This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: 53/4/708    most recent HYPERTENSIONAHA.108.126805v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Garciarena, C. D. Articles by Ennis, I. L. Search for Related Content PubMed PubMed Citation Articles by Garciarena, C. D. Articles by Ennis, I. L. Pubmed/NCBI databases Substance via MeSH Medline Plus Health Information High Blood Pressure Related Collections Animal models of human disease Cell signalling/signal transduction Hypertrophy Exercise/exercise testing/rehabilitation

(Hypertension. 2009;53:708.)
© 2009 American Heart Association, Inc.

Original Articles

Endurance Training in the Spontaneously Hypertensive Rat

Conversion of Pathological into Physiological Cardiac Hypertrophy

Carolina D. Garciarena; Oscar A. Pinilla; Mariela B. Nolly; Ruben P. Laguens; Eduardo M. Escudero; Horacio E. Cingolani; Irene L. Ennis

From the Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Buenos Aires, Argentina.

Correspondence to Irene L. Ennis, Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, UNLP, 60 y 120 (1900) La Plata, Argentina. E-mail iennis{at}med.unlp.edu.ar

The effect of endurance training (swimming 90 min/d for 5 days a week for 60 days) on cardiac hypertrophy was investigated in the spontaneously hypertensive rat (SHR). Sedentary SHRs (SHR-Cs) and normotensive Wistar rats were used as controls. Exercise training enhanced myocardial hypertrophy assessed by left ventricular weight/tibial length (228±7 versus 251±5 mg/cm in SHR-Cs and exercised SHRs [SHR-Es], respectively). Myocyte cross-sectional area increased 40%, collagen volume fraction decreased 50%, and capillary density increased 45% in SHR-Es compared with SHR-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 and SHR-Es, respectively). The expression of sarcoplasmic reticulum Ca²⁺ pump was significantly augmented, whereas that of Na⁺/Ca²⁺ exchanger was unchanged (93±7% versus 167±8% and 158±13% versus 157±7%, sarcoplasmic reticulum Ca²⁺ pump and Na⁺/Ca²⁺ exchanger in SHR-Cs and SHR-Es, respectively; P<0.05). Endurance training inhibited apoptosis, as reflected by a decrease in caspase 3 activation and poly(ADP-ribose) polymerase-1 cleavage, and normalized calcineurin activity without inducing significant changes in the phosphatidylinositol 3-kinase/Akt pathway. The swimming routine improved midventricular shortening determined by echocardiography (32.4±0.9% versus 36.9±1.1% in SHR-Cs and SHR-Es, respectively; P<0.05) and decreased the left ventricular free wall thickness/left ventricular cavity radius toward an eccentric model of cardiac hypertrophy (0.59±0.02 versus 0.53±0.01 in SHR-Cs and SHR-Es, respectively; P<0.05). In conclusion, we present data demonstrating the effectiveness of endurance training to convert pathological into physiological hypertrophy improving cardiac performance. The reduction of myocardial fibrosis and calcineurin activity plus the increase in capillary density represent factors to be considered in determining this beneficial effect.

Key Words: exercise training • cardiac hypertrophy • hypertension • calcium handling • apoptosis • signaling pathways

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