title: Exercise preconditioning attenuates pressure overload-induced pathological cardiac hypertrophy.
abstract: Pathological cardiac hypertrophy, a common response of the heart to a variety of cardiovascular diseases, is typically associated with myocytes remodeling and fibrotic replacement, cardiac dysfunction. Exercise preconditioning (EP) increases the myocardial mechanical load and enhances tolerance of cardiac ischemia-reperfusion injury (IRI), however, is less reported in pathological cardiac hypertrophy. To determine the effect of EP in pathological cardiac hypertrophy, Male 10-wk-old Sprague-Dawley rats (n=30) were subjected to 4 weeks of EP followed by 4-8 weeks of pressure overload (transverse aortic constriction, TAC) to induce pathological remodeling. TAC in untrained controls (n=30) led to pathological cardiac hypertrophy, depressed systolic function. We observed that left ventricular wall thickness in end diastole, heart size, heart weight-to-body weight ratio, heart weight-to-tibia length ratio, cross-sectional area of cardiomyocytes and the reactivation of fetal genes (atrial natriuretic peptide and brain natriuretic peptide) were markedly increased, meanwhile left ventricular internal dimension at end-diastole, systolic function were significantly decreased by TAC at 4 wks after operation (P < 0.01), all of which were effectively inhibited by EP treatment (P < 0.05), but the differences of these parameters were decreased at 8 wks after operation. Furthermore, EP treatment inhibited degradation of IκBα, and decreased NF-κB p65 subunit levels in the nuclear fraction, and then reduced IL2 levels in the myocardium of rats subject to TAC. EP can effectively attenuate pathological cardiac hypertrophic responses induced by TAC possibly through inhibition of degradation of IκB and blockade of the NF-κB signaling pathway in the early stage of pathological cardiac hypertrophy.
authors.affiliation: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University Shanghai, China ; Department of Cardiothoracic Surgery, No.401 Hospital of PLA Qingdao, China.
authors.forename: Tongyi
authors.initials: T
authors.lastname: Xu
authors.affiliation: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University Shanghai, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Tang
authors.affiliation: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University Shanghai, China.
authors.forename: Ben
authors.initials: B
authors.lastname: Zhang
authors.affiliation: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University Shanghai, China.
authors.forename: Chengliang
authors.initials: C
authors.lastname: Cai
authors.affiliation: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University Shanghai, China.
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University Shanghai, China.
authors.forename: Qingqi
authors.initials: Q
authors.lastname: Han
authors.affiliation: Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University Shanghai, China.
authors.forename: Liangjian
authors.initials: L
authors.lastname: Zou
mesh_terms: D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology* / Q000517:prevention & control; D020672:I-kappa B Proteins / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000502:physiology
chemical_list: D020672:I-kappa B Proteins; D020097:Natriuretic Peptide, Brain; D009320:Atrial Natriuretic Factor
keywords: Exercise preconditioning; IκB; NF-κB; pathological cardiac hypertrophy; pressure-overload