It is commonly held that the structural capacity of the normal lung is "overbuilt" and exceeds the demand for pulmonary O2 and CO2 transport in the healthy, exercising human. On the other hand, the adaptability of pulmonary system structures to habitual physical training is substantially less than are other links in the O2 transport system. Accordingly, in some highly fit, and even in some not so fit habitually active individuals, the lung's diffusion surface, airways, and/or chest-wall musculature are underbuilt relative to the demand for maximal O2 transport. Two specific pulmonary limitations to exercise performance are proposed: (1) exercise-induced arterial hypoxemia secondary to excessive widening of the alveolar to arterial O2 difference, inadequate hyperventilation, and metabolic acidosis; and (2) highly fatiguing levels of respiratory muscle work which effectively steals blood flow from locomotor muscles via sympathetically mediated reflexes and heightens the perception of limb discomfort and dyspnea. In this brief review, we describe the characteristics and causes of each of these proposed pulmonary limitations and their consequences to maximal O2 uptake and exercise performance.