title: Exercise tolerance in rats with aortic stenosis and ventricular diastolic and/or systolic dysfunction.
abstract: BACKGROUND
  Physical stress tolerance (ST) is a measurement of cardiorespiratory fitness. Aerobic capacity is reduced in heart failure (HF) although there is no data available on this parameter in animals with ventricular dysfunction and no signs of HF.
  
  
  OBJECTIVE
  Evaluate ST in rats with ventricular diastolic dysfunction isolated or associated with systolic dysfunction induced by ascending aortic stenosis (AoS).
  
  
  METHODS
  Young male Wistar rats (20-30 days old), divided in: control group (CG, n=11) and AoSG group, (n=12). Animals were assessed at 6 and 18 weeks after AoS surgery. Treadmill exercise test was until exhaustion and evaluated treadmill speed and lactate concentration [LAC] at lactate threshold, treadmill speed and [LAC] at exhaustion, and total testing time.
  
  
  RESULTS
  Echocardiography data revealed remodeling of the left atrium and left ventricular concentric hypertrophy at 6 and 18 weeks. Endocardial fractional shortening was greater in AoSG than CG at 6 and 18 weeks. Midwall fractional shortening was greater in AoSG than in CG only 6 week. Cardiac index was similar in CG and AoSG at 6 and 18 weeks and decreased between from 6 to 18 weeks in both groups. The E wave to A wave ratio was greater in CG than in AoSG at both periods and did not change in both groups between week 6 and 18. Treadmill stress testing parameters were similar in both groups at 6 or 18 weeks.
  
  
  CONCLUSIONS
  Although AoS promotes isolated diastolic dysfunction or associated with systolic dysfunction at 6 or 18 weeks, it is not sufficient to modify physical stress tolerance.
authors.affiliation: Departamento de Clínica Médica, Faculdade de Medicina, Universidade Estadual Paulista, Botucatu, SP, Brasil.
authors.forename: Olga Castro
authors.initials: OC
authors.lastname: Mendes
authors.forename: Mario Mateus
authors.initials: MM
authors.lastname: Sugizaki
authors.forename: Dijon Salomé
authors.initials: DS
authors.lastname: Campos
authors.forename: Ricardo Luiz
authors.initials: RL
authors.lastname: Damatto
authors.forename: André Soares
authors.initials: AS
authors.lastname: Leopoldo
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Lima-Leopoldo
authors.forename: Vilmar
authors.initials: V
authors.lastname: Baldissera
authors.forename: Carlos Roberto
authors.initials: CR
authors.lastname: Padovani
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
authors.forename: Antonio Carlos
authors.initials: AC
authors.lastname: Cicogna
mesh_terms: D000818:Animals; D001024:Aortic Valve Stenosis / Q000503:physiopathology*; D003971:Diastole / Q000502:physiology; D004452:Echocardiography; D017079:Exercise Tolerance / Q000502:physiology*; D019344:Lactic Acid / Q000097:blood; D008297:Male; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000502:physiology*; D013599:Systole / Q000502:physiology; D013997:Time Factors; D018754:Ventricular Dysfunction / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000502:physiology
chemical_list: D019344:Lactic Acid