title: Exercise training improves biventricular oxidative metabolism and left ventricular efficiency in patients with dilated cardiomyopathy.
abstract: OBJECTIVE
  The aim of this study was to determine the effect of exercise training on myocardial oxidative metabolism and efficiency in patients with idiopathic dilated cardiomyopathy (DCM) and mild heart failure (HF).
  
  
  BACKGROUND
  Exercise training is known to improve exercise tolerance and quality of life in patients with chronic HF. However, little is known about how exercise training may influence myocardial energetics.
  
  
  METHODS
  Twenty clinically stable patients with DCM (New York Heart Association classes I through III) were prospectively separated into a training group (five-month training program; n = 9) and a non-trained control group (n = 11). Oxidative metabolism in both the right and left ventricles (RV and LV) was measured using [(11)C]acetate and positron emission tomography. Myocardial work power was measured using echocardiography. Myocardial efficiency for forward work was calculated as myocardial work power per mass/LV oxidative metabolism.
  
  
  RESULTS
  Significant improvements were noted in exercise capacity (VO(2)) and ejection fraction in the training group, whereas no changes were observed in the non-trained group. Exercise training reduced both RV and LV oxidative metabolism and elicited a significant increase in LV forward work efficiency, although no significant changes were observed in the non-trained group.
  
  
  CONCLUSIONS
  Exercise training improves exercise tolerance and LV function. This is accompanied by a decrease in biventricular oxidative metabolism and enhanced forward work efficiency. Therefore, exercise training elicits an energetically favorable improvement in myocardial function and exercise tolerance in patients with DCM.
authors.affiliation: Turku PET Centre, University of Turku and Turku University Central Hospital, FIN-20521 Turku, Finland.
authors.forename: Kira Q
authors.initials: KQ
authors.lastname: Stolen
authors.forename: Jukka
authors.initials: J
authors.lastname: Kemppainen
authors.forename: Heikki
authors.initials: H
authors.lastname: Ukkonen
authors.forename: Kari K
authors.initials: KK
authors.lastname: Kalliokoski
authors.forename: Matti
authors.initials: M
authors.lastname: Luotolahti
authors.forename: Pertti
authors.initials: P
authors.lastname: Lehikoinen
authors.forename: Helena
authors.initials: H
authors.lastname: Hämäläinen
authors.forename: Tiina
authors.initials: T
authors.lastname: Salo
authors.forename: K E Juhani
authors.initials: KE
authors.lastname: Airaksinen
authors.forename: Pirjo
authors.initials: P
authors.lastname: Nuutila
authors.forename: Juhani
authors.initials: J
authors.lastname: Knuuti
mesh_terms: D000328:Adult; D002311:Cardiomyopathy, Dilated / Q000175:diagnosis / Q000378:metabolism* / Q000628:therapy*; D004452:Echocardiography; D004734:Energy Metabolism / Q000502:physiology*; D005081:Exercise Therapy; D005260:Female; D006333:Heart Failure / Q000175:diagnosis / Q000378:metabolism* / Q000628:therapy*; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012720:Severity of Illness Index; D013997:Time Factors; D014055:Tomography, Emission-Computed; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis / Q000378:metabolism* / Q000628:therapy*