G. C. Liggins

Pulmonary metabolism during diving: conditioning blood for the brain.

During experimental diving by the awake Weddell seal, blood glucose concentration falls consistently. A large fraction of the glucose consumed from the central circulating blood appears as lactate. During diving, the lung utilizes blood lactate in preference to blood glucose as a source of both carbon and energy, and it is able to release glucose into pulmonary venous blood to supplement the supply available for brain metabolism.

Protective metabolic mechanisms during liver ischemia: Transferable lessons from long-diving animals

During periods of O2 lack in liver of seals, mitochondrial respiration and adenosine triphosphate (ATP) synthesis are necessarily arrested. During such electron transfer system (ETS) arrest, the mitochondria are suspended in functionally protected states; upon resupplying O2 and adenosine diphosphate (ADP), coupled respiration and ATP synthesis can resume immediately, implying that mitochondrial electrochemical potentials required for ATP synthesis are preserved during ischemia. A similar situation occurs in the rest of the cell since ion gradients also seem to be maintained across the plasma membrane; with ion-specific channels seemingly relatively inactive, ion fluxes (e.g., K+ efflux and Ca++ influx) can be reduced, consequently reducing ATP expenditure for ion pumping. The need for making up energy shortfalls caused by ETS arrest is thus minimized, which is why anaerobic glycolysis can be held in low activity states (anaerobic ATP turnover rates being reduced in ischemia to less than 1/100 of typical normoxic rates in mammalian liver and to about 1/10 the rates expected during liver hypoperfusion in prolonged diving). As in many ectotherms, an interesting parallelism (channel arrest coupled with a proportionate metabolic arrest at the level of both glycolysis and the ETS) appears as the dominant hypoxia defense strategy in a hypoxia-tolerant mammalian organ.

Breathing pattern, CO2 elimination and the absence of exhaled NO in freely diving Weddell seals.

UNLABELLED Weddell seals undergo lung collapse during dives below 50 m depth. In order to explore the physiological mechanisms contributing to restoring lung volume and gas exchange after surfacing, we studied ventilatory parameters in three Weddell seals between dives from an isolated ice hole on McMurdo Sound, Antarctica. METHODS Lung volumes and CO(2) elimination were investigated using a pneumotachograph, infrared gas analysis, and nitrogen washout. Thoracic circumference was determined with a strain gauge. Exhaled nitric oxide was measured using chemiluminescence. RESULTS Breathing of Weddell seals was characterized by an apneustic pattern with end-inspiratory pauses with functional residual capacity at the end of inspiration. Respiratory flow rate and tidal volume peaked within the first 3 min after surfacing. Lung volume reductions before and increases after diving were approximately 20% of the lung volume at rest. Thoracic circumference changed by less than 2% during diving. The excess CO(2) eliminated after dives correlated closely with the duration of the preceding dive. Nitric oxide was not present in the expired gas. CONCLUSION Our data suggest that most of the changes in lung volume during diving result from compression and decompression of the gas remaining in the respiratory tract. Cranial shifts of the diaphragm and translocation of blood into the thorax rather than a reduction of thoracic circumference appear to compensate for lung collapse. The time to normalise gas exchange after surfacing was mainly determined by the accumulation of CO(2) during the dive. These findings underline the remarkable adaptations of the Weddell seal for restoring lung volume and gas exchange after diving.

Arterial Oxygen Tensions and Hemoglobin Concentrations of the Free Diving Antarctic Weddell Seal

Diving physiology has interested scientists for over a century (Blix and Folkow 1983). The mammals and birds which dive to great depths for long periods to exploit food sources deep in the ocean have developed remarkable evolutionary adaptations to optimize their diving ability. Some of the respiratory accommodations are obvious to casual inspection, such as a small-lung-volume-to-body-size ratio, thoracic cage mobility, and circular bronchial cartilages (Kooyman 1981). Some respiratory and circulatory adaptations have been observed in the laboratory; captive seals have been forced to dive while monitored by invasive instrumentation (Swan Ganz catheters, left ventricular catheters) (Zapol et al. 1979) or have been subjected to the pressure of depth (hyperbaric chamber) (Kooyman et al. 1972). However, it has been clear for over 10 years that laboratory diving forces an abnormally profound diving reflex, including intense bradycardia and marked regional arterial vasoconstriction (Blix and Folkow 1983; Zapol et al. 1979). This intense bradycardia is far slower than that recorded in free-swimming seals with an electrocardiogram (ECG) and breakoff leads (Kooyman and Campbell 1972).