Key result
Combined resistance and moderate continuous training improves LV systolic function and reduces fibrosis in HF mice.
Why the study?
Does resistance training alone or combined with aerobic training improve cardiac structure, function, and myocardial mitophagic activity in a mouse model of chronic heart failure?
Does resistance training alone or combined with aerobic training improve cardiac structure, function, and myocardial mitophagic activity in a mouse model of chronic heart failure?
In a mouse model of heart failure, moderate-intensity continuous training combined with resistance training provided optimal cardioprotection via the HIF1α-Parkin-mitophagy pathway, whereas high-intensity interval training combined with resistance training showed no protective effect.
Answers are grounded in this paper and cite their sources.
Should not yet change HF exercise prescriptions; leaves open translation of training-type differences to patients.
Resistance exercise is an indispensable mode of exercise rehabilitation for heart failure. Here we elucidate the cardiac effects of resistance training alone or combined with different aerobic trainings on heart failure and explore the critical regulation of mitophagy. The chronic heart failure model was constructed by transverse aortic constriction surgery, followed by 8 wk of resistance training (RT), moderate-intensity continuous training combined with resistance training (MRT), and high-intensity interval training combined with resistance training (HRT), and subsequently analyzed the changes of maximum load, cardiac structure and function, and myocardial mitophagic activity. The role and signaling of mitophagy in exercise protection of heart failure were investigated by knockdown of Hif1α and Parkin genes in primary neonatal cardiomyocytes. RT and especially MRT improved maximum load (P < 0.0001), myocardial morphology and fibrosis (P < 0.0001), reduced left ventricular diameter and enhanced left ventricular systolic function (P < 0.01), and enhanced myocardial mitophagic activity and HIF1α expression (P < 0.05) in heart failure mice. However, HRT had no obvious protective effect on ventricular diameter and function or mitophagy. The abilities of exercise stimulation to regulate reactive oxygen species, adenosine triphosphate, and brain natriuretic peptide were impaired after knockdown of Hif1α and Parkin genes inhibited mitophagy in failing cardiomyocytes (P < 0.05). Different exercise modalities provide discrepant cardiovascular effects on heart failure, and MRT exhibits optimal protection. The HIF1α-Parkin-mitophagy pathway is involved in the protection and regulation of exercise on heart failure.NEW & NOTEWORTHY Impaired myocardial mitophagy is implicated in the pathogenesis of heart failure. Resistance training alone or combined with different aerobic trainings provide discrepant cardiovascular effects on heart failure, and the cardioprotective function depends on HIF1α-Parkin-mitophagy pathway.
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Guo et al. (2023) studied Heart failure. Resistance training (RT) alone or combined with moderate-intensity continuous training (MRT) or high-intensity interval training (HRT) vs. Untrained heart failure model / alternative exercise modalities was evaluated on Maximum load, cardiac structure and function (left ventricular diameter and systolic function), and myocardial mitophagic activity (p=<0.01). Resistance training combined with moderate-intensity continuous training improved maximum load, fibrosis, LV systolic function, and mitophagy in heart failure mice.
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