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大鼠4周停训后运动诱导的心肌血管生成部分持续存在。

Partial persistence of exercise-induced myocardial angiogenesis following 4-week detraining in the rat.

作者信息

Marini Marina, Falcieri Elisabetta, Margonato Vittoria, Treré Davide, Lapalombella Rosa, di Tullio Simona, Marchionni Cosetta, Burattini Sabrina, Samaja Michele, Esposito Fabio, Veicsteinas Arsenio

机构信息

Department of Histology, Embryology and Applied Biology, University of Bologna, Via Belmeloro, 8, Bologna, Italy.

出版信息

Histochem Cell Biol. 2008 Apr;129(4):479-87. doi: 10.1007/s00418-007-0373-8. Epub 2008 Jan 3.

DOI:10.1007/s00418-007-0373-8
PMID:18172661
Abstract

Enhanced angiogenesis, or capillary growth, has a prominent role among the various beneficial effects of exercise training on the myocardium. The aim of the present study is to assess if training-induced increases in capillarity and vascularization persist after 4 weeks of detraining. Adult male rats were trained to run on a treadmill for 10 weeks at approximately 60% VO2max, which did not induce cardiac hypertrophy, but increased (P < 0.05) the soleus/body weight ratio, left ventricle capillarity and von Willebrand-positive cell density (n = 6). In another group of animals (n = 6) subjected to training followed by 4-week detraining, the soleus/body weight ratio returned to normal, with only partial reversal of left ventricle capillarity and von Willebrand-positive cell density. Markers of angiogenesis (VEGF, KDR/VEGF-R2 and HIF-1alpha mRNA, studied by real-time RT-PCR) were upregulated at the end of training, and returned to baseline value after detraining. Electron microscopy highlighted some morphological features in trained hearts (endothelial cell sprouting and bridges and pericyte detachment), suggestive of endothelial cell proliferation and capillary growth that were absent in untrained and detrained hearts. We conclude that the training-induced increase in cardiac capillarity and vascularization are retained for some time upon cessation of the training program even in the absence of angiogenic stimuli.

摘要

在运动训练对心肌的各种有益作用中,增强血管生成(即毛细血管生长)起着重要作用。本研究的目的是评估在停止训练4周后,训练诱导的毛细血管密度和血管化增加是否仍然持续存在。成年雄性大鼠在跑步机上以约60%最大摄氧量的强度训练10周,该训练未诱导心脏肥大,但增加了(P < 0.05)比目鱼肌/体重比、左心室毛细血管密度和血管性血友病因子阳性细胞密度(n = 6)。在另一组动物(n = 6)中,先进行训练,然后停止训练4周,比目鱼肌/体重比恢复正常,左心室毛细血管密度和血管性血友病因子阳性细胞密度仅部分逆转。血管生成标志物(通过实时逆转录聚合酶链反应研究的VEGF、KDR/VEGF-R2和HIF-1α mRNA)在训练结束时上调,停止训练后恢复到基线值。电子显微镜突出了训练心脏中的一些形态学特征(内皮细胞发芽、桥接和周细胞脱离),提示内皮细胞增殖和毛细血管生长,而未训练和停止训练的心脏中不存在这些特征。我们得出结论,即使在没有血管生成刺激的情况下,训练诱导的心脏毛细血管密度和血管化增加在训练计划停止后仍会保留一段时间。

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