Key result
Chronic low-intensity exercise training prevented cardiomyocyte dysfunction and impaired adrenergic responsiveness in a swine model of chronic pressure overload-induced heart failure.
Why the study?
Does chronic low-intensity exercise training improve cardiomyocyte Ca2+ handling and contractile function in a large animal model of pressure overload-induced heart failure?
Does chronic low-intensity exercise training improve cardiomyocyte Ca2+ handling and contractile function in a large animal model of pressure overload-induced heart failure?
Chronic low-intensity exercise training prevents cardiomyocyte dysfunction and impaired adrenergic responsiveness in a translational large animal model of chronic pressure overload-induced heart failure.
Answers are grounded in this paper and cite their sources.
Does not alter HF exercise guidance; leaves open translation of swine findings to patients.
Exercise improves clinical outcomes in patients diagnosed with heart failure with reduced ejection fraction (HFrEF), in part via beneficial effects on cardiomyocyte Ca 2+ cycling during excitation-contraction coupling (ECC). However, limited data exist regarding the effects of exercise training on cardiomyocyte function in patients diagnosed with heart failure with preserved ejection fraction (HFpEF). The purpose of this study was to investigate cardiomyocyte Ca 2+ handling and contractile function following chronic low-intensity exercise training in aortic-banded miniature swine and test the hypothesis that low-intensity exercise improves cardiomyocyte function in a large animal model of pressure overload. Animals were divided into control (CON), aortic-banded sedentary (AB), and aortic-banded low-intensity trained (AB-LIT) groups. Left ventricular cardiomyocytes were electrically stimulated (0.5 Hz) to assess Ca 2+ homeostasis (fura-2-AM) and unloaded shortening during ECC under conditions of baseline pacing and pacing with adrenergic stimulation using dobutamine (1 μM). Cardiomyocytes in AB animals exhibited depressed Ca 2+ transient amplitude and cardiomyocyte shortening vs. CON under both conditions. Exercise training attenuated AB-induced decreases in cardiomyocyte Ca 2+ transient amplitude but did not prevent impaired shortening vs. CON. With dobutamine, AB-LIT exhibited both Ca 2+ transient and shortening amplitude similar to CON. Adrenergic sensitivity, assessed as the time to maximum inotropic response following dobutamine treatment, was depressed in the AB group but normal in AB-LIT animals. Taken together, our data suggest exercise training is beneficial for cardiomyocyte function via the effects on Ca 2+ homeostasis and adrenergic sensitivity in a large animal model of pressure overload-induced heart failure. NEW & NOTEWORTHY Conventional treatments have failed to improve the prognosis of heart failure with preserved ejection fraction (HFpEF) patients. Our findings show chronic low-intensity exercise training can prevent cardiomyocyte dysfunction and impaired adrenergic responsiveness in a translational large animal model of chronic pressure overload-induced heart failure with relevance to human HFpEF.
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Hiemstra et al. (2018) studied Pressure overload-induced heart failure (HFpEF model). Chronic low-intensity exercise training vs. Sedentary aortic-banded and healthy controls was evaluated on Cardiomyocyte Ca2+ handling, contractile function, and adrenergic sensitivity. Chronic low-intensity exercise training prevented cardiomyocyte dysfunction and impaired adrenergic responsiveness in a swine model of chronic pressure overload-induced heart failure.
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