Hydrostatic lung compression in diving marine mammals, resulting in atelectasis, has been the main theoretical basis for limiting N2 uptake and avoiding gas emboli as they ascend. However, studies of beached and bycaught cetaceans and sea turtles imply that air breathing marine vertebrates may, under unusual circumstances, develop gas emboli that result in gas emboli (decompression sickness symptoms). Theoretical modelling of tissue and blood gas dynamics of breath-hold divers suggests that our current understanding of diving physiology in many species is poor, as the models predict DCS in most of their natural dive profiles. In this lecture published results from marine mammals and turtles are presented present an alternative mechanisms for how marine vertebrates control gas exchange in the lung, through management of the pulmonary distribution of alveolar ventilation ( ) and cardiac output/lung perfusion (Q ), varying the level of / (Q ) mismatch in the lung. Results from studies on anatomy and physiology in animals and humans are combined to develop a novel hypothesis how marine mammals, and cetaceans in particular, could have volitional control of gas exchange during diving. This hypothesis provides an explanation for how man-made disturbances, causing stress, could alter the / Q mismatch level in the lung, resulting in an abnormally elevated uptake of N2, increasing the risk for gas emboli. In addition, this new hypothesis also explains how marine mammals are able to utilize the lung as an O2 store while minimizing N2 uptake and the risk for gas emboli. This hypothesis provides avenues for new areas of research, offers an explanation for how sonar exposure may alter physiology causing gas emboli, and provides a new mechanism for how marine vertebrates can avoid the diving related problems observed in human divers.