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Purpose: Apnea duration is dependent on three factors: oxygen storage, oxygen consumption, hypoxia and hypercapnia tolerance. While current literature focuses on maximal apneas to improve apnea duration, apnea trained individuals use timed-repeated submaximal apneas, called "O2 and CO2 tables". These tables claim to accommodate the body to cope with hypoxia and hypercapnia, respectively. The aim of this study was twofold. First, to investigate the determinants of maximal apnea duration in apnea novices. Second, to compare physiologic responses to maximal apneas, O2 and CO2 tables. Methods: After medical screening, lung function test and hemoglobin mass measurement, twenty-eight apnea novices performed three apnea protocols in random order: maximal apneas, O2 table and CO2 table. During apnea, peripheral oxygen saturation (SpO2), heart rate (HR), muscle (mTOI) and cerebral (cTOI) tissue oxygenation index were measured continuously. End-tidal carbon dioxide (EtCO2) was measured before and after apneas. Results: Larger lung volumes, higher resting cTOI and lower resting EtCO2 levels correlated with longer apnea durations. Maximal apneas induced greater decreases in SpO2 (− 16%) and cTOI (− 13%) than O2 (− 8%; − 8%) and CO2 tables (− 6%; − 6%), whereas changes in EtCO2, HR and mTOI did not differ between protocols. Conclusion: These results suggest that, in apnea novices, O2 and CO2 tables did not induce a more profound hypoxia and hypercapnia, but a similar reduction in oxygen consumption than maximal apneas. Therefore, apnea novices should mainly focus on maximal apneas to improve hypoxia and hypercapnia tolerance. The use of specific lung training protocols can help to increase oxygen storage capacity. [ABSTRACT FROM AUTHOR]

Abstract Background Habitat transitions have considerable consequences in organism homeostasis, as they require the adjustment of several concurrent physiological compartments to maintain stability and adapt to a changing environment. Within the range of molecules with a crucial role in the regulation of different physiological processes, neuropeptides are key agents. Here, we examined the coding status of several neuropeptides and their receptors with pleiotropic activity in Cetacea. Results Analysis of 202 mammalian genomes, including 41 species of Cetacea, exposed an intricate mutational landscape compatible with gene sequence modification and loss. Specifically for Cetacea, in the 12 genes analysed we have determined patterns of loss ranging from species-specific disruptive mutations (e.g. neuropeptide FF-amide peptide precursor; NPFF) to complete erosion of the gene across the cetacean stem lineage (e.g. somatostatin receptor 4; SSTR4). Conclusions Impairment of some of these neuromodulators may have contributed to the unique energetic metabolism, circadian rhythmicity and diving response displayed by this group of iconic mammals.

Competitive swimmers complete 50‐m front crawl swimming without breathing or with a limited number of breaths. Breath holding during exercise can trigger diving reflex including bradycardia and diminished active muscle blood flow, whereas oxygen supply to vital organ such as brain is maintained. We hypothesized that swimmers achieving faster time in 50‐m front crawl with limited number of breaths demonstrate a blunted diving reflex of cardiac and active muscle blood flow responses with elevated cerebral perfusion to counteract peripheral and central fatigues. Twenty‐eight competitive swimmers (12 females) underwent a 50‐m front crawl swimming time trial with minimum respiratory interruptions, following which they were categorized into two groups: Fast (n = 13) and Slow (n = 15). Additionally, they performed knee extension exercises with maximal voluntary breath‐ holding, wherein leg blood flow (Doppler ultrasound), cardiac output (Modelflow), heart rate (electrocardiogram), and middle cerebral artery mean blood velocity (transcranial Doppler ultrasound) were evaluated. The pattern of leg blood flow response differed between the two groups (p = 0.031) with the Fast group experiencing a delayed onset of reductions in leg blood flow (p = 0.035). The onset of bradycardia was also delayed in the Fast group (p = 0.014), with this group demonstrating a higher value of the lowest heart rate (between‐trial difference in average: 15.9 [3.73, 28.2] beats/min) and cardiac output (between‐trial difference in median: 2.84 L/min) (both, p ≤ 0.013). Middle cerebral artery mean blood velocity was similar between the groups (all p ≥ 0.112). We show that swimmers with superior performance in 50‐m front crawl swim with limited breaths display a diminished diving reflex. [ABSTRACT FROM AUTHOR]

Background: Habitat transitions have considerable consequences in organism homeostasis, as they require the adjustment of several concurrent physiological compartments to maintain stability and adapt to a changing environment. Within the range of molecules with a crucial role in the regulation of different physiological processes, neuropeptides are key agents. Here, we examined the coding status of several neuropeptides and their receptors with pleiotropic activity in Cetacea. Results: Analysis of 202 mammalian genomes, including 41 species of Cetacea, exposed an intricate mutational landscape compatible with gene sequence modification and loss. Specifically for Cetacea, in the 12 genes analysed we have determined patterns of loss ranging from species-specific disruptive mutations (e.g. neuropeptide FF-amide peptide precursor; NPFF) to complete erosion of the gene across the cetacean stem lineage (e.g. somatostatin receptor 4; SSTR4). Conclusions: Impairment of some of these neuromodulators may have contributed to the unique energetic metabolism, circadian rhythmicity and diving response displayed by this group of iconic mammals. [ABSTRACT FROM AUTHOR]

Breath-hold diving performances are typically better in men than in women. However, it is still being determined if there are differences in the physiological responses to breath-holding between the sexes. We conducted a study comparing the maximum breath-hold duration, heart rate (HR) reduction, peripheral oxygen saturation (SpO2), and spleen volume and contraction in 37 men and 44 women, all of whom had no prior breath-holding experience. They performed two dry apneas separated by 2 min; the first was limited to 60 s, followed by a maximal effort apnea. HR and SpO2 were measured continuously. Spleen diameters were measured via ultrasonography before and immediately following each apnea. The maximal apneic duration was longer in men (78 ± 19 s) compared with women (61 ± 18 s, p < 0.001), while the HR reduction was similar (women: 16% ± 19% versus men: 16% ± 17%, p = 0.973). The absolute splenic contraction was greater in men (59 ± 56 mL) compared with women (35 ± 28 mL, p < 0.001) in the first apnea, while the relative contraction was similar (women: 21% ± 17% versus men: 23% ± 13%, p = 0.528). In addition, the lowest SpO2 during the maximal apnea was similar between sexes (women: 93.3% ± 4.4%; men: 91.9% ± 4.3%, p = 0.161). We conclude that men have larger spleen size and contraction, lung size, and maximal apneic duration than women. The cardiovascular diving response is similar between sexes for those inexperienced with apneic diving. The longer breath-hold duration in men may be partly due to greater oxygen storage capacity, which results from larger vital capacity and greater spleen size and contraction.

We aimed to determine the relative contribution of hypercapnia and hypoxia to the bradycardic response to apneas. We hypothesized that apneas with hypercapnia would cause greater bradycardia than normoxia, similar to the response seen with hypoxia, and that apneas with hypercapnic hypoxia would induce greater bradycardia than hypoxia or hypercapnia alone. Twenty‐six healthy participants (12 females; 23 ± 2 years; BMI 24 ± 3 kg/m2) underwent three gas challenges: hypercapnia (+5 torr end tidal partial pressure of CO2 [PETCO2]), hypoxia (50 torr end tidal partial pressure of O2 [PETO2]), and hypercapnic hypoxia (combined hypercapnia and hypoxia), with each condition interspersed with normocapnic normoxia. Heart rate and rhythm, blood pressure, PETCO2, PETO2, and oxygen saturation were measured continuously. Hypercapnic hypoxic apneas induced larger bradycardia (−19 ± 16 bpm) than normocapnic normoxic apneas (−11 ± 15 bpm; p = 0.002), but had a comparable response to hypoxic (−19 ± 15 bpm; p = 0.999) and hypercapnic apneas (−14 ± 14 bpm; p = 0.059). Hypercapnic apneas were not different from normocapnic normoxic apneas (p = 0.134). After removal of the normocapnic normoxic heart rate response, the change in heart rate during hypercapnic hypoxia (−11 ± 16 bpm) was similar to the summed change during hypercapnia+hypoxia (−9 ± 10 bpm; p = 0.485). Only hypoxia contributed to this bradycardic response. Under apneic conditions, the cardiac response is driven by hypoxia. [ABSTRACT FROM AUTHOR]

Breath-hold diving has been traditionally practiced for professional and recreational reasons and has recently emerged as a competitive sport. The physiological response during breath-holding, also known as diving response, consists mainly of bradycardia and peripheral vasoconstriction. Elite apneists can suppress the urge to breathe, sustain greater arterial desaturation and develop pronounced bradycardia, thus accomplishing impressively long breath-hold times. This study explored physiological responses during static apnea and their association with apnea duration in breath-hold divers with high physiological adaptations acquired from long-term apnea training. Nine well-trained competitive divers held their breath for as long as possible while floating motionlessly in a swimming pool (26–27 °C), simulating an actual “static apnea competition”. Long apnea durations (302 ± 60 s) as well as severe oxygen desaturation (minSaO2 46 ± 11%) and bradycardia (minHR 49 ± 8 bpm) were achieved. Apnea duration was positively correlated with forced vital capacity (r = 0.771) and apnea duration until initiation of desaturation (r = 0.736) and negatively correlated with minSaO2 (r = −0.672) (p < 0.05). Moreover, minHR during apnea was correlated with pre-apneic hemoglobin concentration (r = 0.685) (p < 0.05). The prolonged apnea durations achieved by the well-trained divers in this study, while performing maximum immersed static apnea under competitive simulated conditions, were related to their high lung volumes and their delayed and profound O2 desaturation, whereas their bradycardic response was not a decisive factor.

Breath-hold diving has been traditionally practiced for professional and recreational reasons and has recently emerged as a competitive sport. The physiological response during breath-holding, also known as diving response, consists mainly of bradycardia and peripheral vasoconstriction. Elite apneists can suppress the urge to breathe, sustain greater arterial desaturation and develop pronounced bradycardia, thus accomplishing impressively long breath-hold times. This study explored physiological responses during static apnea and their association with apnea duration in breath-hold divers with high physiological adaptations acquired from long-term apnea training. Nine well-trained competitive divers held their breath for as long as possible while floating motionlessly in a swimming pool (26–27 °C), simulating an actual "static apnea competition". Long apnea durations (302 ± 60 s) as well as severe oxygen desaturation (minSaO2 46 ± 11%) and bradycardia (minHR 49 ± 8 bpm) were achieved. Apnea duration was positively correlated with forced vital capacity (r = 0.771) and apnea duration until initiation of desaturation (r = 0.736) and negatively correlated with minSaO2 (r = −0.672) (p < 0.05). Moreover, minHR during apnea was correlated with pre-apneic hemoglobin concentration (r = 0.685) (p < 0.05). The prolonged apnea durations achieved by the well-trained divers in this study, while performing maximum immersed static apnea under competitive simulated conditions, were related to their high lung volumes and their delayed and profound O2 desaturation, whereas their bradycardic response was not a decisive factor. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The spleen contracts during apnea, releasing stored erythrocytes, thereby increasing systemic hemoglobin concentration (Hb). We compared apnea and rebreathing periods, of equal sub-maximal duration (mean 137 s; SD 30), in eighteen subjects to evaluate whether respiratory arrest or hypoxic and hypercapnic chemoreceptor stimulation is the primary elicitor of splenic contraction and cardiovascular responses during apnea. Spleen volume, Hb, cardiovascular variables, arterial (SaO2), cerebral (ScO2), and deltoid muscle oxygen saturations (SmO2) were recorded during the trials and end-tidal partial pressure of oxygen (PETO2) and carbon dioxide (PETCO2) were measured before and after maneuvers. The spleen volume was smaller after apnea, 213 (89) mL, than after rebreathing, 239 (95)mL, corresponding to relative reductions from control by 20.8 (17.8) % and 11.6 (8.0) %, respectively. The Hb increased 2.4 (2.0) % during apnea, while there was no significant change with rebreathing. The cardiovascular responses, including bradycardia, decrease in cardiac output, and increase in total peripheral resistance, were augmented during apnea compared to during rebreathing. The PETO2 was higher, and the PETCO2 was lower, after apnea compared to after rebreathing. The ScO2 wasmaintained duringmaneuvers. The SaO2 decreased 3.8 (3.1) % during apnea, and even more, 5.4 (4.4) %, during rebreathing, while the SmO2 decreased less during rebreathing, 2.2 (2.8) %, than during apnea, 8.3 (6.2) %. We conclude that respiratory arrest per se is an important stimulus for splenic contraction and Hb increase during apnea, as well as an important initiating factor for the apnea-associated cardiovascular responses and their oxygen-conserving effects. [ABSTRACT FROM AUTHOR]

The idea of putting astronauts into a hibernation-like state during interplanetary spaceflights has sparked new interest in the evolutionary roots of hibernation and torpor. In this context, it should be noted that mammalian fetuses and neonates respond to the environmental challenges in the perinatal period with a number of physiological mechanisms that bear striking similarity to hibernation and torpor. These include three main points: first, prenatal deviation from the overall metabolic size relationship, which adapts the fetus to the low-oxygen conditions in the womb and corresponds to the metabolic reduction during hibernation and estivation; second, intranatal diving bradycardia in response to shortened O2 supply during birth, comparable to the decrease in heart rate preceding the drop in body temperature upon entry into torpor; and third, postnatal onset of nonshivering thermogenesis in the brown adipose tissue, along with the increase in basal metabolic rate up to the level expected from body size, such as during arousal from hibernation. The appearance of hibernation-like adaptations in the perinatal period suggests that, conversely, hibernation and torpor may be composed of mechanisms shared by all mammals around birth. This hypothesis sheds new light on the origins of hibernation and supports its potential accessibility to nonhibernating species, including humans. [ABSTRACT FROM AUTHOR]

The spleen contracts during apnea, releasing stored erythrocytes, thereby increasing systemic hemoglobin concentration (Hb). We compared apnea and rebreathing periods, of equal sub-maximal duration (mean 137 s; SD 30), in eighteen subjects to evaluate whether respiratory arrest or hypoxic and hypercapnic chemoreceptor stimulation is the primary elicitor of splenic contraction and cardiovascular responses during apnea. Spleen volume, Hb, cardiovascular variables, arterial (SaO2), cerebral (ScO2), and deltoid muscle oxygen saturations (SmO2) were recorded during the trials and end-tidal partial pressure of oxygen (PETO2) and carbon dioxide (PETCO2) were measured before and after maneuvers. The spleen volume was smaller after apnea, 213 (89) mL, than after rebreathing, 239 (95) mL, corresponding to relative reductions from control by 20.8 (17.8) % and 11.6 (8.0) %, respectively. The Hb increased 2.4 (2.0) % during apnea, while there was no significant change with rebreathing. The cardiovascular responses, including bradycardia, decrease in cardiac output, and increase in total peripheral resistance, were augmented during apnea compared to during rebreathing. The PETO2 was higher, and the PETCO2 was lower, after apnea compared to after rebreathing. The ScO2 was maintained during maneuvers. The SaO2 decreased 3.8 (3.1) % during apnea, and even more, 5.4 (4.4) %, during rebreathing, while the SmO2 decreased less during rebreathing, 2.2 (2.8) %, than during apnea, 8.3 (6.2) %. We conclude that respiratory arrest per se is an important stimulus for splenic contraction and Hb increase during apnea, as well as an important initiating factor for the apnea-associated cardiovascular responses and their oxygen-conserving effects.

Understanding the physiology and genetics of human hypoxia tolerance has important medical implications, but this phenomenon has thus far only been investigated in high-altitude human populations. Another system, yet to be explored, is humans who engage in breath-hold diving. The indigenous Bajau people ("Sea Nomads") of Southeast Asia live a subsistence lifestyle based on breath-hold diving and are renowned for their extraordinary breath-holding abilities. However, it is unknown whether this has a genetic basis. Using a comparative genomic study, we show that natural selection on genetic variants in the PDE10A gene have increased spleen size in the Bajau, providing them with a larger reservoir of oxygenated red blood cells. We also find evidence of strong selection specific to the Bajau on BDKRB2, a gene affecting the human diving reflex. Thus, the Bajau, and possibly other diving populations, provide a new opportunity to study human adaptation to hypoxia tolerance. VIDEO ABSTRACT.

Static apneas performed after an overnight fast as opposed to postprandially have been evinced to improve apneic performance. However, no study has explored the effect of dietary intake on apneic performance, cardiovascular or splenic responses over a series of repeated apneas. Ten healthy adults attended the laboratory on three separate occasions (≥48-h apart): after a 14-h fast (F14), 1 h postconsumption of a high-calorie, high-carbohydrate (HCHC) meal, or 1 h postconsumption of a low-calorie, low-carbohydrate (LCLC)-based meal. During each visit, the subjects performed a hyperoxic rebreathing trial and a series of three repeated maximal static apneas. Heart rate, peripheral oxyhemoglobin saturation (SpO2 ), and gas exchange were monitored continuously, whereas splenic volume (SV) and hematology were assessed after the rebreathing and apneas. At rest, after HCHC, the respiratory exchange ratio (0.87 ± 0.17, P ≤ 0.043), expired minute volume of carbon dioxide (CO2; HCHC, 0.35 ± 0.09 L/min, P ≤ 0.014), and SV (227 ± 45 mL, P ≤ 0.031) were higher compared with F14 (0.71 ± 0.08; 0.23 ± 0.04 L/min; 204 ± 49 mL) and LCLC (0.72 ± 0.07; 0.25 ± 0.03 L/min; 199 ± 49 mL). A faster CO2 accumulation was recorded during the HCHC (96 ± 35 s) rebreathing trial (F14, 162 ± 42 s, P = 0.001; LCLC, 151 ± 23 s, P = 0.002). Longer apneas were reported in F14 compared with HCHC (apneas 1-3, P ≤ 0.046) and LCLC (apneas 2-3, P ≤ 0.006). After the first apnea, SV was lower in F14 (141 ± 43 mL, P = 0.015) compared with HCHC (180 ± 34 mL). Moreover, after the third apnea, end-tidal partial pressure of oxygen and nadir SpO2 were lower in F14 (8.6 ± 2.2 kPa, P = 0.028; 77 ± 13%, P = 0.009) compared with HCHC (10.1 ± 1.7 kPa; 84 ± 9%). No differences were measured in end-apneic end-tidal partial pressure of CO2, heart rate nor hematology across diets. Fasting improved apneic performance with apneas being terminated at lower oxygen levels through altering the rate of CO2 accumulation but without affecting the cardiovascular responses. [ABSTRACT FROM AUTHOR]

Lars J Bjertnaes,1,2 Anton Hauge,3 Marianne Thoresen,3,4 Lars Walløe3 1Anesthesia and Critical Care Research Group, Department of Clinical Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, N-9037, Norway; 2Department of Intensive Care Medicine, University Hospital of North Norway, Tromsø, N- 9017, Norway; 3Division of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, 0317, Norway; 4Translational Health Sciences, University of Bristol, Bristol, UKCorrespondence: Lars J BjertnaesAnesthesia and Critical Care Research Group, Department of Clinical Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, N-9037, NorwayTel +47 77627001Fax +47 77626042Email lars.bjertnaes@uit.noBackground: Successful cardiopulmonary resuscitation after drowning or avalanche is often attributed to hypothermia-induced decrease in metabolism, which adapts the oxygen demand to the amount supplied under cardiac compression. Four decades ago, we speculated if oxygen-sparing mechanisms like those found in marine mammals, may improve cerebral oxygenation during acute airway blockade in humans. We investigated hemodynamic changes during steady state ergometer cycling with intermittent periods of apnea and face immersion (AFI) in ice-cold water. During AFI, heart rate (HR) dropped by 58% whereas average blood velocity (ABV) determined by means of a Doppler ultrasound velocity meter (UNIDOP University of Oslo, Oslo, Norway) fell by 85% in the radial artery and rose by 67% in the vertebral artery. Similar changes occured in radial artery ABV, albeit more slowly, when the test subject only held his breath while cycling. When he breathed via a snorkel during face immersion, HR remained unchanged while radial artery ABV fell transiently and subsequently returned to its pre-immersion level. These findings later were confirmed by other investigators. Moreover, a recent study revealed that the seal even has a system for selective brain cooling during the dive.Conclusion: Our research has confirmed prioritized cerebral circulation during AFI in cold water. We hypothesize that these changes may improve brain oxygenation due both to greater blood flow and possibly also to faster brain cooling, as demonstrated in diving seals.Keywords: apnea, breath-hold, cardiopulmonary resuscitation, diving response, hypothermia

Heart rates of air-breathing diving animals can change on a short time scale due to the diving response during submergence. Heart rate is used frequently as a proxy for indirectly estimating metabolic rates on a fine time scale. However, most studies to date have been conducted on endothermic diving animals, and the relationships between metabolic rates and heart rates in ectothermic diving animals have not been well studied. Sea turtles are unique model organisms of diving ectotherms because they spend most of their life in the ocean and perform deep and/or long dives. In this study, we examined the relationship between heart rates and metabolic rates in captive loggerhead turtles, Caretta caretta, to estimate oxygen consumption rates during each dive based on heart rates. The oxygen consumption rates (V̇O2: mlO2 min−1 kg−1) and average heart rates (fH: beats min−1) were measured simultaneously in indoor tanks at water temperatures of 15–25°C. Our results showed that oxygen consumption rate was affected by heart rate and water temperature in loggerhead turtles. Based on the collected data, we formulated the model equation as V̇O2=0.0124fH+0.0047Tw - 0.0791. The equation can be used for estimating fine-scaled field metabolic rates in free-ranging loggerhead turtles. The results of this study will contribute to future comparative studies of the physiological states of ectothermic diving animals.

Increased CO2 sensitivity is common in panic disorder (PD) patients. Free divers who are known for their exceptional breathing control have lower CO2 sensitivity due to training effects. This study aimed to investigate the immediate effects of cold facial immersion (CFI), breath holding and CO2 challenges on panic symptoms. Healthy participants and patients with PD were subjected to four experimental conditions in a randomly assigned order. The four conditions were (a) breath-holding (BH), (b) CFI for 30 s, (c) CO2 challenge, and (d) CO2 challenge followed by CFI. Participants completed a battery of psychological measures, and physiological data (heart rate and respiration rate) were collected following each experimental condition. Participants with PD were unable to hold their breath for as long as normal controls; however, this finding was not significant, potentially due to a small sample size. Significant reductions in both physiological and cognitive symptoms of panic were noted in the clinical group following the CFI task. As hypothesized, the CFI task exerted demonstrable anxiolytic effects in the clinical group in this study by reducing heart rate significantly and lessening self-reported symptoms of anxiety and panic. This outcome demonstrates the promise of the CFI task for clinical applications.

Introduction: Acute apnea evokes bradycardia and peripheral vasoconstriction in order to conserve oxygen, which is more pronounced with face immersion. This response is contrary to the tachycardia and increased blood flow to muscle tissue related to the higher oxygen consumption during exercise. The aim of this study was to investigate cardiovascular and metabolic responses of dynamic dry apnea (DRA) and face immersed apnea (FIA).Methods: Ten female volunteers (17.1 ± 0.6 years old) naive to breath-hold-related sports, performed a series of seven dynamic 30 s breath-holds while cycling at 25% of their peak power output. This was performed in two separate conditions in a randomized order: FIA (15°C) and DRA. Heart rate and muscle tissue oxygenation through near-infrared spectroscopy were continuously measured to determine oxygenated (m[O2Hb]) and deoxygenated hemoglobin concentration (m[HHb]) and tissue oxygenation index (mTOI). Capillary blood lactate was measured 1 min after the first, third, fifth, and seventh breath-hold.Results: Average duration of the seven breath-holds did not differ between conditions (25.3 s ± 1.4 s, p = 0.231). The apnea-induced bradycardia was stronger with FIA (from 134 ± 4 to 85 ± 3 bpm) than DRA (from 134 ± 4 to 100 ± 5 bpm, p < 0.001). mTOI decreased significantly from 69.9 ± 0.9% to 63.0 ± 1.3% (p < 0.001) which is reflected in a steady decrease in m[O2Hb] (p < 0.001) and concomitant increase in m[HHb] (p = 0.001). However, this was similar in both conditions (0.121 < p < 0.542). Lactate was lower after the first apnea with FIA compared to DRA (p = 0.038), while no differences were observed in the other breath-holds.Conclusion: Our data show strong decreases in heart rate and muscle tissue oxygenation during dynamic apneas. A stronger bradycardia was observed in FIA, while muscle oxygenation was not different, suggesting that FIA did not influence muscle oxygenation. An order of mechanisms was observed in which, after an initial tachycardia, heart rate starts to decrease after muscle tissue deoxygenation occurs, suggesting a role of peripheral vasoconstriction in the apnea-induced bradycardia. The apnea-induced increase in lactate was lower in FIA during the first apnea, probably caused by the stronger bradycardia.

Introduction: Acute apnea evokes bradycardia and peripheral vasoconstriction in order to conserve oxygen, which is more pronounced with face immersion. This response is contrary to the tachycardia and increased blood flow to muscle tissue related to the higher oxygen consumption during exercise. The aim of this study was to investigate cardiovascular and metabolic responses of dynamic dry apnea (DRA) and face immersed apnea (FIA). Methods: Ten female volunteers (17.1 ± 0.6 years old) naive to breath-hold-related sports, performed a series of seven dynamic 30 s breath-holds while cycling at 25% of their peak power output. This was performed in two separate conditions in a randomized order: FIA (15°C) and DRA. Heart rate and muscle tissue oxygenation through near-infrared spectroscopy were continuously measured to determine oxygenated (m[O2Hb]) and deoxygenated hemoglobin concentration (m[HHb]) and tissue oxygenation index (mTOI). Capillary blood lactate was measured 1 min after the first, third, fifth, and seventh breath-hold. Results: Average duration of the seven breath-holds did not differ between conditions (25.3 s ± 1.4 s, p = 0.231). The apnea-induced bradycardia was stronger with FIA (from 134 ± 4 to 85 ± 3 bpm) than DRA (from 134 ± 4 to 100 ± 5 bpm, p < 0.001). mTOI decreased significantly from 69.9 ± 0.9% to 63.0 ± 1.3% (p < 0.001) which is reflected in a steady decrease in m[O2Hb] (p < 0.001) and concomitant increase in m[HHb] (p = 0.001). However, this was similar in both conditions (0.121 < p < 0.542). Lactate was lower after the first apnea with FIA compared to DRA (p = 0.038), while no differences were observed in the other breath-holds. Conclusion: Our data show strong decreases in heart rate and muscle tissue oxygenation during dynamic apneas. A stronger bradycardia was observed in FIA, while muscle oxygenation was not different, suggesting that FIA did not influence muscle oxygenation. An order of mechanisms was observed in which, after an initial tachycardia, heart rate starts to decrease after muscle tissue deoxygenation occurs, suggesting a role of peripheral vasoconstriction in the apnea-induced bradycardia. The apnea-induced increase in lactate was lower in FIA during the first apnea, probably caused by the stronger bradycardia. [ABSTRACT FROM AUTHOR]

IntroductionTechnical diving is very popular in Finland throughout the year despite diving conditions being challenging, especially due to arctic water and poor visibility. Cold water, immersion, submersion, hyperoxia, as well as psychological and physiological stress, all have an effect on the autonomic nervous system (ANS).Materials and methodsTo evaluate divers’ ANS responses, short-term (5 min) heart rate variability (HRV) during dives in 2–4°C water was measured. HRV resting values were evaluated from separate measurements before and after the dives. Twenty-six experienced closed circuit rebreather (CCR) divers performed an identical 45-meter decompression dive with a non-physical task requiring concentration at the bottom depth.ResultsActivity of the ANS branches was evaluated with the parasympathetic (PNS) and sympathetic (SNS) indexes of the Kubios HRV Standard program. Compared to resting values, PNS activity decreased significantly on immersion with face out of water. From immersion, it increased significantly with facial immersion, just before decompression and just before surfacing. Compared to resting values, SNS activity increased significantly on immersion with face out of water. Face in water and submersion measures did not differ from the immersion measure. After these measurements, SNS activity decreased significantly over time.ConclusionOur study indicates that the trigeminocardiac part of the diving reflex causes the strong initial PNS activation at the beginning of the dive but the reaction seems to decrease quickly. After this initial activation, cold seemed to be the most prominent promoter of PNS activity – not pressure. Also, our study showed a concurrent increase in both SNS and PNS branches, which has been associated with an elevated risk for arrhythmia. Therefore, we recommend a short adaptation phase at the beginning of cold-water diving before physical activity.

Introduction: Technical diving is very popular in Finland throughout the year despite diving conditions being challenging, especially due to arctic water and poor visibility. Cold water, immersion, submersion, hyperoxia, as well as psychological and physiological stress, all have an effect on the autonomic nervous system (ANS). Materials and methods: To evaluate divers' ANS responses, short-term (5 min) heart rate variability (HRV) during dives in 2–4°C water was measured. HRV resting values were evaluated from separate measurements before and after the dives. Twenty-six experienced closed circuit rebreather (CCR) divers performed an identical 45-meter decompression dive with a non-physical task requiring concentration at the bottom depth. Results: Activity of the ANS branches was evaluated with the parasympathetic (PNS) and sympathetic (SNS) indexes of the Kubios HRV Standard program. Compared to resting values, PNS activity decreased significantly on immersion with face out of water. From immersion, it increased significantly with facial immersion, just before decompression and just before surfacing. Compared to resting values, SNS activity increased significantly on immersion with face out of water. Face in water and submersion measures did not differ from the immersion measure. After these measurements, SNS activity decreased significantly over time. Conclusion: Our study indicates that the trigeminocardiac part of the diving reflex causes the strong initial PNS activation at the beginning of the dive but the reaction seems to decrease quickly. After this initial activation, cold seemed to be the most prominent promoter of PNS activity – not pressure. Also, our study showed a concurrent increase in both SNS and PNS branches, which has been associated with an elevated risk for arrhythmia. Therefore, we recommend a short adaptation phase at the beginning of cold-water diving before physical activity. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Splenic contractions occur in response to apnoea‐induced hypoxia with and without face immersion in water. However, the splenic responses to a series of static or dynamic apnoeas with whole‐body water immersion in non‐divers and elite breath‐hold divers are unknown.What is the main finding and its importance?Static and dynamic apnoeas were equally effective in stimulating splenic contractions across non‐divers and elite breath‐hold divers. These findings demonstrate that the magnitude of the splenic response is largely dictated by the degree of the hypoxemic stress encountered during voluntary apnoeic epochs. Splenic contractions occur in response to apnoea‐induced hypoxia with and without facial water immersion. However, the splenic responses to a series of static (STA) or dynamic (DYN) apnoeas with whole‐body water immersion in non‐divers (NDs) and elite breath‐hold divers (EBHDs) are unknown. EBHD (n = 8), ND (n = 10) and control participants (n = 8) were recruited. EBHD and ND performed a series of five maximal DYN or STA on separate occasions. Control performed a static eupnoeic (STE) protocol to control against any effects of water immersion and diurnal variation on splenic volume and haematology. Heart rate (HR) and peripheral oxygen saturation (SpO2) were monitored for 30 s after each apnoea. Pre‐ and post‐apnoeic splenic volumes were quantified ultrasonically, and blood samples were drawn for haematology. For EBHD and ND end‐apnoeic HR was higher (P < 0.001) and SpO2 was lower in DYN (P = 0.024) versus STA. EBHD attained lower end‐apnoeic SpO2 during DYN and STA than NDs (P < 0.001). Splenic contractions occurred following DYN (EBHD, −47 ± 6%; ND, −37 ± 4%; P < 0.001) and STA (EBHD, −26 ± 4%; ND, −26 ± 8%; P < 0.01). DYN‐associated splenic contractions were greater than STA in EBHD only (P = 0.042). Haemoglobin concentrations were higher following DYN only (EBHD, +5 ± 8g/L , +4 ± 2%; ND, +8 ± 3 g/L , +4.9 ± 3%; P = 0.019). Haematocrit remained unchanged after each protocol. There were no between group differences in post‐apnoeic splenic volume or haematology. In both groups, splenic contractions occurred in response to STA and DYN when combined with whole‐body immersion. DYN apnoeas, were effective at increasing haemoglobin concentrations but not STA apnoeas. Thus, the magnitude of the splenic response relates to the hypoxemic stress encountered during apnoeic epochs. [ABSTRACT FROM AUTHOR]

Global biotic and abiotic threats, particularly from pervasive human activities, are progressively pushing large, apex carnivorous mammals into the functional role of mesopredator. Hunters are now becoming the hunted. Despite marked impacts on these animals and the ecosystems in which they live, little is known about the physiological repercussions of this role downgrading from ultimate to penultimate predator.Here we examine how such ecological role reversals alter the physiological processes associated with energy expenditure, and ultimately the cost of survival during peak performance.Taxonomic group, preferred habitat and domestication affected the capacity of the oxygen pathway to support high levels of aerobic performance by carnivorous mammals. Fear responses associated with anthropogenic threats also impacted aerobic performance.Allometric trends for three energetic metrics [maximum oxygen consumption, field metabolic rates (FMRs) and the cost per stride or stroke], showed distinct trends in aerobic capacity for different evolutionary lineages of mammalian predators. Cursorial canids that chase down prey demonstrated the highest relative maximum oxygen consumption rates (10–25 times resting levels) and FMRs, while ambush predators (i.e. felids) and diving marine mammals had aerobic capacities that were similar to or lower than sedentary domestic mammals of comparable size.The maximum energetic cost of performance for apex predators depended on whether the animals were hunters or the hunted. Escape responses were exceptionally costly for marine (narwhal Monodon monoceros) and terrestrial (mountain lion Puma concolor) locomotor specialists, as well as semi‐aquatic (polar bear Ursus maritimus) species; all showed a nearly two‐fold increase in peak energy expenditure when avoiding threats.As the duration and frequency of threats to wild species continue to grow, cumulative energetic costs are becoming more apparent. In view of this, attention to the energy demands of apex predators will provide vital predictive power to anticipate mismatches between a species' functional design and human‐induced pressures, and allow for the development of conservation strategies based on how species are built to survive. A free Plain Language Summary can be found within the Supporting Information of this article. [ABSTRACT FROM AUTHOR]

Purpose: Acute breath-holding deprives the human body from oxygen. In an effort to protect the brain, the diving response is initiated, coupling several physiological responses. The aim of this study was to describe the physiological responses to apnea at the cardiac, peripheral and cerebral level. Methods: 31 physically active subjects (17 male, 14 female, 23.3 ± 1.8 years old) performed a maximal static breath-hold in a seated position. Heart rate (HR), muscle and cerebral oxygenation (by means of near-infrared spectroscopy, NIRS) were continuously measured. RM MANOVA's were used to identify changes in HR, peripheral (mTOI) and cerebral (cTOI) tissue oxygenation and oxygenated (O2Hb) and deoxygenated (HHb) hemoglobin during apnea. Results: Average apnea duration was 157 ± 41 s. HR started decreasing after 10 s (p < 0.001) and dropped on average by 27 ± 14 bpm from baseline (p < 0.001). mTOI started decreasing 10 s after apnea (p < 0.001) and fell by 8.6 ± 4.0% (p < 0.001). Following an immediate drop after 5 s (p < 0.001), cTOI increased continuously, reaching a maximal increase of 3.7 ± 2.4% followed by a steady decrease until the end of apnea. cTOI fell on average 5.4 ± 8.3% below baseline (p < 0.001). Conclusion: During apnea, the human body elicits several protective mechanisms to protect itself against the deprivation of oxygen. HR slows down, decreasing O2 demand of the cardiac muscle. The decrease in mTOI and increase in cTOI imply a redistribution of blood flow prioritizing the brain. However, this mechanism is not sufficient to maintain cTOI until the end of apnea. [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Does facial cooling‐mediated stimulation of cutaneous trigeminal afferents associated with the diving response increase cerebral blood flow or are factors associated with breath‐holding (e.g. arterial carbon dioxide accumulation, pressor response) more important in humans?What is the main finding and its importance?Physiological factors associated with breath‐holding such as arterial carbon dioxide accumulation and the pressor response, but not facial cooling (trigeminal nerve stimulation), make the predominant contribution to diving response‐mediated increases in cerebral blood flow in humans. Diving evokes a pattern of physiological responses purported to preserve oxygenated blood delivery to vital organs such as the brain. We sought to uncouple the effects of trigeminal nerve stimulation on cerebral blood flow (CBF) from other modifiers associated with the diving response, such as apnoea and changes in arterial carbon dioxide tension. Thirty‐seven young healthy individuals participated in separate trials of facial cooling (FC, 3 min) and cold pressor test (CPT, 3 min) under poikilocapnic (Protocol 1) and isocapnic conditions (Protocol 2), facial cooling while either performing a breath‐hold (FC +BH) or breathing spontaneously for a matched duration (FC −BH) (Protocol 3), and BH during facial cooling (BH +FC) or without facial cooling (BH −FC) (Protocol 4). Under poikilocapnic conditions neither facial cooling nor CPT evoked a change in middle cerebral artery blood flow velocity (MCA vmean; transcranial Doppler) (P > 0.05 vs. baseline). Under isocapnic conditions, facial cooling did not change MCA vmean (P > 0.05), whereas CPT increased MCA vmean by 13% (P < 0.05). Facial cooling with a concurrent BH markedly increased MCA vmean (Δ23%) and internal carotid artery blood flow (ICAQ; duplex Doppler ultrasound) (Δ26%) (P < 0.001), but no change in MCA vmean and ICAQ was observed when facial cooling was accompanied by spontaneous breathing (P > 0.05). Finally, MCA vmean and ICAQ were similarly increased by BH either with or without facial cooling. These findings suggest that physiological factors associated with BH, and not facial cooling (i.e. trigeminal nerve stimulation) per se, make the predominant contribution to increases in CBF during diving in humans. [ABSTRACT FROM AUTHOR]

IntroductionDiving close to the Arctic circle means diving in cold water regardless of the time of year. The human body reacts to cold through autonomous nervous system (ANS)-mediated thermoregulatory mechanisms. Diving also induces ANS responses as a result of the diving reflex.Materials and MethodsIn order to study ANS responses during diving in Arctic water temperatures, we retrospectively analyzed repeated 5-min heart rate variability (HRV) measures and the mean body temperature from dives at regular intervals using naval diving equipment measurement tests in 0°C water. Three divers performed seven dives without physical activity (81–91 min), and two divers performed four dives with physical activity after 10 min of diving (0–10 min HRV recordings were included in the study).ResultsOur study showed a significant increase in parasympathetic activity (PNS) at the beginning of the dives, after which PNS activity decreased significantly (measure 5–10 min). Subsequent measurements (15–20 min and onward) showed a significant increase in PNS activity over time.ConclusionOur results suggest that the first PNS responses of the human diving reflex decrease quickly. Adverse effects of PNS activity should be considered on long and cold dives. To avoid concurrent sympathetic (SNS) and PNS activity at the beginning of dives, which in turn may increase the risk of arrhythmia in cold water, we suggest a short adaptation phase before physical activity. Moreover, we suggest it is prudent to give special attention to cardiovascular risk factors during pre-dive examinations for cold water divers.

Introduction: Diving close to the Arctic circle means diving in cold water regardless of the time of year. The human body reacts to cold through autonomous nervous system (ANS)-mediated thermoregulatory mechanisms. Diving also induces ANS responses as a result of the diving reflex. Materials and Methods: In order to study ANS responses during diving in Arctic water temperatures, we retrospectively analyzed repeated 5-min heart rate variability (HRV) measures and the mean body temperature from dives at regular intervals using naval diving equipment measurement tests in 0°C water. Three divers performed seven dives without physical activity (81–91 min), and two divers performed four dives with physical activity after 10 min of diving (0–10 min HRV recordings were included in the study). Results: Our study showed a significant increase in parasympathetic activity (PNS) at the beginning of the dives, after which PNS activity decreased significantly (measure 5–10 min). Subsequent measurements (15–20 min and onward) showed a significant increase in PNS activity over time. Conclusion: Our results suggest that the first PNS responses of the human diving reflex decrease quickly. Adverse effects of PNS activity should be considered on long and cold dives. To avoid concurrent sympathetic (SNS) and PNS activity at the beginning of dives, which in turn may increase the risk of arrhythmia in cold water, we suggest a short adaptation phase before physical activity. Moreover, we suggest it is prudent to give special attention to cardiovascular risk factors during pre-dive examinations for cold water divers. [ABSTRACT FROM AUTHOR]

Purpose: Serum 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.Methods: Participants 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.Results: No 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.Conclusions: The 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. [ABSTRACT FROM AUTHOR]

• Blood pressure response to apnoea overlaps in air and in O 2. • In O 2 , apnoeas show a milder response in heart rate and peripheral resistances. • CO 2 rise may trigger the pressure increase in phase III. To check whether the evolution of alveolar pressures of O 2 (P A O 2) and CO 2 (P A CO 2) explains the cardiovascular responses to apnoea, eight divers performed resting apnoeas of increasing duration in air and in O 2. We measured heart rate (f H), arterial pressure (AP), and peripheral resistances (TPR) beat-by-beat, P A O 2 and P A CO 2 at the end of each apnoea. The three phases of the cardiovascular response to apnoea were observed. In O 2 , TPR increase (9 ± 4 mmHg min l−1) and f H decrease (-11 ± 8 bpm) were lower than in air (15 ± 5 mmHg min l−1 and -28 ± 13 bpm, respectively). At end of maximal apnoeas in air, P A O 2 and P A CO 2 were 50 ± 9 and 48 ± 5 mmHg, respectively; corresponding values in O 2 were 653 ± 8 mmHg and 55 ± 5 mmHg. At end of phase II, P A O 2 and P A CO 2 in air were 90 ± 13 mmHg and 42 ± 4 mmHg respectively; corresponding values in O 2 were 669 ± 7 mmHg and 47 ± 6 mmHg. The P A CO 2 increase may trigger the AP rise in phase III. [ABSTRACT FROM AUTHOR]

Most terrestrial animals demonstrate an autonomic reflex that facilitates survival during prolonged submersion under water. This diving response is characterized by bradycardia, apnea and selective increases in peripheral vascular resistance. Stimulation of the nose and nasal passages is thought to be primarily responsible for providing the sensory afferent signals initiating this protective reflex. Consequently, the primary objective of this research was to determine the central terminal projections of nerves innervating the external nose, nasal vestibule and nasal passages of rats. We injected wheat germ agglutinin (WGA) into specific external nasal locations, into the internal nasal passages of rats both with and without intact anterior ethmoidal nerves (AENs), and directly into trigeminal nerves innervating the nose and nasal region. The central terminations of these projections within the medulla were then precisely mapped. Results indicate that the internal nasal branch of the AEN and the nasopalatine nerve, but not the infraorbital nerve (ION), provide primary innervation of the internal nasal passages. The results also suggest afferent fibers from the internal nasal passages, but not external nasal region, project to the medullary dorsal horn (MDH) in an appropriate anatomical way to cause the activation of secondary neurons within the ventral MDH that express Fos protein during diving. We conclude that innervation of the anterior nasal passages by the AEN and nasopalatine nerve is likely to provide the afferent information responsible for the activation of secondary neurons within MDH during voluntary diving in rats. [ABSTRACT FROM AUTHOR]

Rhythmic ventilation is an automatic process controlled by the central nervous system. Groups of cells in the brainstem, predominantly the ventral and dorsal respiratory groups, are responsible for generating basic respiratory rhythm. This basic rhythm is subject to modulation by both conscious and reflex actions. In normal individuals the respiratory minute volume is set to closely regulate arterial carbon dioxide tension (PaCO 2 ) at approximately 5.3 kPa, predominantly via a negative feedback reflex involving the central chemoreceptors. A separate group of chemoreceptors, the arterial chemoreceptors, are responsible for initiating the increased ventilatory response to counter arterial hypoxia, but a brisk response is not seen until PaO 2 levels fall to approximately 8.0 kPa from the normal 13.3 kPa. Combined hypercarbia and hypoxia (asphyxia) is a very powerful stimulus to breathe as the two inputs interact in a synergistic manner. The chemoreceptor reflexes can be modified when the need arises (e.g. blockade of the respiratory part of the arterial chemoreflex by the trigeminal reflex as part of the diving response). Other reflexes such as the Hering–Breuer reflex contribute to setting the balance between tidal volume and respiratory rate to attain a given minute volume, although this reflex does not appear to play a major role in humans at resting tidal volumes. Superimposed on this ‘tonic’ control, additional protective reflexes (e.g. from receptors in the upper airways) are recruited to protect the lungs and airways with responses such as coughs and sneezes when required. [ABSTRACT FROM AUTHOR]

In cetaceans, diving behavior immediately induces a change in blood circulation to favor flow to the brain and heart; this is achieved by intense vasoconstriction of the blood vessels that serve other organs. This blood circulation response is allied to a decrease in heart rate in order to optimize oxygen usage during diving. Vasoconstrictors are present in all mammals and stimulate the contraction of the smooth muscle in the walls of blood vessels. The most important of these vasoconstrictors are the hormones adrenaline (A), noradrenaline (NA), and angiotensin II (ANG II). At present, the contribution of these hormones to vasoconstriction during diving in cetaceans is unclear. To elucidate their possible roles, changes in serum levels of A, NA and ANG II were monitored together with heart rate in the Indo-Pacific bottlenose dolphin Tursiops aduncus during 90 and 180 s dives. Both brief diving periods induced an increase in serum NA concentration and a decrease in heart rate; however, no changes were detected in serum levels of A or ANG II. These data indicate that NA may play a role in diving-induced vasoconstriction. [ABSTRACT FROM AUTHOR]

With the high prevalence of obstructive sleep apnea, the issue of developing a practical tool for obstructive sleep apnea screening has been raised. Conventional obstructive sleep apnea screening tools are limited in their ability to help clinicians make rational decisions due to their inability to predict the apnea-hypopnea index. Our study aimed to develop a new prediction model that can provide a reliable apnea-hypopnea index value during wakefulness. We hypothesized that patients with more severe obstructive sleep apnea would exhibit more attenuated waking vagal tone, which may result in lower effectiveness in decreasing heart rate as a response to deep inspiration breath-holding. Prior to conducting nocturnal in-laboratory polysomnography, 30 non-obstructive sleep apnea (apnea-hypopnea index < 5 events/h) subjects and 246 patients with obstructive sleep apnea participated in a 75-second experiment that consisted of a 60-second baseline measurement and consecutive 15-second deep inspiration breath-hold sessions. Two apnea-hypopnea index predictors were devised by considering the vagal activities reflected in the electrocardiographic recordings acquired during the experiment. Using the predictors obtained from 184 individuals, regression analyses and k -fold cross-validation tests were performed to develop an apnea-hypopnea index prediction model. For the remaining 92 individuals, the developed model provided an absolute error (mean ± SD) of 3.53 ± 2.67 events/h and a Pearson's correlation coefficient of 0.99 ( P < 0.01) between the apnea-hypopnea index predictive values and the reference values reported by polysomnography. Our study is the first to achieve reliable and time-efficient prediction of the apnea-hypopnea index during wakefulness. [ABSTRACT FROM AUTHOR]

Diving response is a powerful integrative response targeted toward survival of the hypoxic/anoxic conditions. Being present in all animals and humans it allows to survive adverse conditions like diving. Earlier we discovered that forehead stimulation affords neuroprotective effect decreasing infarction volume triggered by permanent occlusion of the middle cerebral artery in rats. We hypothesized that cold stimulation of the forehead induces diving response in rats, which, in turn, exerts neuroprotection. We compared autonomic (AP, HR, CBF) and EEG responses to the known diving response-triggering stimulus, ammonia stimulation of the nasal mucosa, cold stimulation of the forehead, and cold stimulation of the glabrous skin of the tail base in anesthetized rats. Responses in AP, HR, CBF and EEG to cold stimulation of the forehead and ammonia vapors instillation into the nasal cavity were comparable and differed significantly from responses to the cold stimulation of the tail base. Excitotoxic lesion of the subthalamic vasodilator area, which is known to participate in CBF regulation and to afford neuroprotection upon excitation, failed to affect autonomic components of the diving response evoked by forehead cold stimulation or nasal mucosa ammonia stimulation. We conclude that cold stimulation of the forehead triggers physiological response comparable to the response evoked by ammonia vapor instillation into the nasal cavity, which considered as stimulus triggering protective diving response. These observations may explain the neuroprotective effect of the forehead stimulation. Data demonstrate that subthalamic vasodilator area does not directly participate in the autonomic adjustments accompanying diving response, however, it is involved in diving-evoked modulation of EEG. We suggest that forehead stimulation can be employed as a stimulus capable of triggering oxygen-conserving diving response and can be used for neuroprotective therapy.

This research was designed to investigate the role of the anterior ethmoidal nerve (AEN) during repetitive trained diving in rats, with specific attention to activation of afferent and efferent brainstem nuclei that are part of this reflexive response. The AEN innervates the nose and nasal passages and is thought to be an important component of the afferent limb of the diving response. Male Sprague-Dawley rats (N=24) were trained to swim and dive through a 5 m underwater maze. Some rats (N=12) had bilateral sectioning of the AEN, others a Sham surgery (N=12). Twelve rats (6 AEN cut and 6 Sham) had 24 post-surgical dive trials over 2 hrs to activate brainstem neurons to produce Fos, a neuronal activation marker. Remaining rats were non-diving controls. Diving animals had significantly more Fos-positive neurons than non-diving animals in the caudal pressor area, ventral medullary dorsal horn, ventral paratrigeminal nucleus, nucleus tractus solitarius, rostral ventrolateral medulla, Raphe nuclei, A5, Locus Coeruleus, and Kölliker-Fuse area. There were no significant differences in brainstem Fos labeling in rats diving with and without intact AENs. Thus the AENs are not required for initiation of the diving response. Other nerve(s) that innervate the nose and nasal passages, and/or suprabulbar activation of brainstem neurons, may be responsible for the pattern of neuronal activation observed during repetitive trained diving in rats. These results help define the central neuronal circuitry of the mammalian diving response.

Diving response (DR) is a powerful integrative response targeted toward survival of the hypoxic/anoxic conditions. Being present in all animals and humans, it allows to survive adverse conditions like diving. Earlier, we discovered that forehead stimulation affords neuroprotective effect, decreasing infarction volume triggered by permanent occlusion of the middle cerebral artery in rats. We hypothesized that cold stimulation of the forehead induces DR in rats, which, in turn, exerts neuroprotection. We compared autonomic [AP, heart rate (HR), cerebral blood flow (CBF)] and EEG responses to the known DR-triggering stimulus, ammonia stimulation of the nasal mucosa, cold stimulation of the forehead, and cold stimulation of the glabrous skin of the tail base in anesthetized rats. Responses in AP, HR, CBF, and EEG to cold stimulation of the forehead and ammonia vapors instillation into the nasal cavity were comparable and differed significantly from responses to the cold stimulation of the tail base. Excitotoxic lesion of the subthalamic vasodilator area (SVA), which is known to participate in CBF regulation and to afford neuroprotection upon excitation, failed to affect autonomic components of the DR evoked by forehead cold stimulation or nasal mucosa ammonia stimulation. We conclude that cold stimulation of the forehead triggers physiological response comparable to the response evoked by ammonia vapor instillation into nasal cavity, which is considered as stimulus triggering protective DR. These observations may explain the neuroprotective effect of the forehead stimulation. Data demonstrate that SVA does not directly participate in the autonomic adjustments accompanying DR; however, it is involved in diving-evoked modulation of EEG. We suggest that forehead stimulation can be employed as a stimulus capable of triggering oxygen-conserving DR and can be used for neuroprotective therapy. [ABSTRACT FROM AUTHOR]