Department of Cardiology, Antwerp University Hospital, Edegem, Belgium.
Basic Res Cardiol. 2010 Sep;105(5):665-76. doi: 10.1007/s00395-010-0105-4. Epub 2010 May 28.
Alterations in circulating angiogenic cells (CAC) and endothelial progenitor cells (EPC), known to contribute to endothelial repair, could explain the reversal of endothelial function in response to exercise training. Moreover, training-induced vascular remodeling might affect the acute response of EPC and CAC following a single exercise bout. We studied the impact of exercise training on CAC function and numbers of CD34(+)/KDR(+) EPC in patients with chronic heart failure (CHF) and we assessed the effect of acute exercise on CAC and EPC in sedentary and trained patients. Twenty-one sedentary CHF patients underwent 6-month exercise training and were compared to a non-trained control group (n = 17) and 10 healthy age-matched subjects. At baseline and follow-up, flow-mediated dilation was assessed and graded exercise testing (GXT) was performed. Before and immediately after GXT, CAC migratory capacity was assessed in vitro and circulating CD34(+)/KDR(+) EPC were quantified using flow cytometry. At baseline, CAC migration was significantly impaired in sedentary CHF patients but normalized acutely after GXT. Training corrected endothelial dysfunction, which coincided with a 77% increase in CAC migration (P = 0.0001). Moreover, the GXT-induced improvement detected at baseline was no longer observed after training. Numbers of CD34(+)/KDR(+) EPC increased following 6-month exercise training (P = 0.021), but were not affected by GXT, either prior or post-training. In conclusion, the present findings demonstrate for the first time that exercise training in CHF reverses CAC dysfunction and increases numbers of CD34(+)/KDR(+) EPC, which is accompanied by improvement of peripheral endothelial function. The acute exercise-induced changes in CAC function wane with exercise training, suggesting that repetitive exercise bouts progressively lead to functional endothelial repair.
循环血管生成细胞（CAC）和内皮祖细胞（EPC）的改变，已知有助于内皮修复，可能解释了运动训练对内皮功能的逆转。此外，训练诱导的血管重塑可能会影响单次运动后 EPC 和 CAC 的急性反应。我们研究了运动训练对慢性心力衰竭（CHF）患者 CAC 功能和 CD34(+)/KDR(+)EPC 数量的影响，评估了急性运动对久坐和训练患者 CAC 和 EPC 的影响。21 名久坐的 CHF 患者接受了 6 个月的运动训练，并与未经训练的对照组（n = 17）和 10 名年龄匹配的健康受试者进行了比较。在基线和随访时，评估了血流介导的扩张，并进行了分级运动测试（GXT）。在 GXT 之前和之后，体外评估 CAC 迁移能力，并使用流式细胞术定量循环 CD34(+)/KDR(+)EPC。在基线时，久坐的 CHF 患者 CAC 迁移明显受损，但 GXT 后急性恢复正常。训练纠正了内皮功能障碍，同时 CAC 迁移增加了 77%（P = 0.0001）。此外，训练后基线时检测到的 GXT 诱导的改善不再观察到。经过 6 个月的运动训练，CD34(+)/KDR(+)EPC 的数量增加（P = 0.021），但无论在训练前还是训练后，GXT 都没有影响。总之，本研究首次证明，CHF 中的运动训练可逆转 CAC 功能障碍并增加 CD34(+)/KDR(+)EPC 的数量，同时改善外周内皮功能。急性运动引起的 CAC 功能变化随着运动训练而减弱，这表明重复的运动可导致功能性内皮修复。
