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PubMed1981

Venous gas bubble production following cold stress during a no-decompression dive.

The effect of cold stress on venous gas bubble production was studied using Doppler ultrasonic monitoring. Ten subjects participated in four exposure regimes carried out at 78 fsw on an underwater platform for 38 min of light exercise in 10 degrees C water. Two cold exposures (1/8-in. wet suit) and two warm exposures (insulated dry suit) were each followed by rewarming in a heated bath or by endogenous heat production while insulated in a sleeping bag. Results showed that for the cold dives compared to warm dives, air consumption increased 29%, rectal temperature dropped 0.8 degrees C by the end of the dive, mean skin temperature dropped 11 degrees C, and cooling rate correlated with mean skin fold and endomorphy (P less than 0.001). A threefold increase in bubble scores (P less than 0.025) was observed following the warm dives compared to the cold dives. The results suggest that inert gas uptake is reduced as a result of peripheral vasoconstriction when the cold stress is induced at the onset of the dive and maintained throughout.

Adult↗
PubMed1995

Dissociation of the behavioral and subjective components of nitrogen narcosis and diver adaptation.

We investigated adaptation to nitrogen narcosis by compressing 11 highly experienced divers in a hyperbaric chamber to the equivalent of 54.6 meters of seawater once a day for 5 consecutive days. The behavioral component of narcosis was assessed with a serial choice-reaction time (RT) task, and the subjective component with a global magnitude estimate. Supplementary magnitude estimates were obtained with adjectives describing work effectiveness and body sensations. The results showed that there was no adaptation on the RT task, although learning was evident. In contrast, the global estimate dissociated from RT and showed clear adaptation by Day 3. The work effectiveness adjectives followed RT and did not show adaptation. Some body sensation adjectives showed clear adaptation, but others did not. These results lead to the conclusion that the anecdotal reports of adaptation by divers can probably be attributed to the subjective rather than the behavioral component of narcosis. Dissociation of these components suggests mediation by different brain mechanisms, and it is speculated that the gamma-aminobutyric acidA/benzodiazepine receptor complex, which has been implicated in both the anesthetic and anxiolytic properties of agents such as nitrous oxide, may be involved.

Adaptation, Physiological↗
PubMed1976

The control of breathing in birds with particular reference to the initiation and maintenance of diving apnea.

Avian respiratory pacemaker activity is dependent on some form of peripheral input but it may be inhibited by both central and peripheral stimulation. At present the results of central nervous stimulation are difficult to interpret but, aside from cortical influences, diving apnea appears to be maintained, in the face of increasing chemoreceptor input, by noxious stimulation of the upper respiratory tract and depression of the output of medullary respiratory neurons by advancing hypercapnia. If this is so, an obvious problem for future research is what initiates the prompt onset of hyperpnea when the animal surfaces and breathes. It is known that post-dive hyperpnea is little affected by either carotid body or pulmonary denervation, so peripheral chemoreceptors are unlikely to play a major role in this response.

Action Potentials↗
PubMed1997

Decompression sickness from saturation diving: a case control study of some diving exposure characteristics.

A comprehensive computerized database of diving activity for a Norwegian offshore diving contractor [Stolt-Nielsen Seaway (SNS)] covering the years 1983-1990 has been established. The database contains detailed dive information about 12,087 surface-oriented and 2,622 saturation dives. During this period a majority of the divers were permanently employed. Preliminary analysis had suggested that decompression sickness (DCS) might be the result of exposure to factors causing pathophysiologic effects which accumulate over the course of a single dive or a series of dives. This concept evolved into the HADES (Highest Accumulated Decompression Score) theory which assumes that DCS is predictable once the underlying exposure factors are understood. The incidence of DCS among the SNS divers from saturation diving in the North Sea was studied by use of a "nested" case-control design. Twenty-one case dives (i.e., dives where DCS occurred) were compared with 41 randomly selected control dives. For these dives, several saturation dive characteristics were established. The relative pressure change between maximum and minimum storage depths was significantly greater among the cases. For each 1% increase in the relative pressure change there was a 5% increase in the probability of a saturation dive resulting in DCS. Significantly more cases than controls performed a saturation dive with more than one storage depth, and the data suggested that there were more and greater ascending and descending changes in storage depth conditions among the affected divers.

Case-Control Studies↗
PubMed1979

Diffusion and nucleation of gas in gel and some implications for the development of decompression procedures.

Attention is directed to certain incongruities among accepted diving procedures in order to emphasize the need for a more complete understanding of the interactions between the factors involved in diving and decompression and in the onset of decompression sickness. It is suggested that physiological responses derived from the effects of diffusion and nucleation of gas in tissue might be interpreted in terms of similar events in specimens of gelatin subjected to patterns of compression and decompression. A model for behavior of specimens in gel is developed and conformity with the results of a program of experimentation is demonstrated. With the insight provided by this model, a substantial analogy between important aspects of the behavior of gel and tissue is claimed and application of this model to the refinement and development of diving and decompression procedures is proposed.

Decompression↗
PubMed1986

Metabolic arrest.

In hypoxia sensitive cells and tissues, the rates of glucose and O2 consumption are inversely related (Pasteur Effect). Under O2 limiting conditions the demands for glucose (glycogen) in such cells may drastically rise as a means for maintaining ATP turnover close to normoxic rates; nevertheless ion and electrical potentials cannot be sustained due to energy insufficiency and high membrane permeability; metabolic and membrane functions, in effect, are decoupled. 'Good' animal anaerobes resolve these problems with a number of biochemical and physiological mechanisms; of these metabolic arrest and stabilized membrane functions are the most effective strategies for extending hypoxia tolerance. Metabolic arrest is achievable by means of a reversed or negative Pasteur Effect (reduced or unchanging glycolytic flux at reduced O2 availability) while coupling of metabolic and membrane function is achievable in spite of the lower energy turnover rates by maintaining membranes of low permeability (probably via reduced densities of ion-specific channels). Although the strategy of combining metabolic arrest with channel arrest has been recognized as a possible intervention, to date success has been minimal, mainly because cold depression of metabolism is the usual arrest mechanism used and this hypothermia in itself perturbs controlled cell function in most endotherms. The only endothermic systems currently known which appear able to use the dual strategy for extending hypoxia tolerance are hypoperfused hypometabolic tissues and organs of diving marine mammals.

Acute Kidney Injury↗
PubMed2003

Simulated human diving and heart rate: making the most of the diving response as a laboratory exercise.

Laboratory exercises in which students examine the human diving response are widely used in high school and college biology courses despite the experience of some instructors that the response is unreliably produced in the classroom. Our experience with this exercise demonstrates that the bradycardia associated with the diving response is a robust effect that can easily be measured by students without any sophisticated measurement technology. We discuss measures that maximize the success of the exercise by reducing individual variation, designing experiments that are minimally affected by change in the response over time, collecting data in appropriate time increments, and applying the most powerful statistical analysis. Emphasis is placed on pedagogical opportunities for using this exercise to teach general principles of physiology, experimental design, and data analysis. Data collected by students, background information for instructors, a discussion of the relevance of the diving reflex to humans, suggestions for additional experiments, and thought questions with sample answers are included.

Apnea↗
PubMed2004

[Scuba diving and the heart. Cardiac aspects of sport scuba diving].

Diving with self-contained underwater breathing apparatus (scuba) has become a popular recreational sports activity throughout the world. A high prevalence of cardiovascular disorders among the population makes it therefore likely that subjects suffering from cardiovascular problems may want to start scuba diving. Although scuba diving is not a competitive sport requiring athletic health conditions, a certain medical fitness is recommended because of the physical peculiarities of the underwater environment. Immersion alone will increase cardiac preload by central blood pooling with a rise in both cardiac output and blood pressure, counteracted by increased diuresis. Exposure to cold and increased oxygen partial pressure during scuba diving will additionally increase afterload by vasoconstrictive effects and may exert bradyarryhthmias in combination with breath-holds. Volumes of gas-filled body cavities will be affected by changing pressure (Figure 1), and inert gas components of the breathing gas mixture such as nitrogen in case of air breathing will dissolve in body tissues and venous blood with increasing alveolar inert gas pressure. During decompression a free gas phase may form in supersaturated tissues, resulting in the generation of inert gas microbubbles that are eliminated by the venous return to the lungs under normal circumstances. Certain cardiovascular conditions may have an impact on these physiological changes and pose the subject at risk of suffering adverse events from scuba diving. Arterial hypertension may be aggravated by underwater exercise and immersion. Symptomatic coronary artery disease and symptomatic heart rhythm disorders preclude diving. The occurrence of ventricular extrasystoles according to Lown classes I and II, and the presence of atrial fibrillation are considered relative contraindications in the absence of an aggravation following exercise. Asymptomatic subjects with Wolff-Parkinson-White syndrome may be allowed to dive, but in case of paroxysmal supraventricular tachycardia they must refrain from diving. Pacemakers will fail with increasing pressure, but some manufacturers have proven their products safe for pressure equivalents of up to 30 m of seawater, so that patients may dive uneventfully when staying within the 0-20 m depth range. Significant aortic or mitral valve stenosis will preclude diving, whereas regurgitation only will not be a problem. Right-to-left shunts have increasingly gained attention in diving medicine, since they may allow venous gas microbubbles to spill over to the arterial side of the circulation enabling the possibility of arterial gas embolism. Significant shunts thus preclude diving. The highly prevalent patent foramen ovale is considered a relative contraindication only when following certain recommendations for safe diving (Table 2). Metabolic disorders are of concern, since adiposity is associated with both, higher bubble grades in Doppler ultrasound detection after scuba dives when compared to normal subjects, and an increased epidemiologic risk of suffering from decompression illness. In conclusion, cardiovascular aspects are important in the assessment of fitness to dive, and certain cardiovascular conditions preclude scuba diving. Any history of cardiac disease or abnormalities detected during the routine medical examination should prompt to further evaluation and specialist referral.

Coronary Artery Disease↗
PubMed1968

Pulmonary and circulatory adjustments determining the limits of depths in breathhold diving.

Data on pulmonary gas exchange were collected in breathhold dives to 90 feet in a tank and in open-sea breathhold dives to depths of 217.5 and 225 feet. Thoracic blood volume displacements were measured at depths of 25, 50, 90, and 130 feet, by use of the impedance plethysmograph. The open-sea dives were carried out with an average speed of descent of 3.95 feet per second and an average rate of ascent of 3.50 feet per second. End-dive alveolar oxygen tensions did not fall below 36 millimeters of mercury, while alveolar carbon dioxide tension did not rise above 40 millimeters of mercury except in one case. These findings indicate that for diver Croft, who has unusual lung capacity, neither hypoxia nor hypercapnia determined the depth limits under those conditions. At depths of 90 and 130 feet blood was forced into the thorax, amounting to 1047 and 850 milliliters respectively.

Adaptation, Physiological↗
PubMed1981

A study of unusual incidents in a well-documented series of dives.

We have analysed 43 unusual incidents, which occurred, during 1303 well-documented dives, according to the environmental factors involved. The objective was to find some indication of the causes of otherwise unexplained loss of consciousness in working divers. It was concluded that rapid compression may handicap divers if adequate time for recovery is not allowed in those adversely affected. Air diving deeper than 48 m (160 ft) appears to be unduly hazardous. A significant proportion of incidents studied may result from an interaction between the physiological effects of oxygen and carbon dioxide, especially in periods of hard work. The possibility was also raised that pressure alone might adversely lower acute oxygen toxicity thresholds. Diving with a Po2 below 1.3 bar prevents acute oxygen toxicity, while a Po2 exceeding 1.6 bar is potentially hazardous.

Air Pressure↗
PubMed2003

Adaptations to diving hypoxia in the heart, kidneys and splanchnic organs of harbor seals (Phoca vitulina).

Pinnipeds (seals and sea lions) have an elevated mitochondrial volume density [VV(mt)] and elevated citrate synthase (CS) and beta-hydroxyacyl-CoA dehydrogenase (HOAD) activities in their swimming muscles to maintain an aerobic, fat-based metabolism during diving. The goal of this study was to determine whether the heart, kidneys and splanchnic organs have an elevated VV(mt) and CS and HOAD activities as parallel adaptations for sustaining aerobic metabolism and normal function during hypoxia in harbor seals (Phoca vitulina). Samples of heart, liver, kidney, stomach and small intestine were taken from 10 freshly killed harbor seals and fixed in glutaraldehyde for transmission electron microscopy or frozen in liquid nitrogen for enzymatic analysis. Samples from dogs and rats were used for comparison. Within the harbor seal, the liver and stomach had the highest VV(mt). The liver also had the highest CS activity. The kidneys and heart had the highest HOAD activities, and the liver and heart had the highest lactate dehydrogenase (LDH) activities. Mitochondrial volume densities scaled to tissue-specific resting metabolic rate [VV(mt)/RMR] in the heart, liver, kidneys, stomach and small intestine of harbor seals were elevated (range 1.2-6.6x) when compared with those in the dog and/or rat. In addition, HOAD activity scaled to tissue-specific RMR in the heart and liver of harbor seals was elevated compared with that in the dog and rat (3.2x and 6.2x in the heart and 8.5x and 5.5x in the liver, respectively). These data suggest that organs such as the liver, kidneys and stomach possess a heightened ability for aerobic, fat-based metabolism during hypoxia associated with routine diving. However, a heightened LDH activity in the heart and liver indicates an adaptation for the anaerobic production of ATP on dives that exceed the animal's aerobic dive limit. Hence, the heart, liver, kidneys and gastrointestinal organs of harbor seals exhibit adaptations that promote an aerobic, fat-based metabolism under hypoxic conditions but can provide ATP anaerobically if required.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2005

Physiological ischemia/reperfusion phenomena and their relation to endogenous melatonin production: a hypothesis.

Ischemia/reperfusion is a frequently encountered phenomenon in organisms. Prolonged ischemia followed then by reperfusion results in severe oxidative injury in tissues and organs; however, some species can tolerate such events better than others. In nature, arousal from hibernation and resurfacing from diving causes animals to experience classic ischemia/reperfusion and, somehow, these animals cope well with the potential oxidative stress. It has been documented that during these physiological ischemia/reperfusion events, the activities of several antioxidant enzymes and the levels of some small-molecular-weight antioxidants become elevated. For example, the potent small-molecular-weight antioxidant melatonin often attains especially high levels during these physiological ischemia/reperfusion events including during arousal from hibernation or in the newborns during delivery. Highly elevated melatonin production during these physiological ischemia/reperfusion episodes exhibits several features. First, this high melatonin production is transient and fits well with the time schedule of the physiological ischemia/reperfusion period; therefore, it is not related to the normal endogenous melatonin rhythm. Yet, this transient peak protects the animals from destructive oxidative processes that occur during these transition periods. Second, these high levels of melatonin seem to derive from several organs since pinealectomy does not totally reduce circulating levels of this agent. Third, high melatonin production present at arousal from hibernation or in the newborns at birth does not appear to be controlled by light, i.e., it occurs both during the day and at night, and the amplitudes of elevated melatonin levels are equivalent at these times. The significance of these findings is discussed herein. Based on currently available data, we hypothesize that melatonin plays an important role in the physiological ischemia/reperfusion, i.e., as a member of antioxidant defense system, to protect against the potential oxidative injury induced by the physiological ischemia/reperfusion.

Animals↗