Endurance training in the SHR: conversion of pathologic into physiologic cardiac hypertrophy

GARCIARENA CD; PINILLA OA; NOLLY MB; LAGUENS RP; ESCUDERO EM; CINGOLANI HE; ENNIS IL

HYPERTENSION

Lippincott Williams & Wilkins

Lugar: Baltimore, EE.UU:; Año: 2009 vol. 53 p. 708 - 714

0194-911X

Abstract—The effect of endurance training (swimming 90 min/d for 5 days a week for 60 days) on cardiac hypertrophy wasinvestigated in the spontaneously hypertensive rat (SHR). Sedentary SHRs (SHR-Cs) and normotensive Wistar rats were usedas controls. Exercise training enhanced myocardial hypertrophy assessed by left ventricular weight/tibial length (228
7versus 251
5 mg/cm in SHR-Cs and exercised SHRs [SHR-Es], respectively). Myocyte cross-sectional area increased40%, collagen volume fraction decreased 50%, and capillary density increased 45% in SHR-Es compared withSHR-Cs. The mRNA abundance of atrial natriuretic factor and myosin light chain 2 was decreased by the swimming routine(100
19% versus 41
10% and 100
8% versus 61
9% for atrial natriuretic factor and myosin light chain 2 in SHR-Cs andSHR-Es, respectively). The expression of sarcoplasmic reticulum Ca2 pump was significantly augmented, whereas that ofNa/Ca2 exchanger was unchanged (93
7% versus 167
8% and 158
13% versus 157
7%, sarcoplasmic reticulumCa2 pump and Na/Ca2 exchanger in SHR-Cs and SHR-Es, respectively; P0.05). Endurance training inhibited apoptosis,as reflected by a decrease in caspase 3 activation and poly(ADP-ribose) polymerase-1 cleavage, and normalized calcineurinactivity without inducing significant changes in the phosphatidylinositol 3-kinase/Akt pathway. The swimming routineimproved midventricular shortening determined by echocardiography (32.4
0.9% versus 36.9
1.1% in SHR-Cs andSHR-Es, respectively; P0.05) and decreased the left ventricular free wall thickness/left ventricular cavity radius toward aneccentric model of cardiac hypertrophy (0.59
0.02 versus 0.53
0.01 in SHR-Cs and SHR-Es, respectively; P0.05). Inconclusion, we present data demonstrating the effectiveness of endurance training to convert pathological into physiologicalhypertrophy improving cardiac performance. The reduction of myocardial fibrosis and calcineurin activity plus the increasein capillary density represent factors to be considered in determining this beneficial effect. (