title: Cardiac benefits of exercise training in aging spontaneously hypertensive rats.
abstract: OBJECTIVE
  To evaluate the effect of low-intensity chronic exercise training (ExT) on blood pressure (BP), as well as the cardiac alterations associated with hypertension in aging hypertensive rats.
  
  
  METHODS
  Male spontaneously hypertensive rats (SHR; 21 months old) and their normotensive control Wistar-Kyoto (WKY) rats were submitted to low-intensity training protocol for 13 weeks. BP, cardiac morphological and morphometric analysis, as well as gene expression of fibrotic and inflammatory factors were analyzed at the end of the training period.
  
  
  RESULTS
  ExT reduced BP and heart rate in aged SHR. Left ventricle hypertrophy, collagen volume fraction and wall-to-lumen ratio of myocardium arterioles were also decreased in trained SHR. However, ExT was unable to reverse the either reduced capillary density or the cardiac myocyte hypertrophy observed in SHR as compared with WKY rats. Trained SHR showed higher metalloproteinase-2/tissue inhibitor metalloproteinase-2 (MMP-2/TIMP-2) ratio and lower levels of α-smooth muscle actin, but similar levels of connective tissue growth factor, transforming growth factor beta or IL-1 beta to that of nontrained SHR.
  
  
  CONCLUSIONS
  Low to moderate-intensity chronic ExT reverses the cardiac alterations associated with hypertension: myocardial arteriole, left ventricle hypertrophy, collagen content and tachycardia. These changes could be consequence or cause of the reduction in BP observed in trained SHR. In addition, ExT does not worsen the underlying inflammatory burden associated with hypertension. Therefore, the data support a beneficial effect of ExT in aging SHR similar to that reported in young or middle-aged individuals, confirming that exercise is a healthy habit that induces cardiac improvements independently of age.
authors: Department of Physiology and Biophysics, Institute of Biomedical Science, University of Sao Paulo, São Paulo, Brazil.
authors: Luciana V
authors: LV
authors: Rossoni
authors: Raphael A F
authors: RA
authors: Oliveira
authors: Rene R
authors: RR
authors: Caffaro
authors: Maria
authors: M
authors: Miana
authors: David
authors: D
authors: Sanz-Rosa
authors: Márcia K
authors: MK
authors: Koike
authors: Sandra L
authors: SL
authors: Do Amaral
authors: Lisete C
authors: LC
authors: Michelini
authors: Vicente
authors: V
authors: Lahera
authors: Victoria
authors: V
authors: Cachofeiro
mesh_terms: D000199:Actins / Q000378:metabolism; D000375:Aging / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003094:Collagen / Q000378:metabolism; D003331:Coronary Vessels / Q000473:pathology; D015870:Gene Expression; D006321:Heart / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000473:pathology / Q000503:physiopathology; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000235:genetics / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D010805:Physical Conditioning, Animal; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000235:genetics / Q000378:metabolism
chemical_list: D000199:Actins; D012333:RNA, Messenger; D019716:Tissue Inhibitor of Metalloproteinase-2; D003094:Collagen; D020778:Matrix Metalloproteinase 2