Resistance training attenuates salt overload-induced cardiac remodeling and diastolic dysfunction in normotensive rats.

D.L.M Barretti,E.M Oliveira,S.F.S Melo,V.G Barauna

doi:10.1590/1414-431x20176146

D.L.M Barretti, E.M Oliveira + Show 2 more

Open Access

https://doi.org/10.1590/1414-431x20176146

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Abstract

Elevated salt intake induces changes in the extracellular matrix collagen, leading to myocardial stiffness and impaired relaxation. Resistance training (RT) has been used as a remarkably successful strategy in the treatment of heart disease. Therefore, the aim of this study was to investigate the effects of RT on preventing pathological adaptation of the left ventricle (LV) induced by salt overload. Male Wistar rats (10 weeks old) were distributed into four groups (n=8/group): control (CO), control+1% salt (CO+SALT), RT and RT+1% salt (RT+SALT). The RT protocol consisted of 4×12 bouts of squat training, 5/week for 8 weeks, with 80% of one repetition maximum (1RM). Echocardiographs were analyzed and interstitial collagen volume fraction (CVF) was determined in the LV. The 1RM tests in the RT and RT+SALT groups increased 145 and 137%, respectively, compared with the test performed before the training program. LV weight-to-body weight ratio and LV weight-to-tibia length ratio were greater in the RT and RT+SALT groups, respectively, compared with the CO group. Although there was no difference in the systolic function between groups, diastolic function decreased 25% in the CO+SALT group compared with the CO group measured by E/A wave ratio. RT partially prevented this decrease in diastolic function compared with the CO+SALT group. A 1% salt overload increased CVF more than 2.4-fold in the CO+SALT group compared with the CO group and RT prevented this increase. In conclusion, RT prevented interstitial collagen deposition in LV rats subjected to 1% NaCl and attenuated diastolic dysfunction induced by salt overload independent of alterations in blood pressure.

Highlights

Many studies have demonstrated that salt intake is an important determinant of cardiovascular remodeling, such as ventricular hypertrophy and fibrosis [1,2]
Maximal strength In the initial 1RM test, all groups lifted a similar weight (Table 1). Both the Resistance training (RT) (145%) and RT+1% salt (RT+SALT) (137%) groups increased their maximal 1RM at the end of the protocol (Table 1)
This study demonstrated that RT attenuated left ventricular (LV) diastolic dysfunction induced by adding 1% salt in the diet

Summary

Introduction

Many studies have demonstrated that salt intake is an important determinant of cardiovascular remodeling, such as ventricular hypertrophy and fibrosis [1,2]. The effects of high salt intake were initially associated with its ability to elevate blood pressure (BP), later studies have shown that salt intake may have cardiac effects independent of increased pressure load or sympathetic activity [3]. Various mechanisms have been suggested to explain these adverse cardiovascular effects of dietary salt excess, and some evidence supports the role of the local renin-angiotensin system in their development [1]. Salt loading has been shown to induce cardiac remodeling and left ventricular (LV) dysfunction in many animal strains, at all ages, and both in normotensive and hypertensive models [4,5,6]. LV fibrosis, rather than LV hypertrophy, determinates myocardial stiffness and diastolic dysfunction [7,8]

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