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Effect of Exercise Training on Mobilization and Functionality of Endothelial Progenitor Cells undergoing Hypoxic Stress
Author(s) -
Wang JongShyan
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.839.6
Subject(s) - progenitor cell , medicine , endothelial progenitor cell , hypoxia (environmental) , endothelial stem cell , endothelium , endothelial dysfunction , stem cell , cardiology , chemistry , biology , microbiology and biotechnology , biochemistry , oxygen , in vitro , organic chemistry
Exercise training improves endothelium‐dependent vasodilation, whereas hypoxic stress causes vascular endothelial dysfunction. This study investigates how high‐intensity interval (HIT) and moderate intensity‐continuous (MCT) exercise training affect mobilization and functionality of endothelial progenitor cells undergoing hypoxic stress. Forty healthy sedentary males were randomized to engage either HIT (3‐minute intervals at 40% and 80%VO 2max , n=20) or MCT (sustained 60%VO 2max , n=20) for 30 minutes/day, 5 days/week for 6 weeks. Characteristics and functionality of circulating progenitor cells (CPCs) under hypoxic exercise (HE, 100W under 12%O 2 ) were determined before and after various interventions. The results demonstrated that both HIT and MCT regimens significantly increased endothelial progenitor cell (EPC) cell count, whereas only HIT considerably increased hemangioblast stem cell (HSC) and endothelial precursor cell (CEP) cell counts at rest and following HE. Moreover, HIT, rather than MCT, significantly diminished the extent of endothelial shedding caused by HE. The HIT regimen also increased resting and HE‐related tube cover area, tube length, and tube count of CPCs. However, MCT did not change migration of CPCs and modestly increased resting tube formation of CPCs at rest or following HE. Therefore, we conclude that HIT is superior to MCT for enhancing functionality of CPCs and suppressing endothelial injury undergoing hypoxia. Support or Funding Information National Science Council of Taiwan (grant number NSC 100‐2314‐B‐182‐004‐MY3), Chang Gung Medical Research Program (grant number CMRPD1A0132 and CMRPD2C0161), and Healthy Aging Research Center, Chang Gung University (grant number EMRPD1A0841)