Cerebral hemodynamic and systemic physiological changes in trained freedivers completing sled-assisted dives to two different depths.

While existing literature covers significant detail on the physiology of human freediving, the lack of standardized protocols has hindered comparisons due to confounding variables such as exercise and depth. By accounting for these variables, direct depth-dependent impacts on cardiovascular and blood oxygen regulation can be investigated. In this study, depth-dependent effects on 1) cerebral hemodynamic and oxygenation changes, 2) arterial oxygen saturation (SpO2), and 3) heart rate during breath-hold diving without confounding effects of exercise were investigated. Six freedivers (51.0 ± 12.6 years; mean ± s.d.), instrumented with continuous-wave near-infrared spectroscopy for monitoring cerebral hemodynamic and oxygenation measurements, heart rate and SpO2, performed sled-assisted breath-hold dives to 15 m and 42 m. Arterial blood gas tensions were validated through cross-sectional periodic blood sampling. Cerebral hemodynamic changes were characteristic of breath-hold diving, with changes during ascent from both depths likely driven by decreasing SpO2 due to lung expansion. While SpO2 was significantly lower following 42 m dives (t(5) = -4.183, p < 0.05), mean cerebral arterial-venous blood oxygen saturation remained at 74% following dives to both depths. Cerebral oxygenation during ascent from 42 m may have been maintained through increased arterial delivery. Heart rate was variable with no significant difference in minimum heart rate between both depths (t(5) = -1.017, p > 0.05). This study presents a standardized methodology, which could provide a basis for future research on human freediving physiology and uncover ways in which freedivers can reduce potential risks of the sport.

Oxy-Inflammation in Humans during Underwater Activities.

Underwater activities are characterized by an imbalance between reactive oxygen/nitrogen species (RONS) and antioxidant mechanisms, which can be associated with an inflammatory response, depending on O2 availability. This review explores the oxidative stress mechanisms and related inflammation status (Oxy-Inflammation) in underwater activities such as breath-hold (BH) diving, Self-Contained Underwater Breathing Apparatus (SCUBA) and Closed-Circuit Rebreather (CCR) diving, and saturation diving. Divers are exposed to hypoxic and hyperoxic conditions, amplified by environmental conditions, hyperbaric pressure, cold water, different types of breathing gases, and air/non-air mixtures. The "diving response", including physiological adaptation, cardiovascular stress, increased arterial blood pressure, peripheral vasoconstriction, altered blood gas values, and risk of bubble formation during decompression, are reported.

Cardiovascular effects of breath-hold diving at altitude.

Hypoxia, centralization of blood in pulmonary vessels, and increased cardiac output during physical exertion are the pathogenetic pathways of acute pulmonary edema observed during exposure to extraordinary environments. This study aimed to evaluate the effects of breath-hold diving at altitude, which exposes simultaneously to several of the stimuli mentioned above. To this aim, 11 healthy male experienced divers (age 18-52y) were evaluated (by Doppler echocardiography, lung echography to evaluate ultrasound lung B-lines (BL), hemoglobin saturation, arterial blood pressure, fractional NO (Nitrous Oxide) exhalation in basal condition (altitude 300m asl), at altitude (2507m asl) and after breath-hold diving at altitude. A significant increase in E/e' ratio (a Doppler-echocardiographic index of left atrial pressure) was observed at altitude, with no further change after the diving session. The number of BL significantly increased after diving at altitude as compared to basal conditions. Finally, fractional exhaled nitrous oxide was significantly reduced by altitude; no further change was observed after diving. Our results suggest that exposure to hypoxia may increase left ventricular filling pressure and, in turn, pulmonary capillary pressure. Breath-hold diving at altitude may contribute to interstitial edema (as evaluated by BL score), possibly because of physical efforts made during a diving session. The reduction of exhaled nitrous oxide at altitude confirms previous reports of nitrous oxide reduction after repeated exposure to hypoxic stimuli. This finding should be further investigated since reduced nitrous oxide production in hypoxic conditions has been reported in subjects prone to high-altitude pulmonary edema.

Arterial Gas Embolism in Breath-Hold Diver.

An arterial gas embolism (AGE) is a potentially fatal complication of scuba diving that is related to insufficient exhalation during ascent. During breath-hold diving, an arterial gas embolism is unlikely because the volume of gas in the lungs generally cannot exceed the volume at the beginning of the dive. However, if a diver breathes from a gas source at any time during the dive, they are at risk for an AGE or other pulmonary overinflation syndromes (POIS). In this case report, a breath-hold diver suffered a suspected AGE due to rapidly ascending without exhalation following breathing from an air pocket at approximately 40 feet.

Consistent changes in muscle metabolism underlie dive performance across multiple lineages of diving ducks.

Diving animals must sustain high activity with limited O2 stores to successfully capture prey. Studies suggest that increasing body O2 stores supports breath-hold diving, but less is known about metabolic specializations that underlie underwater locomotion. We measured maximal activities of 10 key enzymes in locomotory muscles (gastrocnemius and pectoralis) to identify biochemical changes associated with diving in pathways of oxidative and substrate-level phosphorylation and compared them across three groups of ducks-the longest diving sea ducks (eight spp.), the mid-tier diving pochards (three spp.) and the non-diving dabblers (five spp.). Relative to dabblers, both diving groups had increased activities of succinate dehydrogenase and cytochrome c oxidase, and sea ducks further showed increases in citrate synthase (CS) and hydroxyacyl-CoA dehydrogenase (HOAD). Both diving groups had relative decreases in capacity for anaerobic metabolism (lower ratio of lactate dehydrogenase to CS), with sea ducks also showing a greater capacity for oxidative phosphorylation and lipid oxidation (lower ratio of pyruvate kinase to CS, higher ratio of HOAD to hexokinase). These data suggest that the locomotory muscles of diving ducks are specialized for sustaining high rates of aerobic metabolism, emphasizing the importance of body O2 stores for dive performance in these species.

Effects of hyperventilation on oxygenation, apnea breaking points, diving response, and spleen contraction during serial static apneas.

PURPOSE: Hyperventilation is considered a major risk factor for hypoxic blackout during breath-hold diving, as it delays the apnea breaking point. However, little is known about how it affects oxygenation, the diving response, and spleen contraction during serial breath-holding. METHODS: 18 volunteers with little or no experience in freediving performed two series of 5 apneas with cold facial immersion to maximal duration at 2-min intervals. In one series, apnea was preceded by normal breathing and in the other by 15 s of hyperventilation. End-tidal oxygen and end-tidal carbon dioxide were measured before and after every apnea, and peripheral oxygen saturation, heart rate, breathing movements, and skin blood flow were measured continuously. Spleen dimensions were measured every 15 s. RESULTS: Apnea duration was longer after hyperventilation (133 vs 111 s). Hyperventilation reduced pre-apnea end-tidal CO2 (17.4 vs 29.0 mmHg) and post-apnea end-tidal CO2 (38.5 vs 40.3 mmHg), and delayed onset of involuntary breathing movements (112 vs 89 s). End-tidal O2 after apnea was lower in the hyperventilation trial (83.4 vs 89.4 mmHg) and so was the peripheral oxygen saturation nadir after apnea (90.6 vs 93.6%). During hyperventilation, the nadir peripheral oxygen saturation was lower in the last apnea than in the first (94.0% vs 86.7%). There were no differences in diving response or spleen volume reduction between conditions or across series. CONCLUSIONS: Serial apneas  revealed a previously undescribed aspect of hyperventilation; a progressively increased desaturation across the series, not observed after normal breathing and could heighten the risk of a blackout.

Arterial blood gases' analysis in elite breath-hold divers at extreme depths.

PURPOSE: To showcase results of arterial blood gases' analysis in elite breath-hold divers sampled at depths where their total lung capacities are below their residual lung volume on surface. METHODS: Three male elite breath-hold divers performed body plethysmographies to determine their lung volumes. Two dives were performed, one on normal inhalation to 60 m of depth and the second on complete exhalation to 10 m of depth. Blood samples were taken on five occasions; before the first dive, at 60 and 10 m of depth and immediately after resurfacing after both dives. RESULTS: Arterial blood gases' analysis at 60 m of depth showed an increase in partial pressures of oxygen and carbon dioxide, a consequent decrease in pH and an increase in concentration of HCO3-. After resurfacing, in two divers, values mostly returned to normal; hypoxemia was observed in one diver. At 10 m of depth, all values showed similar variation, and hypoxemia was observed in the same diver but at depth. Upon resurfacing, all values returned to normal. CONCLUSION: This is the first study performed at depths where the total lung capacities of participants are below their residual lung volumes at the surface. Partial pressure of carbon dioxide increases at depth to higher than normal values causing pH to decrease thus exceeding the buffering potential of the blood. In addition, previous assumptions that maximum depth in breath-hold divers is where total lung capacity is reduced to their residual volume proved wrong as our group of divers had no symptoms after resurfacing.

Unlocking the depths: multiple factors contribute to risk for hypoxic blackout during deep freediving.

PURPOSE: To examine the effect of freediving depth on risk for hypoxic blackout by recording arterial oxygen saturation (SpO2) and heart rate (HR) during deep and shallow dives in the sea. METHODS: Fourteen competitive freedivers conducted open-water training dives wearing a water-/pressure proof pulse oximeter continuously recording HR and SpO2. Dives were divided into deep (> 35 m) and shallow (10-25 m) post-hoc and data from one deep and one shallow dive from 10 divers were compared. RESULTS: Mean ± SD depth was 53 ± 14 m for deep and 17 ± 4 m for shallow dives. Respective dive durations (120 ± 18 s and 116 ± 43 s) did not differ. Deep dives resulted in lower minimum SpO2 (58 ± 17%) compared with shallow dives (74 ± 17%; P = 0.029). Overall diving HR was 7 bpm higher in deep dives (P = 0.002) although minimum HR was similar in both types of dives (39 bpm). Three divers desaturated early at depth, of which two exhibited severe hypoxia (SpO2 ≤ 65%) upon resurfacing. Additionally, four divers developed severe hypoxia after dives. CONCLUSIONS: Despite similar dive durations, oxygen desaturation was greater during deep dives, confirming increased risk of hypoxic blackout with increased depth. In addition to the rapid drop in alveolar pressure and oxygen uptake during ascent, several other risk factors associated with deep freediving were identified, including higher swimming effort and oxygen consumption, a compromised diving response, an autonomic conflict possibly causing arrhythmias, and compromised oxygen uptake at depth by lung compression possibly leading to atelectasis or pulmonary edema in some individuals. Individuals with elevated risk could likely be identified using wearable technology.

A randomized trial of one versus three hyperbaric oxygen sessions for acute carbon monoxide poisoning.

Introduction: Hyperbaric oxygen (HBO2) improves outcome in patients with acute carbon monoxide (CO) poisoning, but optimal dose/timing are unknown. In this double-blind, sham-controlled randomized trial, we compared neuropsychological sequelae at six weeks and six months in patients receiving three HBO2 sessions or one HBO2 session and two sham chamber sessions after acute CO poisoning. Methods: After completing one HBO2 session (3.0 ATA, 60 minutes, 2.0 ATA, 65 minutes), CO-poisoned patients were randomized (1:1): two sham chamber sessions (1 ATA air, 120 minutes) or two additional HBO2sessions (2.0 ATA, 90 minutes at pressure, 120 minutes in chamber) completed within 24 hours. Eligible patients were >24 hours from accidental poisoning, English-speaking, and not intubated. We planned 150 participants. Results: The study was stopped early for enrollment futility. From 2006 to 2016, we screened 395 patients: 136 were deemed eligible to participate, and 75 signed informed consent. Two were later withdrawn for past brain injury/PTSD (one sham, one HBO2), and one for performance validity (sham). Of the 72 analyzed, mean age was 42 ± 15 years, 40 (56%) were male, 20 (28%) had loss of consciousness, and mean initial carboxyhemoglobin was 22 ± 9%. The rate of six-week neuropsychological sequelae was 50% in the one-HBO2 session group and 55% in the three-HBO2 sessions group (p = 0.80), and at six months was 42% versus 46%, respectively (p = 0.76). Conclusions: There was no difference in the rate of neuropsychological sequelae in those who received three HBO2 sessions and those who received one HBO2 sessions and two sham sessions. The higher rate of neuropsychological sequelae compared to an earlier study may be due to neuropsychological test-retest effects or previously identified risk factors for cognitive sequelae (age, duration of poisoning, cerebellar dysfunction). This study's rates of cognitive difficulties, affective complaints, and other symptoms suggest brain injury after CO poisoning is common.

Cerebral arterial gas embolism and neurogenic stunned myocardium in a previously healthy freediver.

Cardiomyopathy is a known but rare sequelae of diving-related cerebral arterial gas embolism (CAGE). In previously reported cases, patient findings have been consistent with takotsubo cardiomyopathy (TCM) per the revised Mayo Clinic's diagnostic criteria. A lesser-known variant of stress-related cardiomyopathy is neurogenic stunned myocardium (NSM), which occurs after a neurological event such as subarachnoid hemorrhage and typically presents in younger patients. Presentation tends to differ slightly to TCM with non-specific left ventricular dysfunction and T wave inversions. This case adds to the rare numbers of reported cardiomyopathy from diving and is the first reported case of suspected NSM associated with CAGE.

The use of dive computers in forensic investigations of fatal breath-hold diving accidents: a case study.

Freediving is a type of diving in which divers rely solely on how long they can hold their breath underwater during their dive, which is why it can also be referred to as 'breath-hold diving'. Unlike scuba (self-contained underwater breathing apparatus) diving, individuals do not require training or licencing to perform freediving and may not be aware of the risks of this activity. This paper presents a case in which coastguards retrieved a free diver's lifeless body from the seafloor. In most cases such as this, the deceased individual's cause of death would be ruled as drowning. With the deceased diver's dive computer, we concluded that a shallow water blackout caused him to drown. Data from the dive computer were extracted, graphed, and analysed to explain how a skilled swimmer and diver drowned on one of his seemingly ordinary diving trips. The dive computer can be the sole witness to a fatal dive event and provide invaluable information to forensic scientists since the diver is almost always alone. To our knowledge of the available literature, dive computers have been used in scuba diving fatality investigations; however, we believe that they have not been used in death investigations of breath-hold divers. Deficient or hasty conclusions are often based solely on autopsy findings without data collected by diving technicians and investigators. It is crucial to wait to draw conclusions until all possible dive information has been gathered and studied. This study discusses the deficiency in presenting a reasonable idea to the grieving family and friends of how their beloved relative could have drowned even though he was known to be a fit and skilled diver and avid swimmer.

Profound hypercapnia but only moderate hypoxia found during underwater rugby play.

Background: Underwater rugby is a team sport where players try to score points with a negatively buoyant ball while submerged in a swimming pool. Reports of syncope incidents at the Swedish Championships led to us to investigate end-tidal oxygen and carbon dioxide levels during simulated match play. Methods: Eight male underwater rugby club players of varying experience participated. Repetitive measurements were made while players were defending during simulated match play. Each time a player surfaced they exhaled through a mouthpiece connected to a flow meter and a gas analyzer to measure tidal volume, PETO2 and PETCO2. Results: Measurements were made over 12 dives, with an average dive duration of 18.5 seconds. The mean maximal PETCO2 across the eight participants was 10.0 kPa (~75 mmHg) (range, 9.1-11.7 [~68-88]). The corresponding mean minimum PETO2 was 7.6 kPa (~57 mmHg) (6.3-10.4 [~47-78)). PETCO2 drifted upward, with the mean upward change from the first to last dive for each participant being +1.8 (~13.5 mmHg) (SD 1.74) kPa. A similar trend for PETO2 was not detected, with a mean change of -0.1 (~0.75 mmHg) (SD 3.79) kPa. Conclusion: Despite high PETCO2 values that were close to narcotic being recorded, these players seemed to regulate their urge to breathe based on hypoxia rather than hypercapnia.

Acute Cardiovascular and Metabolic Effects of Different Warm-Up Protocols on Dynamic Apnea.

The aim of this study was to evaluate the acute physiological response to different warm-up protocols on the dynamic apnea performance. The traditional approach, including a series of short-mid dives in water (WET warm-up), was compared to a more recent strategy, consisting in exercises performed outside the water (DRY warm-up). Nine athletes were tested in two different sessions, in which the only difference was the warm-up executed before 75m of dynamic apnea. Heart rate variability, baroreflex sensitivity, hemoglobin, blood lactate and the rate of perceived exertion were recorded and analyzed. With respect to WET condition, DRY showed lower lactate level before the dive (1.93 vs. 2.60 mmol/L, p = 0.006), higher autonomic indices and lower heart rate during the subsequent dynamic apnea. A significant correlation between lactate produced during WET with the duration of the subsequent dynamic apnea, suggests that higher lactate levels could affect the dive performance (72 vs. 70 sec, p = 0.028). The hemoglobin concentration and the rate of perceived exertion did not show significant differences between conditions. The present findings partially support the claims of freediving athletes who adopt the DRY warm-up, since it induces a more pronounced diving response, avoiding higher lactate levels and reducing the dive time of a dynamic apnea.

Physiology, pathophysiology and (mal)adaptations to chronic apnoeic training: a state-of-the-art review.

Breath-hold diving is an activity that humans have engaged in since antiquity to forage for resources, provide sustenance and to support military campaigns. In modern times, breath-hold diving continues to gain popularity and recognition as both a competitive and recreational sport. The continued progression of world records is somewhat remarkable, particularly given the extreme hypoxaemic and hypercapnic conditions, and hydrostatic pressures these athletes endure. However, there is abundant literature to suggest a large inter-individual variation in the apnoeic capabilities that is thus far not fully understood. In this review, we explore developments in apnoea physiology and delineate the traits and mechanisms that potentially underpin this variation. In addition, we sought to highlight the physiological (mal)adaptations associated with consistent breath-hold training. Breath-hold divers (BHDs) are evidenced to exhibit a more pronounced diving-response than non-divers, while elite BHDs (EBHDs) also display beneficial adaptations in both blood and skeletal muscle. Importantly, these physiological characteristics are documented to be primarily influenced by training-induced stimuli. BHDs are exposed to unique physiological and environmental stressors, and as such possess an ability to withstand acute cerebrovascular and neuronal strains. Whether these characteristics are also a result of training-induced adaptations or genetic predisposition is less certain. Although the long-term effects of regular breath-hold diving activity are yet to be holistically established, preliminary evidence has posed considerations for cognitive, neurological, renal and bone health in BHDs. These areas should be explored further in longitudinal studies to more confidently ascertain the long-term health implications of extreme breath-holding activity.

Arterial blood gases in divers at surface after prolonged breath-hold.

PURPOSE: Adaptations during voluntary breath-hold diving have been increasingly investigated since these athletes are exposed to critical hypoxia during the ascent. However, only a limited amount of literature explored the pathophysiological mechanisms underlying this phenomenon. This is the first study to measure arterial blood gases immediately before the end of a breath-hold in real conditions. METHODS: Six well-trained breath-hold divers were enrolled for the experiment held at the "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Before the experiment, an arterial cannula was inserted in the radial artery of the non-dominant limb. All divers performed: a breath-hold while moving at the surface using a sea-bob; a sled-assisted breath-hold dive to 42 m; and a breath-hold dive to 42 m with fins. Arterial blood samples were obtained in four conditions: one at rest before submersion and one at the end of each breath-hold. RESULTS: No diving-related complications were observed. The arterial partial pressure of oxygen (96.2 ± 7.0 mmHg at rest, mean ± SD) decreased, particularly after the sled-assisted dive (39.8 ± 8.7 mmHg), and especially after the dive with fins (31.6 ± 17.0 mmHg). The arterial partial pressure of CO2 varied somewhat but after each study was close to normal (38.2 ± 3.0 mmHg at rest; 31.4 ± 3.7 mmHg after the sled-assisted dive; 36.1 ± 5.3 after the dive with fins). CONCLUSION: We confirmed that the arterial partial pressure of oxygen reaches hazardously low values at the end of breath-hold, especially after the dive performed with voluntary effort. Critical hypoxia can occur in breath-hold divers even without symptoms.

Changes in PUFA and eicosanoid metabolism during/after apnea diving: a prospective single-center study.

Background: The popularity of apneic diving is continually growing. As apnea diving substantially burdens the cardiovascular system, special focus is warranted. Regarding inflammation processes and associated inflammatory-related diseases (e.g., cardiovascular diseases), eicosanoids play an important role. This study aims to investigate polyunsaturated fatty acids (PUFAs) and eicosanoids in voluntary apnea divers, and so to further improve understanding of pathophysiological processes focusing on proinflammatory effects of temporarily hypercapnic hypoxia.. Methods: The concentration of PUFAs and eicosanoids were investigated in EDTA plasma in apnea divers (n=10) before and immediately after apnea, 0.5 hour and four hours later, applying liquid chromatography-tandem mass spectrometry (LC-MS/MS). Results: Mean age was 41±10 years, and divers performed a mean breath-hold time of 317±111 seconds. PUFAs, eicosanoids and related lipids could be classified in four different kinetical reaction groups following apnea. The first group (e.g., Ω-6 and Ω-3-PUFAs) showed an immediate concentration increase followed by a decrease below baseline four hours after apnea. The second group (e.g., thromboxane B2) showed a slower increase, with its maximum concentration 0.5 hour post-apnea followed by a decrease four hours post-apnea. Group 3 (9- and 13-hydroxyoctadecadienoic acid) is characterized by two concentration increase peaks directly after apnea and four hours afterward compared to baseline. Group 4 (e.g., prostaglandin D2) shows no clear response. Conclusion: Changes in the PUFA metabolism after even a single apnea revealed different kinetics of pro- and anti-inflammatory regulations and changes for oxidative stress levels. Due to the importance of these mediators, apnea diving should be evaluated carefully and be performed only with great caution against the background of cardiovascular diseases and inflammation processes.

Whole-body cold tolerance in older Korean female divers "haenyeo" during cold air exposure: effects of repetitive cold exposure and aging.

This study was conducted to investigate the effects of chronic and repetitive diving in cold sea water on physiological responses to cold in older Korean female divers, Haenyeo, who have been exposed to cold water through breath-hold diving since their teens. Young and older females, who have no experience of swimming in cold sea water, were recruited as control groups: older haenyeos (N = 10, 70 ± 3 years of age), young non-diving females (N = 10, 23 ± 2 years), and older non-diving females (N = 6, 73 ± 4 years). For the test of cold exposure, all subjects were exposed to cold in an air temperature of 12 °C with 45% RH in a sitting position for 60 min. The changes in core temperature showed no significant differences between older haenyeos and the other two groups. The decreases in mean skin temperature were greater for older haenyeos than the other two groups (P < 0.01). Older haenyeos had significantly lower energy expenditure during cold exposure when compared to older non-diving females (P < 0.05). Heart rate was significantly lower in older haenyeos than that of young non-diving females (P < 0.05). Older haenyeos felt cooler at the face with lower face temperature when compared with older non-diving females. The results indicate that older haenyeos respond to cold through reducing heat loss from the skin rather than increasing metabolic rate. These responses are distinctive features from the cold defensive system of young or older non-diving females.

Blood lactate accumulation during competitive freediving and synchronized swimming.

A number of competitive water sports are performed while breath-holding (apnea). Such performances put large demands on the anaerobic system, but the study of lactate accumulation in apneic sports is limited. We therefore aimed to determine and compare the net lactate accumulation (NLA) during competition events in six disciplines of competitive freediving (FD) and three disciplines of synchronized swimming (SSW). The FD disciplines were: static apnea (STA; n = 14); dynamic apnea (DYN; n = 19); dynamic apnea no fins (DNF; n = 16); constant weight (CWT; n = 12); constant weight no fins (CNF; n = 8); free immersion (FIM; n =10). The SSW disciplines were solo (n = 21), duet (n = 31) and team (n = 34). Capillary blood lactate concentration was measured before and three minutes after competition performances, and apneic duration and performance variables were recorded. In all nine disciplines NLA was observed. The highest mean (SD) NLA (mmol·L-1) was found in CNF at 6.3 (2.2), followed by CWT at 5.9 (2.3) and SSW solo at 5 (1.9). STA showed the lowest NLA 0.7 (0.7) mmol·L-1 compared to all other disciplines (P ⟨ 0.001). The NLA recorded shows that sports involving apnea involve high levels of anaerobic activity. The highest NLA was related to both work done by large muscle groups and long apneic periods, suggesting that NLA is influenced by both the type of work and apnea duration, with lower NLA in SSW due to shorter apneic episodes with intermittent breathing.

The association of kidney function with repetitive breath-hold diving activities of female divers from Korea, Haenyeo.

BACKGROUND: Voluntary apnea during breath-hold diving (BHD) induces cardiovascular changes including bradycardia, reduced cardiac output, and arterial hypertension. Although the impacts of repetitive BHD on cardiovascular health have been studied previously, the long-term risk for kidney dysfunction has never been investigated. METHODS: A cross-sectional propensity score-matched study was performed to evaluate the influence of repetitive long-lasting BHD on kidney function. Using matching propensity scores (PS), 715 breath-hold female divers (Haenyeo) and non-divers were selected for analysis from 1,938 female divers and 3,415 non-divers, respectively. The prevalence of chronic kidney disease (CKD) defined as an estimated glomerular filtration rate (eGFR) calculated to be less than 60 ml/min/1.73 m2 was investigated in both diver and non-diver groups. RESULTS: The prevalence of CKD was significantly higher in breath-hold divers compared with non-divers after PS matching (12.6% vs. 8.0%, P = 0.004). In multivariate analysis, BHD activity was significantly associated with the risk of CKD in an unmatched cohort (OR, 1.976; 95% CI, 1.465-2.664). In the PS-matched cohort, BHD remained the independent risk factor for CKD even after adjusting for multiple covariates (OR 1.967; 95% CI, 1.341-2.886). CONCLUSION: Shallow but repetitive intermittent apnea by BHD, sustained for a long period of time, may potentially cause a deterioration in kidney function, as a long-term consequence.

Blood pooling in extrathoracic veins after glossopharyngeal insufflation.

PURPOSE: Trained breath-hold divers hyperinflate their lungs by glossopharyngeal insufflation (GPI) to prolong submersion time and withstand lung collapse at depths. Pulmonary hyperinflation leads to profound hemodynamic changes. METHODS: Thirteen divers performed preparatory breath-holds followed by apnea with GPI. Filling of extrathoracic veins was determined by ultrasound and magnetic resonance imaging and peripheral extravasation of fluid was assessed by electrical impedance. Femoral vein diameter was measured by ultrasound throughout the easy-going and struggle phase of apnea with GPI in eight divers in a sub-study. RESULTS: After GPI, pulmonary volume increased by 0.8 ± 0.6 L above total lung capacity. The diameter of the superior caval (by 36 ± 17%) and intrathoracic part of the inferior caval vein decreased (by 21 ± 16%), while the diameters of the internal jugular (by 53 ± 34%), hepatic (by 28 ± 40%), abdominal part of the inferior caval (by 28 ± 28%), and femoral veins (by 65 ± 50%) all increased (P < 0.05). Blood volume of the internal jugular, the hepatic, the abdominal part of the inferior caval vein, and the combined common iliac and femoral veins increased by 145 ± 115, 80 ± 88, 61 ± 60, and 183 ± 197%, respectively. In the sub-study, femoral vein diameter increased by 44 ± 33% in the easy-going phase of apnea with GPI, subsequently decreasing by 20 ± 16% during the struggle phase. Electrical impedance remained unchanged over the thigh and forearm, thus excluding peripheral fluid extravasation. CONCLUSIONS: GPI leads to heart and pulmonary vessel compression, resulting in redistribution of blood to extrathoracic capacitance veins proximal to venous valves. This is partially reversed by the onset of involuntary breathing movements.