Heart rates and diving behavior of leatherback sea turtles in the eastern pacific ocean

Heart rates and diving behavior of leatherback sea turtles (Dermochelys coriacea) were monitored at sea during the internesting interval. Instruments that recorded the electrocardiogram and the depth and duration of dives were deployed on six female leatherback turtles as they laid eggs at Playa Grande, Costa Rica. Turtles dived continually for the majority of the internesting interval and spent 57-68 % of the time at sea submerged. Mean dive depth was 19+/-1 m (mean +/- s.d.) and the mean dive duration was 7.4+/-0.6 min. Heart rate declined immediately upon submergence and continued to fall during descent. All turtles showed an increase in heart rate before surfacing. The mean heart rate during dives of 17.4+/-0.9 beats min-1 (mean +/- s.d.) was significantly lower than the mean heart rate at the surface of 24.9+/-1.3 beats min-1 (P<0.05). Instantaneous heart rates as low as 1.05 beats min-1 were recorded during a 34 min dive. The mean heart rate over the entire dive cycle (dive + succeeding surface interval; 19.4+/-1.3 beats min-1) was more similar to the heart rate during diving than to the heart rate at the surface. Although dive and surface heart rates were significantly different from each other, heart rates during diving were 70 % of heart rates at the surface, showing that leatherback turtles do not experience a dramatic bradycardia during routine diving.

Control of gill ventilation and air-breathing in the bowfin amia calva

The purpose of this study was to investigate the roles of branchial and gas bladder reflex pathways in the control of gill ventilation and air-breathing in the bowfin Amia calva. We have previously determined that bowfin use two distinct air-breathing mechanisms to ventilate the gas bladder: type I air breaths are characterized by exhalation followed by inhalation, are stimulated by aquatic or aerial hypoxia and appear to regulate O2 gas exchange; type II air breaths are characterized by inhalation alone and possibly regulate gas bladder volume and buoyancy. In the present study, we test the hypotheses (1) that gill ventilation and type I air breaths are controlled by O2-sensitive chemoreceptors located in the branchial region, and (2) that type II air breaths are controlled by gas bladder mechanosensitive stretch receptors. Hypothesis 1 was tested by examining the effects of partial or complete branchial denervation of cranial nerves IX and X to the gill arches on gill ventilation frequency (fg) and the proportion of type I air breaths during normoxia and hypoxia; hypothesis II was tested by gas bladder inflation and deflation. Following complete bilateral branchial denervation, fg did not differ from that of sham-operated control fish; in addition, fg was not significantly affected by aquatic hypoxia in sham-operated or denervated fish. In sham-operated fish, aquatic hypoxia significantly increased overall air-breathing frequency (fab) and the percentage of type I breaths. In fish with complete IX-X branchial denervation, fab was also significantly increased during aquatic hypoxia, but there were equal percentages of type I and type II air breaths. Branchial denervation did not affect the frequency of type I air breaths during aquatic hypoxia. Gas bladder deflation via an indwelling catheter resulted in type II breaths almost exclusively; furthermore, fab was significantly correlated with the volume removed from the gas bladder, suggesting a volume-regulating function for type II air breaths. These results indicate that chronic (3-4 weeks) branchial denervation does not significantly affect fg or type I air-breathing responses to aquatic hypoxia. Because type I air-breathing responses to aquatic hypoxia persist after IX-X cranial nerve denervation, O2-sensitive chemoreceptors that regulate air-breathing may be carried in other afferent pathways, such as the pseudobranch. Gas bladder deflation reflexly stimulates type II breaths, suggesting that gas bladder volume-sensitive stretch receptors control this particular air-breathing mechanism. It is likely that type II air breaths function to regulate buoyancy when gas bladder volume declines during the inter-breath interval.