EXERCISE TRAINING IN PATIENTS WITH SEVERE LEFT-VENTRICULAR DYSFUNCTION - HEMODYNAMIC AND METABOLIC EFFECTS
EXERCISE TRAINING IN PATIENTS WITH SEVERE LEFT-VENTRICULAR DYSFUNCTION - HEMODYNAMIC AND METABOLIC EFFECTS
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DOI：
10.1161/01.cir.78.3.506
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发表时间：
1988-09-01
期刊：
影响因子：
37.8
通讯作者：
COBB, FR
中科院分区：
文献类型：
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作者：
SULLIVAN, MJ;HIGGINBOTHAM, MB;COBB, FR
我们研究了运动训练对因左心功能不全(射血分数，24.+-)引起的慢性心力衰竭患者的影响。10%)。12例症状稳定的非卧床患者接受了4-6个月的训练，锻炼4.1+-。0.6小时/周，心率相当于峰值耗氧量的75%。在训练前后，患者接受最大限度的自行车运动试验，直接测量中枢血流动力学、腿部血流量和代谢反应。运动训练导致安静时和次极量运动时心率降低，峰值耗氧量从16.8±-增加了23%。3.8至20.6+-。4.7ml/kg/min(p<；0.01)。训练结束后，心率、动脉血乳酸和呼吸交换率无明显变化。最大心输出量有由8.9.+-增加的趋势。2.7至9.9+-3.2 1次/min，部分患者峰值氧耗量有所改善，但差异无统计学意义(p=0.13)。静息和运动测量的左心室射血分数、左心室舒张末容量和左心室收缩末容量没有变化。训练后右心房、肺动脉、肺毛细血管楔形和体动脉压无明显差异。训练诱导了几个重要的外周适应，有助于提高运动成绩。在运动高峰期，体循环动静脉血氧差由13.1±-增加。1.4至14.6。+-。2.3ml/dl(p<；0.05)。这一增加与峰值运动腿部血流量从2.5+-增加有关。0.7至3.0。+-0.8 L/分钟(p<；0.01)，小腿动静脉血氧差由14.5±-增加。1.3至16.1+-1.9ml/dl(p=0.07)。在训练后的次极量运动中，动脉和股静脉乳酸水平显著降低，即使心输出量和腿部血流量在这些工作负荷下保持不变。因此，慢性心力衰竭的门诊患者可以通过长期锻炼达到显著的训练效果。外周适应，包括运动腿部峰值血流量的增加，在提高运动耐量方面发挥了重要作用。这一发现表明，在慢性心力衰竭患者中，外周代谢或血管因素在决定乳酸产生的开始方面是重要的，并且可能独立于中枢血流动力学，影响运动耐量。
We studied the effects of exercise training in patients with chronic heart failure attributed to left ventricular dysfunction (ejection fraction, 24 .+-. 10%). Twelve ambulatory patients with stable symptoms underwent 4-6 months of conditioning by exercising 4.1 .+-. 0.6 hr/wk at a heart rate corresponding to 75% of peak oxygen consumption. Before and after training, patients underwent maximal bicycle exercise testing with direct measurement of central hemodynamic, leg blood flow, and metabolic responses. Exercise training resulted in a decrease in heart rate at rest and submaximal exercise and a 23% increase in peak oxygen consumption from 16.8 .+-. 3.8 to 20.6 .+-. 4.7 ml/kg/min (p < 0.01). Heart rate, arterial lactate, and respiratory exchange ratio were unchanged peak exercise after training. Maximal cardiac output tended to increase from 8.9 .+-. 2.7 to 9.9 .+-. 3.2 1/min and contributed to improved peak oxygen consumption in some patients, although this change did not reach statistical significance (p = 0.13). Rest and exercise measurements of left ventricular ejection fraction, left ventricular end-diastolic volume, and left ventricular end-systolic volume were unchanged. Right atrial, pulmonary arterial, pulmonary capillary wedge, and systemic arterial pressures were not different after training. Training induced several important peripheral adaptations that contributed to improved exercise performance. At peak exercise, systemic arteriovenous oxygen difference increased from 13.1 .+-. 1.4 to 14.6 .+-. 2.3 ml/dl (p < 0.05). This increase was associated with an increase in peak-exercise leg blood flow from 2.5 .+-. 0.7 to 3.0 .+-. 0.8 l/min (p < 0.01) and an increase in leg arteriovenous oxygen difference from 14.5 .+-. 1.3 to 16.1 .+-. 1.9 ml/dl (p = 0.07). Arterial and femoral venous lactate levels were markedly reduced during submaximal exercise after training, even though cardiac output and leg blood flow were unchanged at these workloads. Thus, ambulatory patients with chronich heart failure can achieve a significant training effect from long-term exercise. Peripheral adaptations, including an increase in peak blood flow to the exercising leg, played an important role in improving exercise tolerance. The finding that blood lactate at submaximal exercise were reduced without improvements in cardiac output suggests that in patients with chronic heart failure, peripheral metabolic or vascular factors are important in determining the onset of lactate production and may, independent of central hemodynamics, influence exercise tolerance.