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Substrate-deprived ventricular myocytes exhibit oscillatory activation of sarcolemmal ATP-sensitive potassium current (IK,ATP). This effect can account for reduced action potential duration in ischemic regions that can increase the chance for cardiac arrhythmia. Evidence shows that the oscillations appear only within a certain range of the cell nutrition level. Correlation between oscillations of the sarcolemmal IK,ATP, NADH, and inner mitochondrial membrane (IMM) potential suggests the phenomenon originates in the mitochondrial metabolism. Experiments with IMM ion channels show that the periodic behavior can be suppressed by blocking the family of inner membrane anion channels (MAC). In this work, a mathematical model is developed that suggests a possible mechanism of the oscillatory behavior that involves the regulation of the low-conductance IMAC by Mg2+ and pH. Other important features of the model include the phosphate carrier, the F1F0-ATPase, the electron transport chain, and the interaction of Mg2+ and P1 in the mitochondrial matrix. Oscillations can be expected when insufficient energy supply causes impairment in the mitochondrial metabolic pathway. The principle of the proposed mechanism is expressed by kinetic model, which shows limit cycle behavior within certain range of ATP synthesis level. The model predicts matrix pH oscillations, confirmed by other experimental evidence.