Abstract The utilization of energy by the working heart has been studied extensively over the years. Because the conversion of chemical energy to mechanical work by the heart is highly dependent on oxygen, the oxygen required and the oxygen available for this conversion are considered to form the conceptual framework of the metabolic demand and supply of the heart, respectively. The oxygen requirement of the myocardium, as assessed by the rate of oxygen consumed (MVO 2), is a function of the mechanical components of ventricular contraction and include: (1) the force developed and sustained by the muscular wall during its contraction; (2) the rate of force development; and (3) the frequency of generating force in the wall per unit time. The oxygen available to the mitochondria, which satisfies this requirement, is primarily determined by the oxygen delivered per unit of time (that is, coronary flow) and the oxygen extracted. Collectively, the response in flow and oxygen extraction represent the metabolic reserve of the heart. Normally, during increments in work, coronary vascular resistance decreases permitting an increment in flow; oxygen extraction (65 to 70 percent) changes little under these circumstances. However, when the response in coronary vascular resistance is limited or at its optimal value, further increments in oxygen requirements are accompanied by an increase in oxygen extraction to 80 to 85 percent; oxygen extraction may exceed 90 percent in the presence of a reduced oxygen-carrying capacity. Stressed beyond the limits of its metabolic reserve (that is, minimum coronary vascular resistance and maximal oxygen extraction) the oxygen available to the heart becomes insufficient and, hence, an aerobic limit is reached. As a consequence, anaerobic metabolism commences, ventricular performance declines and pulsus alternans appear. The concept of inappropriate oxygen demand relative to oxygen supply would appear to be central not only to the patient with coronary artery disease whose oxygen delivery may be compromised, but also to patients with chronic hemodynamic overload (for example, aortic stenosis) whose hypertrophied ventricle is now failing. Moreover, the implications of an aerobic limit may also explain the limits of hypertrophy.