BackgroundThe maximum metabolic rate (MMR) of mammals is approximately proportional to M0.9, where M is the mammal's body weight. Therefore, MMR increases with body weight faster than does the basal metabolic rate (BMR), which is approximately proportional to M0.7. MMR is strongly associated with the capacity of the cardiovascular system to deliver blood to capillaries in the systemic circulation, but properties of this vascular system have not produced an explanation for the scaling of MMR.ResultsHere we focus on the pulmonary circulation where resistance to blood flow (impedance) places a limit on the rate that blood can be pumped through the lungs before pulmonary edema occurs. The maximum pressure gradient that does not produce edema determines the maximum rate that blood can flow through the pulmonary veins without compromising the diffusing capacity of oxygen. We show that modeling the pulmonary venous tree as a fractal-like vascular network leads to a scaling equation for maximum cardiac output that predicts MMR as a function of M as well as the conventional power function aMb does and that least-squares regression estimates of the equation's slope-determining parameter correspond closely to the value of the parameter calculated directly from Murray's law.ConclusionThe assumption that cardiac output at the MMR is limited by pulmonary capillary pressures that produce edema leads to a model that is in agreement with experimental measurements of MMR scaling, and the rate of blood flow in pulmonary veins may be rate-limiting for the pathway of oxygen.