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Exercise Training in Patients with Heart Failure A Randomized, Controlled Trial

Steven J. Keteyian, PhD; Arlene B. Levine, MD; Clinton A. Brawner, BS; Takeshi Kataoka, MD; Felix J. Rogers, DO; John R. Schairer, DO; Paul D. Stein, MD; T. Barry Levine, MD; and Sidney Goldstein, MD
[+] Article and Author Information

From Henry Ford Heart and Vascular Institute, Detroit, Michigan. Grant Support: In part by a grant from Astra Merck. Requests for Reprints: Steven J. Keteyian, PhD, Henry Ford Heart and Vascular Institute, Suite 1107, 2921 West Grand Boulevard, Detroit, MI 48202. Current Author Addresses: Drs. Keteyian, Kataoka, and Stein and Mr. Brawner: Henry Ford Heart and Vascular Institute, 2921 West Grand Boulevard, Suite 1107, Detroit, MI 48202.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1996;124(12):1051-1057. doi:10.7326/0003-4819-124-12-199606150-00004
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Objective: To assess the benefit of exercise training in patients with heart failure caused by left ventricular systolic dysfunction and to further describe the physiologic changes associated with exercise training in these patients.

Design: Randomized, controlled trial.

Setting: Urban outpatient clinic.

Patients: 40 men with compensated heart failure who were receiving standard medical therapy were randomly assigned to an exercise-training group or to a control group that did not exercise. Fifteen of the 21 patients assigned to exercise training and 14 of the 19 patients assigned to the control group completed the study.

Intervention: Patients assigned to exercise training participated in a program of three exercise sessions per week for 24 weeks.

Measurements: Symptom-limited exercise tests with gas exchange analysis done just before randomization, at week 12, and at week 24.

Results: At week 24, the following changes (mean ± SE) were seen in patients in the exercise group and patients in the control group, respectively: exercise duration, 2.8 ± 0.6 minutes and 0.5 ± 0.5 minutes; peak oxygen consumption (VO2), 231 ± 54 L/min and 58 ± 38 L/min; peak ventilation, 12 ± 3 L/min and minus4 ± 3 L/min; peak heart rate, 10 ± 4 beats/min and minus2 ± 4 beats/min; and peak power output, 20 ± 6 W and 2 ± 5 W. Differences between the increases occurring in the exercise group and the changes occurring in the control group were significant (P < 0.05). Among patients in the exercise group, 85% of the increase in peak VO2 occurred by week 12, and 46% of the increase in peak VO2 was caused by the increase in peak heart rate.

Conclusions: Exercise training does not appear to be contraindicated in patients with compensated heart failure. Exercise training improved exercise tolerance, as measured by increases in peak VO2, exercise duration, and power output. This improved exercise tolerance was caused in part by an increase in peak heart rate.

Figures

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Figure 1.
Peak oxygen consumption in patients with compensated heart failure who did not have exercise training (control group, n = 14) and who did have exercise training (exercise group, n = 15).P

The heavy line represents the mean value across time, with a significant difference noted between groups (analysis of variance; < 0.05).

Grahic Jump Location
Grahic Jump Location
Figure 2.
Exercise duration in patients with compensated heart failure who did not have exercise training (control group, n = 14) and who did have exercise training (exercise group, n = 15).P

The heavy line represents the mean value across time, with a significant difference noted between groups (analysis of variance; < 0.05).

Grahic Jump Location
Grahic Jump Location
Figure 3.
Peak heart rate in patients with compensated heart failure who had exercise training (exercise group, n = 14) and did not have exercise training (control group, n = 13).P

A significant difference over time was seen between groups (analysis of variance; < 0.05). Values are expressed as means with 95% Cls.

Grahic Jump Location

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