title: Exercise training in patients with heart failure. A randomized, controlled trial.
abstract: 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.
  
  
  METHODS
  Randomized, controlled trial.
  
  
  METHODS
  Urban outpatient clinic.
  
  
  METHODS
  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.
  
  
  METHODS
  Patients assigned to exercise training participated in a program of three exercise sessions per week for 24 weeks.
  
  
  METHODS
  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 -4 +/- 3 L/min; peak heart rate, 10 +/- 4 beats/min and -2 +/- 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.
authors.affiliation: Henry Ford Heart and Vascular Institute, Detroit, Michigan, USA.
authors.forename: S J
authors.initials: SJ
authors.lastname: Keteyian
authors.forename: A B
authors.initials: AB
authors.lastname: Levine
authors.forename: C A
authors.initials: CA
authors.lastname: Brawner
authors.forename: T
authors.initials: T
authors.lastname: Kataoka
authors.forename: F J
authors.initials: FJ
authors.lastname: Rogers
authors.forename: J R
authors.initials: JR
authors.lastname: Schairer
authors.forename: P D
authors.initials: PD
authors.lastname: Stein
authors.forename: T B
authors.initials: TB
authors.lastname: Levine
authors.forename: S
authors.initials: S
authors.lastname: Goldstein
mesh_terms: D000328:Adult; D000368:Aged; D002303:Cardiac Output, Low / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D003131:Combined Modality Therapy; D005081:Exercise Therapy; D017079:Exercise Tolerance; D006339:Heart Rate; D006801:Humans; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption; D010349:Patient Compliance; D012119:Respiration; D018487:Ventricular Dysfunction, Left / Q000150:complications