Metabolic responses to exercise in patients with heart failure

Metabolic and hemodynamic responses to exercise were evaluated in 10 patients with chronic congestive heart failure. We utilized an exercise protocol in which the work rate was increased continuously and oxygen uptake (VO2) kinetics were characterized by linear, first-order dynamics. VO2 at peak exercise (VO2max) was depressed at 12.8 +/- 2.3 ml/min/kg and the anaerobic threshold occurred at 63 +/- 10% of the VO2max. A significant correlation was observed between the VO2 at the anaerobic threshold and the resting cardiac index (r = .74, p less than .05). Ventilation-perfusion relationships improved during exercise, despite the presence of a widened alveolar-arterial gradient in oxygen tension and elevation of the physiologic dead space/tidal volume ratio. At peak exercise, a large breathing reserve (maximal voluntary ventilation-minute ventilation), a decline in arterial carbon dioxide tension, and a slight increase in arterial oxygen tension were observed. Plasma epinephrine levels at peak exercise correlated directly with VO2max (r = .74, p less than .05). Thus, although disturbances in ventilation-perfusion relationships occur in association with heart failure, exercise is not limited by an impairment in pulmonary function. The glycogenolytic action of epinephrine may play an important role in determining peak exercise capacity since glycogen stores are increasingly utilized at work rates above the anaerobic threshold.