title: Controlled trial of physical training in chronic heart failure. Exercise performance, hemodynamics, ventilation, and autonomic function.
abstract: BACKGROUND
  Many secondary abnormalities in chronic heart failure (CHF) may reflect physical deconditioning. There has been no prospective, controlled study of the effects of physical training on hemodynamics and autonomic function in CHF.
  
  
  RESULTS
  In a controlled crossover trial of 8 weeks of exercise training, 17 men with stable moderate to severe CHF (age, 61.8 +/- 1.5 years; left ventricular ejection fraction, 19.6 +/- 2.3%), increased exercise tolerance (13.9 +/- 1.0 to 16.5 +/- 1.0 minutes, p less than 0.001), and peak oxygen uptake (13.2 +/- 0.9 to 15.6 +/- 1.0 ml/kg/min, p less than 0.01) significantly compared with controls. Training increased cardiac output at submaximal (5.9-6.7 l/min, p less than 0.05) and peak exercise (6.3-7.1 l/min, p less than 0.05), with a significant reduction in systemic vascular resistance. Training reduced minute ventilation and the slope relating minute ventilation to carbon dioxide production (-10.5%, p less than 0.05). Sympathovagal balance was altered by physical training when assessed by three methods: 1) RR variability (+19.2%, p less than 0.05); 2) autoregressive power spectral analysis of the resting ECG divided into low-frequency (-21.2%, p less than 0.01) and high-frequency (+51.3%, p less than 0.05) components; and 3) whole-body radiolabeled norepinephrine spillover (-16%, p less than 0.05). These measurements all showed a significant shift away from sympathetic toward enhanced vagal activity after training.
  
  
  CONCLUSIONS
  Carefully selected patients with moderate to severe CHF can achieve significant, worthwhile improvements with exercise training. Physical deconditioning may be partly responsible for some of the associated abnormalities and exercise limitation of CHF, including abnormalities in autonomic balance.
authors.affiliation: Department of Cardiac Medicine, National Heart and Lung Institute, London, UK.
authors.forename: A J
authors.initials: AJ
authors.lastname: Coats
authors.forename: S
authors.initials: S
authors.lastname: Adamopoulos
authors.forename: A
authors.initials: A
authors.lastname: Radaelli
authors.forename: A
authors.initials: A
authors.lastname: McCance
authors.forename: T E
authors.initials: TE
authors.lastname: Meyer
authors.forename: L
authors.initials: L
authors.lastname: Bernardi
authors.forename: P L
authors.initials: PL
authors.lastname: Solda
authors.forename: P
authors.initials: P
authors.lastname: Davey
authors.forename: O
authors.initials: O
authors.lastname: Ormerod
authors.forename: C
authors.initials: C
authors.lastname: Forfar
mesh_terms: D001341:Autonomic Nervous System / Q000502:physiology; D004562:Electrocardiography / Q000379:methods; D005080:Exercise Test; D005081:Exercise Therapy; D006333:Heart Failure / Q000503:physiopathology / Q000534:rehabilitation*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012815:Signal Processing, Computer-Assisted
chemical_list: D009638:Norepinephrine