title: Swimming exercise in infancy has beneficial effect on the hearts in cardiomyopathic Syrian hamsters.
abstract: The phenotypic expression of cardiomyopathy is greatly influenced by extrinsic factors other than intrinsic genetic defects, such as environmental stress. Exercise is assumed to be an important extrinsic factor, since sudden death is sometimes seen during exercise in young patients with hypertrophic cardiomyopathy (HCM). However, the long-term effects of mild exercise on phenotypic expression in cardiomyopathy remain unclear. To evaluate the effects of exercise performed during infancy or adolescence in cardiomyopathic patients, cardiomyopathic Syrian hamsters (BIO14.6) were subjected to swimming. BIO14.6 and age-matched congenic normal hamsters (CN) as controls were divided into three groups: sedentary (Sed), and trained during infancy (Inf) and during adolescence (Ado). Histological and biochemical analysis of 41-week-old hamsters revealed that (1) the relative level of beta-myosin heavy chain mRNA was significantly lower in the Inf group than in the Sed and Ado groups of BIO14.6. The level in the Inf group of BIO14.6 was compatible with that in the age-matched Sed group of the CN strain; (2) in BIO14.6, degenerative mitochondrial change in the cardiomyocytes was not seen in the Inf group while it was common in the Sed and Ado groups; (3) calcineurin phosphatase activity in the swimming group in 10-week-old CN was significantly higher than that of the age-matched sedentary group, and was as much as that of the swimming and sedentary groups in 10- and 41-week-old BIO14.6.
authors.affiliation: Department of Cardiology, Heart Institute of Japan, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan.
authors.forename: Mariko
authors.initials: M
authors.lastname: Tatsuguchi
authors.forename: Eriko
authors.initials: E
authors.lastname: Hiratsuka
authors.forename: Shuichi
authors.initials: S
authors.lastname: Machida
authors.forename: Toshio
authors.initials: T
authors.lastname: Nishikawa
authors.forename: Shin-Ichiro
authors.initials: S
authors.lastname: Imamura
authors.forename: Satoru
authors.initials: S
authors.lastname: Shimizu
authors.forename: Masahiko
authors.initials: M
authors.lastname: Nishimura
authors.forename: Issei
authors.initials: I
authors.lastname: Komuro
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Furutani
authors.forename: Michiko
authors.initials: M
authors.lastname: Furutani
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Nagao
authors.forename: Keiko
authors.initials: K
authors.lastname: Komatsu
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kasanuki
authors.forename: Rumiko
authors.initials: R
authors.lastname: Matsuoka
mesh_terms: D000367:Age Factors; D000818:Animals; D001835:Body Weight; D002312:Cardiomyopathy, Hypertrophic / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D048429:Cell Size; D006224:Cricetinae; D004195:Disease Models, Animal; D006352:Heart Ventricles / Q000737:chemistry / Q000503:physiopathology*; D066298:In Vitro Techniques; D008647:Mesocricetus; D009206:Myocardium / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000648:ultrastructure; D018995:Myosin Heavy Chains / Q000235:genetics; D009929:Organ Size; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D013550:Swimming / Q000502:physiology; D013997:Time Factors; D016276:Ventricular Function; D024723:Ventricular Myosins / Q000235:genetics
chemical_list: D012333:RNA, Messenger; C120817:calcineurin phosphatase; D010744:Phosphoric Monoester Hydrolases; D024723:Ventricular Myosins; D018995:Myosin Heavy Chains