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首页> 外文期刊>European journal of preventive cardiology >Obesity and hemoglobin content impact peak oxygen uptake in human heart failure
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Obesity and hemoglobin content impact peak oxygen uptake in human heart failure

机译：肥胖症和血红蛋白含量影响人心力衰竭中的氧气吸收

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Background Exercise intolerance, obesity, and low hemoglobin (hemoglobin13 and 12 g/dl, men/women, respectively) are common features of heart failure. Despite serving as potent contributors to metabolic dysfunction, the impact of obesity and low hemoglobin on exercise intolerance is unknown. This study tested the hypotheses, compared with non-obese (NO) heart failure with normal hemoglobin, (a) counterparts with low hemoglobin and obesity or non-obesity will demonstrate reduced peak exercise oxygen uptake; (b) obese with normal hemoglobin will demonstrate decreased peak exercise oxygen uptake; (c) compared across stratifications, obese with low hemoglobin will demonstrate the sharpest decrement in peak exercise oxygen uptake. Methods Adults with heart failure (n = 315; left ventricular ejection fraction = 40%; 77% men) (Group 1: normal hemoglobin and non-obese, n = 137; Group 2: low hemoglobin and non-obese, n = 51; Group 3: normal hemoglobin+obesity, n = 89; Group 4, n = 38: low hemoglobin+obesity; body mass index = 26 +/- 3, 26 +/- 2, 34 +/- 4, 34 +/- 4 kg/m(2), respectively) completed treadmill cardiopulmonary exercise testing as part of routine clinical management. Peak exercise oxygen uptake was measured via standard metabolic system. Results There were no group-wise differences for heart failure class, gender, left ventricular ejection fraction, and resting cardiopulmonary function. Group 1 demonstrated increased peak exercise oxygen uptake versus Groups 2-4 (20 +/- 6 versus 17 +/- 6, 17 +/- 5, 13 +/- 4 ml/kg/min, respectively; all p 0.001); whereas Group 4 peak exercise oxygen uptake was reduced versus all groups (p 0.001). Additionally, both body mass index (R-2 = 0.10) and hemoglobin (R-2 = 0.12) were significant predictors of peak exercise oxygen uptake in Group 1; which were relationships not mirrored for Groups 2-4. Conclusion These data suggest obesity together with low hemoglobin are potent contributors to impaired peak exercise oxygen uptake and, hence, oxidative metabolic capacity. In diverse populations of heart failure where obesity and/or low hemoglobin are present, it is important to consider these features together when interpreting peak exercise oxygen uptake and underlying exercise limitations.
机译：背景锻炼不耐受，肥胖和低血红蛋白（分别是血红蛋白＆ 12 g / dl，男性/女性）是心力衰竭的常见特征。尽管用作代谢功能障碍的有效贡献，但肥胖症和低血红蛋白对运动不耐受的影响是未知的。该研究测试了假设，与非肥胖（NO）心力衰竭与正常血红蛋白相比，（a）低血红蛋白和肥胖或非肥胖的对应物将证明峰值运动氧气吸收降低; （b）具有正常血红蛋白的肥胖将展示降低的峰值运动氧气吸收; （c）在分层上比较，低血红蛋白的肥胖将展示峰值运动氧吸收的最敏锐的衰落。方法具有心力衰竭的成虫（n = 315;左心室喷射馏分= 40％; 77％的男性）（第1组：正常血红蛋白和非肥胖，n = 137;第2组：低血红蛋白和非肥胖，n = 51;第3组：正常血红蛋白+肥胖，n = 89;第4组，n = 38：低血红蛋白+肥胖;体重指数= 26 +/- 3,26 +/- 2,34 +/- 4,34 +/- 4千克/米（2），分别完成了跑步机心肺运动测试作为常规临床管理的一部分。通过标准代谢系统测量峰值运动氧吸收。结果心力衰竭阶级，性别，左心室喷射分数和休息心肺功能没有群体明显差异。第1组分别证明了峰值运动氧摄取和组2-4（20 +/- 6对17 +/- 6,13 +/- 4ml / kg / min;所有P <0.001 ）;虽然第4组峰值运动氧摄取与所有基团相比（P <0.001）降低。另外，体重指数（R-2 = 0.10）和血红蛋白（R-2 = 0.12）都是第1组中峰运动氧摄取的显着预测因子;这是第2-4组没有镜像的关系。结论这些数据表明肥胖以及低血红蛋白是有效的贡献者，峰值运动氧气吸收，因此，氧化代谢能力。在存在肥胖和/或低血红蛋白的心力衰竭的不同群体中，重要的是在解释峰值运动氧气摄取和潜在的运动限制时将这些特征在一起。

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