Forced Dives Research Articles

The role of cognition as a factor regulating the diving responses of animals, including humans.

The dive response involves three main components - breath holding, reduced heart rate and increased peripheral vasoconstriction - and is ubiquitous during forced dives in air-breathing vertebrates; however, numerous studies in free-diving animals have shown that the heart rate response to diving varies considerably in a manner that suggests cognitive control. Furthermore, studies on free-diving animals and controlled experiments in trained animals both indicate that the dive response can be conditioned, such that the reduction in heart rate begins before submergence and the extent of the reduction is set early in the dive. In addition, numerous species also experience an increase in heart rate and blood flow during ascent at the end of a dive, a phenomenon commonly called 'ascent tachycardia'. Collectively, these data suggest that although the dive response is under autonomic control, many species can vary its magnitude depending on the length and type of the planned dive - an indication of a role for cognition in the overall physiological responses associated with diving. Here, we provide examples of the conditioned cardiac responses - including anticipatory changes in heart rate - in several diving species and propose potential underlying mechanisms. We also discuss how the anticipatory cardiovascular responses not only improve diving capacity, but also prevent diving-related problems, such as decompression sickness or barotrauma, through a mechanism described by the selective gas exchange hypothesis.

Adaptations to deep and prolonged diving in phocid seals.

This Review focuses on the original papers that have made a difference to our thinking and were first in describing an adaptation to diving, and less on those that later repeated the findings with better equipment. It describes some important anatomical peculiarities of phocid seals, as well as their many physiological responses to diving. In so doing, it is argued that the persistent discussions on the relevance and differences between responses seen in forced dives in the laboratory and those during free diving in the wild are futile. In fact, both are two sides of the same coin, aimed at protecting the body against asphyxic insult and extending diving performance.

The cardiovascular and endocrine responses to voluntary and forced diving in trained and untrained rats

The mammalian diving response, consisting of apnea, bradycardia, and increased total peripheral resistance, can be modified by conscious awareness, fear, and anticipation. We wondered whether swim and dive training in rats would 1) affect the magnitude of the cardiovascular responses during voluntary and forced diving, and 2) whether this training would reduce or eliminate any stress due to diving. Results indicate Sprague-Dawley rats have a substantial diving response. Immediately upon submersion, heart rate (HR) decreased by 78%, from 453 +/- 12 to 101 +/- 8 beats per minute (bpm), and mean arterial pressure (MAP) decreased 25%, from 143 +/- 1 to 107 +/- 5 mmHg. Approximately 4.5 s after submergence, MAP had increased to a maximum 174 +/- 3 mmHg. Blood corticosterone levels indicate trained rats find diving no more stressful than being held by a human, while untrained rats find swimming and diving very stressful. Forced diving is stressful to both trained and untrained rats. The magnitude of bradycardia was similar during both voluntary and forced diving, while the increase in MAP was greater during forced diving. The diving response of laboratory rats, therefore, appears to be dissimilar from that of other animals, as most birds and mammals show intensification of diving bradycardia during forced diving compared with voluntary diving. Rats may exhibit an accentuated antagonism between the parasympathetic and sympathetic branches of the autonomic nervous system, such that in the autonomic control of HR, parasympathetic activity overpowers sympathetic activity. Additionally, laboratory rats may lack the ability to modify the degree of parasympathetic outflow to the heart during an intense cardiorespiratory response (i.e., the diving response).

Cardiovascular responses to voluntary and forced underwater submergence in trained and untrained rats

The mammalian diving response consists of apnea, a parasympathetically‐induced bradycardia and a sympathetically‐induced increase in peripheral resistance. Although initiation of this autonomic response is a trigeminally mediated reflex, we wanted to determine if the magnitudes of the cardiovascular responses to diving are altered by the nature of the dive or previous diving experience. Six rats were trained in both voluntary and forced diving, while 6 other rats received no training. All rats were implanted with telemetric transmitters to record mean arterial blood pressure (BP, in mm Hg) and heart rate (HR, in beats per minute). In trained rats undergoing voluntary dives HR immediately decreased from 468 ± 14 to 128 ± 16 and BP increased from 145 ± 1 to a maximum of 169 ± 4, while in untrained rats HR immediately decreased from 468 ± 21 to 98 ± 11 and BP increased from 136 ± 4 to a maximum of 173 ± 4. In trained rats undergoing forced dives HR immediately decreased from 442 ± 4 to 125 ± 16 and BP increased from 132 ± 4 to a maximum of 191 ± 8, while in untrained rats HR immediately decreased from 452 ± 14 to 115 ± 9 and BP increased from 125 ± 4 to a maximum of 194 ± 5. We conclude that the type of dive and previous experience alters the magnitude of the HR and BP responses to underwater submergence. This suggests that cortical input can modify both the parasympathetic and sympathetic limb of this autonomic reflex. Supported by NIH R15 HL080007.

To what extent might N2 limit dive performance in king penguins?

A mathematical model was used to explore if elevated levels of N2, and risk of decompression sickness (DCS), could limit dive performance (duration and depth) in king penguins (Aptenodytes patagonicus). The model allowed prediction of blood and tissue (central circulation, muscle, brain and fat) N2 tensions (P(N2)) based on different cardiac outputs and blood flow distributions. Estimated mixed venous P(N2) agreed with values observed during forced dives in a compression chamber used to validate the assumptions of the model. During bouts of foraging dives, estimated mixed venous and tissue P(N2) increased as the bout progressed. Estimated mean maximum mixed venous P(N2) upon return to the surface after a dive was 4.56+/-0.18 atmospheres absolute (ATA; range: 4.37-4.78 ATA). This is equivalent to N2 levels causing a 50% DCS incidence in terrestrial animals of similar mass. Bout termination events were not associated with extreme mixed venous N2 levels. Fat P(N2) was positively correlated with bout duration and the highest estimated fat P(N2) occurred at the end of a dive bout. The model suggested that short and shallow dives occurring between dive bouts help to reduce supersaturation and thereby DCS risk. Furthermore, adipose tissue could also help reduce DCS risk during the first few dives in a bout by functioning as a sink to buffer extreme levels of N2.

Stroke volume and cardiac output in juvenile elephant seals during forced dives

The aim of this study was to examine the effect of forced diving on cardiac dynamics in a diving mammal by evaluating cardiac output and heart rate. We used MR Imaging and phase contrast flow analysis to obtain accurate flow measurements from the base of the aorta. Heart rate (fh) and cardiac output (Q) were measured before, during and after dives in four restrained juvenile northern elephant seals, Mirounga angustirostris, and stroke volume (Vs) was calculated (Vs=Q/fh). Mean Q during diving (4011+/-387 ml min(-1)) and resting (6530+/-1018 ml min(-1)) was not significantly different (paired t-test; P<0.055). Diving was accompanied by a 20% increase in Vs over the pre-dive level. Pre-dive, post-dive or diving fh was not significantly correlated with Vs during any state. Diving Vs correlated negatively with the bradycardic ratio (diving fh to pre-dive fh). In this study, the degree of bradycardia during diving was less than in previous pinniped studies, suggesting that the reduction in vagal input may contribute to the observed increase in Vs.

Effects of forced diving on the spleen and hepatic sinus in northern elephant seal pups.

In phocid seals, an increase in hematocrit (Hct) accompanies diving and periods of apnea. The variability of phocid Hct suggests that the total red cell mass is not always in circulation, leading researchers to speculate on the means of blood volume partitioning. The histology and disproportionate size of the phocid spleen implicates it as the likely site for RBC storage. We used magnetic resonance imaging on Northern elephant seals to demonstrate a rapid contraction of the spleen and a simultaneous filling of the hepatic sinus during forced dives (P < 0.0001, R(2) = 0.97). The resulting images are clear evidence demonstrating a functional relationship between the spleen and hepatic sinus. The transfer of blood from the spleen to the sinus provides an explanation for the disparity between the timing of diving-induced splenic contraction ( approximately 1-3 min) and the occurrence of peak Hct (15-25 min). Facial immersion was accompanied by an immediate and profound splenic contraction, with no further significant decrease in splenic volume after min 2 (Tukey-Kramer HSD, P = 0.05). At the conclusion of the dive, the spleen had contracted to 16% of its predive volume (mean resting splenic volume = 3,141 ml +/- 68.01 ml; 3.54% of body mass). In the postdive period, the spleen required 18-22 min to achieve resting volume, indicating that this species may not have sufficient time to refill the spleen when routinely diving at sea, which is virtually continuous with interdive surface intervals between 1 and 3 min.

Effect of temperature on oxygen stores during aerobic diving in the freshwater turtle Mauremys caspica leprosa.

Oxygen stores available for aerobic diving were studied in the freshwater turtle (Mauremys caspica leprosa) at three constant body temperatures (15 degrees, 25 degrees, and 35 degrees C) and during the thermal transient (30 degrees-15 degrees C) induced by immersion in cold water. The term "aerobic dive limit" has been defined as the maximal duration of the dive before lactate increases. This increase occurs when a critical PO2 value is reached, and it is well characterized at lung level by a sharp increase in the lung apnoeic respiratory quotient. Kinetic analysis of lung gas composition during forced dives at fixed body temperature shows that critical PO2 values rise with temperature and that the postventilatory PO2 at the beginning of a dive decreases, so that the two temperature-dependent factors lead to a significant decrease with temperature in the lung O2 stores available for aerobic diving. During dives with transient body cooling, a natural condition in M. caspica leprosa, temperature equilibration occurs fast enough to expand aerobic scope by bearing the critical PO2 to the same value obtained at a fixed temperature of 15 degrees C. These dives are characterized by reversed CO2 transport (from lung to tissues) and therefore by negative values of the lung respiratory quotient; a decrease in temperature increases CO2 capacitance of tissues, resulting in a fall in PCO2 at constant CO2 content. Because this does not occur in the gas phase, PCO2 difference can lead to diffusion in the direction opposite from normal. This pattern may favour lung-to-tissue O2 transfer, through the Bohr effect. Therefore, the aerobic dive limit is reduced at high temperature not only through a metabolic rate effect but also through a marked decrease in the available O2 stores; fast body cooling (30 degrees-15 degrees C) associated with immersion in cold water extends the O2 stores available for aerobic diving to a level similar to that of immersions at constant body temperatures that are in equilibrium with water temperature.

Autonomic nervous control of heart rate in muskrats during exercise in air and under water.

Neural control of the cardiac responses to exercise in air (running) and under water (diving) was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine and the beta-adrenergic blocker nadolol. Saline injection was used as a control. Controls running on a treadmill showed a marked increase in heart rate with exercise. Atropine-treated animals had a higher resting heart rate than controls, but heart rate still increased with running. Nadolol-treated animals had a lower resting heart rate than controls and displayed a less pronounced increase in heart rate with running than controls. Animals treated with a combination of atropine and nadolol had a resting heart rate similar to that of controls but their heart rate was unaffected by running. Thus, exercise tachycardia in muskrats is due to activation of the sympathetic system and also to a reduction in parasympathetic tone. Heart rate decreased markedly during voluntary submergence in controls but rose as muskrats swam submerged against increasing water flows. Nevertheless, diving bradycardia was still present. Free-diving bradycardia and the relative increase in heart rate with underwater exercise were abolished by atropine and unaffected by nadolol. Hence, unlike the cardiac response to exercise in air, the cardiac response to underwater exercise is due only to a reduction in parasympathetic tone. Injection of the beta-adrenergic agonist isoproterenol markedly increased heart rate in air but had little effect during voluntary and forced dives, indicating a marked decrease in the sensitivity of cardiac cells to adrenergic stimulation during submergence. These results strongly suggest that accentuated antagonism between the two branches of the autonomic nervous system occurs during diving so that parasympathetic influences on the heart predominate and inhibit any chronotropic response to adrenergic stimulation.

Effect of pharmacological blockade on cardiovascular responses to voluntary and forced diving in muskrats.

Neural control of free and forced diving bradycardia and peripheral resistance was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine, the alpha-adrenergic blocker phentolamine and the beta-adrenergic blockers nadolol and propranolol. Saline injection was used as a control. Heart rate in control animals increased before voluntary dives and dropped markedly as soon as the animals submerged. Heart rate started increasing towards the end of voluntary dives and reached pre-dive values within the first 5 s of recovery. Pre-dive and post-dive tachycardia were reduced in beta-blocked animals, emphasizing the role of the sympathetic system during the preparatory and recovery periods of voluntary dives. Diving bradycardia and the acceleration in heart rate before surfacing were abolished by atropine and unaffected by nadolol, demonstrating the importance of vagal efferent activity during diving. The results after blockade with nadolol suggest that there is an accentuated antagonism between the two branches of the autonomic nervous system during diving, so that parasympathetic influences on the heart predominate. Propranolol-treated muskrats had a higher diving heart rate than saline- and nadolol-treated animals, which may be due to a sedative effect caused by propranolol crossing the blood-brain barrier, a blockade of central catecholaminergic pathways or a peripheral neural effect, due to the anaesthetic properties of propranolol. Phentolamine did not affect diving bradycardia, indicating that diving bradycardia occurs independently of peripheral vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic responses to forced dives in Pekin duck measured by indirect calorimetry and 31P-MRS.

We tested the hypothesis that forced-dived ducks experience a reduction in metabolic rate during prolonged submergence. Unidirectionally ventilated conscious ducks were subjected to forced dives by temporarily stopping the airflow in the ventilation system and simultaneously filling a face mask with cold water. A typical cardiovascular response to submergence was observed: bradycardia and maintained arterial blood pressure. Phosphorylated metabolite concentrations in the pectoral muscle were measured noninvasively by phosphorus magnetic resonance spectroscopy (31P-MRS). ATP content was constant, and phosphocreatine was depleted via the creatine kinase reaction at a rate similar to the resting rate of ATP turnover, which was estimated to be 0.9 mumol.min-1 x g-1 in resting perfused pectoral muscle of pentobarbital-anesthetized ducks. Oxygen from myoglobin supplied at most 12% of the ATP required by the resting muscle during dives. Whole animal postdive excess oxygen consumption and blood lactic acid accumulation suggested that the shortfall in aerobic metabolism during forced dives was compensated by an increase in anaerobic metabolism.

Voluntary diving metabolism and ventilation in the loggerhead sea turtle

Ventilation and gas exchange patterns were examined during voluntary dives in the loggerhead sea turtle Caretta caretta (L.) and contrasted with the changes that occur during forced submergence. Turtles spent 86% of their time submerged, with a mean dive length of 16.1 ± 6.0 ( sd) min. During voluntary dives lasting 5–40 min, arterial blood P O2 fell to a minimum of 23 torr but turtles often surfaced before P O2 levels reached 50 torr. Arterial P CO2 increased typically < 10 torr while pH was held nearly constant, decreasing ⩽0.03-0.1U⪷dive −1. In voluntary submergence, aerobic limits were much longer than that of forced dives. The changes in blood acid-base status during voluntary submergence differed substantially from those reported in turtles forcibly submerged, and may account for the apparently reduced submersion endurance of sea turtles accidentally captured in shrimp trawls.

Cortical Influences on Diving Bradycardia in Muskrats (Ondatra zibethicus)

Muskrats (Ondatra zibethicus) freely diving for food in an indoor tank were monitored with a video camera and a VCR unit. The EKG was telemetered from the animals and recorded on the audio channel of the VCR tape. Heart rate responses to voluntary dives were analyzed and compared with those from escape andforced dives. Heart rate responses from decorticate and sham-operated muskrats were also recorded to elucidate the role that the cerebral cortex plays in the dive response. In intact animals voluntary, escape, and forced submergence resulted in progressively greater decreases in heart rate. At 5 s into the dive, heart rate had fallen by 56% in voluntary dives, 65% in escape dives, and 73% in forced dives. Intensification of the bradycardia in escape and forced dives to a lower heart rate than that seen in voluntary dives was mediated by the cerebral cortex. Heart rate in decorticate muskrats in escape and forced dives did not fall below that seen in voluntary dives. However, there appeared to be a recovery of cortical function in decorticate muskrats because intensification of bradycardia in forced dives reappeared with time after surgery. Diving bradycardia was not due to fear or stress but occurred as a result ofsubmersion per se, although there was a marked cortical influence on the response in that bradycardia was intensified in escape and forced dives.

The source of circulating catecholamines in forced dived ducks

Plasma catecholamines have been measured in chronically adrenalectomized (ADX) ducks, in chronically adrenal-denervated ducks (DNX), and in their respective shamoperated controls (SH-adx, SH-dnx) after 3 min forced submergence. The results showed that 100% of the plasma epinephrine (EP) and 70 to 80% of plasma norepinephrine (NE) released during the dive came from the adrenal glands. Only 20 to 30% of plasma NE came from the endings of the autonomic vascular sympathetic nerves which are strongly stimulated during diving. Adrenal catecholamines were released by nerve activation only; nonneural mechanisms did not play any role in their release. The action of adrenal catecholamines on the cardiovascular system during dives was investigated by measuring heart rate and arterial blood pressure in operated and sham-operated ducks. Cardiovascular adjustments, associated with 3 min of forced diving, were not affected by any differences in the levels of plasma catecholamines.

Thermoregulatory control of expired air temperature in diving harp seals.

Expired air temperature (Tex), metabolic rate (MR), and skin (Ts) and body (Tb; rectal) temperatures were recorded in four or five young (1-2 yr) harp seals (Phoca groenlandica) in air [mean air temperature (Ta) = -30, -10, or 10 degrees C] and in water [mean water temperature (Tw) = 2.3 or 24.8 degrees C, with Ta = -30, -10, 0, or 10 degrees C]. Apparent lower critical temperature was below -10 degrees C in air. Above this Ta, mean MR was 5.85 W.kg-0.75 (2.23 W.kg-1), while mean MR was 12.56 W.kg-0.75 (4.69 W.kg-1) at Ta -30 degrees C. When seals were immersed in water of 2.3 degrees C, mean MR was 6.13 W.kg-0.75 (2.31 W.kg-1), regardless of Ta. At Ta -30, -10, and 10 degrees C, mean Tex in air were 9.5, 13.0, and 25.0 degrees C, respectively. The corresponding values for seals in water (Tw = 2.3 degrees C) were 8.0, 9.5, and 15.5 degrees C, respectively. The low Tex recorded at Ta -30 and -10 degrees C in air and at all Ta in water (Tw = 2.3 degrees C) suggests that heat was conserved by nasal heat exchange. At Ta 10 degrees C, mean Tex of seals in air was approximately 10 degrees C higher than mean Tex of seals in water (Tw = 2.3 degrees C). Furthermore, seals subjected to a Tw of 24.8 degrees C at Ta 0 degrees C had a mean Tex 10 degrees C higher than when subjected to Tw 2.3 degrees C at the same Ta. These observations suggest that Tex in seals is under thermoregulatory control. In a series of forced dives of up to 5-min duration Tex was found to be the same before and after the dive regardless of dive duration and Ta.

The effect of breathing oxygen and air on diving bradycardia in cormorants (Phalacrocorax auritus).

ABSTRACT Cardiovascular chemoreceptors are crucial for the development of forced diving responses in dabbling ducks such as the mallard (Anas platyrhynchos). Denervation of the peripheral chemoreceptors or allowing the duck to breath 100 % oxygen before a forced dive eliminates or considerably delays the onset of noticeable bradycardia (Jones &amp; Purves, 1970; Mangalam &amp; Jones, 1984). These procedures have no effect on the level of bradycardia established after 10 s or so underwater in diving ducks or cormorants in forced dives (Butler &amp; Woakes, 1982; Mangalam &amp; Jones, 1984; Furilla &amp; Jones, 1986). The afferent neural pathway for the dive response is unclear in cormorants, but in diving ducks it is the stimulation of nasal receptors with water that causes dive bradycardia (Furilla &amp; Jones, 1986). When forced dives are prolonged, then peripheral chemoreceptors appear to affect heart rate in diving ducks. Heart rate is elevated in ducks (Aythya fuligula) in which the carotid body has been denervated, compared with intact ducks, after 50 s or so of forced submergence (Butler &amp; Woakes, 1982). The purpose of the present study was to investigate whether chemoreflexes also influence heart rate in cormorants in forced dives of up to 120s duration.

Forced and voluntary diving in ducks: cardiovascular adjustments and their control

Diving ducks submerge voluntarily for less than 1 min yet, in forced dives in the laboratory, redhead ducks can endure at least 8 min underwater. This is much longer than a dabbling duck of the same body mass can endure and is a result of the quicker onset of oxygen-conserving cardiovascular responses in divers. Oxygen conservation during forced dives is indicated by a profound bradycardia as blood flow is restricted to cerebral and central cardiovascular areas. In voluntary dives, on the other hand, heart rate is frequently above resting rates, and blood flow is preferentially directed to the working muscles of the hind limbs. Profound bradycardia only occurs in unrestrained ducks when they are trapped underwater. Since leg movements cease within 30 s after ducks are trapped, blood flow must at that time be directed away from the working muscles, as in the "classical" oxygen-conserving dive response. Cardiovascular adjustments to forced diving are caused by stimulation of nasal receptors in diving ducks. In dabblers, arterial chemoreceptor stimulation is crucial to the response, although an intact barostatic system may be necessary for development of profound bradycardia. Baroreceptors are essential for the cardiac response observed when dabblers are trained to dive for food, although neither baro-, chemo-, nor naso-receptors appear to have much to do with the cardiac adjustments to voluntary submergence in diving ducks. Nevertheless, in divers, cardiac adjustments to dabbling and forced, voluntary, and trapped dives are linearly related on a plot of dive (trapped) against the logarithm of predive (pretrap) heart rate. This relationship is due to a similar increase in vagal activity, of some 50% of maximum, in all types of diving manoeuvers. Phychogenic factors, long thought to be important in cardiac responses to forced diving, would appear to underpin this relationship.

Circulatory responses of seals to periodic breathing: heart rate and breathing during exercise and diving in the laboratory and open sea

In terms of a seal's success as a predator, the ability to spend a high fraction of time submerged and yet remain in a steady state is at least as important as that to make long dives. This aspect of seal physiology has received much less attention than has the ability to dive for extended periods and yet is important to the context in which dive-related morphological and physiological specializations are considered. We found, in seals exercising in the laboratory, that as [Formula: see text] increased, heart rate during breathing bouts was high and unchanging. Heart rate during dives was 25 to 33% of the rate during breathing and was insensitive to metabolic rate. However, the fraction of time seals spent breathing and overall average heart rate increased with exercise. We have confirmed these patterns using very high frequency and acoustic telemetry in freely diving harbour seals in the open sea. Heart rate at the surface was virtually constant at 120 beats/min and independent of dive duration. While the seals were diving, heart rate fell to 40 beats/min. Average heart rate depended almost entirely on the proportion of time spent below the surface and only to a minor extent on dive length. The exceedingly low heart rates seen during forced dives in the laboratory were never observed at sea.

Visualizing metabolic transitions in aquatic mammals: does apnea plus swimming equal "diving"?

While diving, aquatic mammals must balance the oxygen conservation requirements of apnea with the oxygen utilization requirements of exercise. The resulting metabolic state depends on a complex range of behavioral, physiological, and metabolic conditions as required by the particular dive profile. Thus, at the one extreme of long duration diving, oxygen conservation requirements will outweigh those of exercise, while under conditions of rapid, short diving or propoising, exercise parameters will probably be of more importance than those of oxygen conservation. In the last several years, techniques for monitoring radioactively tagged plasma metabolites have allowed the visualization of metabolic variation throughout various diving and surface exercise regimes in aquatic mammals. By comparing such tracer turnover dilution curves under conditions of surface exercise, quiet forced diving, free diving, and sleep apnea, patterns emerge that demonstrate the extreme metabolic plasticity of the diving response. These comparisons have led to the conclusions that even short diving periods probably involve a marked change in metabolic steady state, and that aerobic diving is not simply analogous to aerobic exercise.

Adrenal gland denervation and diving in ducks.

The extreme elevation in plasma levels of free norepinephrine (NE) and free epinephrine (EP), which occurs during forced diving of ducks (Anas platyrhynchos), was studied before and after denervation of the adrenal glands. In intact animals both NE and EP concentration increased by up to two orders of magnitude in a 4-min dive but by a significantly lesser amount if the duck breathed O2 before the dive. Denervating the adrenal glands reduced the amounts of both catecholamines (CA) released during dives, plasma EP decreased to 10%, and NE to 50% of values obtained before denervation. Breathing O2 before a dive virtually eliminated CA release in denervates, indicating that hypoxia was the important non-neural releasing agent. Hypoxia was also the most important neural releasing agent compared with hypercapnia, acidosis, or hypoglycemia. Adrenal denervation did not cause significant changes in heart rate, blood pressure, arterial blood gas tensions, pH, or plasma glucose during dives, although denervation caused increased variation in some of these variables. In ducks CA release in dives is largely due to decreasing arterial O2 partial pressure, and full expression of the response is dependent on intact innervation of the adrenal gland.