Key result
Exercise training rescued dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restored exercise capacity in a mouse model of cardiometabolic HFpEF.
Why the study?
Does exercise training reverse skeletal muscle metabolic dysfunction and improve exercise intolerance in a mouse model of cardiometabolic HFpEF?
Does exercise training reverse skeletal muscle metabolic dysfunction and improve exercise intolerance in a mouse model of cardiometabolic HFpEF?
Exercise training improves exercise intolerance in cardiometabolic HFpEF primarily through peripheral adaptations, specifically by rescuing skeletal muscle metabolic and mitochondrial dysfunction.
[Figure: see text] [Figure: see text]
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Upadhya et al. (2024) conducted an editorial in Cardiometabolic Heart Failure with Preserved Ejection Fraction (HFpEF). Exercise training vs. Sedentary control was evaluated. Exercise training rescued dysfunctional skeletal muscle lipid and branched-chain amino acid oxidation and restored exercise capacity in a mouse model of cardiometabolic HFpEF.
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