Myers J, Dziekan G, Goebbels U, Dubach P
Cardiology Division, Kantonsspital Chur, Switzerland.
Med Sci Sports Exerc. 1999 Jul;31(7):929-37. doi: 10.1097/00005768-199907000-00003.
Exercise training increases exercise capacity in patients with reduced ventricular function in part through improved skeletal muscle metabolism, but the effect training might have on abnormal ventilatory and gas exchange responses to exercise has not been clearly defined.
Twenty-five male patients with reduced ventricular function after a myocardial infarction were randomized to either a 2-month high-intensity residential exercise training program or to a control group. Before and after the study period, upright exercise testing was performed with measurements of ventilatory gas exchange, lactate, arterial blood gases, cardiac output, and pulmonary artery and wedge pressures.
In the exercise group, peak VO2 and VO2 at the lactate threshold increased 29 and 39%, respectively, whereas no increases were observed among controls. Maximal cardiac output increased only in the exercise group (1.7 L x min(-1), P < 0.05), and no changes in rest or peak exercise pulmonary pressures were observed in either group. At baseline, modest inverse relationships were observed between pulmonary wedge pressure and peak VO2 both at rest (r = -0.56, P < 0.05) and peak exercise (r = -0.43, P < 0.05). Maximal VE/VCO2 was inversely related to maximal cardiac output (r = -0.72, P < 0.001). Training did not have a significant effect on these relationships. Training lowered VE/VO2, heart rate, and blood lactate levels at matched work rates throughout exercise and tended to lower maximal Vd/Vt. The slope of the relationship between VE and VCO2 was reduced after training in the exercise group (0.33 pre vs 0.27 post, P < 0.01), whereas control patients did not differ.
Exercise training among patients with reduced left ventricular function results in a systematic improvement in the ventilatory response to exercise. Training increased maximal cardiac output, tended to lower Vd/Vt, and markedly improved the efficiency of ventilation. Peak VO2 and ventilatory responses to exercise were only modestly related to pulmonary vascular pressures, and training had no effect on the relationships between exercise capacity, ventilatory responses, and pulmonary pressures.
运动训练可部分通过改善骨骼肌代谢来提高心室功能降低患者的运动能力，但训练对运动时异常通气和气体交换反应的影响尚未明确界定。
25名心肌梗死后心室功能降低的男性患者被随机分为两组，一组接受为期2个月的高强度住院运动训练计划，另一组为对照组。在研究期前后，进行直立运动测试，测量通气气体交换、乳酸、动脉血气、心输出量以及肺动脉和楔压。
运动组中，峰值VO2和乳酸阈值时的VO2分别增加了29%和39%，而对照组未观察到增加。仅运动组的最大心输出量增加（1.7L·min⁻¹，P<0.05），两组在静息或运动峰值时的肺压均无变化。基线时，静息（r=-0.56，P<0.05）和运动峰值（r=-0.43，P<0.05）时肺楔压与峰值VO2之间均观察到适度的负相关关系。最大VE/VCO2与最大心输出量呈负相关（r=-0.72，P<0.001）。训练对这些关系无显著影响。训练降低了整个运动过程中匹配工作率下的VE/VO2、心率和血乳酸水平，并倾向于降低最大Vd/Vt。运动组训练后VE与VCO2关系曲线的斜率降低（训练前为0.33，训练后为0.27，P<0.01），而对照组患者无差异。
左心室功能降低患者的运动训练可使运动通气反应得到系统性改善。训练增加了最大心输出量，倾向于降低Vd/Vt，并显著提高了通气效率。峰值VO2和运动通气反应与肺血管压力仅存在适度关联，且训练对运动能力、通气反应和肺压之间的关系无影响。
