Beneficial effects of moderate exercise in arterial hypertension.
Beneficial effects of moderate exercise in arterial hypertension.
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适度运动对动脉高血压的有益作用。
DOI：
10.1161/hypertensionaha.109.128652
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Schulze,PChristian
中科院分区：
文献类型：
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作者：
Schulze,PChristian
长期以来，运动和心肺健康与明显健康的个体和预先存在心血管疾病的患者的心血管死亡率和总体寿命降低有关。它是早期心血管疾病患者生活方式改变的一般建议的一部分，并与多种心脏风险因素的变化相关，如脂质代谢，胰岛素抵抗，体重，炎症和心理社会变量。3、4运动对血压的影响为轻度至中度，收缩压平均降低J10 mmHg，舒张压平均降低J8 mmHg。然而，运动作为一种特定的治疗干预措施，很难评估和剂量。[3]对于特定的运动形式，如有氧运动与阻力训练，以及作为生活方式干预方案的特定运动形式的强度、持续时间和训练间隔，存在争议。4来自高血压患者的动物模型和临床数据的实验证据表明，高血压患者的心脏和血管重塑受到运动的积极影响，但在高血压动物模型中也显示出与过度运动相关的有害结果。5 Miyachi等人6在已建立的高血压导致心力衰竭的动物模型（雄性盐敏感性Dahl大鼠）中研究了适度运动对心血管重塑和功能的影响。大鼠每天游泳1小时，每周5天，持续9周，高盐饮食的久坐动物作为对照组，而第二个对照组由低盐饮食的Dahl大鼠组成（不发展高血压）。运动方案从9周的相对年轻的年龄开始，持续9周。通过尾袖测量，运动组动物的血压与久坐对照组相似，在研究期间逐渐升高。在运动方案的早期阶段，运动降低了盐诱导高血压动物的静息心率，这是一种潜在的有益效果，然而，随着时间的推移而丧失。患有盐诱导高血压的久坐动物组的总体死亡率很高（56%），而研究中运动组的死亡率则显着降低（12%）。这一令人兴奋的发现本身就证明了运动在高血压和心力衰竭动物模型中的强大有益作用。通过他们对心脏功能、结构、组织形态学和分子信号模式的仔细和集中的分析，作者对引发他们研究运动作为预防高血压心力衰竭发作的干预措施的问题提供了几个答案。运动组动物的左心室和右心室壁厚度较小，但左心室略有扩大，表明心肌肥厚较少与久坐不动的人相比，最值得注意的是，左心室舒张末期压在久坐组中增加，作为心力衰竭发展的指标，但在运动组和对照组中保持在相同的水平。运动组的肺质量正常，而久坐组的肺质量显著增加。
Exercise and cardiorespiratory fitness have long been associated with reduced cardiovascular mortality and overall longevity in apparently healthy individuals and also in patients with pre-existing cardiovascular diseases. 1, 2 It is part of the general recommendations for lifestyle modifications in patients with early forms of cardiovascular disease and has been associated with changes in multiple cardiac risk factors, such as lipid metabolism, insulin resistance, weight, inflammation, and psychosocial variables. 3, 4 Effects of exercise on blood pressure are mild to moderate, with an average reduction of J10 mmHg systolic and J8 mmHg diastolic. However, exercise as a specific therapeutic intervention is difficult to evaluate and dose. 3 Controversy exists on the specific form of exercise, such as aerobic versus resistance training, as well as the intensity, duration, and training intervals of the specific form of exercise chosen as a lifestyle intervention regimen. 4 Experimental evidence from animal models and clinical data in individuals with hypertension suggest that cardiac and vascular remodeling in hypertension are positively influenced by exercise but also showed detrimental results associated with excessive exercise in an animal model of hypertension. 5 Miyachi et al6 studied the effects of moderate exercise on cardiovascular remodeling and function in an established animal model of hypertension with resulting heart failure (male salt-sensitive Dahl rats). Rats were exercised by swimming for 1 hour per day, 5 days per week, for 9 weeks, and sedentary animals on a high-salt diet served as controls, whereas a second control group consisted of Dahl rats on a low-salt diet (that do not develop hypertension). The exercise regimen started at the relatively young age of 9 weeks and lasted for 9 weeks. Animals in the exercise group had similar blood pressure as measured by tail cuff compared with the sedentary control group with progressive increase over the study period. Exercise lowered the resting heart rate of animals with salt-induced hypertension in the early phase of the exercise regimen, a potentially beneficial effect that was, however, lost over time. Overall mortality was high in the sedentary group of animals with salt-induced hypertension (56%) and was dramatically reduced in the exercise arm of the study (12%). This exciting finding alone argues for strong beneficial effects of exercise in this animal model of hypertension and heart failure. Through their careful and focused analysis of cardiac function, structure, histomorphology, and molecular signaling pattern, the authors provide several answers to the questions that triggered their investigation of exercise as an intervention to prevent the onset of heart failure in hypertension.Animals in the exercise group also had less hypertrophy indicated by smaller wall thickness of both the left and the right ventricle but slightly enlarged left ventricles compared with their sedentary counterparts. Most notably, left ventricular end-diastolic pressure increased in the sedentary group as an indicator of the development of heart failure but remained at the same level in both the exercise group and in the control group. This was accompanied by normal lung mass in the exercise group, with significantly increased lung mass in the sedentary group.