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Purpose: Heart failure is one of the most prevalent causes of death in the western world. Caveolin1 knockout mice (cav1-/-) develop a severe hypertrophic cardiomyopathy with functional impairment especially in cardiac output and ejection fraction. Behavior observation during the breeding of this mouse line revealed, that the animals showed a markedly reduced activity. Physiological inactivity can also contribute to heart diseases. The aim of the current study was to test, if moderate physical activity (swim training) can improve heart function and reverse cardiac morphological alterations in this particular model. The efficiency of training was unclear, because caveolin-1 deficiency is associated with eNOS hyperactivation. Hyperactivation of eNOS can lead to massive radical production. Overexpression of eNOS has been described to be counteracting the beneficial effects of training with respect to improved cardiovascular function.

Methods and results: Echocardiographic measurements of 8 week old animals show that cav1-/- mice had an increased left ventricular posterior wall thickness resulting in a reduced left ventricular volume. Previous data from our group have demonstrated that this left ventricular hypertrophy leads to a reduced cardiac function (reduced stroke volume and cardiac output) in older mice combined with reduced physical ability in swimming tests compared to wild type mice. Six weeks of moderate training (2 weeks 5 min/day, 2 weeks 10 min/day and 2 weeks 15 min/day) resulted in markedly prolonged swim duration (untrained: 11±4 min vs. training: 50±12 min) in cav1-/- mice. In line with this, the functional parameters following training showed that stroke volume and cardiac output (measured by echocardiography) were comparable to wild type littermates. Furthermore, the left ventricular wall thickness was reduced in during the training period leading to a significantly higher intraventricular volume. None the less, heart and lung weight of these animals were still significantly elevated.

Conclusions: In conclusion the present study documents that moderate training can inhibit the progression of heart failure in a hypertrophic mouse model with elevated eNOS activity. It remains to be established, if the beneficial effects are mediated by direct cardiac mechanisms, or if alterations in the peripheral circulation e.g. in blood viscosity or in peripheral resistance are involved here.

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The European Society of Cardiology
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