Search

Plasticity in the cardiac function of a marine mammal facilitates rapid adjustments to the contrasting metabolic demands of breathing at the surface and diving during an extended apnea. By matching their heart rate ( f H ) to their immediate physiological needs, a marine mammal can improve its metabolic efficiency and maximize the proportion of time spent underwater. Respiratory sinus arrhythmia (RSA) is a known modulation of f H that is driven by respiration and has been suggested to increase cardiorespiratory efficiency. To investigate the presence of RSA in cetaceans and the relationship between f H , breathing rate ( f R ) and body mass ( M b ), we measured simultaneous f H and f R in five cetacean species in human care. We found that a higher f R was associated with a higher mean instantaneous f H (i f H ) and minimum i f H of the RSA. By contrast, f H scaled inversely with M b such that larger animals had lower mean and minimum i f H s of the RSA. There was a significant allometric relationship between maximum i f H of the RSA and M b , but not f R , which may indicate that this parameter is set by physical laws and not adjusted dynamically with physiological needs. RSA was significantly affected by f R and was greatly reduced with small increases in f R . Ultimately, these data show that surface f H s of cetaceans are complex and the f H patterns we observed are controlled by several factors. We suggest the importance of considering RSA when interpreting f H measurements and particularly how f R may drive f H changes that are important for efficient gas exchange. This article is part of the theme issue ‘Measuring physiology in free-living animals (Part I)’.

We measured respiratory flow rates, and expired O2in 32 (2–34 years, body mass [Mb] range: 73–291 kg) common bottlenose dolphins (Tursiops truncatus) during voluntary breaths on land or in water (between 2014 and 2017). The data were used to measure the resting O2consumption rate (V˙O2, range: 0.76–9.45 ml O2 min−1 kg−1) and tidal volume (VT, range: 2.2–10.4 l) during rest. For adult dolphins, the restingVT, but notV˙O2, correlated with body mass (Mb, range: 141–291 kg) with an allometric mass-exponent of 0.41. These data suggest that the mass-specificVTof larger dolphins decreases considerably more than that of terrestrial mammals (mass-exponent: 1.03). The average restingsV˙O2was similar to previously published metabolic measurements from the same species. Our data indicate that the resting metabolic rate for a 150 kg dolphin would be 3.9 ml O2 min−1 kg−1, and the metabolic rate for active animals, assuming a multiplier of 3–6, would range from 11.7 to 23.4 ml O2 min−1 kg−1.\absbreak Our measurements provide novel data for resting energy use and respiratory physiology in wild cetaceans, which may have significant value for conservation efforts and for understanding the bioenergetic requirements of this species.

Decompression sickness (DCS; ‘the bends’) is a disease associated with gas uptake at pressure. The basic pathology and cause are relatively well known to human divers. Breath-hold diving marine mammals were thought to be relatively immune to DCS owing to multiple anatomical, physiological and behavioural adaptations that reduce nitrogen gas (N2) loading during dives. However, recent observations have shown that gas bubbles may form and tissue injury may occur in marine mammals under certain circumstances. Gas kinetic models based on measured time-depth profiles further suggest the potential occurrence of high blood and tissue N2 tensions. We review evidence for gas-bubble incidence in marine mammal tissues and discuss the theory behind gas loading and bubble formation. We suggest that diving mammals vary their physiological responses according to multiple stressors, and that the perspective on marine mammal diving physiology should change from simply minimizing N2 loading to management of the N2 load. This suggests several avenues for further study, ranging from the effects of gas bubbles at molecular, cellular and organ function levels, to comparative studies relating the presence/absence of gas bubbles to diving behaviour. Technological advances in imaging and remote instrumentation are likely to advance this field in coming years. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Bubbles in supersaturated tissues and blood occur in beaked whales stranded near sonar exercises, and post-mortem in dolphins bycaught at depth and then hauled to the surface. To evaluate live dolphins for bubbles, liver, kidneys, eyes and blubber–muscle interface of live-stranded and capture-release dolphins were scanned with B-mode ultrasound. Gas was identified in kidneys of 21 of 22 live-stranded dolphins and in the hepatic portal vasculature of 2 of 22. Nine then died or were euthanized and bubble presence corroborated by computer tomography and necropsy, 13 were released of which all but two did not re-strand. Bubbles were not detected in 20 live wild dolphins examined during health assessments in shallow water. Off-gassing of supersaturated blood and tissues was the most probable origin for the gas bubbles. In contrast to marine mammals repeatedly diving in the wild, stranded animals are unable to recompress by diving, and thus may retain bubbles. Since the majority of beached dolphins released did not re-strand it also suggests that minor bubble formation is tolerated and will not lead to clinically significant decompression sickness.

Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N2uptake 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 N2levels 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 ofin different regions of the lung. Man-made disturbances, causing stress, could alter themismatch 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.