Abstract
Tight regulation of cardiac oxidative phosphorylation to ensure fast and accurate adaptation to myocardial metabolic demand is of vital importance. There has been much discussion during the last decade on the nature of the signals that stimulate the mitochondria in the heart muscle to increase mitochondrial ATP synthesis when the workload to the heart is increased. The classic view is that ADP, the direct product of ATP hydrolysis, stimulates the mitochondria to increase ATP synthesis when muscle work increases. This is very likely correct in skeletal muscle but was challenged for cardiac muscle tissue (Balaban et al., 1986). Here we will review recent data that throw new light on this issue. We will particularly consider what happens in the first minute during the dynamic adaptation of ATP synthesis to a sudden change in workload to the heart.
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© 1996 Plenum Press, New York
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van Beek, J.H.G.M., Tian, X. (1996). What Determines Cardiac Oxygen Consumption and How is it Regulated?. In: Ince, C., Kesecioglu, J., Telci, L., Akpir, K. (eds) Oxygen Transport to Tissue XVII. Advances in Experimental Medicine and Biology, vol 388. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0333-6_34
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DOI: https://doi.org/10.1007/978-1-4613-0333-6_34
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