Delayed attainment of peak oxygen consumption after the end of exercise in patients with chronic heart failure.

Peak oxygen uptake (VO2) is attained at peak exercise in normal subjects. Recently, it was shown that the kinetics of the VO2 increase during exercise is slowed in chronic heart failure (CHF). We hypothesized that this may delay maximal VO2 after the end of exercise. We studied 21 patients who attained their peak VO2 15 s or more after cessation of a graded bicycle exercise test with breath-by-breath gas analysis (group 1). They were compared with 21 age- and sex-matched CHF patients who did not do so (group 2) and 21 normal subjects (group 3). Peak VO2 occurred 30 +/- 10 s (15-45) after exercise and was 10 +/- 7% (3-31) higher than end-exercise VO2 (P < 0.001) in group 1. Group 1 patients had poorer functional status (NYHA class 3.0 +/- 0.2 vs. 2.4 +/- 0.5), a smaller ejection fraction (21 +/- 6 vs. 26 +/- 8%), a lower end-exercise VO2 (1156 +/- 251 vs. 1535 +/- 508 ml/min), a lower anaerobic threshold (762 +/- 183 vs. 970 +/- 265 ml/min), and an identical respiratory exchange ratio (1.09 +/- 0.13 vs. 1.06 +/- 0.12) relative to group 2 patients. The delta VO2/delta workrate ratio was lower (9.5 +/- 2.0 vs. 11.2 +/- 1.1 ml/W) and the half-time of VO2 recovery was longer (156 +/- 27 vs. 95 +/- 27 s) in group 1 than in group 2 (P < 0.05, P < 0.01 group 1 vs. group 2). Slow kinetics of the VO2 increase with exercise may delay achievement of peak VO2 beyond the maximal workrate achieved. Gas exchanges should thus be measured also during recovery so as not to underestimate the true peak VO2, especially in severe CHF patients referred for heart transplantation.

Transient fall in oxygen intake during exercise in congestive heart failure.

We report four cases in which oxygen intake abruptly decreased during a graded exercise test. In all these cases, there was an acute event (arrhythmia, mitral regurgitation) that had very likely resulted in a decrease in cardiac output. These studies provide new evidence of oxygen intake dependence on oxygen transport, even in nonsteady-state situations.

Serial assessment of cardiopulmonary exercise capacity after cardiomyoplasty for either ischemic or idiopathic dilated cardiomyopathy.

Cardiomyoplasty is a surgical procedure aimed at assisting the left ventricle during ejection. We describe the long-term effects of cardiomyoplasty on peak exercise capacity, with serial assessments for up to 3 years after operation. Sixteen patients (12 in New York Heart Association class III and 4 in class IV) were enrolled. The mean left ventricular ejection fraction was 18 +/- 8%. Bicycle exercise tests with respiratory gas analysis were performed preoperatively and 6, 12, 18, 24, and 36 months after operation. Mean follow-up was 12 +/- 5 months (range 6 to 24). At 6 months, peak oxygen consumption and the ventilatory threshold were unchanged (from 17.8 +/- 5.8 to 15.8 +/- 5.3 ml/min/kg, and from 12.1 +/- 2.7 to 11.4 +/- 3.4 ml/min/kg, respectively). Ventilation at 50 W, viewed as an index of polypnea at submaximal exercise, was also unchanged. Serial assessment of exercise capacity thereafter showed no changes. However, ejection fraction tended to increase from 18 +/- 8% to 21 +/- 9% (p=0.08) and 14 patients reported an improvement in their functional status, resulting in a significant change in New York Heart Association functional class (3.3 +/- 0.5 to 2.2 +/- 0.4 at 6 months and 2.4 +/- 0.4 at the last visit, p <0.005) and improvement in quality-of-life scores. Thus, cardiomyoplasty does not appear to increase peak exercise capacity in the long term, despite an improvement in the left ventricular ejection fraction. Symptoms and quality of life, however, appear to improve. This may be related in part to an insufficient number of assisted systoles during exercise, persistent deconditioning, or changes in pulmonary mechanics.

Prolonged kinetics of recovery of oxygen consumption after maximal graded exercise in patients with chronic heart failure. Analysis with gas exchange measurements and NMR spectroscopy.

BACKGROUND: Patients with chronic heart failure (CHF) often complain of prolonged dyspnea after exercise. The determinants of oxygen consumption after exercise in these patients are unknown. We hypothesized that the kinetics of oxygen consumption recovery after graded exercise was prolonged in parallel with the recovery of muscle energy stores, was not affected by the exercise level, and could be used to assess the circulatory response to exercise. METHODS AND RESULTS: Seventy-two patients with CHF in Weber's class A (n = 28), B (n = 21), and C/D (n = 23) and 13 healthy subjects performed maximal upright bicycle exercise with breath-by-breath respiratory gas analysis. Kinetics of recovery of ventilation (VE), oxygen consumption (VO2), and CO2 production (VCO2) after exercise were characterized by T1/2, the time to reach 50% of the peak value. T1/2 VO2 (seconds) increased with the severity of CHF (97 +/- 17 for CHF A [P < .05 versus CHF B, P < .05 versus CHF C/D], 119 +/- 22 for CHF B [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF C/D], 155 +/- 55 for CHF C/D [P < .05 versus control subjects, P < .05 versus CHF A, and P < .05 versus CHF B] compared with 77 +/- 17 for control subjects). T1/2 VCO2 and T1/2 VE also increased similarly with the worsening of CHF. T1/2 VO2 was correlated negatively with peak VO2 (r = .65) and was reproducible (r = .96). To study the relation between T1/2 VO2 and the duration of exercise, 10 healthy subjects and 22 patients underwent a second graded test at 75% and/or 50% of peak workload. T1/2 VO2 was minimally shortened, at only 50% of peak workload (P = .02). Finally, 19 patients underwent 31P nuclear magnetic resonance spectroscopy of the anterior compartment of the leg during exercise; the half-time of recovery of the ratio of inorganic phosphate to creatine phosphate (T1/2 Pi/PCr), reflecting the level of involvement of oxidative metabolism in the restoration of energetic metabolites after exercise, was linearly correlated with the half-time of VO2 recovery (r = .70, P < .01). CONCLUSIONS: Postexercise T1/2 VO2 increases when CHF worsens, perhaps in part a result of slower kinetics of recovery of muscle energy stores. The time course of oxygen consumption recovery may represent a simple new criterion for measuring the impairment of the circulatory response to exercise in CHF, even submaximal exercise.