Oxygen uptake kinetics during exercise in chronic heart failure: influence of peripheral vascular reserve

Exercise performance in chronic heart failure is severely impaired, due in part to a peripherally mediated limitation. In addition to impaired maximal exercise capacity, the O₂ uptake (O₂) response during submaximal exercise may be affected, with a greater reliance on anaerobiosis leading to early fatigue. However, the response of O₂ kinetics to submaximal exercise in chronic heart failure has not been studied extensively; in particular, the relationship between oxygen utilization and the peripheral response to exercise has not been studied. The present investigation examined the time-constant (τ, corresponding to 63% of the total response fitted from exercise onset) of the O₂ kinetics on-response to submaximal exercise and its relationship to maximal peripheral blood flow in patients with chronic heart failure, and compared responses with those in healthy sedentary subjects. Subjects were 10 patients with chronic heart failure (NYHA class II/III). The mean age was 50±12 years, with a mean resting left ventricular ejection fraction of 25±9%. Controls were 10 age-matched healthy subjects. O_2(max) was first determined for all subjects. Repeated transitions from rest to exercise were performed on a cycle ergometer while measuring breath-by-breath responses of O₂ at a fixed work rate of 50% of O_2(max) (heart failure patients and healthy controls) and at a work rate equivalent to the average in heart failure patients (65 W; healthy controls only). On a separate occasion, post-maximal ischaemic exercise calf blood flow was measured (strain-gauge plethysmography).Whereas heart failure subjects displayed a significantly prolonged O₂ kinetics response at a similar absolute workload (i.e. 65 W), as indicated by a longer τ value (42 s, compared with 22 s in controls; P< 0.01), there was no difference in τ at a similar relative work rate [50% of O_2(max)]. In addition, heart failure subjects demonstrated a lower maximal calf blood flow (P< 0.05) than control subjects. These results indicate that patients with heart failure have a prolonged O₂ kinetics on-response compared with healthy subjects at a similar absolute work rate (i.e. 65 W), but not at a similar relative work rate [50% of O_2(max)]. Thus, despite a reduced maximal calf blood flow response associated with heart failure, it does not appear that this contributes to an impairment of the submaximal exercise response beyond that explained by a reduced maximal exercise capacity [O_2(max)].