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Articles in PresS, published online ahead of print July 12, 2002
J Appl Physiol, 10.1152/jap.00376.2002
Submitted on April 30, 2002
Accepted on July 6, 2002
1 Institute of Respiratory Pathophysiology, CNR, Palermo, Italy
2 Dpt. of Experimental Medicine, University of Palermo, Palermo, Italy
3 Dpt. of Hematology, V. Cervello Hospital, Palermo, Italy
4 Laboratory of Clinical Pathology, V. Cervello Hospital, Palermo, Italy
5 Dpt. of Hematology, Istituto Superiore di Sanita', Rome, Italy
6 University of British Columbia, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: marisa{at}ifr.pa.cnr.it.
Because endurance exercise causes release of mediators/growth factors active on the bone marrow, we asked whether it might affect circulating hematopoietic progenitor cells (HPCs) in amateur runners (n=16, mean age±SD: 41.8±13.5 yr, training: 93.8±31.8 km/week) as compared to sedentary controls (n=9, age: 39.4±10.2 yr). HPCs, plasma cortisol, interleukin-6 (IL-6), granulocyte colony stimulating factor (G-CSF), and the growth factor flt3-ligand were measured at rest and after a Marathon (M, n=8) or Half-Marathon (HM, n=8) race. Circulating HPC counts (i.e. CD34+ cells and their subpopulations) were three- to four-fold higher in runners than in controls at baseline. They were unaffected by HM or M acutely, but decreased the morning post-race. 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 to HM, whereas cortisol and flt3-ligand increased similarly post-race. Our data suggest that increased HPCs reflect an adaptation response to recurrent, exercise-associated release of neutrophils and stress/inflammatory mediators, indicating modulation of bone marrow activity by habitual running.
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