title: Abnormal cardiac response to exercise in a murine model of familial hypertrophic cardiomyopathy.
abstract: Clinical outcome in familial hypertrophic cardiomyopathy (FHC) may be influenced by modifying factors such as exercise. Transgenic mice which overexpress the human disease-causing cTnI gene mutation, Gly203Ser (designated cTnI-G203S), develop all the characteristic phenotypic features of FHC. To study the modifying effect of exercise in early disease, mice underwent swimming exercise at an early age prior to the development of the FHC phenotype. In non-transgenic and cTnI-wt mice, swimming resulted in a significant increase in left ventricular wall thickness and contractility on echocardiography, consistent with a physiological hypertrophic response to exercise. In contrast, cTnI-G203S mice showed no increase in these parameters, indicating an abnormal response to exercise. The lack of a physiological response to exercise may indicate an important novel mechanistic insight into the role of exercise in triggering adverse events in FHC.
authors.forename: Lan
authors.initials: L
authors.lastname: Nguyen
authors.forename: Jessica
authors.initials: J
authors.lastname: Chung
authors.forename: Lien
authors.initials: L
authors.lastname: Lam
authors.forename: Tatiana
authors.initials: T
authors.lastname: Tsoutsman
authors.forename: Christopher
authors.initials: C
authors.lastname: Semsarian
mesh_terms: D000818:Animals; D024741:Cardiomyopathy, Hypertrophic, Familial / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D004452:Echocardiography; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation; D013550:Swimming / Q000502:physiology*; D019210:Troponin I / Q000502:physiology
chemical_list: D019210:Troponin I