Abstract
Mitochondrial TCA cycle dehydrogenases have been shown to be stimulated by calcium under various substrate and ADP incubation conditions in an attempt to determine and understand the role of calcium in maintaining energy homeostasis in working hearts. The present study tests the hypothesis that at physiological temperature and 1 mM extramitochondrial free magnesium concentration, calcium can stimulate the overall mitochondrial NADH generation flux in rat heart mitochondrial utilizing pyruvate/malate or 2-oxoglutarate as substrates. In both cases we find that in the physiological regime of mitochondrial oxygen consumption observed in the intact animal, and in the physiological range of cytosolic calcium concentration averaged per beat from 1–6 Hz heart rate, calcium has no apparent effect on the mitochondrial respiratory system. Modest stimulatory effects observed over the sub-physiological calcium range are not sufficient to explain the range of oxygen consumption that can be attained in an intact animal due to feedback from the products of ATP hydrolysis.
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