Effect of endurance training on the determinants of peak exercise oxygen consumption in elderly patients with stable compensated heart failure and preserved ejection fraction.
Effect of endurance training on the determinants of peak exercise oxygen consumption in elderly patients with stable compensated heart failure and preserved ejection fraction.
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DOI：
10.1016/j.jacc.2012.02.055
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发表时间：
2012-07-10
影响因子：
24
通讯作者：
Kitzman, Dalane W.
中科院分区：
文献类型：
--
作者：
Haykowsky, Mark J.;Brubaker, Peter H.;Stewart, Kathryn P.;Morgan, Timothy M.;Eggebeen, Joel;Kitzman, Dalane W.
评估心力衰竭和射血分数保留（HFPEF）老年患者耐力运动训练（ET）后运动能力改善的机制。背景资料：运动不耐受，通过降低峰值耗氧量（VO 2）客观地测量，是HFPEF的主要慢性症状，并通过ET改善。然而，机制尚不清楚。在基线和ET（n=22）或注意力控制（n=18）4个月后，对40例稳定、代偿HFPEF门诊患者（平均年龄69 ± 6岁）进行了检查。VO 2及其决定因素进行了评估，在休息和峰值直立周期运动。ET后，峰值VO 2高于对照组（16.3 ± 2.6 vs. 13.1 ± 3.4 ml/kg/min; p=0.002）。这与较高的峰值心率有关（139 ± 16 vs. 131 ± 20次/min; p=0.03），但舒张末期峰值容积无差异（77 ± 18 vs. 77 ± 17 ml; p=0.51）、每搏输出量（48 ± 9 vs. 46 ± 9 ml; p=0.83）或心输出量（6.6 ± 1.3 vs. 5.9 ± 1.5 L/min; p=0.32）。然而，ET组的估计动脉-静脉血氧峰值差（A-VO 2 Diff）显著较高（19.8 ± 4.0 vs. 17.3 ± 3.7 ml/dl; p=0.03）。ET对心输出量的影响导致峰值VO 2改善< 15%。在老年稳定代偿HFPEF患者中，ET后A-VO 2 Diff峰值较高，是VO 2峰值改善的主要原因。这表明外周机制（改善的微血管和/或骨骼肌功能）有助于HFPEF中ET后运动能力的改善。
Evaluate the mechanism(s) for improved exercise capacity after endurance exercise training (ET) in elderly patients with heart failure and preserved ejection fraction (HFPEF). Background: Exercise intolerance, measured objectively by reduced peak oxygen consumption (VO2), is the primary chronic symptom in HFPEF and is improved by ET. However, the mechanism(s) are unknown. Forty stable, compensated HFPEF outpatients (mean age 69 ± 6 yrs) were examined at baseline and after 4 months of ET (n=22) or attention control (n=18). VO2 and its determinants were assessed during rest and peak upright cycle exercise. Following ET, peak VO2 was higher than controls (16.3 ± 2.6 vs. 13.1 ± 3.4 ml/kg/min; p=0.002). This was associated with higher peak heart rate (139 ± 16 vs. 131 ± 20 beats/min; p=0.03), but no difference in peak end-diastolic volume (77 ± 18 vs. 77 ± 17 ml; p=0.51), stroke volume (48 ± 9 vs. 46 ± 9 ml; p=0.83), or cardiac output (6.6 ± 1.3 vs. 5.9 ± 1.5 L/min; p=0.32). However, estimated peak arterial-venous oxygen difference (A-VO2 Diff) was significantly higher in ET (19.8 ± 4.0 vs. 17.3 ± 3.7 ml/dl; p=0.03). The effect of ET on cardiac output was responsible for < 15% of the improvement in peak VO2. In elderly stable compensated HFPEF patients, peak A-VO2 Diff was higher following ET and was the primary contributor to improved peak VO2. This suggests that peripheral mechanisms (improved microvascular and/or skeletal muscle function) contribute to the improved exercise capacity after ET in HFPEF.
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