Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats
Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats
复制标题
DOI：
10.1152/ajpheart.00526.2005
复制
发表时间：
2005-11-01
影响因子：
4.8
通讯作者：
Moore, RL
中科院分区：
文献类型：
--
作者：
Emter, CA;McCune, SA;Moore, RL
关于慢性运动训练在改善充血性心力衰竭(CHF)患者生存方面的有效性的数据尚不确定。因此，我们使用瘦削的雄性自发性高血压心衰(SHHF)大鼠进行了一项研究，以确定运动训练对心力衰竭(HF)动物模型存活率的影响。在这个模型中，动物通常在18到23个月龄之间出现失代偿、扩张的心衰。SHHF大鼠在9个月龄和16个月龄时被分成久坐组和运动组。运动训练包括6mo的低强度跑步机跑步。运动训练延迟了显性心衰的发生并改善了存活率(P<；0.01)，与对大鼠高血压状态的任何影响无关。训练延缓了肌球蛋白重链(MyHC)亚型从α-MyHC到β-MyHC的转变，这种转变在久坐不动的动物身上可以看到。运动与心肌细胞长度(约6%)、宽度和面积的同时增加有关，并阻止了在心衰久坐动物中出现的长宽比的增加。低强度运动训练可抑制心力衰竭大鼠尿蛋白、血浆心钠素和血清瘦素水平的升高。肌浆网钙三磷酸腺苷酶、磷蛋白或钠/钙交换蛋白的表达在训练过程中未见明显变化。我们的结果表明，6个月的低强度运动训练延缓了失代偿性心衰的发生，并提高了雄性SHHF大鼠的存活率。同样，运动干预阻止或抑制了几个关键变量的变化，这些变量通常伴随着显性心力衰竭的发展而发生。这些数据支持这样一种观点，即运动可能是治疗心力衰竭的一种有用且廉价的干预措施。
Data regarding the effectiveness of chronic exercise training in improving survival in patients with congestive heart failure ( CHF) are inconclusive. Therefore, we conducted a study to determine the effect of exercise training on survival in a well- defined animal model of heart failure ( HF), using the lean male spontaneously hypertensive HF ( SHHF) rat. In this model, animals typically present with decompensated, dilated HF between similar to 18 and 23 mo of age. SHHF rats were assigned to sedentary or exercise- trained groups at 9 and 16 mo of age. Exercise training consisted of 6 mo of low- intensity treadmill running. Exercise training delayed the onset of overt HF and improved survival ( P < 0.01), independent of any effects on the hypertensive status of the rats. Training delayed the myosin heavy chain ( MyHC) isoform shift from alpha- to beta- MyHC that was seen in sedentary animals that developed HF. Exercise was associated with a concurrent increase in cardiomyocyte length ( approximate to 6%), width, and area and prevented the increase in the length- to- width ratio seen in sedentary animals in HF. The increases in proteinuria, plasma atrial natriuretic peptide, and serum leptin levels observed in rats with HF were suppressed by low- intensity exercise training. No significant alterations in sarco ( endo) plasmic reticulum Ca2+ ATPase, phospholamban, or Na+/ Ca2+ exchanger protein expression were found in response to training. Our results indicate that 6 mo of low- intensity exercise training delays the onset of decompensated HF and improves survival in the male SHHF rat. Similarly, exercise intervention prevented or suppressed alterations in several key variables that normally occur with the development of overt CHF. These data support the idea that exercise may be a useful and inexpensive intervention in the treatment of HF.