Search PubMedSearch

SEARCH · Search PubMed

Results for “Repetitive diving”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Venous gas emboli and complement activation after deep repetitive air diving.

Complement activity has been linked to decompression sickness (DCS), but the effects of intravascular bubbles on complement activation are poorly understood. We have investigated intravascular complement activation by measuring red blood cell (RBC)-bound C3d after repetitive air diving in man. Subjects were exposed to a single, 20 min, 170 fsw (feet of sea water) dive, or to 2 such dives with a 6-h surface interval. Doppler monitoring for venous gas emboli was performed postdive. Predive blood samples were studied to determine sensitivity of complement to activation by air bubbles. Other predive and postdive venous samples were evaluated for intravascular complement activation. No cases of DCS occurred in 39 dives. Baseline complement sensitivity appeared normally distributed, thus "sensitive" and "insensitive" subjects were not clearly distinguishable. RBC-bound C3d did not increase after 1 dive but did increase after the repetitive dive (P less than 0.05). Furthermore, maximum bubble grade was independent of complement activation.

Adult

Behavior of freely diving animals.

While diving animals are capable of both long-duration and deep dives, their normal behavior does not routinely approach these limits of time and depth. Studies of the physiologic and biochemical capabilities of diving species have defined the maximum limits of their underwater periods. However, by also studying their diving behavior, we can examine how diving animals most efficiently work within those limits. If we assume for example that the behavioral goal of a foraging seal is to spend as much time underwater as possible, then it must also minimize time at the surface and make many repetitive dives instead of single, longer dives that require long surface recovery periods. To understand the efficiency of bout diving, we must study the physiologic impact of many repetitive dives and how the seal manipulates its behavior to both stay within its physiologic limits and to maximize time underwater.

Animals

Hormonal changes during decompression sickness.

Changes in plasma hormone levels were studied in anesthetized dogs during decompression sickness. Hormone levels were measured in 4 groups: control (no dive, n = 9); air group (air dive, ventilated with air postdive, n = 6); helium-oxygen (He-O2) group (air dive, ventilation changed to He-O2 at 30 min postdive, n = 9); nonsurvivor group (air dive, died within 30 min postdive, n = 9). Dived animals were subjected to repetitive dives until pulmonary artery pressure doubled. Plasma epinephrine (Epi) and norepinephrine (NE) concentrations rapidly increased postdive in all animals. Serum angiotensin-converting enzyme (ACE) activity increased postdive in the He-O2 group only, and these increases were small. Diving did not alter serum concentrations of cortisol, thyroxine (T4), or triiodothyronine (T3); however, T4 and T3 fell in all animals, probably as a consequence of anesthesia. He-O2 breathing did not affect concentrations of Epi, NE, cortisol, T4, T3, or serum ACE activity.

Animals

Factors in 171 navy diving decompression accidents occurring between 1960-1969.

Comparisons were made between the incidence of specific factors in U.S. Navy decompression accidents and the incidence of these factors in routine (nonexperimental) U.S. Navy operational dives. It was found that decompression accidents are disproportionately high among a) air dives less than 140 ft which have bottom times of 30 min or less and air dives greater than 140 ft which have bottom times of more than 15 min, b) Divers First Class, c) older divers, and d) dives which do not involve work or divers which require heavy work. Repetitive dives have a lower decompression accident rate than expected. Decompression accidents were not disproportionately high for any category of body build. These results indicate that the present U.S. Navy decompression tables are extremely safe (5 decompression accidents/10,000 dives), and do not appear to require modification. Future decompression research may be directed toward analyzing the relationship of work and aging to physiological processes involved in decompression. In addition, the present findings should be cross-validated using more recent accident and operational diving data.

Accidents

Pulmonary blood flow regulation in an aquatic snake.

Regulation of pulmonary blood flow was studied during voluntary diving in the aquatic file snake, Acrochordus granulatus. Measurements of pressure and blood flow in pulmonary and systemic vessels indicate that blood flow completely bypasses the lung for significant periods during prolonged and quiescent submergence (greater than 30 minutes). When the lung is ventilated, pulmonary blood flow increases to 36 milliliters per minute per kilogram of body mass (measured in the anterior pulmonary artery), and the cardiac output largely bypasses the systemic circulation. These reciprocating patterns of preferential blood flow reflect inverse relations between flow and vascular resistance, with the result that systemic and pulmonary arterial pressures remain virtually constant throughout repetitive dive cycles. Neuropharmacological studies of freely diving snakes and isolated, perfused lung preparations show that pulmonary blood flow is regulated by an interplay of adrenergic vasodilatation and cholinergic vasoconstriction within the densely innervated lung vasculature. The patterns of blood circulation shown by diving Acrochordus reflect an unusual lability of intracardiac shunts.

Animals

Failure of heparin, superoxide dismutase, and catalase to protect against decompression sickness.

The effects of heparin (HEP), superoxide dismutase (SOD), and catalase (CAT) on the course of decompression sickness (DCS) were studied in anesthetized dogs (Canis familiaris). Animals were divided into 4 groups: a drug assay group (n = 4) received HEP + SOD or HEP + SOD + CAT but were not dived; a control group (n = 14) was dived without drug treatment; a HEPSOD group (n = 11) received HEP + SOD predive and postdive; and a HEPSODCAT group (n = 15) received HEP + SOD + CAT before diving. All dived animals were subjected to repetitive air dives to 10 ATA until pulmonary artery pressure at least doubled within 10 min postdive. Physiologic variables were measured for 3 h postdive or until death. Animals were not recompressed. More early deaths occurred in the HEPSOD (7/11) and HEPSODCAT (8/15) groups than in the control group (5/14). All dived animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, acidosis, hypoxemia, and interstitial pulmonary edema postdive. Drug therapy did not alter these responses to decompression. We conclude that without recompression, treatment with either HEP + SOD OR HEP + SOD + CAT does not improve the outcome of severe DCS in this animal model.

Animals

Cardiovascular responses elicited by simulated diving and their habituation in man.

The cardiovascular responses of 24 subjects were investigated under various simulated diving conditions. Muscle blood flow in forearm and calf, arterial pressure, heart rate and intrathoracic pressure were monitored. Breath holding with face immersion in water at 18 degrees C gave a typical diving response at intrathoracic pressure of 0 and 20 mmHg, (23% bradycardia, greater than 60% muscle vasoconstriction). Breath holding alone at 20 mmHg intrathoracic pressure resulted in vasoconstriction (50%) and bradycardia (4%). Breath holding at 0 mmHg intrathoracic pressure induced a muscle vasoconstriction (5%). These results indicate that both increased intrathoracic pressure and facial immersion can produce a typical diving response individually but that the full 'diving response' requires the presence of both conditions. Diving often activated two responses, the typical 'diving response' and a superimposed defence reaction. Cardiovascular components of the defence reaction (muscle vasodilatation and tachycardia) which was elicited in some divers masked the diving response. In those subjects in whom the diving response was initially absent during repetition of diving manoeuvres the cardiovascular components of the defence reaction were habituated and the characteristic diving response gradually emerged: the initial tachycardia diminished and was replaced by bradycardia, while vasodilatation in the forearm and calf was replaced by vasoconstriction.

Adolescent

Dolphin lung collapse and intramuscular circulation during free diving: evidence from nitrogen washout.

Intramuscular nitrogen tensions in Tursiops truncatus after a schedule of repetitive ocean dives suggest a lung collapse depth of about 70 meters and suggest that intramuscular circulation is maintained during unrestrained diving in the open ocean. Therefore, the bottle-nosed dolphin is not protected by lung collapse from the decompression hazards of dives to depths shallower than 70 meters.

Adipose Tissue

Adaptations to breath-hold diving: from traditional divers to elite athletes.

Breath-hold diving exposes humans to repeated episodes of profound hypoxia and hypercapnia, eliciting physiological adaptations that enable prolonged underwater performance. This article summarises current knowledge on chronic adaptations in elite breath-hold athletes and traditional diving populations, including the Bajau sea nomads of Southeast Asia and the Korean Haenyeo divers. Evidence indicates that repeated apnoea induces adaptations across multiple physiological systems. Haematological changes include increased spleen size and enhanced splenic contraction, augmenting circulating haemoglobin and oxygen stores during apnoea. In elite divers, structured training can increase resting spleen volume, whereas the Bajau exhibit genetically associated splenic enlargement linked to variants near the PDE10A gene. Cardiopulmonary adaptations include modified pulmonary vascular responses to hypoxia, improved oxygen conservation, and metabolic shifts favoring efficient mitochondrial energy production. Molecular adaptations involve enhanced antioxidant defenses and activation of hypoxia-responsive pathways that may mitigate oxidative stress associated with repeated hypoxia-reoxygenation cycles. Emerging evidence also suggests neural plasticity and possible structural brain adaptations, although the long-term neurological consequences of chronic intermittent hypoxia exposure remain uncertain. Studies of traditional diving populations indicate that both phenotypic plasticity and genetic selection contribute to diving capacity, highlighting interactions between training and evolution. Despite these benefits, breath-hold diving also carries risks, including hypoxic blackout, decompression sickness, and potential neurological injury. Understanding the mechanisms underlying human tolerance to extreme hypoxia may have implications beyond diving physiology, including applications in cardiovascular medicine, hypoxic diseases, and rehabilitation. Further longitudinal, genomic, and mechanistic studies are needed to clarify the limits, benefits, and clinical relevance of these adaptations.

Humans

Splenic contraction during breath-hold diving in the Korean ama.

Major increases of hemoglobin concentration and hematocrit, possibly secondary to splenic contraction, have been noted during diving in the Weddell seal. We sought to learn whether this component of the diving response could be present in professional human breath-hold divers. Splenic size was measured ultrasonically before and after repetitive breath-hold dives to approximately 6-m depth in ten Korean ama (diving women) and in three Japanese male divers who did not routinely practice breath-hold diving. Venous hemoglobin concentration and hematocrit were measured in nine of the ama and all Japanese divers. In the ama, splenic length and width were reduced after diving (P = 0.0007 and 0.0005, respectively) and calculated splenic volume decreased 19.5 +/- 8.7% (mean +/- SD, P = 0.0002). Hemoglobin concentration and hematocrit increased 9.5 +/- 5.9% (P = 0.0009) and 10.5 +/- 4% (P = 0.0001), respectively. In Japanese male divers, splenic size and hematocrit were unaffected by repetitive breath-hold diving and hemoglobin concentration increased only slightly over baseline (3.0 +/- 0.6%, P = 0.0198). Splenic contraction and increased hematocrit occur during breath-hold diving in the Korean ama.

Adult

Nitrogen tensions in brachial vein blood of Korean ama divers.

Intravascular bubble formation and symptoms of decompression sickness have been reported during repetitive deep breath-hold diving. Therefore we examined the pattern of blood N2 kinetics during and after repetitive breath-hold diving. To study muscle N2 uptake and release, we measured brachial venous N2 partial pressure (PN2) in nine professional Korean breath-hold divers (ama) during a 3-h diving shift at approximately 4 m seawater depth and up to 4 h after diving. PN2 was determined with the manometric Van Slyke method. Diving time and depth were recorded using a backpack computer-assisted dive longer that allowed calculating the surface-to-depth time ratio to derive the effective depth. With the assumption that forearm muscle N2 kinetics follow the general Haldanian principles of compression and decompression, i.e., forearm muscle is a single compartment with a uniform tissue PN2 equal to venous PN2, PN2 data were fitted to monoexponential functions of time. In the early phase of the diving shift, PN2 rapidly increased to 640 Torr (half time = 6 min) and then slowly declined to baseline levels (half time = 36 min) after the work shift. Peak PN2 levels approximated the alveolar PN2 derived from the effective depth. We conclude that forearm muscle N2 kinetics are well described by a Haldanian single-compartment model. Decompression sickness is theoretically possible in the ama; it did not occur because the absolute PN2 remained low due to the shallow working depth of the ama we studied.

Diving

Fatal dissecting aneurysm of the aorta in a diver.

A 20-yr-old trained sports diver developed severe chest pain shortly after decompressing from a 40 m repetitive freshwater sinkhole dive, and died 6 h later. An autopsy examination showed a dissecting aneurysm of the aorta with rupture into the left pleural cavity. The relationship between the fatal event and the diving is discussed.

Adult

Converting standard air decompression tables for no-stop diving from altitude or habitat.

Using the phase equilibration theory of Hills (1966), as modified by Hennessy and Hempleman (1977), it is possible to predict formulas for converting standard air decompression tables for no-stop diving at altitude or from a normoxic habitat, breathing air. For diving following equilibration at altitude, the Royal Navy, Royal Naval Physiological Laboratory, and Haldane-type rules appear to be too conservative, with the opposite result for diving after excursion to altitude. Predictions in the latter case are in fair agreement with the Swiss (Boni, Schibli, Nussberger, and Bühlmann 1976) no-stop altitude tables. In the case of habitats, close agreement is found between the Hamilton, Kenyon, Freitag, and Schreiner (1973) normoxic tables for no-stop downward excursions and indefinite dive upward-excursions on air. In the case of flying directly after no-stop diving, the US Navy rule of using repetitive group D appears to be conservative for dives less than 50 fsw, and possibly unsafe for dives over 50 fsw. It is concluded that for no-stop diving a single tissue and single safe ascent pressure formula are all that is necessary to generate equivalent air dives. This enforces the hypothesis that it is the volume of gas released on ascent that governs marginal type I bends, and that in a no-stop ascent, all excess dissolved gas is released in the worst case.

Aerospace Medicine

Habituation of the cardiac response to involuntary diving in diving and dabbling ducks.

1. Bradycardia in response to forced submergence was habituated in dabbling (Anas platyrhynchos, Linnaeus) and diving (Aythya americana, Eyton) ducks by repetitively submerging the animals, each day for several days, for periods of 40 and 20 s, respectively. The onset of pronounced bradycardia was delayed with each successive trial, until little or no bradycardia occurred during submergence. Diving bradycardia is driven by chemoreceptors in the dabbler and caused by stimulation of narial receptors in the diver. 2. Mean arterial blood pressure in dives was unchanged from pre-dive levels in both naive and trained dabbling ducks. PaO2, PaCO2 and pHa at the end of a dive were similar before and after habituation training. 3. Bradycardia occurred in dives by habituated dabbling ducks if the animal breathed 15% O2 before submergence. The ventilatory responses to breathing high and low levels of oxygen were unaffected by habituation training. 4. The changes in blood gases during dives by naive and habituated dabbling ducks were the same: therefore, in the absence of a demonstrated decrement in receptor chemosensitivity or efferent potency, the locus of habituation must reside in the central nervous system.

Animals

Numerical phase algorithm for decompression computers and application.

Present generation decompression computers employ a simplified algorithm, limiting dissolved gas build-up in tissue and blood according to a method proposed by Haldane 80 years ago. Such a model works well for single dives, but is usually liberal and theoretically incomplete for multiple exposures within 24 hr spans. Using the critical phase hypothesis in a bubble model, we have extended the classical model of Haldane to multi-exposures. This model is discussed, and a decomputer algorithm described for multi-diving. The focus is permissible bubble excess, not just dissolved gas per se, with phase constraints affecting all tissues, fast and slow, and requiring a systematic lowering of repetitive tissue tensions. Deep repetitive and shallow multi-day exposures are impacted most by the procedure. Within nucleation theory deeper-than-first dives are also treated. A set of multi-diving fractions, xi, accounting for micronuclei excitation and regeneration, reduced bubble elimination in repetitive activity, and coupled effects on tissue tension, are proposed, with xi representing a set of multiplicative factors (less than one) applied to critical tissue tensions for multi-exposures. These factors affect repetitive activity over short time spans, deeper-than-previous and continuous multi-day activities, compared to standard computer software, and are easily encoded into existing decompression meters, potentially extending their range and flexibility over exposure regimes.

Algorithms

Modeling dissolved and free phase gas dynamics under decompression.

Dissolved and free gases do not behave the same way in tissue under pressure, and their interaction is complex. Differences are highlighted, particularly with respect to time scales, gradients and transport. Impacts of free phases on diving are described, contrasting increased off-gassing pressures, slower ascent rates, safety stops and reduced repetitive exposures as consistent practical measures within Haldane models (limited supersaturation) which can be played off against buildup of dissolved gas. Simple computations illustrate the points.

Algorithms

Effect of mental task load on fronto-central theta activity in a deep saturation dive to 450 msw.

The increase of theta activity (4-7 Hz) in the electroencephalogram (EEG) during deep diving is commonly attributed to pathophysiologic mechanisms underlying the high pressure neurologic syndrome. The aim of this study was to clarify whether more precise cognitive aspects of the condition may be described in which theta activity occurs during a deep dive. Among 4 divers who were repeatedly examined during the GUSI 14 dive to 450 msw, 3 divers exhibited a pronounced correlation between short-term memory load, as varied by the memory set size of Sternberg's memory search task (MST), and the size of a distinct peak in the theta band of the EEG-power spectrum. The power of this peak was greatest in the fronto-central electrode position (Fz), increased dramatically during MST-performance at pressure, and failed to subside fully 1 day before surfacing. Despite the close dependency of observed theta activity on cognitive demands, no consistent correlation with performance measures (mean reaction time and errors) was found. In one diver, theta waves of similar morphology appeared in the resting EEG and increased significantly during the dive. We suggest two alternative explanations for the positive interaction of memory load and hyperbaric exposure on Fz-theta: a) Both factors induce a state of increased mental effort or selectivity of attention, known to be accompanied by frontal theta activity from normobaric studies. b) Pressure abnormally facilitates or patterns rhythmical excitations underlying theta activity that would occur naturally to a lesser extent during certain mental activities, learning, or repetitive short-term memory operations.

Adult