Fueling Normal and Diseased Hearts: Myocardial Bioenergetics
Cardiac contractile performance depends upon: (1) the delivery of carbon substrates and oxygen present in the blood to the cardiac extracellular space (via the coronary circulation), (2) the ability of the cardiomyocytes to efficiently extract these subst
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Arthur H.L. From and Robert J. Bache
Abstract
Cardiac contractile performance depends upon: (1) the delivery of carbon substrates and oxygen present in the blood to the cardiac extracellular space (via the coronary circulation), (2) the ability of the cardiomyocytes to efficiently extract these substrates from the extracellular space, and (3) the pathways via which the chemical energy stored within the carbon substrates is transferred to adenosine triphosphate (ATP), an energy storage molecule that can be directly utilized by most chemical energy driven processes. Importantly, ATP synthetic capacity must be sufficient to support a wide range of energy demands with high rates of ATP generation and must not be associated with destabilization of cytosolic and intra- organelle chemical milieus. The latter characteristic is crucial if the performance of the contractile apparatus and intracellular organelles is to remain optimal over the broad range of cardiac work states required by a physically active organism. Hence, even a high rate of myocardial energy expenditure must not induce the fatigue that is known to develop in heavily working skeletal muscle. This chapter describes the ways in which the chemical energy stored in ingested carbon substrates (glucose, fatty acids, and, to a modest extent, proteins) is transferred to ATP and reviews some of the regulatory systems which integrate the function of these pathways and make them responsive to changes in ATP demand without destabilizing the intracellular chemical milieu. The generation of toxic by-products of the metabolic processes and mechanisms that limit their adverse effects are also reviewed. Last of all, the effects of several physiological states and diseases on these processes are briefly discussed, and the concept that the diseased heart may be energy limited is presented. Keywords
Adenosine triphosphate • Myocardial blood flow • Glucose metabolism • Fatty acid metabolism • Electron transport • Oxidative phosphorylation • Regulatory processes • Stable intracellular chemical milieu reactive oxygen species
Abbreviations
A.H.L. From, MD (*) • R.J. Bache, MD Department of Medicine (Cardiovascular Division), Lillihei Heart Institute and Center for Magnetic Resonance Research, University of Minnesota, 2021 6th St. SE, Minneapolis, MN 55455, USA e-mail: [email protected]
ADP AMP AMPK ATP FADH2 LDH NADH NEFA
Adenosine diphosphate Adenosine monophosphate Adenosine monophosphate-activated kinase Adenosine triphosphate Flavin adenine dinucleotide Lactic acid dehydrogenase Nicotinamide adenine dinucleotide Nonesterified free fatty acids
© Springer International Publishing Switzerland 2015 P.A. Iaizzo (ed.), Handbook of Cardiac Anatomy, Physiology, and Devices, DOI 10.1007/978-3-319-19464-6_21
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PDH ROS TCA VLCAD
A.H.L. From and R.J. Bache
Pyruvate dehydrogenase Reactive oxygen species Tricarboxylic acid Very long-chain acyl-CoA dehydrogenase
21.1 Introduction In the interest of putting the subject of myocardial metabolism into a broader perspect
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