Journalartikel

Jahr der Veröffentlichung: 2012

Seiten: 5389-5400

Zeitschrift: The Journal of Physiology

Bandnummer: 590

Heftnummer: 21

ISSN: 0022-3751

eISSN: 1469-7793

Open Access Status: Green

DOI Link: https://doi.org/10.1113/jphysiol.2012.241141

Verlag: Wiley

Abstract: 
In the present study it was hypothesized that voluntary aerobic exercise favours a pro-fibrotic phenotype and promotes adverse remodelling in hearts from spontaneously hypertensive rats (SHRs) in an angiotensin II-dependent manner. To test this, female SHRs at the age of 1 year were started to perform free running wheel exercise. Captopril was used to inhibit the reninangiotensin system (RAS). Normotensive rats and SHRs kept in regular cages were used as sedentary controls. Training intensity, expressed as mean running velocity, was positively correlated with the left ventricular mRNA expression of TGF-beta 1, collagen-III and biglycan but negatively correlated with the ratio of sarcoplasmic reticulum Ca2+-ATPase (SERCA)2a to Na+-Ca2+ exchanger (NCX). A pro-fibrotic phenotype was verified by Picrosirius red staining. Sixty-seven per cent of SHRs performing free running wheel exercise died either spontaneously or had to be killed during a 6 month follow-up. In the presence of captopril, aerobic exercise did not show a similar positive correlation between training intensity and the expression of fibrotic markers. Moreover, in SHRs receiving captopril and performing free running wheel exercise, a training intensity-dependent reverse remodelling of the SERCA2a-to-NCX ratio was observed. None of these rats died spontaneously or had to be killed. In captopril-treated SHRs performing exercise, expression of mRNA for decorin, a natural inhibitor of TGF-beta(1), was up-regulated. Despite these differences between SHR-training groups with and without captopril, positive training effects (lower resting heart rate and no progression of hypertension) were found in both groups. In conclusion, high aerobic exercise induces an angiotensin II-dependent adverse remodelling in chronic pressure overloaded hearts. However, high physical activity can potentially induce reverse remodelling in the presence of RAS inhibition.

Harvard-Zitierstil: Rebelo, R., Schreckenberg, R. and Schlueter, K. (2012) Adverse cardiac remodelling in spontaneously hypertensive rats: acceleration by high aerobic exercise intensity, The Journal of Physiology, 590(21), pp. 5389-5400. https://doi.org/10.1113/jphysiol.2012.241141

APA-Zitierstil: Rebelo, R., Schreckenberg, R., & Schlueter, K. (2012). Adverse cardiac remodelling in spontaneously hypertensive rats: acceleration by high aerobic exercise intensity. The Journal of Physiology. 590(21), 5389-5400. https://doi.org/10.1113/jphysiol.2012.241141