initials: MD
authors.lastname: Ross
authors.forename: Antony L
authors.initials: AL
authors.lastname: Wekesa
authors.forename: John P
authors.initials: JP
authors.lastname: Phelan
authors.forename: Michael
authors.initials: M
authors.lastname: Harrison
mesh_terms: D016179:Granulocyte Colony-Stimulating Factor / Q000097:blood; D006339:Heart Rate; D055018:Hemangioblasts; D006801:Humans; D019344:Lactic Acid / Q000097:blood; D008297:Male; D020782:Matrix Metalloproteinases / Q000097:blood*; D005082:Physical Exertion / Q000502:physiology*; D042787:Receptor, TIE-2 / Q000097:blood; D055070:Resistance Training; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood; D042442:Vascular Endothelial Growth Factors / Q000097:blood*; D055815:Young Adult
chemical_list: D042442:Vascular Endothelial Growth Factors; D016179:Granulocyte Colony-Stimulating Factor; D019344:Lactic Acid; D042787:Receptor, TIE-2; D040281:Vascular Endothelial Growth Factor Receptor-1; D020782:Matrix Metalloproteinases