Premium
Exercise training inhibits inflammatory cytokines and more than prevents myocardial dysfunction in rats with sustained β‐adrenergic hyperactivity
Author(s) -
Serra Andrey J.,
Santos Marília H. H.,
Bocalini Danilo S.,
Antônio Ednei L.,
Levy Rozeli F.,
Santos Alexandra A.,
Higuchi Maria L.,
Silva Jr. José A.,
Magalhães Flávio C.,
Baraúna Valério G.,
Krieger José E.,
Tucci Paulo J. F.
Publication year - 2010
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.187310
Subject(s) - proinflammatory cytokine , medicine , endocrinology , muscle hypertrophy , contractility , ventricle , isoprenaline , inflammation , stimulation
Myocardial hypertrophy and dysfunction occur in response to excessive catecholaminergic drive. Adverse cardiac remodelling is associated with activation of proinflammatory cytokines in the myocardium. To test the hypothesis that exercise training can prevent myocardial dysfunction and production of proinflammatory cytokines induced by β‐adrenergic hyperactivity, male Wistar rats were assigned to one of the following four groups: sedentary non‐treated (Con); sedentary isoprenaline treated (Iso); exercised non‐treated (Ex); and exercised plus isoprenaline (Iso+Ex). Echocardiography, haemodynamic measurements and isolated papillary muscle were used for functional evaluations. Real‐time RT‐PCR and Western blot were used to quantify tumour necrosis factor α, interleukin‐6, interleukin‐10 and transforming growth factor β 1 (TGF‐β 1 ) in the tissue. NF‐κB expression in the nucleus was evaluated by immunohistochemical staining. The Iso rats showed a concentric hypertrophy of the left ventricle (LV). These animals exhibited marked increases in LV end‐diastolic pressure and impaired myocardial performance in vitro , with a reduction in the developed tension and maximal rate of tension increase and decrease, as well as worsened recruitment of the Frank–Starling mechanism. Both gene and protein levels of tumour necrosis factor α and interleukin‐6, as well as TGF‐β 1 mRNA, were increased. In addition, the NF‐κB expression in the Iso group was significantly raised. In the Iso+Ex group, the exercise training had the following effects: (1) it prevented LV hypertrophy; (ii) it improved myocardial contractility; (3) it avoided the increase of proinflammatory cytokines and improved interleukin‐10 levels; and (4) it attenuated the increase of TGF‐β 1 mRNA. Thus, exercise training in a model of β‐adrenergic hyperactivity can avoid the adverse remodelling of the LV and inhibit inflammatory cytokines. Moreover, the cardioprotection is related to beneficial effects on myocardial performance.