scholarly journals Postnatal development of diving physiology: implications of anthropogenic disturbance for immature marine mammals

2020 ◽  
Vol 223 (17) ◽  
pp. jeb227736
Author(s):  
Shawn R. Noren
Keyword(s):  
Postnatal Development ◽  
Marine Mammals ◽  
Decompression Sickness ◽  
Swimming Performance ◽  
Small Body ◽  
Food Limitation ◽  
Breath Hold ◽  
Oxygen Utilization ◽  
Diving Physiology ◽  
Oxygen Stores

ABSTRACTMarine mammals endure extended breath-holds while performing active behaviors, which has fascinated scientists for over a century. It is now known that these animals have large onboard oxygen stores and utilize oxygen-conserving mechanisms to prolong aerobically supported dives to great depths, while typically avoiding (or tolerating) hypoxia, hypercarbia, acidosis and decompression sickness (DCS). Over the last few decades, research has revealed that diving physiology is underdeveloped at birth. Here, I review the postnatal development of the body's oxygen stores, cardiorespiratory system and other attributes of diving physiology for pinnipeds and cetaceans to assess how physiological immaturity makes young marine mammals vulnerable to disturbance. Generally, the duration required for body oxygen stores to mature varies across species in accordance with the maternal dependency period, which can be over 2 years long in some species. However, some Arctic and deep-diving species achieve mature oxygen stores comparatively early in life (prior to weaning). Accelerated development in these species supports survival during prolonged hypoxic periods when calves accompany their mothers under sea ice and to the bathypelagic zone, respectively. Studies on oxygen utilization patterns and heart rates while diving are limited, but the data indicate that immature marine mammals have a limited capacity to regulate heart rate (and hence oxygen utilization) during breath-hold. Underdeveloped diving physiology, in combination with small body size, limits diving and swimming performance. This makes immature marine mammals particularly vulnerable to mortality during periods of food limitation, habitat alterations associated with global climate change, fishery interactions and other anthropogenic disturbances, such as exposure to sonar.

scholarly journals Deadly diving? Physiological and behavioural management of decompression stress in diving mammals

2011 ◽  
Vol 279 (1731) ◽  
pp. 1041-1050 ◽  
Author(s):  
S. K. Hooker ◽  
A. Fahlman ◽  
M. J. Moore ◽  
N. Aguilar de Soto ◽  
Y. Bernaldo de Quirós ◽  
...  
Keyword(s):  
Marine Mammal ◽  
Marine Mammals ◽  
Multiple Stressors ◽  
Decompression Sickness ◽  
Tissue Injury ◽  
Bubble Formation ◽  
Gas Bubbles ◽  
Breath Hold ◽  
Technological Advances ◽  
Measured Time

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 (N 2 ) 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 N 2 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 N 2 loading to management of the N 2 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.

scholarly journals Pulmonary ventilation–perfusion mismatch: a novel hypothesis for how diving vertebrates may avoid the bends

2018 ◽  
Vol 285 (1877) ◽  
pp. 20180482 ◽  
Author(s):  
Daniel Garcia Párraga ◽  
Michael Moore ◽  
Andreas Fahlman
Keyword(s):  
Gas Exchange ◽  
Marine Mammals ◽  
Decompression Sickness ◽  
Large Fraction ◽  
Pulmonary Ventilation ◽  
Flow Distribution ◽  
Theoretical Modelling ◽  
Breath Hold ◽  
Air Breathing ◽  
Marine Vertebrates

Hydrostatic lung compression in diving marine mammals, with collapsing alveoli blocking gas exchange at depth, has been the main theoretical basis for limiting N 2 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 N 2 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 N 2 , 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.

Comparative seabird diving physiology: first measures of haematological parameters and oxygen stores in three New Zealand Procellariiformes

2015 ◽  
Vol 523 ◽  
pp. 187-198 ◽  
Author(s):  
BJ Dunphy ◽  
GA Taylor ◽  
TJ Landers ◽  
RL Sagar ◽  
BL Chilvers ◽  
...  
Keyword(s):  
New Zealand ◽  
Haematological Parameters ◽  
Diving Physiology ◽  
Oxygen Stores

Hyperbaric treatment of air or gas embolism: current recommendations

2019 ◽  
pp. 673-683
Author(s):  
Richard E. Moon ◽  
Keyword(s):  
Animal Studies ◽  
Decompression Sickness ◽  
Bubble Formation ◽  
Endothelial Damage ◽  
Neurological Deficits ◽  
Breath Hold ◽  
Gas Embolism ◽  
Hyperbaric Treatment ◽  
Pulmonary Capillaries ◽  
Venous Gas Embolism

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac “vapor lock” and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence-based review of adjunctive therapies is presented.

scholarly journals Effect of Dietary Nitrate Supplementation on Swimming Performance in Trained Swimmers

2017 ◽  
Vol 27 (4) ◽  
pp. 377-384 ◽  
Author(s):  
Sam Lowings ◽  
Oliver Michael Shannon ◽  
Kevin Deighton ◽  
Jamie Matu ◽  
Matthew John Barlow
Keyword(s):  
Nitric Oxide ◽  
Repeated Measures ◽  
Swimming Performance ◽  
Time Trial ◽  
Mean Difference ◽  
Breath Hold ◽  
Double Blind ◽  
Nitric Oxide Concentration ◽  
Nitrate Supplementation ◽  
Maximal Effort

Nitrate supplementation appears to be most ergogenic when oxygen availability is restricted and subsequently may be particularly beneficial for swimming performance due to the breath-hold element of this sport. This represents the first investigation of nitrate supplementation and swimming time-trial (TT) performance. In a randomized double-blind repeated-measures crossover study, ten (5 male, 5 female) trained swimmers ingested 140ml nitrate-rich (~12.5mmol nitrate) or nitrate-depleted (~0.01mmol nitrate) beetroot juice. Three hours later, subjects completed a maximal effort swim TT comprising 168m (8 × 21m lengths) backstroke. Preexercise fractional exhaled nitric oxide concentration was significantly elevated with nitrate compared with placebo, Mean (SD): 17 (9) vs. 7 (3)p.p.b., p = .008. Nitrate supplementation had a likely trivial effect on overall swim TT performance (mean difference 1.22s; 90% CI -0.18–2.6s; 0.93%; p = .144; d = 0.13; unlikely beneficial (22.6%), likely trivial (77.2%), most unlikely negative (0.2%)). The effects of nitrate supplementation during the first half of the TT were trivial (mean difference 0.29s; 90% CI -0.94–1.5s; 0.46%; p = .678; d = 0.05), but there was a possible beneficial effect of nitrate supplementation during the second half of the TT (mean difference 0.93s; 90% CI 0.13–1.70s; 1.36%; p = .062; d = 0.24; possibly beneficial (63.5%), possibly trivial (36.3%), most unlikely negative (0.2%)). The duration and speed of underwater swimming within the performance did not differ between nitrate and placebo (both p > .30). Nitrate supplementation increased nitric oxide bioavailability but did not benefit short-distance swimming performance or the underwater phases of the TT. Further investigation into the effects of nitrate supplementation during the second half of performance tests may be warranted.

Diving and swimming performance of white whales, Delphinapterus leucas: an assessment of plasma lactate and blood gas levels and respiratory rates.

1997 ◽  
Vol 200 (24) ◽  
pp. 3091-3099 ◽  
Author(s):  
S A Shaffer ◽  
D P Costa ◽  
T M Williams ◽  
S H Ridgway
Keyword(s):  
High Speed ◽  
Swimming Performance ◽  
Lactate Concentration ◽  
Delphinapterus Leucas ◽  
Breath Hold ◽  
Plasma Lactate ◽  
Post Exercise ◽  
Test Platform ◽  
Plasma Lactate Concentration ◽  
Breath Hold Duration

The white whale Delphinapterus leucas is an exceptional diver, yet we know little about the physiology that enables this species to make prolonged dives. We studied trained white whales with the specific goal of assessing their diving and swimming performance. Two adult whales performed dives to a test platform suspended at depths of 5-300 m. Behavior was monitored for 457 dives with durations of 2.2-13.3 min. Descent rates were generally less than 2 m s-1 and ascent rates averaged 2.2-3 m s-1. Post-dive plasma lactate concentration increased to as much as 3.4 mmol l-1 (4-5 times the resting level) after dives of 11 min. Mixed venous PO2 measured during voluntary breath-holds decreased from 79 to 20 mmHg within 10 min; however, maximum breath-hold duration was 17 min. Swimming performance was examined by training the whales to follow a boat at speeds of 1.4-4.2 m s-1. Respiratory rates ranged from 1.6 breaths min-1 at rest to 5.5 breaths min-1 during exercise and decreased with increasing swim speed. Post-exercise plasma lactate level increased to 1.8 mmol l-1 (2-3 times the resting level) following 10 min exercise sessions at swimming speeds of 2.5-2.8 m s-1. The results of this study are consistent with the calculated aerobic dive limit (O2 store/metabolic rate) of 9-10 min. In addition, white whales are not well adapted for high-speed swimming compared with other small cetaceans.

State of the art review: from the seaside to the bedside: insights from comparative diving physiology into respiratory, sleep and critical care

Thorax ◽  
2019 ◽  
Vol 74 (5) ◽  
pp. 512-518 ◽  
Author(s):  
Paul J Ponganis
Keyword(s):  
Critical Care ◽  
Marine Mammals ◽  
Recent Progress ◽  
State Of The Art ◽  
Extreme Environments ◽  
Human Medicine ◽  
Potential Treatment ◽  
Diving Physiology ◽  
Physiological Adaptations ◽  
Insight Into

Anatomical and physiological adaptations of animals to extreme environments provide insight into basic physiological principles and potential therapies for human disease. In that regard, the diving physiology of marine mammals and seabirds is especially relevant to pulmonary and cardiovascular function, and to the pathology and potential treatment of patients with hypoxaemia and/or ischaemia. This review highlights past and recent progress in the field of comparative diving physiology with emphasis on its potential relevance to human medicine.

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