Department of Kinesiology, University of Maryland College Park School of Public Health, College Park, MD 20742, U.S.A.
Clin Sci (Lond). 2010 Feb;118(4):303-11. doi: 10.1042/CS20090253.
Exercise may contribute to the maintenance of vascular function via enhanced liberation and action of bone-marrow-derived progenitor cells. Activity related changes in oxidative stress may also influence the number and function of these cells. In the present study, we sought to determine (i) whether adaptations in reactive hyperaemic FBF (forearm blood flow) response associated with long-term endurance exercise and short-term detraining were related to resting putative progenitor cell number and function, and (ii) whether oxidative stress affected these factors. Participants included men with a history of more than 30 years of moderate-to-high intensity exercise (HI group) and healthy low-active age- and BMI (body mass index)-matched control subjects (LO group). Vascular reactive hyperaemic FBF response, resting CD34+ and CD34+/VEGFR2+ (vascular endothelial growth factor receptor 2+] cell number, CFU-EC (colony forming unit-endothelial cell) count and CFU-EC senescence were evaluated. Oxidative stress measures included OxLDL (oxidized low-density lipoprotein) and TAC (total antioxidant capacity).These measures were assessed following 10 days of detraining in the HI group. The HI group had greater peak reactive hyperaemic FBF responses compared with the LO group, despite no difference in resting CD34+ cell number, CD34+/VEGFR2+ cell number, CFU-EC colonies or CFU-EC senescence. With detraining in the HI group, CD34+ cells declined 44 %, and the percentage change in CD34+/VEGFR2+ cells was positively correlated with the change in FBF response to reactive hyperaemia. The percentage change in CD34+/VEGFR2+ cells and the percentage change in EPC (endothelial progenitor cell) senescence with detraining were related to the percentage change in TAC. These results reveal that changes in reactive hyperaemic FBF are closely related to activity dependent dynamic changes in CD34+/VEGFR2+ cell number, which may be influenced by alterations in oxidative stress.
运动可能通过增强骨髓源性祖细胞的释放和作用来维持血管功能。与活动相关的氧化应激变化也可能影响这些细胞的数量和功能。在本研究中，我们试图确定（i）长期耐力运动和短期停训与静息推测祖细胞数量和功能相关的反应性充血 FBF（前臂血流）反应适应性是否相关，以及（ii）氧化应激是否影响这些因素。参与者包括有 30 多年中高强度运动史的男性（HI 组）和健康的低活动年龄和 BMI（体重指数）匹配的对照组受试者（LO 组）。评估了血管反应性充血 FBF 反应、静息 CD34+和 CD34+/VEGFR2+（血管内皮生长因子受体 2+）细胞数量、CFU-EC（集落形成单位-内皮细胞）计数和 CFU-EC 衰老。氧化应激指标包括 OxLDL（氧化低密度脂蛋白）和 TAC（总抗氧化能力）。在 HI 组中进行 10 天停训后评估了这些指标。尽管 HI 组的静息 CD34+细胞数量、CD34+/VEGFR2+细胞数量、CFU-EC 集落或 CFU-EC 衰老无差异，但 HI 组的最大反应性充血 FBF 反应更大。在 HI 组中停训后，CD34+细胞下降了 44%，而 CD34+/VEGFR2+细胞的变化百分比与反应性充血的 FBF 反应变化呈正相关。随着 HI 组停训，CD34+/VEGFR2+细胞和 EPC（内皮祖细胞）衰老的变化百分比与 TAC 的变化百分比相关。这些结果表明，反应性充血 FBF 的变化与依赖于活动的 CD34+/VEGFR2+细胞数量的动态变化密切相关，这可能受氧化应激变化的影响。
