Abstract

Endothelial progenitor cells (EPC) play a critical role in vascular repair and its depletion is usually associated with endothelial dysfunction. In addition, regular moderate‐intensity aerobic exercise increases EPC mobilization from bone marrow to peripheral blood and, consequently, improves endothelial function. Therefore, this is a potential mechanism by which exercise reduces the risk of atherosclerosis in patients with cardiometabolic risk (CMR). However, it is unclear whether exercise‐induced EPC mobilization is preserved in patients with CMR and whether EPC mobilization is associated with endothelial function in this population. Accordingly, healthy subjects (CT group; n=3) and patients with CMR (CMR group; n=7) were studied. Circulating EPC were evaluated quantitatively (flow cytometry) and qualitatively (immunofluorescence) before and 20 min after a 40‐ min bout of cycling exercise. Endothelial function was evaluated by flow‐mediated dilation (FMD, Doppler). The CMR group had a significant reduction in CD34 cells (P=0.02) and a trend of reduction in CD34/VEGFR2 cells (P=0.09) after exercise. Moreover, there was a marginal correlation between mobilization of CD34/VEGFR2 cells and FMD (r=0.55; P=0.10). These preliminary results suggest that a bout of aerobic exercise reduced circulating EPC in patients with CMR and EPC mobilization tended to be associated with endothelial function.Supported by CNPq, FAPERJ, FINEP and CAPES.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.