Efeitos de uma única sessão de exercício resistido na contratilidade miocárdica e na reatividade vascular de ratos espontaneamente hipertensos.

• Autor(a) principal: Lizardo, Juliana Hott de Fúcio
• Data de Publicação: 2008
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/5160
• topic: Fisiologia; 612

The regular exercise elicits beneficial adaptations in the cardiovascular system, for example reducing resting arterial pressure (AP) and improving vascular and ventricular function. Recently, we investigated the effects of acute exercise after a single bout. After a single endurance exercise session a decrease of resting AP and of vascular reactivity occurs. However, the underlying mechanisms of cardiac and vascular effects evoked by a single resistance exercise (RE) session are unknown. Therefore, the aim of the present study was evaluate the AP, myocardial contractility and vascular reactivity after a single RE session. Spontaneously hypertensive rats (SHR) with 3 months of age weighting 250-300 g were used. The AP was measured in conscious animals. In vitro, we evaluated the tail and aortic vascular contractile responses, the contractility of papillary muscles of left ventricle (LV) and of the isolated heart perfused by the Langendorff technique after an acute RE, in 2 experimental groups: control (Ct) and exercise (Ex). The animals were exercised in an apparatus described previously by Tamaki e cols. (1992). A single RE session caused pronounced decrease of systolic and diastolic AP when compared to pre-exercise conditions (∆ - 79 ± 1.8; - 23 ± 2.3 mmHg, respectively; P<0.05). In the tail artery, the vasodilator response induced by acetylcholine increased the sensitivity (EC50) of dose-response curve in Ex animals (EC50 = 9.8 ± 0.06 log M, P<0.05) when compared to Ct animals (EC50 = 8.7 ± 0.1 log M). The maximal response (Rmax) to phenylephrine decreased after the exercise session (Ex: 276 ± 22 mm Hg vs. Ct: 439 ± 18 mm Hg, P<0.05). This response was abolished after endothelial damage, as well as after L-NAME and indomethacin administration. In aortic rings, the exercise decrease the EC50 (Ex= -5.9 ± 0.07 vs. Ct= -5.3 ± 0.06 log M; P<0.0001) and the Rmax to ACh (Ex= 53 ± 1.6 % vs. Ct= 73 ± 1.5 %; P<0.0001). These responses were abolished in presence of an adenosine receptor antagonist (EC50: Ex= -5.9 ± 0.07 vs. Ct= -5.3 ± 0.06 log M; P<0.0001. Rmax: Ex= 53 ± 1.6 vs. Ct= 73 ± 1.5 %; P<0.0001). The Rmax to FE was reduced after exercise (95 ± 7.9 % vs. Ct 120 ± 4.2 %; P<0,008). This reduction was abolished after endothelial damage and after L-NAME administration. The exercise increased the force development of isolated papillary muscles (Ex: 1.0 ± 0.1 vs. Ct: 0.63 ± 0.2 g/mg, P<0.05). In this preparation, the post-rest contraction (PRC) was greater in exercised animals (4.1 ± 0.4% g/mg vs. Ct: 1.7 ± 0.2% g/mg, P<0.05). Moreover, papillary muscles of exercised animals developed greater force with increasing isoproterenol concentrations (P<0.05). However, the contractile machinery activity evaluated by tetanic contraction was not altered after exercise (Ex: 0.24 ± 0.05 vs. Ct: 0.28 ± 0.05 g/mg, P>0.05). In the isolated perfused heart the exercise increased the left ventricle isovolumetric systolic pressure (LVISP) in baseline conditions (∆ +39 mmHg; P<0.05). Exercised rats presented a greater response to the Frank-Starling mechanism with the progressive increase of diastolic pressure (P<0.05). Under positive inotropic intervention to calcium and isoproterenol the LVISP was greater in Ex animals (P<0.05). The results obtained in the present study showed that a single RE session decrease the resting AP, improves the endothelial function and increases myocardial contractility in SHR.