title: Moderate exercise training improves survival and ventricular remodeling in an animal model of left ventricular volume overload.
abstract: BACKGROUND
  Exercise training has beneficial effects in patients with heart failure, although there is still no clear evidence that it may impact on their survival. There are no data regarding the effects of exercise in subjects with chronic left ventricular (LV) volume overload. Using a rat model of severe aortic valve regurgitation (AR), we studied the effects of long-term exercise training on survival, development of heart failure, and LV myocardial remodeling.
  
  
  RESULTS
  One hundred sixty male adult rats were divided in 3 groups: sham sedentary (n=40), AR sedentary (n=80), and AR trained (n=40). Training consisted in treadmill running for up to 30 minutes, 5 times per week for 9 months, at a maximal speed of 20 m/minute. All sham-operated animals survived the entire course of the protocol. After 9 months, 65% of trained animals were alive compared with 46% of sedentary ones (P=0.05). Ejection fractions remained in the normal range (all above 60%) and LV masses between AR groups were similar. There was significantly less LV fibrosis in the trained group and lower LV filling pressures and improved echocardiographic diastolic parameters. Heart rate variability was also improved by exercise.
  
  
  CONCLUSIONS
  Our data show that moderate endurance training is safe, does not increase the rate of developing heart failure, and most importantly, improves survival in this animal model of chronic LV volume overload. Exercise improved LV diastolic function, heart rate variability, and reduced myocardial fibrosis.
authors.affiliation: Groupe de Recherche en Valvulopathies, Centre de Recherche, Institut universitaire de cardiologie et de pneumologie de Québec, Université Laval, Québec, Canada.
authors.forename: Dominic
authors.initials: D
authors.lastname: Lachance
authors.forename: Eric
authors.initials: E
authors.lastname: Plante
authors.forename: Andrée-Anne
authors.initials: AA
authors.lastname: Bouchard-Thomassin
authors.forename: Serge
authors.initials: S
authors.lastname: Champetier
authors.forename: Elise
authors.initials: E
authors.lastname: Roussel
authors.forename: Marie-Claude
authors.initials: MC
authors.lastname: Drolet
authors.forename: Marie
authors.initials: M
authors.lastname: Arsenault
authors.forename: Jacques
authors.initials: J
authors.lastname: Couet
mesh_terms: D000818:Animals; D001022:Aortic Valve Insufficiency / Q000150:complications* / Q000503:physiopathology; D001794:Blood Pressure; D004195:Disease Models, Animal; D005081:Exercise Therapy; D005355:Fibrosis; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D006339:Heart Rate; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012720:Severity of Illness Index; D013997:Time Factors; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D017725:Ventricular Pressure; D020257:Ventricular Remodeling
chemical_list: D012333:RNA, Messenger