Chest
Volume 105, Issue 6, June 1994, Pages 1693-1700
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Cardiology: Clinical Investigations
Dynamics of Oxygen Uptake for Submaximal Exercise and Recovery in Patients With Chronic Heart Failure

https://doi.org/10.1378/chest.105.6.1693Get rights and content

Study design and objectives

Attainment of a steady state for oxygen uptake ( V˙o2) during constant work rate exercise has been reported to take longer for patients with chronic heart failure (CHF) compared with normal. The steady state is also delayed in normal subjects during high-intensity exercise compared with moderate exercise, however, and the delay correlates with the degree of associated lactic acidosis. To determine whether prolonged kinetics of V˙o2 are attributable solely to the reduction of exercise capacity in CHF, V˙o2 kinetics were compared for patients with CHF and normal subjects, both for exercise of matched absolute work rate and for matched relative work intensity.

Subjects

Eighteen men with CHF and 10 normal men.

Methods and results

Subjects performed 6 min of constant work rate cycle ergometry with breath-by-breath measurement of V˙o2. Patients were studied using 25 W, and a work rate midway between the lactic acidosis threshold and maximal capacity (50 percent A). Normal subjects were tested similarly, and also at a work rate matched to the patients’ average 50 percent A work rate. The V˙o2 kinetics were characterized by the mean response time (MRT) to attain the 6 min V˙o2 value. Rates of recovery of V˙o2 were analyzed for 2 min following exercise. For the same absolute work rate, V˙o2 MRTs were significantly longer for patients than controls (25 W, 67±26 vs 37±25 s; ˜60 W, 87±20 vs 54±27 s), but there was no significant difference in V˙o2 MRT between the two groups at a matched intensity of 50 percent A (87±20 vs 81±18 s). However, the decrease in V˙o2 during 2 min of recovery was slower for the patients on all comparisons, even for matched exercise intensity.

Conclusion

The V˙o2 dynamics for submaximal exercise are slowed in CHF. The slower dynamics are not entirely accounted for by the relatively higher intensity of a given work rate, since delayed recovery is evident even at a matched relative work intensity. Exercise intolerance in CHF is characterized not only by decreased maximal exercise capacity, but also by slower adaptations to and from submaximal levels of exercise.

Section snippets

Subjects

Patients were selected on the basis of having a clinical history of CHF, and a resting left ventricular ejection fraction of 40 percent or less. All were judged to be clinically stable and compensated on medical therapy at the time of study. None was taking adrenergic antagonists or other medications known to affect the dynamic responses measured, and none had exertional angina or conditions contraindicating exercise. Ten male subjects who served as control subjects were selected on the basis

RESULTS

Patient characteristics are summarized in Table 1. Etiology of heart failure was idiopathic in eight, ischemic in seven, hypertensive in two, and rheumatic in one. No patient had significant valvular stenosis. Their left ventricular ejection fractions measured at rest averaged 26±7 percent. The patients’ peak V˙o2 values averaged 1,380±399 ml/min (18.2±6 ml/min/kg), which represented 65±18 percent of their age- and size-based predicted values.14 The LAT was apparent from analysis of gas

DISCUSSION

In 1923, Hill and Lupton16 introduced the concept that persistent elevation of V˙o2 following cessation of exercise represented the repaying of an “O2 debt,” incurred because of the delay in attainment of the steady-state V˙o2 requirements of the work in the early minutes of exercise. The O2 debt is thus similar, though not necessarily identical,17 to the corresponding O2 deficit at exercise onset. The deficit may be attributed to: (1) a circulatory delay between the consumption of O2

ACKNOWLEDGMENTS

The authors gratefully acknowledge the assistance of Medical Graphics Corporation for technical support and development of the data analysis software.

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    Supported in part by NIH grants HL11907 and HL01642 and the Ciba-Giegy Corporation.

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