BACKGROUND: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. METHODS: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. RESULTS: 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. CONCLUSIONS: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.
RCT Entities:
BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
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