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1Department of Cardiology and 2Center for Cellular Therapy and Regenerative Medicine (CCRG), Antwerp University Hospital; and 3Vaccine and Infectious Disease Institute (VIDI), Laboratory for Experimental Hematology, University of Antwerp, Antwerp, Belgium
Submitted 13 November 2007 ; accepted in final form 24 January 2008
Mobilization of bone marrow-derived endothelial progenitor cells (EPC) might explain exercise-induced improvement of endothelial function. We assessed whether a maximal exercise bout could alter the number of circulating EPC in healthy subjects and whether this effect is related to their cardiovascular risk profile. Additionally, we investigated possible mediators of this effect, namely nitric oxide (NO) bioavailability and vascular endothelial growth factor (VEGF) release. Healthy subjects (group 1, n = 11; group 2, n = 14) performed a symptom-limited cardiopulmonary exercise test on a bicycle ergometer. Numbers of CD34+/kinase insert domain receptor (KDR)+ cells were determined by flow-cytometric analysis, either after magnetic separation of CD34+ cells (group 1) or starting from whole blood (group 2). Serum concentrations of VEGF and NO metabolites were measured by using ELISA. Following exercise, EPC increased by 76% (15.4 ± 10.7 cells/ml vs. 27.2 ± 13.7 cells/ml; P = 0.01) in group 1 and by 69% in group 2 (30.9 ± 14.6 cells/ml vs. 52.5 ± 42.6 cells/ml; P = 0.03). The increase in EPC correlated positively with LDL and total cholesterol/HDL ratio and negatively with peak oxygen consumption and oxygen consumption at anaerobic threshold. VEGF levels increased with exercise, with a strong trend toward significance (P = 0.055). NO levels remained unchanged. The present study demonstrates that a maximal bout of exercise induces a significant shift in CD34+ cells toward CD34+/KDR+ cells. This response was larger in subjects with a less favorable lipid profile.
acute exercise; endothelial function
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