Background: 

Studies investigating the effects of continuously performed exercise on the progression of pressure induced heart failure have not revealed a clear picture. Animal experiments as well as guidelines of several cardiac societies partially contradict each other. These discrepancies are mainly based on different protocols in animal studies with respect to the age and sex of animals, duration of exercise and exercise protocols. The aim of this study was to investigate the combined effect of exercise and standard therapy (ACE Inhibitor) on cardiac remodelling in rats with established hypertension.

Methods: 

Female spontaneously hypertensive rats were included in this study at an age of 12 months and followed up to 6 months. Exercise was performed by free access to running wheels and running activities were monitored by a computerized system. mRNA expression of genes linked to metabolism, hypertrophy, apoptosis and fibrosis were quantified by real time RT-PCR.

Results: 

The mean weekly running distance of the SHR und SHR+Captopril group was 41.7 and 45.7 km/week with a mean running velocity of 2.30 and 2.29 km/h. As expected running activity induced adaptive metabolic changes which are responsible for the beneficial effects of endurance exercise in hypertensives (upregulation of eNOS: 4.2- and 3.1-fold, PGC-1a: 3.8- and 2.4- fold and Nrf-1: 2.3- and 2.4- fold). Within the first eight weeks training was responsible for a reduction of the resting heart rate (388 vs. 438 bpm). From the beginning of week 20 SHR performing exercise showed a successive decompensation. Despite metabolic adaption exercise induced a myocardial hypertrophy and fibrosis (e.g. Collagen-1 mRNA Expression 18,2- fold). Captopril treatment prevented the decompensation of SHR and attenuated the exercise dependent pro-fibrotic and pro-hypertrophic events. Captopril lowered blood pressure in SHRs not performing exercise but not in those that performed exercise.

Conclusion: 

Exercise led to a cardiac decompensation in rats with established hypertension but the addition of standard therapy with ACE inhibition preserves the positive metabolic adaption and attenuates the corresponding pro-hypertrophic and pro-fibrotic events.