Chapter

Myocardial energetics

Peter H. Sugden and Stephen J. Fuller

in Oxford Textbook of Heart Failure

Published on behalf of Oxford University Press

ISBN: 9780199577729
Published online July 2011 | e-ISBN: 9780199697809 | DOI: http://dx.doi.org/10.1093/med/9780199577729.003.0011

Series: Oxford Textbooks

Myocardial energetics

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The heart is an example of a specialized type I (‘red’) striated muscle in that it is continuously active and reliant principally on aerobic metabolism for its energy supply. Although much of the myocyte volume is taken up by myofibrils, the mitochondria constitute about 30%. In the heart, these subcellular organelles regenerate the bulk of ATP from ADP and inorganic phosphate. ATP is an ‘energy transducing molecule’ which couples the energy available from fuel metabolism into external work (principally myofibrillar contraction). In order to maintain fuel oxidation, ATP regeneration, and muscle contraction, a highly developed coronary circulation and uninterrupted coronary blood flow are necessary to ensure adequate delivery of O2 and fuels, and to remove the product of aerobic metabolism, CO2. The heart is omnivorous and utilizes any metabolic fuel presented to it, within the constraints of metabolic regulation. The major substrates for oxidation in humans are lipid-derived fuels (principally long-chain fatty acids (LCFAs) such as palmitate, but also triglycerides and ketone bodies (acetoacetate and its reduction product, 3-hydroxybutyrate) in specialized circumstances) and the carbohydrate-derived fuels (glucose, lactate, and pyruvate).

Although the heart can oxidize amino acids, these are of minor importance. The accepted dogma is that the human heart relies predominantly (70% ) on lipid-derived fuels for its energy supply, but the majority of investigations have involved postabsorptive subjects where lipid metabolism is generally more favoured than in the immediately postprandial state. The role of cardiac energetics and ‘metabolic remodelling’ are discussed with regards to the transition of the healthy heart into failure.

Chapter.  6946 words.  Illustrated.

Subjects: Cardiovascular Medicine

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