title: Chronic exercise partially restores the transmural heterogeneity of action potential duration in left ventricular myocytes of spontaneous hypertensive rats.
abstract: Hypertension leads to electrophysiological changes in the heart. Chronic exercise induced by a treadmill-running programme (TRP) is considered a potential non-pharmacological treatment for hypertension and may have implications in heart remodelling. However, it is not known whether the TRP is able to improve the electrophysiological properties of the heart in spontaneously hypertensive rats (SHR). In the present study, we investigated whether TRP affects the electrical properties of left ventricular (LV) myocytes isolated from different layers of the LV wall of SHR. Male SHR were divided into exercised (chronic treadmill running for 8 weeks; CEX-SHR) and sedentary (SED-SHR) groups. Age-matched normotensive Wistar male rats served as controls. Action potentials (AP) and transient outward potassium current (I(to) ) were recorded in subepicardial (EPI) and subendocardial (ENDO) LV myocytes. In normotensive controls, AP duration (APD) was longer in ENDO cells than in EPI cells. This sort of transmural heterogeneity in the LV was not observed in sedentary SHR and was partially restored in SHR subject to chronic exercise. This partial recovery was associated with an increase in I(to)  density in EPI cells but not in ENDO cells. The electrophysiological changes observed in the CEX-SHR group were not accompanied by either amelioration of systolic blood pressure or a reduction in heart hypertrophy. These findings imply that a TRP is able to improve the electrophysiological parameters of isolated cardiac myocytes in SHR. This sort of adaptation contributes to the overall improvement of heart physiology in this model.
authors.affiliation: Department of Biochemistry and Immunology, Federal University of Minas Gerais, Belo Horizonte, Minas Gerais, Brazil. drcbio@gmail.com
authors.forename: Danilo
authors.initials: D
authors.lastname: Roman-Campos
authors.forename: Miguel A
authors.initials: MA
authors.lastname: Carneiro-Júnior
authors.forename: Thales N
authors.initials: TN
authors.lastname: Prímola-Gomes
authors.forename: Karina A
authors.initials: KA
authors.lastname: Silva
authors.forename: Judson F
authors.initials: JF
authors.lastname: Quintão-Júnior
authors.forename: Antonio Ns
authors.initials: AN
authors.lastname: Gondim
authors.forename: Hugo L
authors.initials: HL
authors.lastname: Duarte
authors.forename: Jader S
authors.initials: JS
authors.lastname: Cruz
authors.forename: Antonio J
authors.initials: AJ
authors.lastname: Natali
mesh_terms: D000200:Action Potentials; D000818:Animals; D006352:Heart Ventricles / Q000166:cytology; D006973:Hypertension / Q000503:physiopathology* / Q000628:therapy*; D008297:Male; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000502:physiology*; D010805:Physical Conditioning, Animal; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D016277:Ventricular Function, Left