HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/H1798    most recent 00347.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Jenkins, N. T. Articles by Hagberg, J. M. PubMed PubMed Citation Articles by Jenkins, N. T. Articles by Hagberg, J. M.

Effects of acute and chronic endurance exercise on intracellular nitric oxide in putative endothelial progenitor cells: role of NAPDH oxidase

Department of Kinesiology, School of Public Health, University of Maryland College Park. College Park, Maryland

Submitted April 9, 2009 ; accepted in final form August 24, 2009

We sought to delineate the effects of acute and chronic exercise on the regulation of intracellular nitric oxide (NO_i) production in putative endothelial progenitor cells (EPCs). Putative EPC colony-forming units (CFU-EC) were cultured from blood drawn before and after 30 min of treadmill exercise at 75% of maximal oxygen uptake in active (n = 8) and inactive (n = 8) men. CFU-EC were similar between groups at baseline, but increased after exercise in active men only (P = 0.04). CFU-EC expressed lower NADPH oxidase subunit gp91^phox mRNA and elevated endothelial nitric oxide synthase mRNA in active relative to inactive men at baseline (P < 0.05). Acute exercise reduced gp91^phox mRNA in CFU-EC of both groups (P < 0.05), whereas p47^phox mRNA levels were reduced in the inactive group only (P = 0.02). There were no differences between groups or with acute exercise in xanthine oxidase, superoxide dismutase isoforms, or gluthathione peroxidase-1 mRNA levels. NO_i was significantly greater in CFU-EC of active men at baseline (P = 0.004). NO_i increased in CFU-EC of inactive men with acute exercise, and in vitro experiments with apocynin indicated the increased NO_i production was caused by suppression of NADPH oxidase. However, the increases in NO_i with the different treatments in the inactive group did not reach the baseline levels in the active group (P < 0.05). We conclude that acute exercise increases NO_i in cells generated by the CFU-EC assay through an NADPH oxidase-inhibition mechanism in sedentary men. However, differences due to chronic exercise must involve additional factors. Our findings support exercise as a means to improve putative EPC function and suggest a novel mechanism that may explain this effect.

physical activity; angiogenesis; oxidative stress