title: Myocardial alterations in senescent mice and effect of exercise training: a strain rate imaging study.
abstract: BACKGROUND
  Aging is accompanied by an alteration in myocardial contractility. However, its noninvasive detection is difficult. The effect of chronic exercise on this decrease is unknown. Murine models of senescence are increasingly used to test therapies in aging. We tested whether strain rate imaging detected left ventricular (LV) systolic dysfunction in aging mice and was able to assess a potential improvement after exercise.
  
  
  RESULTS
  Young (3 weeks), adult (2 to 3 months), and old (6 to 18 months) C57BL6 male mice underwent echocardiograms with strain rate imaging, either in sedentary conditions or before, 2 weeks and 4 weeks after chronic swimming. Hemodynamic parameters of LV function including maximal and end-systolic elastance were obtained before euthanizing. LV fibrosis was measured using Sirius red staining. Conventional echocardiography was unable to detect LV systolic dysfunction in old mice, whereas both systolic strain rate and load-independent hemodynamic parameters such as preload recruitable stroke work and end-systolic elastance were significantly decreased. Both strain rate and load-independent hemodynamic parameters normalized after 4 weeks of exercise. Both endocardial and epicardial fibrosis were increased in the LV of aging mice. Endocardial fibrosis decreased in exercised aged mice.
  
  
  CONCLUSIONS
  Strain rate noninvasively detects LV systolic dysfunction associated with aging in mice, whereas conventional echocardiography does not. Chronic exercise normalizes LV systolic function and decreases fibrosis in old mice. Strain rate imaging in mice may be a useful tool to monitor the effect of new therapeutic strategies preventing the myocardial dysfunction associated with aging.
authors.affiliation: Inserm U886, Université Claude Bernard Lyon I, Lyon, France. genevieve.derumeaux@chu-lyon.fr
authors.forename: Geneviève
authors.initials: G
authors.lastname: Derumeaux
authors.forename: Fumito
authors.initials: F
authors.lastname: Ichinose
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Raher
authors.forename: John G
authors.initials: JG
authors.lastname: Morgan
authors.forename: Tereza
authors.initials: T
authors.lastname: Coman
authors.forename: Candace
authors.initials: C
authors.lastname: Lee
authors.forename: Jose Maria
authors.initials: JM
authors.lastname: Cuesta
authors.forename: Hélène
authors.initials: H
authors.lastname: Thibault
authors.forename: Kenneth D
authors.initials: KD
authors.lastname: Bloch
authors.forename: Michael H
authors.initials: MH
authors.lastname: Picard
authors.forename: Marielle
authors.initials: M
authors.lastname: Scherrer-Crosbie
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D004452:Echocardiography; D005355:Fibrosis; D006352:Heart Ventricles / Q000473:pathology; D006439:Hemodynamics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D009929:Organ Size; D010805:Physical Conditioning, Animal; D016277:Ventricular Function, Left