Low-intensity aerobic exercise improves cardiac remodelling of adult spontaneously hypertensive rats.

Luana U Pagan,Ricardo L Damatto,Marcelo D M Cezar,Felipe C Damatto,Marina P Okoshi,David R A Reyes,Katashi Okoshi,Aline R R Lima,Bertha F Polegato,Mariana J Gomes,Tulio M M Caldonazo

doi:10.1111/jcmm.14530

Abstract

We evaluated the influence of aerobic training on cardiac remodeling in untreated spontaneously hypertensive rats (SHR). Four experimental groups were used: sedentary (W‐SED, n=27) and trained (WEX, n=31) normotensive Wistar rats, and sedentary (SHR‐SED, n=27) and exercised (SHR‐EX, n=32) hypertensive rats. At 13 months old, trained groups underwent treadmill exercise five days a week for four months. Statistical analysis: ANOVA or Kruskal‐Wallis. Exercised groups had higher physical capacity. Hypertensive groups presented left ventricular (LV) concentric hypertrophy with impaired function. Left atrium diameter, LV posterior wall thickness and relative thickness, and isovolumetric relaxation time were lower in SHR‐EX than SHR‐SED. Interstitial collagen fraction and Type I‐Type III collagen ratio were higher in SHR‐SED than W‐SED. In SHR‐EX these parameters had intermediate values between W‐EX and SHRSED with no differences between either group. Myocardial matrix metalloproteinase‐2 activity, evaluated by zymography, was higher in SHR‐SED than W‐SED and SHR‐EX. TIMP‐2 was higher in hypertensive than normotensive groups. In conclusion, low intensity aerobic exercise reduces left atrium dimension and LV posterior wall thickness, and improves functional capacity, diastolic function, and metalloproteinase‐2 activity in adult SHR.

Highlights

Physical exercise plays an important role in attenuating pathological cardiac remodelling.[1]
The fact that exercise did not change blood pressure is in accordance with previous studies in aged spontaneously hypertensive rats (SHR) 2,7 and suggests that uncontrolled long‐term hypertension is not modulated by physical exercise
A decrease in structural parameters observed in exercised SHR (SHR‐EX) was com‐ bined with improved diastolic function, characterized by a lower isovolumetric relaxation time in SHR‐EX than sedentary spontaneously hypertensive rats (SHR‐SED)

Summary

| INTRODUCTION

Physical exercise plays an important role in attenuating pathological cardiac remodelling.[1]. Hy‐ pertensive rats (SHR) subjected to long‐term voluntary wheel running 2-4 have presented worse cardiac remodelling than sedentary SHR. Wheel running SHR usually perform short series of relatively high‐intensity stints reaching many kilometres a day.[5]. It is possible that a high‐intensity exercise programme produces deleteri‐ ous cardiac effects when performed under increased afterload. We observed that light treadmill exercise over four months reduced myocardial fibrosis and attenu‐ ated ventricular dysfunction in ageing SHR.[7]. We evalu‐ ated the influence of physical training performed before heart failure. As the effects of physical exercise on extracellular matrix changes during cardiac re‐ modelling have been poorly addressed, our focus was on myocardial collagen tissue

| METHODS

| DISCUSSION