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Exercise training prevents β‐adrenergic hyperactivity‐induced myocardial hypertrophy and lesions
Author(s) -
Serra Andrey J.,
Higuchi Maria L.,
Ihara Silvia S.M.,
Antônio Ednei L.,
Santos Marília H.H.,
Bombig Maria T.N.M.,
Tucci Paulo J.F.
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2008.03.016
Subject(s) - medicine , cardioprotection , ventricle , muscle hypertrophy , myocardial hypertrophy , adrenergic , cardiac hypertrophy , endocrinology , heart failure , cardiology , treadmill , myocardial infarction , receptor
Background Sustained β‐adrenoreceptor activation promotes cardiac hypertrophy and cellular injury. Aims To evaluate the cardioprotective effect of exercise on damage induced by β‐adrenergic hyperactivity. Methods Male Wistar rats were randomised into four groups ( n =8 per group): sedentary non‐treated control (C), sedentary treated with isoproterenol 0.3 mg/kg/day administered subcutaneously for 8 days (I), exercised non‐treated (E) and exercised plus isoproterenol administered during the last eight days of exercise (IE). Exercised animals ran on a treadmill for 1 h daily 6 times a week for 13 weeks. Results Isoproterenol caused increases in left ventricle (LV) wet and dry weight/body weight ratio, LV water content and cardiomyocyte transverse diameter. Additionally, isoproterenol induced severe cellular lesions, necrosis, and apoptosis, increased collagen content and reduced capillary and fibre fractional areas. Notably, all of these abnormalities were completely prevented by exercise. Conclusion Our data have demonstrated that complete cardioprotection is possible through exercise training; by preventing β‐adrenergic hyperactivity‐induced cardiac hypertrophy and structural injury.