When the heart fails, it is unable to produce enough energy, leaving the body in an energy-starved state with reduced functioning. Numerous modifications to the metabolic pathways in the failing heart that result in a decrease in the oxidation of either glucose or fatty acid substrates have been found in studies. Diminished energy production is needed to mediate cardiac contraction as a result of this reduced oxidation, which results from abnormalities in mitochondrial activities and/or oxidative phosphorylation. Early-stage clinical studies have demonstrated that fatty acid oxidation inhibitors and antioxidants that target the mitochondria improve cardiac function during failure by increasing compensatory glucose oxidation. Adrenergic receptors (α1 and β) are a crucial regulator of the sympathetic nervous system that controls heart function. Both β-AR blockers and α-1A-AR agonists have potential therapeutic use in the treatment of heart failure. In addition to regulating inotropy and chronotropy, the heart's α1- and β2-adrenergic receptors also regulate metabolic processes that have a positive impact on the heart. In this review, we highlight new research that show how metabolic pathways regulated by adrenergic receptors may be able to restore cardiac energetics to non-failing levels, suggesting potential treatment approaches.
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