Abstract
Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N2 uptake and avoiding gas emboli (GE) as they ascend. However, studies of beached and bycaught cetaceans and sea turtles imply that air-breathing marine vertebrates may, under unusual circumstances, develop GE that result in decompression sickness (DCS) symptoms. Theoretical modelling of tissue and blood gas dynamics of breath-hold divers suggests that changes in perfusion and blood flow distribution may also play a significant role. The results from the modelling work suggest that our current understanding of diving physiology in many species is poor, as the models predict blood and tissue N2 levels that would result in severe DCS symptoms (chokes, paralysis and death) in a large fraction of natural dive profiles. In this review, we combine published results from marine mammals and turtles to propose 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 (), varying the level of in different regions of the lung. Man-made disturbances, causing stress, could alter the mismatch level in the lung, resulting in an abnormally elevated uptake of N2, increasing the risk for GE. Our hypothesis provides avenues for new areas of research, offers an explanation for how sonar exposure may alter physiology causing GE and provides a new mechanism for how air-breathing marine vertebrates usually avoid the diving-related problems observed in human divers.
Highlights
Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N2 uptake and avoiding gas emboli (GE) as they ascend
Studies of beached and bycaught cetaceans and sea turtles imply that airbreathing marine vertebrates may, under unusual circumstances, develop GE that result in decompression sickness (DCS) symptoms
The results from the modelling work suggest that our current understanding of diving physiology in many species is poor, as the models predict blood and tissue N2 levels that would result in severe DCS symptoms in a large fraction of natural dive profiles
Summary
While exposure to high pressure is a common challenge among breath-hold divers, there is large variation in respiratory anatomy, function and capacity between genera and even species [1,2,3]. Scholander [10] argued that passive compression of the highly compliant alveolus and rigid conducting airways would result in cessation of gas exchange, which would prevent N2 uptake and reduce the risk of gas emboli (GE) Until recently, this lung compression/alveolar collapse model has been the main hypothesis as to how marine mammals prevent excessive uptake of N2 and avoid divingrelated complications, such as DCS and N2 narcosis. We aim to summarize past studies that have attempted to assess how lung compression and atelectasis alter gas dynamics From this synthesis, we provide an alternative perspective as to how cetaceans, and possibly 2 other marine mammals, and sea turtles, may manage a pulmonary shunt through alteration in alveolar ventilation (V_ A) and perfusion (Q_ ) that allows selective gas exchange during natural dives. We will provide additional data to make a general case as to how volitional V_ A=Q_ regulation could be a common trait to manage gas exchange in cetaceans in particular, and as a general mechanism in other breath-hold divers
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