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Circulating hematopoietic progenitor cells in runners

  • Autori: Bonsignore, M.; Morici, G.; Santoro, A.; Pagano, M.; Cascio, L.; Bonanno, A.; Abate, P.; Mirabella, F.; Profita, M.; Insalaco, G.; Gioia, M.; Vignola, A.; Majolino, I.; Testa, U.; Hogg, J.
  • Anno di pubblicazione: 2002
  • Tipologia: Articolo in rivista (Articolo in rivista)
  • Parole Chiave: Cytokines; Endurance training; Growth factors; Marathon; Physiology; Endocrinology; Orthopedics and Sports Medicine; Physical Therapy, Sports Therapy and Rehabilitation
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Because endurance exercise causes release of mediators and growth factors active on the bone marrow, we asked whether it might affect circulating hematopoietic progenitor cells (HPCs) in amateur runners [n = 16, age: 41.8 ± 13.5 (SD) yr, training: 93.8 ± 31.8 km/wk] compared with sedentary controls (n = 9, age: 39.4 ± 10.2 yr). HPCs, plasma cortisol, interleukin (IL)-6, granulocyte colony-stimulating factor (G-CSF), and the growth factor fms-like tyrosine kinase-3 (flt3)-ligand were measured at rest and after a marathon (M; n = 8) or half-marathon (HM; n = 8). Circulating HPC counts (i.e., CD34+ cells and their subpopulations) were three- to fourfold higher in runners than in controls at baseline. They were unaffected by HM or M acutely but decreased the morning postrace. Baseline cortisol, flt3-ligand, IL-6, and G-CSF levels were similar in runners and controls. IL-6 and G-CSF increased to higher levels after M compared with HM, whereas cortisol and flt3-ligand increased similarly postrace. Our data suggest that increased HPCs reflect an adaptation response to recurrent, exercise-associated release of neutrophils and stress and inflammatory mediators, indicating modulation of bone marrow activity by habitual running.