Breath-hold Divers Research Articles

Comparison of lung function between breath-holding diving and non-breath-holding diving fishermen in Ambon city

Breath-hold diving is a traditional method used by fishermen to catch fish or other marine organisms. When humans hold their breath during diving, generally their body will develop physiological changes, and with regular exercise, this can improve the lung function. Based on many studies reported, there is an increase in lung function in breath-hold diving fishermen. The objective of this study was to analyze the comparison of pulmonary function between breath-hold diving fishermen and non-divers fishermen in Ambon. This study uses analytical methods with a cross-sectional approach using primary data of 15 breath-hold divers and 15 non-divers fishermen sample with same background of healthy behavior. The pulmonary function differences between breath-hold diving fishermen and non-diving fishermen were analyzed using t-student test. Pulmonary function parameters i.e. VC, FVC, and FEV1% was measured using spirometer. The results of this study showed that mean value of lung function comparison between breath-hold diving fishermen and non-breath lung function fishermen in vital capacity (VC) ratio was 3.48 ± 0.5 vs. 3.01 ± 0.63 (tα(2)0.05:P = 0‘03), forced vital capacity (FVC) was 2.19 ± 0.45 vs. 1.84 ± 0.46 (tα(2)0.05:P = 0.045), and forced expiratory volume in one second (FEV1%) was 91.46 ± 9.12 vs. 83.44 ± 10.3 (tα(2)0.05:P = 0.03). The lung function comparison in breath-hold diving fishermen and non-diver fishermen showed that there is a significant difference in lung function between breath-hold fishermen and non-diver fishermen. The conclusion of the research is, with the same background of life behavior, the lung function of breath-hold diving fishermen is better than non-diver fishermen.

Assessment of sensory sensitivity through critical flicker fusion frequency thresholds after a maximum voluntary apnoea.

The influence of acute exercise on sensory sensitivity (SS) differs according to the type and duration of exercise performed. In the present study, we assessed changes on SS soon after a maximal dynamic apnoea. Thirty-nine experienced male breath-hold divers were recruited. Critical flicker fusion frequency (CFFF) thresholds were used to measure SS. Thresholds were determined before and after a maximal dynamic apnoea. Immediately after surfacing, heart rate and oxygen saturation (SpO2) were recorded for two minutes. After maximal dynamic apnoea, SpO2 was significantly decreased (from mean 97.3% pre-dive to mean 63.1% post-dive; P < 0.0001; η2 P = 0.86), but this acute hypoxaemia did not trigger changes in SS (post-dive value 102% of baseline; P = 0.22; η2 P = 0.03). Pearson correlation analysis revealed a moderate association between SS with swimming speed (r = 0.423) and apnoea time (r = -0.404). A maximal dynamic apnoea did not produce changes in central nervous system fatigue or cortical arousal. We found no relationship between the hypoxaemia level reached after a maximal apnoea and changes in the CFFF thresholds. This study suggests that the time of exposure to hypoxia during a maximal voluntary apnoea is not enough to produce changes in SS.

Snorkelling and breath-hold diving fatalities in Australia, 2001 to 2013. Demographics, characteristics and chain of events.

The aim of this study was to identify characteristics of victims of fatal snorkelling and breath-hold diving accidents in Australia from 2001-2013, inclusive, to determine underlying factors and risks associated with such activities and inform appropriate countermeasures. The National Coronial Information System (NCIS) was searched to identify snorkelling and breath-hold diving-related cases reported to Australian coroners for the years 2001-2013, inclusive. Coronial data in the form of findings, witness and police reports, medical histories and autopsies were collected and collated, and descriptive statistics were used to analyse these data. A chain of events analysis was used to determine the likely sequence of events. There were 175 identified snorkelling-related fatalities during the study period. Most victims were middle-aged males (mean age 49 years). Pre-existing health conditions were possible contributors to 41% of the deaths, the main being ischaemic heart disease. The majority of deaths occurred in Queensland in inexperienced snorkellers, often in commercial settings. The victim's plight often went unnoticed as they were alone, or poorly supervised, when the incident occurred. Apnoeic hypoxia appeared to have been associated with at least 12.5% of the deaths. The main disabling injuries were asphyxia (40%) and cardiac incidents (35%). Human factors, such as chronic health conditions, poor skills and inexperience and poor planning can play a substantial role throughout the chain of events leading to a snorkelling fatality. It is important to educate the community, doctors and dive industry professionals about potential problems associated with the interaction between certain health-related conditions, especially cardiovascular conditions, and snorkelling. Close supervision is strongly recommended for inexperienced snorkellers due to their likely poor skills, as well as for experienced breath-hold divers due to the potential for apnoeic hypoxia.

Erythropoietic responses to a series of repeated maximal dynamic and static apnoeas in elite and non-breath-hold divers

PurposeSerum erythropoietin (EPO) concentration is increased following static apnoea-induced hypoxia. However, the acute erythropoietic responses to a series of dynamic apnoeas in non-divers (ND) or elite breath-hold divers (EBHD) are unknown.MethodsParticipants were stratified into EBHD (n = 8), ND (n = 10) and control (n = 8) groups. On two separate occasions, EBHD and ND performed a series of five maximal dynamic apnoeas (DYN) or two sets of five maximal static apnoeas (STA). Control performed a static eupnoeic (STE) protocol to control against any effects of water immersion and diurnal variation on EPO. Peripheral oxygen saturation (SpO2) levels were monitored up to 30 s post each maximal effort. Blood samples were collected at 30, 90, and 180 min after each protocol for EPO, haemoglobin and haematocrit concentrations.ResultsNo between group differences were observed at baseline (p > 0.05). For EBHD and ND, mean end-apnoea SpO2 was lower in DYN (EBHD, 62 ± 10%, p = 0.024; ND, 85 ± 6%; p = 0.020) than STA (EBHD, 76 ± 7%; ND, 96 ± 1%) and control (98 ± 1%) protocols. EBHD attained lower end-apnoeic SpO2 during DYN and STA than ND (p < 0.001). Serum EPO increased from baseline following the DYN protocol in EBHD only (EBHD, p < 0.001; ND, p = 0.622). EBHD EPO increased from baseline (6.85 ± 0.9mlU/mL) by 60% at 30 min (10.82 ± 2.5mlU/mL, p = 0.017) and 63% at 180 min (10.87 ± 2.1mlU/mL, p = 0.024). Serum EPO did not change after the STA (EBHD, p = 0.534; ND, p = 0.850) and STE (p = 0.056) protocols. There was a significant negative correlation (r = − 0.49, p = 0.003) between end-apnoeic SpO2 and peak post-apnoeic serum EPO concentrations.ConclusionsThe novel findings demonstrate that circulating EPO is only increased after DYN in EBHD. This may relate to the greater hypoxemia achieved by EBHD during the DYN.

Skeletal muscle, haematological and splenic volume characteristics of elite breath-hold divers

PurposeThe aim of the study was to provide an evaluation of the oxygen transport, exchange and storage capacity of elite breath-hold divers (EBHD) compared with non-divers (ND).MethodsTwenty-one healthy males’ (11 EBHD; 10 ND) resting splenic volumes were assessed by ultrasound and venous blood drawn for full blood count analysis. Percutaneous skeletal muscle biopsies were obtained from the m. vastus lateralis to measure capillarisation, and fibre type-specific localisation and distribution of myoglobin and mitochondrial content using quantitative immunofluorescence microscopy.ResultsSplenic volume was not different between groups. Reticulocytes, red blood cells and haemoglobin concentrations were higher (+ 24%, p < 0.05; + 9%, p < 0.05; + 3%, p < 0.05; respectively) and mean cell volume was lower (− 6.5%, p < 0.05) in the EBHD compared with ND. Haematocrit was not different between groups. Capillary density was greater (+ 19%; p < 0.05) in the EBHD. The diffusion distance (R95) was lower in type I versus type II fibres for both groups (EBHD, p < 0.01; ND, p < 0.001), with a lower R95 for type I fibres in the EBHD versus ND (− 13%, p < 0.05). Myoglobin content was higher in type I than type II fibres in EBHD (+ 27%; p < 0.01) and higher in the type I fibres of EBHD than ND (+ 27%; p < 0.05). No fibre type differences in myoglobin content were observed in ND. Mitochondrial content was higher in type I than type II fibres in EBHD (+ 35%; p < 0.05), with no fibre type differences in ND or between groups.ConclusionsIn conclusion, EBDH demonstrate enhanced oxygen storage in both blood and skeletal muscle and a more efficient oxygen exchange capacity between blood and skeletal muscle versus ND.

Oxidative stress assessment in breath-hold diving.

Breath-hold diving results in significant changes in blood gases' levels. Challenging variations in oxygen partial pressures may induce reactive oxygen species (ROS) production that exacerbate oxidative stress and, consequently, affect endothelial function. The aim of this study was to investigate the effects of breath-hold diving on oxidative stress damage, assessing ROS production. Nitric oxide metabolites, inducible nitric oxide synthase (iNOS), aminothiols, and renal function were evaluated too as markers of redox status and renal damage. ROS production was assessed with electron paramagnetic resonance. Oxidative status values were measured at pre- and post-40m dive in a deep swimming pool (Y-40) from six divers (mean age 46.6 ± 9.3years; height 176 ± 4cm; BMI 25 ± 2.9kg/m2). Significant (p < 0.05) increases at post-dive of ROS production rate (0.158 ± 0.003 vs 0.195 ± 0.006μmolmin-1), lipid peroxidation (8-isoprostane: 375.67 ± 195.62 vs 420.49 ± 232.31pgmg-1 creatinine), nitrate (27.91 ± 19.71 vs 30.80 ± 20.44μM), iNOS (31.30 ± 4.52 vs 35.68 ± 6.72IUmL-1) and neopterin concentration (96.20 ± 40.41 vs 118.76 ± 27.84μmolmol-1 creatinine) were recorded. Conversely, the antioxidant capacity significantly decreased (3.423 ± 0.089 vs 3.015 ± 0.284mM) after immersion. Overproduction of ROS and consequent oxidative damage to lipids of membrane and antioxidant capacity decreasing reflect also a hypoxic condition, which in the breath-hold diving typically occurs in the last few meters below the surface. iNOS produces NO in large quantities under the examined extreme conditions. Neopterin and creatinine concentration level increased, suggesting an "impairment of renal function" as a likely physiological response to PaO2 variations during dive activity.

De novo Assembly and Annotation of the Blood Transcriptome of the Southern Elephant Seal Mirounga leonina from the South Shetland Islands, Antarctica

The southern elephant seal Mirounga leonina is the largest member of the phocid seals and is a highly sexually dimorphic predator at circumpolar regions. In this study, we generated the first high-quality de novo assembly of the blood transcriptome of M. leonina using the Illumina MiSeq platform. A total of 40.5 million raw reads were obtained and assembled using the Oases assembly platform, resulting in 46,445 contigs with an N50 value of 634 bp. We performed functional gene annotations through pathway analyses of the Gene Ontology (GO), Eukaryotic Orthologous Groups (KOG), and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases. Ortholog comparison revealed that a high proportion of the M. leonina blood transcriptome had significant sequence homology within pinnipeds. M. leonine, a deep and long-diving seal, is routinely exposed to progressive hypoxia during dives. KEGG analyses detected an intact hypoxia-inducible factor-1 (HIF-1) signaling pathway, which is a key metabolism pathway in the adaptive homeostatic responses to hypoxia. In the blood transcriptome, many essential genes involved in innate immunity were detected, which suggests that the blood serves as a host defense modulator against exogenous infections in M. leonina. This genomic resource will be useful for understanding adaptive metabolism upon repeated breath-hold dives and determining the health status of southern elephant seals without the need to sacrifice them in experiments.

Technical Freediving: An Emerging Breath-Hold Diving Technique

Technical freediving can be defined as freediving augmented by the use of oxygen-enriched gases or oxygen before, during, or after a freedive. As a result of these techniques, breath-hold divers can visit and enjoy underwater wrecks, reefs, and other diving locations previously located at depths unreachable to apnea divers. By pre-breathing oxygen-enriched gases in conjunction with hyperventilation—which decreases the partial pressure of carbon dioxide (PCO2)—the technical freediver now has additional oxygen to facilitate aerobic respiration during the dive. In addition, pre-breathing oxygen decreases tissue nitrogen tensions, which limits inert gas loading and decreases the risk of decompression sickness (DCS). Finally, this technique decreases PCO2, which diminishes the urge to breathe. Consequently, a diver may be able to dive longer before critical hypoxia or hypercarbia forces an ascent. Technical freediving can also be complemented by the use of a diver propulsion vehicle to increase the speed of descent and ascent and minimize exertion. The techniques of technical freediving may be associated with increased risks in central nervous system oxygen toxicity, DCS, and arterial gas embolism. As the boundaries of apnea diving continue to expand, there will be considerable opportunities to investigate the physiological limits of the human body and to determine the safest methodologies to practice this evolving discipline.

Impaired dynamic cerebral autoregulation in trained breath-hold divers.

Breath-hold divers (BHD) experience repeated bouts of severe hypoxia and hypercapnia with large increases in blood pressure. However, the impact of long-term breath-hold diving on cerebrovascular control remains poorly understood. The ability of cerebral blood vessels to respond rapidly to changes in blood pressure represents the property of dynamic autoregulation. The current investigation tested the hypothesis that breath-hold diving impairs dynamic autoregulation to a transient hypotensive stimulus. Seventeen BHD (3 women, 11 ± 9 yr of diving) and 15 healthy controls (2 women) completed two or three repeated sit-to-stand trials during spontaneous breathing and poikilocapnic conditions. Heart rate (HR), finger arterial blood pressure (BP), and cerebral blood flow velocity (BFV) from the right middle cerebral artery were measured continuously with three-lead electrocardiography, finger photoplethysmography, and transcranial Doppler ultrasonography, respectively. End-tidal carbon dioxide partial pressure was measured with a gas analyzer. Offline, an index of cerebrovascular resistance (CVRi) was calculated as the quotient of mean BP and BFV. The rate of the drop in CVRi relative to the change in BP provided the rate of regulation [RoR; (∆CVRi/∆T)/∆BP]. The BHD demonstrated slower RoR than controls (P ≤ 0.001, d = 1.4). Underlying the reduced RoR in BHD was a longer time to reach nadir CVRi compared with controls (P = 0.004, d = 1.1). In concert with the longer CVRi response, the time to reach peak BFV following standing was longer in BHD than controls (P = 0.01, d = 0.9). The data suggest impaired dynamic autoregulatory mechanisms to hypotension in BHD. NEW & NOTEWORTHY Impairments in dynamic cerebral autoregulation to hypotension are associated with breath-hold diving. Although weakened autoregulation was observed acutely in this group during apneic stress, we are the first to report on chronic adaptations in cerebral autoregulation. Impaired vasomotor responses underlie the reduced rate of regulation, wherein breath-hold divers demonstrate a prolonged dilatory response to transient hypotension. The slower cerebral vasodilation produces a longer perturbation in cerebral blood flow velocity, increasing the risk of cerebral ischemia.

Differences in Vital Capacity and Length of a Dive in Dynamics with and without Glossopharyngeal Insufflation in Breath-hold Divers

The purpose of this study was to determine differences between vital capacity and length of a dive in dynamics (DYN) with and without glossopharyngeal insufflation in breath-hold divers. The sample consisted of 15 elite breath-hold divers (12 male subjects and 3 female subjects) who were in regular training process and members of national team in Croatia. The sample of variables consisted two measures for estimating valuation of vital capacity (VC and VCP) and two measures for determining length of a dive in meters (URON and URONP). All variables have standard their basic statistic parameters and were tested to determine statistically significant differences between the vital capacity and length of a dive with and without glossopharyngeal insufflation as technique of air packaging. One-sided t- test for dependent samples was used and with results (significance level of p = 0.00) it can be concluded that there is a statistically significant difference between vital capacity and length of a dive with and without glossopharyngeal insufflation. Technique of packing air (glossopharyngeal insufflation) is producing better results for competitors, but with this advantage athletes must be aware of disadvantages of using this technique which can cause injuries to respiratory system and its organs.

Non‐Invasive Pulmonary Gas Exchange Measurements Following Deep Breath‐Hold Diving

Breath‐hold diving is a ubiquitous activity, with recreational, fishing, military and competitive divers. During a dive, immersion and the increasing hydrostatic pressure of descent facilitate cardiovascular adjustments that promote a blood volume shift into the heart and chest vasculature, further augmenting autonomic responses (i.e. diving bradycardia, peripheral vasoconstriction, and splenic contraction) to conserve O2. Exceeding the compliant capacity of the lung and associated tissues can result in pulmonary injury called squeeze, which is characterized by post‐dive coughing, wheezing and hemoptysis. To provide insight into the consequences of such lung squeeze, our objective was to evaluate the time‐course of a maximal deep dive on pulmonary gas exchange, pulmonary artery systolic pressures (PASP), and ultrasound lung comets (ULCs). Ten healthy trained breath‐hold divers (33±9 yr; 80±15 kg; 185±9 cm) performed a maximal effort dive (55±12 m; range 40–76 m). Pulmonary gas exchange and PASP were performed at baseline, and repeated at 10 and 60 min post dive. Pulmonary gas exchange was non‐invasively measured by collecting end‐tidal PO2 and PCO2 during steady‐state breathing, and derived arterial PO2 via pulse oximetry. O2 deficit was defined as the difference between end‐tidal and calculated arterial PO2; consistent with the Bohr effect by utilizing end‐tidal PCO2. The ULCs were collected bilaterally, parasternal to mid‐axillary, at baseline and again 2.5 h post dive. Following the dive, although there was an impairment of pulmonary gas exchange, evident by an increase in O2 deficit from 10.9±4.5 mmHg at baseline to 22.9±5.1 mmHg 10‐min post dive (p=0.02), this deficit had normalized by 60‐min post. There was persistent hyperventilation up to 60 min post dive, reflected by reductions in end‐tidal PCO2 (p=0.02). PASP was unaltered post‐dive. Although ULCs trended to increase from baseline to 2.5 h post dive (3.7±3 to 10.4±13.2 comets; p=0.09), the delta change in ULC from baseline to post‐dive was positively correlated with depth (r=0.67, p=0.04) and, to a lesser extent, with both change in SpO2 (r=−0.62, p=0.06) and O2 deficit (r=0.58, p=0.08). The findings of this novel study suggest impairment in pulmonary gas exchange is present following diving to depth, even up to 10 min after surfacing. The mechanism(s) driving the slight hyperventilation are unclear, but potentially could be mediated via mild pulmonary edema and/or stimulation of juxtapulmonary capillary receptors. Together, there is transient impairment in gas exchange and associations with ULC during ‘modest’ dives. The development of pathological pulmonary edema, and severe and sustained impairment in pulmonary gas exchange, would seem likely at the forefront of breath‐hold diving performances (e.g, &gt;100 m). There remains little data regarding safe return‐to‐dive practices following a squeeze, and non‐invasive pulmonary gas exchange monitoring could provide valuable utility.Support or Funding InformationCanada Research Chair, NSERCThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Marine Mammals' NMDA Receptor Structure: Possible Adaptation to High Pressure Environment.

Divers that are exposed to high pressure (HP) above 1.1 MPa suffer from High Pressure Neurological Syndrome (HPNS), which is implicated with central nervous system (CNS) malfunction. Marine mammals performing extended and deep breath-hold dives are exposed to almost 20 MPa without apparent HPNS symptoms. N-methyl-D-aspartate receptor (NMDAR) has repeatedly been implicated as one of the major factors in CNS hyperexcitability as part of HPNS. Electrophysiological studies in rat brain slices at He HP showed a significant increase in the synaptic NMDAR response, followed by postsynaptic excitability changes. Molecular studies of Rattus norvegicus NMDARs have revealed that different subunit combinations of the NMDAR exhibit different, increased or decreased, current responses under He HP conditions. The purpose of the present research was to disclose if the breath-hold deep diving mammals exhibit NMDAR structural modifications related to HP. We used sequence alignment and homology structure modeling in order to compare deep diving marine mammals’ NMDARs to those of terrestrial mammals. We discovered that deep diving mammals have a special tertiary TMD structure of the GluN2A subunit that differs from that of the terrestrial mammals. In addition, the GluN2A subunit has a group of four conserved a.a. substitutions: V68L (N-terminal domain, NTD) and V440I (agonist-binding domain, ABD) are cetacean specific, E308D (N-terminal domain, NTD) and I816V (transmembrane domain, TMD) were also singularly found in some terrestrial mammals. Since I816V is localized in M4 α-helix region, which is critical for NMDAR activation and desensitization, we hypothesize that the presence of all 4 substitutions rather than a single one, is the combination that may enable HP tolerance. Furthermore, additional special substitutions that were found in the marine mammals’ NTD may affect the Zn2+ binding site, suggesting less or no voltage-independent inhibition by this ion. Our molecular studies of NMDARs containing the GluN2A subunit showed that HP removal of the Zn2+ voltage-independent inhibition could be the mechanism explaining its current increase at HP. Thus, this mechanism could play a crucial role in the CNS hyperexcitability at HP. Less or no voltage-independent Zn2+ inhibition, different conformations of the TMD, and special mutation in the M4 α-helix region of cetaceans’ NMDAR, may give them the advantage they need in order to perform such deep dives without CNS malfunction.

Arterial Blood Gas Analysis in Breath-Hold Divers at Depth.

The present study aimed to evaluate the partial pressure of arterial blood gases in breath-hold divers performing a submersion at 40 m. Eight breath-hold divers were enrolled for the trials held at “Y-40 THE DEEP JOY” pool (Montegrotto Terme, Padova, Italy). Prior to submersion, an arterial cannula in the radial artery of the non-dominant limb was positioned. All divers performed a sled-assisted breath-hold dive to 40 m. Three blood samplings occurred: at 10 min prior to submersion, at 40 m depth, and within 2 min after diver’s surfacing and after resuming normal ventilation. Blood samples were analyzed immediately on site. Six subjects completed the experiment, without diving-related problems. The theoretically predicted hyperoxia at the bottom was observed in 4 divers out of 6, while the other 2 experienced a reduction in the partial pressure of oxygen (paO2) at the bottom. There were no significant increases in arterial partial pressure of carbon dioxide (paCO2) at the end of descent in 4 of 6 divers, while in 2 divers paCO2 decreased. Arterial mean pH and mean bicarbonate () levels exhibited minor changes. There was a statistically significant increase in mean arterial lactate level after the exercise. Ours was the first attempt to verify real changes in blood gases at a depth of 40 m during a breath-hold descent in free-divers. We demonstrated that, at depth, relative hypoxemia can occur, presumably caused by lung compression. Also, hypercapnia exists at depth, to a lesser degree than would be expected from calculations, presumably because of pre-dive hyperventilation and carbon dioxide distribution in blood and tissues.

Evaluation of fatal diving accidents in Turkey

In any kind of diving there is a risk of accidents, as the move from the topside environment to underwater can affect a diver’s physiological and psychological condition. It is important to investigate dive accidents to clarify the causative factors and determine preventive measures. In this study, autopsy files of fatal dive accident cases were reviewed to evaluate demographic data, type of diving, purpose of dive, seasonal distribution, autopsy findings, and causes of death. We reviewed 56 fatal dive accident files from autopsy units in cities where dive activities are concentrated and from the archive of the Turkish Underwater Federation. Four cases were excluded from the study since we were unable to obtain autopsy reports. Of 52 cases there were 20 scuba divers, two surface-supplied divers and 30 breath-hold divers. The majority of cases involved males (94%). The average age of 50 cases was 38.6; age estimation for two cases could not be determined due to advanced putrefaction. Of these fatal dive accidents 75% took place over a period of six months between May and October. Drowning was recorded as the primary cause of death in these cases. X-ray imaging was used in four (8%) cases. A special autopsy technique was used for nine (17%) cases, to detect possible pulmonary barotrauma and arterial gas embolism. The forensic specialist who is planning to conduct the autopsy for a dive fatality should have knowledge and experience about dive physics and physiology as well as physiopathology of dysbaric injuries.

Provisional report on diving-related fatalities in Australian waters in 2012.

An individual case review of known diving-related deaths that occurred in Australia in 2012 was conducted. The case studies were compiled using statements from witnesses and reports of the police and coroners. In each case, the particular circumstances of the accident and details from the post-mortem examination, where available, are provided. There were 26 reported fatalities (four less than the previous year). Only two of the victims were female (one snorkeller and one scuba diver). Fourteen deaths occurred while snorkelling and/or breath-hold diving, 11 while scuba diving and one diver died while using surface supplied breathing apparatus in a commercial pearl diving setting. Two breath-hold divers likely drowned as a result of apnoeic hypoxia. Cardiac-related issues were thought to have contributed to the deaths of at least three and possibly seven snorkellers and four scuba divers. Pre-existing medical conditions; poor organisation, planning and supervision; equipment-related problems; snorkelling or diving alone or with loose buddy oversight and apnoeic hypoxia were features in several deaths in this series.

Oxygen conserving mitochondrial adaptations in the skeletal muscles of breath hold divers.

BackgroundThe performance of elite breath hold divers (BHD) includes static breath hold for more than 11 minutes, swimming as far as 300 m, or going below 250 m in depth, all on a single breath of air. Diving mammals are adapted to sustain oxidative metabolism in hypoxic conditions through several metabolic adaptations, including improved capacity for oxygen transport and mitochondrial oxidative phosphorylation in skeletal muscle. It was hypothesized that similar adaptations characterized human BHD. Hence, the purpose of this study was to examine the capacity for oxidative metabolism in skeletal muscle of BHD compared to matched controls.MethodsBiopsies were obtained from the lateral vastus of the femoral muscle from 8 Danish BHD and 8 non-diving controls (Judo athletes) matched for morphometry and whole body VO2max. High resolution respirometry was used to determine mitochondrial respiratory capacity and leak respiration with simultaneous measurement of mitochondrial H2O2 emission. Maximal citrate synthase (CS) and 3-hydroxyacyl CoA dehydrogenase (HAD) activity were measured in muscle tissue homogenates. Western Blotting was used to determine protein contents of respiratory complex I-V subunits and myoglobin in muscle tissue lysates.ResultsMuscle biopsies of BHD revealed lower mitochondrial leak respiration and electron transfer system (ETS) capacity and higher H2O2 emission during leak respiration than controls, with no differences in enzyme activities (CS and HAD) or protein content of mitochondrial complex subunits myoglobin, myosin heavy chain isoforms, markers of glucose metabolism and antioxidant enzymes.ConclusionWe demonstrated for the first time in humans, that the skeletal muscles of BHD are characterized by lower mitochondrial oxygen consumption both during low leak and high (ETS) respiration than matched controls. This supports previous observations of diving mammals demonstrating a lower aerobic mitochondrial capacity of the skeletal muscles as an oxygen conserving adaptation during prolonged dives.

Taravana, vestibular decompression illness, and autochthonous distal arterial bubbles

Decompression bubbles can develop only from pre-existing gas micronuclei. These are the nanobubbles which appear on active hydrophobic spots (AHS) found on the luminal aspect of all blood vessels. Following decompression, with the propagation of blood along the arterial tree, diffusion parameters cause increased transfer of nitrogen from the tissue into the artery, and more so if perfusion is low. Taravana is a neurological form of decompression illness (DCI) prevalent in repeated breath-hold diving. A nanobubble on an AHS in a distal artery of the brain may receive an influx of nitrogen after each dive until it occludes the arterial blood flow. The vestibular organ has very low perfusion compared with the brain and the cochlea of the inner ear. We suggest that a nanobbubble on an AHS in the distal artery of the vestibular organ will receive a high influx of nitrogen from the surrounding tissue after decompression due to the low nitrogen clearance, thus expanding to cause vestibular DCI.

Medium term effects of physical conditioning on breath-hold diving performance

The current study aimed to analyze the effects of physical conditioning inclusion on apnea performance after a 22-week structured apnea training program. Twenty-nine male breath-hold divers participated and were allocated into: (1) cross-training in apnea and physical activity (CT; n = 10); (2) apnea training only (AT; n = 10); and control group (CG; n = 9). Measures were static apnea (STA), dynamic with fins (DYN) and dynamic no fins (DNF) performance, body composition, hemoglobin, vital capacity (VC), maximal aerobic capacity (VO2max), resting metabolic rate, oxygen saturation, and pulse during a static apnea in dry conditions at baseline and after the intervention. Total performance, referred as POINTS (constructed from the variables STA, DNF and DYN) was used as a global performance variable on apnea indoor diving. + 30, +26 vs. + 4 average POINTS of difference after-before training for CT, AT and CG respectively were found. After a discriminant analysis, CT appears to be the most appropriate for DNF performance. The post-hoc analysis determined that the CT was the only group in which the difference of means was significant before and after training for the VC (p < 0.01) and VO2max (p < 0.05) variables. Inclusion of physical activity in apnea training increased VC and VO2max in breath hold divers; divers who followed a mixed training, physical training and hypoxic training, achieved increased DNF performance.

Resting Metabolic Rate and Lung Function in Wild Offshore Common Bottlenose Dolphins, Tursiops truncatus, Near Bermuda.

Diving mammals have evolved a suite of physiological adaptations to manage respiratory gases during extended breath-hold dives. To test the hypothesis that offshore bottlenose dolphins have evolved physiological adaptations to improve their ability for extended deep dives and as protection for lung barotrauma, we investigated the lung function and respiratory physiology of four wild common bottlenose dolphins (Tursiops truncatus) near the island of Bermuda. We measured blood hematocrit (Hct, %), resting metabolic rate (RMR, l O2 ⋅ min-1), tidal volume (VT, l), respiratory frequency (fR, breaths ⋅ min-1), respiratory flow (l ⋅ min-1), and dynamic lung compliance (CL, l ⋅ cmH2O-1) in air and in water, and compared measurements with published results from coastal, shallow-diving dolphins. We found that offshore dolphins had greater Hct (56 ± 2%) compared to shallow-diving bottlenose dolphins (range: 30–49%), thus resulting in a greater O2 storage capacity and longer aerobic diving duration. Contrary to our hypothesis, the specific CL (sCL, 0.30 ± 0.12 cmH2O-1) was not different between populations. Neither the mass-specific RMR (3.0 ± 1.7 ml O2 ⋅ min-1 ⋅ kg-1) nor VT (23.0 ± 3.7 ml ⋅ kg-1) were different from coastal ecotype bottlenose dolphins, both in the wild and under managed care, suggesting that deep-diving dolphins do not have metabolic or respiratory adaptations that differ from the shallow-diving ecotypes. The lack of respiratory adaptations for deep diving further support the recently developed hypothesis that gas management in cetaceans is not entirely passive but governed by alteration in the ventilation-perfusion matching, which allows for selective gas exchange to protect against diving related problems such as decompression sickness.

Medical Management and Risk Reduction of the Cardiovascular Effects of Underwater Diving.

Undersea diving is a sport and commercial industry. Knowledge of potential problems began with Caisson disease or "the bends", first identified with compressed air in the construction of tunnels under rivers in the 19th century. Subsequently, there was the commercially used old-fashioned diving helmet attached to a suit, with compressed air pumped down from the surface. Breathhold diving, with no supplementary source of air or other breathing mixture, is also a sport as well as a commercial fishing tool in some parts of the world. There has been an evolution to self-contained underwater breathing apparatus (SCUBA) diving with major involvement as a recreational sport but also of major commercial importance. Knowledge of the physiology and cardiovascular plus other medical problems associated with the various forms of diving have evolved extensively. The major medical catastrophes of SCUBA diving are air embolism and decompression sickness (DCS). Understanding of the essential referral to a hyperbaric recompression chamber for these problems is critical, as well as immediate measures until that recompression is achieved. These include the administration of 100% oxygen and rehydration with intravenous normal saline. Undersea diving continues to expand, especially as a sport, and a basic understanding of the associated preventive and emergency medicine will decrease complications and save lives.