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首页> 外文期刊>American Journal of Physiology >Muscle angiogenic growth factor gene responses to exercise in chronic renal failure.
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Muscle angiogenic growth factor gene responses to exercise in chronic renal failure.

机译：慢性肾功能衰竭运动中的肌肉血管生成生长因子基因反应。

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Patients with chronic renal failure (CRF) have impaired exercise capacity even after erythropoietin treatment. We recently showed that although this is explained in part by reduced convective O(2) delivery to muscles, there is also an impairment of O(2) transport from muscle capillaries to the mitochondria. Given the importance of the capillary surface area for capillary mitochondrial O(2) transport and reports of reduced capillarity in CRF, we hypothesized that the angiogenic gene response to exercise is impaired in such patients. Six patients with CRF and six control subjects matched for age, size, and sedentary lifestyle exercised on a single occasion for 1 h at similar work intensities averaging 50% of maximal capacity. Exercise was confined to the knee extensors of a single leg by means of a specially designed leg-kick ergometer. A percutaneous biopsy of the quadriceps was taken within 30 min of cessation of exercise and compared with a similar biopsy done at different times without any prior exercise for 24 h. Conventional Northern blots were prepared and probed for vascular endothelial growth factor (VEGF; the major putative angiogenic growth factor for muscle), basic fibroblast growth factor (bFGF), and transforming growth factor (TGF)-beta(1). Data during both rest and exercise were successfully obtained in four subjects of each group. We also assessed muscle capillarity and mitochondrial oxidative capacity to relate to these changes. Mitochondrial oxidative capacity was normal, whereas capillary number per fiber was 12% lower than in normal subjects. VEGF mRNA abundance was increased after exercise by about one order of magnitude, with no reduction in response in CRF. For bFGF and TGF-beta(1), exercise elicited no response in either group. Reduced muscle capillarity in CRF does not, therefore, stem from reduced transcription of VEGF. To the extent that VEGF is important to exercise-induced angiogenesis in muscle, we suspect a posttranscriptional aberration in this response occurs in CRF to explain reduced capillarity.
机译：即使在促红细胞生成素治疗后，慢性肾功能衰竭（CRF）患者的运动能力也会受损。我们最近显示，尽管这可以部分通过对流O（2）传递至肌肉的方式来解释，但O（2）从肌肉毛细血管到线粒体的运输也存在损害。鉴于毛细管表面积对于毛细管线粒体O（2）运输的重要性以及CRF中毛细血管减少的报道，我们假设在此类患者中运动对血管生成的基因反应受到损害。六名患有CRF的患者和六名对照受试者按年龄，体型和久坐的生活方式进行了一次匹配，分别以相同的工作强度锻炼了1小时，平均强度为最大容量的50％。通过专门设计的腿部测力计，运动仅限于单腿的膝盖伸肌。在停止运动后30分钟内对四头肌进行经皮活检，并将其与在不进行任何事先运动24小时的不同时间进行的类似活检进行比较。制备了常规的Northern印迹，并检测了血管内皮生长因子（VEGF;肌肉的主要假定血管生成生长因子），碱性成纤维细胞生长因子（bFGF）和转化生长因子（TGF）-β（1）。在每组的四个受试者中成功获得了休息和运动期间的数据。我们还评估了与这些变化有关的肌肉毛细血管扩张和线粒体氧化能力。线粒体的氧化能力正常，而每根纤维的毛细管数比正常人低12％。运动后，VEGF mRNA的丰度增加了大约一个数量级，而CRF的反应却没有降低。对于bFGF和TGF-beta（1），运动在任何一组中均未引起反应。因此，CRF的肌肉毛细血管减少并非源于VEGF转录减少。就VEGF对运动引起的肌肉血管生成很重要的程度而言，我们怀疑CRF中此反应的转录后异常发生，可以解释毛细血管减少。

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