Department of Medical Sciences, Centre of Clinical and Basic Research, IRCCS San Raffaele Pisana, Rome, Italy.
Eur J Heart Fail. 2011 Jun;13(6):642-50. doi: 10.1093/eurjhf/hfr026.
Physical training improves endothelial function and exercise capacity in patients with heart failure (HF). Serum from patients with cardiovascular diseases increases apoptosis of human endothelial cells suggesting the importance of humoral factors in the progression of the disease. We evaluated whether exercise training influences the apoptotic capacity of serum from patients with chronic HF (CHF).
The study included 39 patients with HF (NYHA II) and 10 age-matched healthy controls. Patients were allocated to either a structured programme of exercise training (24 patients) or standard care (15 patients). Human umbilical vein endothelial cells (HUVECs) were incubated with a medium containing 20% serum obtained before and after either a 3-week exercise training programme or standard care. At baseline, serum from patients with CHF induced a higher degree of lactate dehydrogenase (LDH) release and apoptosis in HUVECs compared with healthy controls (43 ± 1.5 vs. 16 ± 1.1%, P< 0.001 and 67 ± 5.4 vs. 23 ± 5.8%, P< 0.001, respectively). Exercise training significantly increased performance in the 6 min walking test (+34.7%) and reduced the ability of serum to induce LDH release and apoptosis of HUVECs. The reduction of apoptosis after exercise training correlated with the improvement in functional capacity. The expression of the apoptosis markers Bax and Caspase-3 was significantly reduced in HUVECs exposed to serum collected after exercise training. Circulating tumour necrosis factor-alpha, matrix metalloproteinase-1 (MMP-1), and tissue inhibitor of metalloproteinase-1 (TIMP-1) levels were significantly reduced by exercise training and the MMP-9/TIMP-1 ratio increased.
A short term in-hospital structured cardiovascular training programme reduces the ability of serum-derived factors to induce endothelial cell death in patients with CHF.
身体训练可改善心力衰竭（HF）患者的内皮功能和运动能力。患有心血管疾病的患者的血清会增加人内皮细胞的凋亡，这表明体液因素在疾病进展中的重要性。我们评估了运动训练是否会影响慢性心力衰竭（CHF）患者血清的凋亡能力。
该研究纳入了 39 名 HF（NYHA II）患者和 10 名年龄匹配的健康对照者。患者被分为结构化运动训练计划组（24 名患者）或标准护理组（15 名患者）。将人脐静脉内皮细胞（HUVEC）与含有 20％血清的培养基孵育，该血清是在 3 周运动训练计划或标准护理前后获得的。在基线时，与健康对照组相比，CHF 患者的血清诱导 HUVEC 中乳酸脱氢酶（LDH）释放和凋亡的程度更高（分别为 43 ± 1.5％对 16 ± 1.1％，P<0.001和 67 ± 5.4％对 23 ± 5.8％，P<0.001）。运动训练可显著提高 6 分钟步行测试的表现（增加 34.7％），并降低血清诱导 LDH 释放和 HUVEC 凋亡的能力。运动训练后凋亡的减少与功能能力的改善相关。暴露于运动训练后收集的血清中的凋亡标志物 Bax 和 Caspase-3 的表达明显降低。运动训练可显著降低循环肿瘤坏死因子-α，基质金属蛋白酶-1（MMP-1）和基质金属蛋白酶抑制剂-1（TIMP-1）的水平，并增加 MMP-9/TIMP-1 比值。
短期住院结构化心血管训练方案可降低 CHF 患者血清来源的因子诱导内皮细胞死亡的能力。
