Search

We sought to characterize the patterns of active pressure development of the inspiratory and expiratory rib cage muscles (P(rcm, i) and P(rcm, e)), the diaphragm (P(di, i)), and the expiratory abdominal muscles (P(abm, e)) during maximal "dry" breath holding in trained apnea divers (n = 8). METHODS: Respiratory contractions were assessed via esophageal and gastric manometry. It was expected that inspiratory/expiratory pressures would progressively increase in both magnitude and frequency during the struggle phase, and that inspiratory rib cage muscle pressures would rise at a rate exceeding that of the diaphragm by the break point. RESULTS: P(rcm, i), P(di, i), P(rcm, e), and P(abm, e) significantly increased from the beginning until the end of the struggle phase (P < 0.05). Moreover, P(di, i)/P(rcm, i) and P(abm, e)/P(rcm, e) ratios had declined by the break point (P < 0.05), indicating that rib cage muscles increased their contribution to net inspiratory/expiratory pressure development by the end of the breath hold, relative to that contributed by the diaphragm and abdominal muscles. The pressure-time indices of the diaphragm and inspiratory rib cage muscles continuously increased over the struggle phase (P < 0.05). CONCLUSIONS: The "extradiaphragmatic" shift in inspiratory muscle recruitment, commensurate with increasing P(rcm, e) and P(abm, e), may reflect an extreme loading response to breathing against a heavy elastance (i.e., closed glottis). In addition, the relative intensity of diaphragmatic and inspiratory rib cage muscle contractions approaches potentially "fatiguing" levels by the break point of maximal breath holding.

The purpose of the study was to provide insight in diaphragmatic involuntary breathing movements (IBM) during struggle phase of apnea at total lung capacity (TLC) and functional residual capacity (FRC) using magnetic resonance imaging along with measurements of hemodynamics and arterial oxygenation. The study was performed in eight elite breath-hold divers. There was a similar increase in diaphragmatic cranio-caudal excursions towards the end of TLC and FRC apnea. The greatest diaphragmatic excursion in both apneas and during tidal breathing was in the middle and posterior part of the diaphragm. Diaphragm thickness in elite BHD was within the reference range of normal values suggesting no diaphragmatic hypertrophy in this population. We found that the range of diaphragmatic excursions increases toward the end of apneas. Additionally, our data suggest that the diaphragm participates in IBM occurrence and that various segments of the diaphragm behave nonhomogenously both in tidal breathing and IBMs.

Premature ventricular contractions (PVC) elicit larger bursts of multiunit muscle sympathetic nerve activity (MSNA), reflecting the ability to increase postganglionic axonal recruitment. We tested the hypothesis that chronic heart failure (CHF) limits the ability to recruit postganglionic sympathetic neurons as a response to PVC due to the excessive sympathetic activation in these patients. Sympathetic neurograms of sufficient signal-to-noise ratio were obtained from six CHF patients and from six similarly aged control individuals. Action potentials (APs) were extracted from the multiunit sympathetic neurograms during sinus rhythm bursts and during the post-PVC bursts. These APs were classified on the basis of the frequency per second, the content per burst, and the peak-to-peak amplitude, which formed the basis of binning the APs into active clusters. Compared with controls, CHF had higher APs per burst and higher number of active clusters per sinus rhythm burst ( P < 0.05). Compared with sinus rhythm bursts, both groups increased AP frequency and the number of active clusters in the post-PVC burst ( P < 0 .05). However, compared with controls, the increase in burst integral, AP frequency, and APs per burst during the post-PVC burst was less in CHF patients. Nonetheless, the PVC-induced increase in active clusters per burst was similar between the groups. Thus, these CHF patients retained the ability to recruit larger APs but had a diminished ability to increase overall AP content.

Evidence suggests that the autonomic nervous system may actively regulate the cerebral vasculature. In this study, central hemodynamics and brain oxy-hemoglobin, deoxy-hemoglobin and total hemoglobin changes (bO₂Hb, bdHb and bTHb) were monitored during infusion of epinephrine (0.06 μg/kg/min over 6 min, and 0.12 μg/kg/min for 3 min) in 12 men. Epinephrine decreased mean arterial pressure (MAP) and total peripheral resistance (TPR), while heart rate (HR), stroke volume (SV) and cardiac output (CO) increased, but did not affect bO₂Hb, bdHb or bTHb. However, upon the cessation of epinephrine infusion an increase in both Oxy- and Total Hb occurred which peaked at 3 min post infusion (+6.0±4.6 and +4.9±4.8 μmol/L respectively, P

We tested the hypothesis that breath-hold divers (BHD) attain higher level of sympathetic activation than controls due to the duration of breath-hold rather than a different recruitment strategy. In 6 control subjects and 8 BHD we measured muscle sympathetic neural activity (MSNA) prior to and during functional residual capacity (FRC) and total lung capacity (TLC) breath-holding. On a subset of subjects we applied a new technique for the detection of action potentials (APs) in multiunit MSNA. Compared with controls, BHD group had lower burst AP content (13±7 vs. 6±3AP/burst ; P=0.05) and number of active clusters (5±1 vs. 3±1clusters/burst ; P=0.05) at baseline. However, the overall sympathetic AP/unit-time was comparable between the groups (131±105 vs. 173±152AP/min ; P=0.62) due to increased burst frequency in BHD group (20±4bursts/min) vs. controls (13±3bursts/min) (P=0.039). The achieved level in total MSNA during FRC breath-holds was higher in divers (2298±780 vs. 1484±575a.u./min ; P=0.039). Total MSNA at the end of TLC breath-hold was comparable between the groups (157±50 (controls) vs. 214±41s (BHD) ; P=0.61). FRC and TLC breath-holds increased AP frequency, burst AP content and active clusters/bursts in both groups but the response magnitude was determined by the type of the breath-hold. The divers used fewer number of APs/burst and active clusters/burst. In both groups breath-holds resulted in similar increases in MSNA which were reached both by an increase in firing frequency and by recruitment of previously silent, larger (faster conducting) sympathetic neurons, and possibly by repeated firing within the same burst.

SCUBA diving is regularly associated with asymptomatic changes in cardiac, pulmonary and vascular function. The aim of this study was to evaluate the changes in vascular/endothelial function following SCUBA diving and to assess the potential difference between two breathing gases: air and nitrox 36 (36% oxygen and 64% nitrogen). Ten divers performed two 3-day diving series (no-decompression dive to 18 m with 47 min bottom time with air and nitrox, respectively), with 2 weeks pause in between. Arterial/endothelial function was assessed using SphygmoCor and flow-mediated dilation measurements, and concentration of nitrite before and after diving was determined in venous blood. Production of nitrogen bubbles post-dive was assessed by ultrasonic determination of venous gas bubble grade. Significantly higher bubbling was found after all air dives as compared to nitrox dives. Pulse wave velocity increased slightly (~6%), significantly after both air and nitrox diving, indicating an increase in arterial stiffness. However, augmentation index became significantly more negative after diving indicating smaller wave reflection. There was a trend for post-dive reduction of FMD after air dives ; however, only nitrox diving significantly reduced FMD. No significant differences in blood nitrite before and after the dives were found. We found that nitrox diving affects systemic/vascular function more profoundly than air diving by reducing FMD response, most likely due to higher oxygen load. Both air and nitrox dives increased arterial stiffness, but decreased wave reflection suggesting a decrease in peripheral resistance due to exercise during diving. These effects of nitrox and air diving were not followed by changes in plasma nitrite.

Limited information exists concerning arterial blood pressure (BP) changes in underwater breath-hold diving. Simulated chamber dives to 50 m of freshwater (mfw) reported very high levels of invasive BP in two divers during static apnea (SA), whereas a recent study using a noninvasive subaquatic sphygmomanometer reported unchanged or mildly increased values at 10 m SA dive. In this study we investigated underwater BP changes during not only SA but, for the first time, dynamic apnea (DA) and shortened (SHT) DA in 16 trained breath-hold divers. Measurements included BP (subaquatic sphygmomanometer), ECG, and pulse oxymetry (arterial oxygen saturation, SpO2, and heart rate). BP was measured during dry conditions, at surface fully immersed (SA), and at 2 mfw (DA and SHT DA), whereas ECG and pulse oxymetry were measured continuously. We have found significantly higher mean arterial pressure (MAP) values in SA (∼40%) vs. SHT DA (∼30%). Postapneic recovery of BP was slightly slower after SHT DA. Significantly higher BP gain (mmHg/duration of apnea in s) was found in SHT DA vs. SA. Furthermore, DA attempts resulted in faster desaturation vs. SA. In conclusion, we have found moderate increases in BP during SA, DA, and SHT DA. These cardiovascular changes during immersed SA and DA are in agreement with those reported for dry SA and DA.

Purpose: During SCUBA diving, breathing at increased pressure leads to a greater tissue gas uptake. During ascent, tissues may become supersaturated, and the gas is released in the form of bubbles that typically occur on the venous side of circulation. These venous gas emboli (VGE) are usually eliminated as they pass through the lungs, although their occasional presence in systemic circulation (arterialization) has been reported and it was assumed to be the main cause of the decompression sickness. The aims of the present study were to assess the appearance of VGE after air dives where no stops in coming to the surface are required and to assess their potential occurrence and frequency in the systemic circulation. Methods: Twelve male divers performed six dives with 3 d of rest between them following standard no-decompression dive procedures: 18/60, 18/70, 24/30, 24/40, 33/15, and 33/20 (the first value indicates depth in meters of sea water and the second value indicates bottom time in minutes). VGE monitoring was performed ultrasonographically every 20 min for 120 min after surfacing. Results: Diving profiles used in this study produced unexpectedly high amounts of gas bubbles, with most dives resulting in grade 4 (55/69 dives) on the bubble scale of 0-5 (no to maximal bubbles). Arterializations of gas bubbles were found in 5 (41.7%) of 12 divers and after 11 (16%) of 69 dives. These VGE crossovers were only observed when a large amount of bubbles was concomitantly present in the right valve of the heart. Conclusions: Our findings indicate high amounts of gas bubbles produced after no-decompression air dives based on standardized diving protocols. High bubble loads were frequently associated with the crossover of VGE to the systemic circulation. Despite these findings, no acute decompression-related pathology was detected

Glossopharyngeal insufflation (lung packing) is a common maneuver among experienced apnea divers by which additional air is pumped into the lungs. It has been shown that packing may compromise cardiovascular homeostasis. We tested the hypothesis that the packing-mediated increase in intrathoracic pressure enhances the baroreflex-mediated increase in muscle sympathetic nerve activity (MSNA) in response to an exaggerated drop in cardiac output (CO). We compared changes in hemodynamics and MSNA (peroneal microneurography) during maximal breath-holds without and with prior moderate packing (0.79 ± 0.40 liters) in 14 trained divers (12 men, 2 women, 26.7 ± 4.5 yr, body mass index 24.8 ± 2.4 kg/m2). Packing did not change apnea time (3.8 ± 1.0 vs. 3.8 ± 1.2 min), hemoglobin oxygen desaturation (−17.6 ± 12.3 vs. −18.7 ± 12.8%), or the reduction in CO (1 min: −3.65 ± 1.83 vs. −3.39 ± 1.96 l/min; end of apnea: −2.44 ± 1.33 vs. −2.16 ± 1.44 l/min). On the other hand, packing dampened the early, i.e., 1-min increase in mean arterial pressure (MAP, 1 min: 9.2 ± 8.3 vs. 2.4 ± 11.0 mmHg, P < 0.01) and in total peripheral resistance (relative TPR, 1 min: 2.1 ± 0.5 vs. 1.9 ± 0.5, P < 0.05) but it augmented the concomitant rise in MSNA (1 min: 28.0 ± 11.7 vs. 39.4 ± 12.7 bursts/min, P < 0.001; 32.8 ± 16.4 vs. 43.9 ± 14.8 bursts/100 heart beats, P < 0.01; 3.3 ± 2.1 vs. 4.8 ± 3.2 au/min, P < 0.05). We conclude that the early sympathoactivation 1 min into apnea after moderate packing is due to mechanisms other than excessive reduction in CO. We speculate that lower MAP despite increased MSNA after packing might be explained by vasodilator substances released by the lungs. This idea should be addressed in future studies.

SCUBA diving is associated with generation of gas emboli due to gas release from the supersaturated tissues during decompression. Gas emboli arise mostly on the venous side of circulation, and they are usually eliminated as they pass through the lung vessels. Arterialization of venous gas emboli (VGE) is seldom reported, and it is potentially related to neurological damage and development of decompression sickness. The goal of the present study was to evaluate the generation of VGE in a group of divers using a mixture of compressed oxygen, helium, and nitrogen (trimix) and to probe for their potential appearance in arterial circulation. Seven experienced male divers performed three dives in consecutive days according to trimix diving and decompression protocols generated by V-planner, a software program based on the Varying Permeability Model. The occurrence of VGE was monitored ultrasonographically for up to 90 min after surfacing, and the images were graded on a scale from 0 to 5. The performed diving activities resulted in a substantial amount of VGE detected in the right cardiac chambers and their frequent passage to the arterial side, in 9 of 21 total dives (42%) and in 5 of 7 divers (71%). Concomitant measurement of mean pulmonary artery pressure revealed a nearly twofold augmentation, from 13.6 ± 2.8, 19.2 ± 9.2, and 14.7 ± 3.3 mmHg assessed before the first, second, and the third dive, respectively, to 26.1 ± 5.4, 27.5 ± 7.3, and 27.4 ± 5.9 mmHg detected after surfacing. No acute decompression-related disorders were identified. The observed high gas bubble loads and repeated microemboli in systemic circulation raise questions about the possibility of long-term adverse effects and warrant further investigation.

An increasing number of recreational self- contained underwater breathing apparatus (SCUBA) divers use trimix of oxygen, helium, and nitrogen for dives deeper than 60 m of sea water. Although it was seldom linked to the development of pulmonary edema, whether SCUBA diving affects the extravascular lung water (EVLW) accumulation is largely unexplored. Methods: Seven divers performed six dives on consecutive days using compressed gas mixture of oxygen, helium, and nitrogen (trimix), with diving depths ranging from 55 to 80 m. The echocardiographic parameters (bubble grade, lung comets, mean pulmonary arterial pressure (PAP), and left ventricular function) and the blood levels of the N-terminal part of pro- brain natriuretic peptide (NT-proBNP) were assessed before and after each dive. Results: Venous gas bubbling was detected after each dive with mean probability of decompression sickness ranging from 1.77% to 3.12%. After each dive, several ultrasonographically detected lung comets rose significantly, which was paralleled by increased pulmonary artery pressure (PAP) and decreased left ventricular contractility (reduced ejection fraction at higher end-systolic and enddiastolic volumes) as well as the elevated NT-proBNP. The number of ultrasound lung comets and mean PAP did not return to baseline values after each dive. Conclusions: This is the first report that asymptomatic SCUBA dives are associated with accumulation of EVLW with concomitant increase in PAP, diminished left ventricular contractility, and increased release of NT- proBNP, suggesting a significant cardiopulmonary strain. EVLW and PAP did not return to baseline during repetitive dives, indicating possible cumulative effect with increasing the risk for pulmonary edema.

Apnea divers are exposed to repeated massive arterial oxygen desaturation, which could perturb chemoreflexes. An earlier study suggested that peripheral chemoreflex regulation of sympathetic vasomotor tone and ventilation may have recovered 4 or more weeks into the off season. Therefore, we tested the hypothesis that peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone is present during the training season. We determined ventilation, heart rate, blood pressure, cardiac stroke volume, and muscle sympathetic nerve activity (MSNA) during isocapnic hypoxia in 10 breath hold divers and 11 matched control subjects. The study was carried out at the end of the season of intense apnea trainings. Baseline MSNA frequency was 30+/-4bursts/min in control subjects and 25+/-4bursts/min in breath hold divers (P=0.053). During hypoxia burst frequency and total sympathetic activity increased similarly in both groups. Sympathetic activity normalized during the 30-minute recovery. Hypoxia-induced stimulation of minute ventilation was similar in both groups, although in divers it was maintained by higher tidal volumes and lower breathing frequency compared with control subjects. In both groups, hypoxia increased heart rate and cardiac output whereas total peripheral resistance decreased. Blood pressure remained unchanged. We conclude that peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone is paradoxically preserved in apnea divers, both, during the off and during the training season. The observation suggests that repeated arterial oxygen desaturation may not be sufficient explaining sympathetic reflex abnormalities similar to those in obstructive sleep apnea patients. Copyright © 2009 Elsevier B.V. All rights reserved.

Recently, an increase in extravascular lung water (EVLW) accumulation with diminished left ventricular contractility within 60 min after SCUBA diving was reported. We have observed previously that diving was associated with reduced diffusing lung capacity for carbon monoxide (DLCO) and arterial oxygen pressure for up to 60-80 min postdive. Here we investigated whether increased EVLW persists 2- 3h after successive deep dives in a group of seven male divers. The echocardiographic indices of pulmonary water accumulation (ultrasound lung comets (ULC)) and left ventricular function, respiratory functional measurements and arterial oxygen saturation (SaO(2)) were assessed 2-3h post diving, while venous gas bubbles (VGB) and the blood levels of NT-proBNP and proANP were analyzed 40 min after surfacing. Spirometry values, flow- volume, DLCO, SaO(2) and ULC were unchanged after each dive, except for significant increase in ULC after the second dive. Left ventricular function was reduced, while NT- proBNP and proANP levels were significantly elevated after majority of dives, suggesting a cardiac strain.

The use of trimix (a mixture of oxygen, helium, and nitrogen) has significantly increased among the diver population. However, data indicating how trimix dives at most common depths affect the cardiovascular function are sparse. The purpose of this study was to investigate the cardiovascular effects of trimix dives and compare them with air dives and to determine whether the repetition of dives in successive days affects their extent.Nine professional divers performed four dives in consecutive days where the dive depth was progressively increased to the maximum of 55 m. Divers used air in the first dive, nitrox 25 in the second, and trimix 20/30 in the third and fourth dives. Echocardiography was performed before and after each dive.After each dive, a significantly decreased left ventricular ejection fraction and fractional shortening and an increased end-systolic volume without a change in end-diastolic volume were found, indicating a depressed systolic function of the left side of the heart. Assessment of the ratio between pulmonary artery acceleration time and right ventricular ejection time (used as an indicator of pulmonary artery pressure (PAP)) revealed an increase in PAP after all the dives. No physiologically relevant cumulative effects of the multiple dives or signs of acclimatization were found.The current study shows that the cardiovascular effects of trimix dives do not differ from those of the dives with compressed air. However, it suggests that even a very safe and conservative trimix diving profile exerts significant cardiovascular effects.

AimsTo examine whether dynamic cerebral autoregulation is acutely impaired during maximal voluntary apnoea in trained divers.MethodsMean arterial pressure (MAP), cerebral blood flow-velocity (CBFV) and end-tidal partial pressures of O2 and CO2 (PETO2 and PETCO2) were measured in eleven trained, male apnoea divers (28 ± 2 yr; 182 ± 2 cm, 76 ± 7 kg) during maximal "dry" breath holding. Dynamic cerebral autoregulation was assessed by determining the strength of phase synchronisation between MAP and CBFV during maximal apnoea.ResultsThe strength of phase synchronisation between MAP and CBFV increased from rest until the end of maximal voluntary apnoea (PConclusionsThis study is the first to report that dynamic cerebral autoregulation is acutely impaired in trained divers performing maximal voluntary apnoea. Furthermore, our data suggest that the impaired autoregulatory response is related to the change in PETCO2, but not PETO2, during maximal apnoea in trained divers.

The current study tested the hypothesis that modification in central hemodynamics during short-term continuous positive airway pressure (CPAP) application was accompanied by altered firing patterns of sympathetic nerve activity in CHF patients and healthy subjects.Muscle sympathetic nerve activity (MSNA), hemodynamic and ventilatory parameters were obtained from 8 healthy middle aged subjects and 7 CHF patients. Action potentials (APs) were extracted from MSNA neurograms, quantified as AP frequency and classified into different sized clusters. While on CPAP at 10cm H2O, multi-unit MSNA, AP frequency and mean burst area/min increased in healthy middle aged subjects (p

The effects of involuntary respiratory contractions on the cerebral blood flow response to maximal apnoea is presently unclear. We hypothesised that while respiratory contractions may augment left ventricular stroke volume, cardiac output and ultimately cerebral blood flow during the struggle phase, these contractions would simultaneously cause marked 'respiratory' variability in blood flow to the brain. Respiratory, cardiovascular and cerebrovascular parameters were measured in ten trained, male apnoea divers during maximal 'dry' breath holding. Intrathoracic pressure was estimated via oesophageal pressure. Left ventricular stroke volume, cardiac output and mean arterial pressure were monitored using finger photoplethysmography, and cerebral blood flow velocity was obtained using transcranial ultrasound. The increasingly negative inspiratory intrathoracic pressure swings of the struggle phase significantly influenced the rise in left ventricular stroke volume (R (2) = 0.63, P

Scuba diving is associated with breathing gas at increased pressure, which often leads to tissue gas supersaturation during ascent and the formation of venous gas emboli (VGE). VGE crossover to systemic arteries (arterialization), mostly through the patent foramen ovale, has been implicated in various diving-related pathologies. Since recent research has shown that arterializations frequently occur in the absence of cardiac septal defects, our aim was to investigate the mechanisms responsible for these events. Divers who tested negative for patent foramen ovale were subjected to laboratory testing where agitated saline contrast bubbles were injected in the cubital vein at rest and exercise. The individual propensity for transpulmonary bubble passage was evaluated echocardiographically. The same subjects performed a standard air dive followed by an echosonographic assessment of VGE generation (graded on a scale of 0–5) and distribution. Twenty-three of thirty-four subjects allowed the transpulmonary passage of saline contrast bubbles in the laboratory at rest or after a mild/moderate exercise, and nine of them arterialized after a field dive. All subjects with postdive arterialization had bubble loads reaching or exceeding grade 4B in the right heart. In individuals without transpulmonary passage of saline contrast bubbles, injected either at rest or after an exercise bout, no postdive arterialization was detected. Therefore, postdive VGE arterialization occurs in subjects that meet two criteria: 1) transpulmonary shunting of contrast bubbles at rest or at mild/moderate exercise and 2) VGE generation after a dive reaches the threshold grade. These findings may represent a novel concept in approach to diving, where diving routines will be tailored individually.

The purpose of this study was to assess the differences in cardiac autonomic modulation during maximal static (SA) and dynamic (DA) underwater apneas. Arterial oxygen saturation (SpO(2)), heart rate (HR) and HR variability (SD1 from Poincare plot and short-term fractal-like scaling exponent, α(1)) were analyzed at the immersed baseline (3 min) and initial, mid- and end-phases (each 30s) of SA and DA in nine elite breath-hold divers. DA and SA lasted 78 ± 8 and 225 ± 20s (mean ± SEM), respectively, and resulted in similar decrements in end-stage SpO(2) (78 ± 3 and 75 ± 3%, p=0.352). During DA, initial increase in HR (from 80 ± 5 to 122 ± 5 bpm, p

In several conditions associated with adrenergic stimulation, an increase in peripheral count of larger platelets has been observed, but the mechanism remained elusive. Larger platelets have greater prothrombotic potential and increase the risk of acute thrombotic events. The human spleen retains one-third of total body platelets, with mean volume (MPV) about 20% greater than that of circulating platelets. We aimed to answer whether low-dose epinephrine infusion results in spleen contraction and MPV increase. We undertook the continuous ultrasonic measurements of spleen volume, hepatic and central circulation with concurrent blood sampling in response to intravenous infusion of epinephrine (6 min of 0·06 µg kg(-1) per min, followed by 3 min of 0·12 µg kg(-1) per min) in nine healthy young subjects. The spleen volume started to decrease immediately after the onset of infusion, in the presence of substantial decreases in peripheral resistance and mean blood pressure and increases in heart rate and cardiac output. The majority of spleen emptying, approximately 25%, (95% CI 71·3- 299·7) was observed 1 min after infusion onset, the hepatic vein flow peaked at the end of infusion for 28·4% (95% CI 1074·6-407·9), while increases in platelet count for approximately 31% (95% CI 187·8-314·8) and MPV for 4·4% (95% CI 7·3-10·9) lagged until 1 min after infusion cessation. We suggest that spleen is a dynamic reservoir of large platelets, which are mobilized even by low-dose epinephrine infusion in conditions of decreased blood pressure.

The growing urge to breathe that occurs during breath-holding results in development of involuntary breathing movements (IBMs). The present study determined whether IBMs are initiated at critical levels of hypercapnia and/or hypoxia during maximal apnoea. Arterial blood gasses at the onset of IBM were monitored during maximal voluntary breath-holds. Eleven healthy men performed breath holds after breathing air, hyperoxic-normocapnia, hypoxic-normocapnia, and normoxic-hypercapnia. Pre-breathing of the gas mixtures facilitated the IBM onset, reducing the time-to-onset for ∼46% (hyperoxic condition) and for ∼80% (hypoxic condition) compared to the normoxic air breathing time. A strong correlation (R=0.83, P=0.002) between arterial partial pressure of CO₂ (PaCO₂) at IBM onset after pre-breathing hyperoxic and hypercapnic gas mixtures was observed, suggesting the existence of a possible IBM PaCO₂ threshold level of ∼6.5 ± 0.5 kPa. No clear "threshold" was observed for partial pressure of arterial O₂(PaO₂). However, we observed that IBM onset was influenced, in part, by an interaction between PaO₂ and PaCO₂ levels during maximal apnoea. This study demonstrated the complex interaction between arterial blood-gases and the physiological response to maximal breath holding.

Testing of decompression procedures has been performed both in the dry and during immersion, assuming that the results can be directly compared. To test this, the aim of the present paper was to compare the number of venous gas bubbles observed following a short, deep and a shallow, long air dive performed dry in a hyperbaric chamber and following actual dives in open water.Fourteen experienced male divers participated in the study; seven performed dry and wet dives to 24 metres' sea water (msw) for 70 minutes; seven divers performed dry and wet dives to 54 msw for 20 minutes. Decompression followed a Bühlmann decompression procedure. Immediately following the dive, pulmonary artery bubble formation was monitored for two hours. The results were graded according to the method of Eftedal and Brubakk.All divers completed the dive protocol, none of them showed any signs of decompression sickness. During the observation period, following the shallow dives, the bubbles increased from 0.1 bubbles per cm ² after the dry dive to 1.4 bubbles per cm ² after the wet dive. Following the deep dives, the bubbles increased from 0.1 bubbles per cm ² in the dry dive to 2.4 bubbles per cm ² in the wet dive. Both results are highly significant (P = 0.0001 or less).The study has shown that diving in water produces significantly more gas bubble formation than dry diving. The number of venous gas bubbles observed after decompression in water according to a rather conservative procedure, indicates that accepted standard decompression procedures nevertheless induce considerable decompression stress. We suggest that decompression procedures should aim at keeping venous bubble formation as low as possible.

INTRODUCTION Increased accumulation of extravascular lung water after repetitive deep trimix dives was recently reported. This effect was evident 40 min post-dive, but in subsequent studies most signs of this lung congestion were not evident 2-3 h post-dive, indicating no major negative effects on respiratory gas exchange following deep dives. Whether this response is unique for trimix dives or also occurs in more frequent air dives is presently unknown. METHODS A single no-decompression field dive to 33 m with 20 min bottom time was performed by 12 male divers. Multiple ultrasound lung comets (ULC), bubble grade (BG), and single-breath lung diffusing capacity (DLCO) measurements were made before and up to 120 min after the dive. RESULTS Median BG was rather high with maximal values observed at 40 min post-dive [median 4 (4-4)]. Arterialization of bubbles from the venous side was observed only in one diver lasting up to 60 min post-dive. Despite high BG, no DCS symptoms were noted. DLCO and ULC were unchanged after the dive at any time point (DLCO(corr) was 33.6 +/- 1.9 ml x min(-1) mmHg(-1) pre-dive, 32.7 +/- 3.8 ml x min(-1) x mmHg(-1) at 60 min post-dive, and 33.2 +/- 5.3 ml x min(-1) x mmHg(-1) at 120 min post-dive; ULC count was 4.1 +/- 1.9 pre-dive, 4.9 +/- 3.3 at 20 min post-dive, and 3.3 +/- 1.9 at 60 min post-dive. DISCUSSION These preliminary findings show no evidence of increased accumulation of extravascular lung water in male divers after a single no-decompression air dive at the limits of accepted Norwegian diving tables.

Purpose: Apnea divers hyperinflate the lung by taking a deep breath followed by glossopharyngeal insufflation. The maneuver can lead to symptomatic arterial hypotension. We tested the hypotheses that glossopharyngeal insufflation interferes with cardiac function further reducing cardiac output (CO) using cardiac magnetic resonance imaging (MRI) to fully sample both cardiac chambers. Methods: Eleven dive athletes (10 men, 1 woman; age = 26 ± 5 yr, body mass index = 23.5 ± 1.7 kg·m-2) underwent cardiac MRI during breath holding at functional residual capacity (baseline), at total lung capacity (apnea), and with submaximal glossopharyngeal insufflation. Lung volumes were estimated from anatomic images. Short-axis cine MR images were acquired to study biventricular function. Dynamic changes were followed by long-axis cine MRI. Results: Left and right ventricular end-diastolic volumes (LVEDV, RVEDV) decreased during apnea with and without glossopharyngeal insufflation (baseline: LVEDV = 198 ± 19 mL, RVEDV = 225 ± 30 mL; apnea: LVEDV = 125 ± 38 mL, RVEDV = 148 ± 37 mL, P < 0.001; glossopharyngeal insufflation: LVEDV = 108 ± 26 mL, RVEDV = 136 ± 29 mL, P < 0.001 vs baseline). CO decreased during apnea (left = -29 ± 4 %, right = -29 ± 4 %) decreasing further with glossopharyngeal insufflation (left = -38% ± 4%, right = -39% ± 4%, P < 0.05). HR increased 16 ± 4 bpm with apnea and 17 ± 5 bpm with glossopharyngeal insufflation (P < 0.01). Ejection fraction moderately decreased (apnea: left = -5% ± 2%, right = -7% ± 2%, glossopharyngeal insufflation: left = -6% ± 2%, right = -10% ± 2%, P < 0.01). With continued apnea with and without glossopharyngeal insufflation, LVEDV and CO increased over time by a similar but small amount (P < 0.01). Conclusions: The major finding of our study was that submaximal glossopharyngeal insufflation decreased CO further albeit by a small amount compared to maximal inspiratory apnea. The response was not associated with severe biventricular dysfunction

The aim of this study was to assess the effects of successive deep dives on endothelial function of large conduit arteries and plasma pro-oxidant and antioxidant activity. Seven experienced divers performed six dives in six consecutive days using a compressed mixture of oxygen, helium and nitrogen (trimix) with diving depths ranging from 55 to 80 m. Before and after first, third and sixth dive, venous gas emboli formation and brachial artery function (flow-mediated dilation, FMD) was assessed by ultrasound. In addition, plasma antioxidant capacity (AOC) was measured by ferric reducing antioxidant power, and the level of oxidative stress was assessed by thiobarbituric acid-reactive substances (TBARS) method. Although the FMD was reduced to a similar extent after each dive, the comparison of predive FMD showed a reduction from 8.6% recorded before the first dive to 6.3% before the third (P = 0.03) and 5.7% before the sixth dive (P = 0.003). A gradual shift in baseline was also detected with TBARS assay, with malondialdehyde values increasing from 0.10 ± 0.02 μmol l⁻¹ before the first dive to 0.16 ± 0.03 before the sixth (P = 0.005). Predive plasma AOC values also showed a decreasing trend from 0.67 ± 0.20 mmol l⁻¹ trolox equivalents (first day) to 0.56 ± 0.12 (sixth day), although statistical significance was not reached (P = 0.08). This is the first documentation of acute endothelial dysfunction in the large conduit arteries occurring after successive deep trimix dives. Both endothelial function and plasma pro-oxidant and antioxidant activity did not return to baseline during the course of repetitive dives, indicating possible cumulative and longer lasting detrimental effects.

Apnea divers increase intrathoracic pressure voluntarily by taking a deep breath followed by glossopharyngeal insufflation. Because apnea divers sometimes experience hypotension and syncope during the maneuver, they may serve as a model to study the mechanisms of syncope. We recorded changes in hemodynamics and sympathetic vasomotor tone with microneurography during breath holding with glossopharyngeal insufflation. Five men became hypotensive and fainted during breath holding with glossopharyngeal insufflation within the first minute. In four divers, heart rate dropped suddenly to a minimum of 38 ± 4 beats/min. Therefore, cardioinhibitory syncope was more common than low cardiac output syncope.

The within-breath modulation of muscle sympathetic nerve activity (MSNA) is well established, with greater activity occurring during expiration and less during inspiration. Whether ventilation per se affects the longer-term (i.e., minute-to-minute) regulation of MSNA has not been determined. We sought to define the specific role of ventilation in regulating sympathetic activation during chemoreflex activation, where both ventilation and MSNA are increased. Ten young healthy subjects performed both asphyxic rebreathing and repeated, rebreathing apneas to cause the same magnitude of chemoreflex stress in the presence or absence of ventilation. Both protocols caused increases in sympathetic burst frequency, burst amplitude, and burst incidence. However, burst frequency was increased more during repeated apneas (12 ± 6 to 25 ± 7 bursts/min) compared with rebreathing (12 ± 5 to 17 ± 7 bursts/min; P < 0.001) due to a greater burst incidence during apneas (36 ± 11 bursts/100 heart beats) vs. rebreathing (26 ± 8 bursts/100 heart beats, P < 0.001). The sympathetic gain to chemoreflex stress was also larger during repeated apneas (2.29 ± 1.29 au/% desaturation) compared with rebreathing (1.44 ± 0.53 au/% desaturation, P < 0.05). The augmented sympathetic response during apneas was associated with a larger pressor response and total peripheral resistance compared with rebreathing. These data demonstrate that ventilation per se restrains sympathetic activation during chemoreflex activation. Further, the augmented sympathetic response during apneas was associated with greater cardiovascular stress and may be relevant to the cardiovascular pathology associated with sleep-disordered breathing. Copyright © 2010 the American Physiological Society.

Sleep apnoea, with repeated periods of hypoxia, results in cardiovascular morbidity and concomitant autonomic dysregulation. Trained apnoea divers also perform prolonged apnoeas accompanied by large lung volumes, large reductions in cardiac output and severe hypoxia and hypercapnia. We tested the hypothesis that apnoea training would be associated with decreased cardiovagal and sympathetic baroreflex gains and reduced respiratory modulation of muscle sympathetic nerve activity (MSNA ; microneurography). Six trained divers and six controls were studied at rest and during asphyxic rebreathing. Despite an elevated resting heart rate (70 ± 14 vs. 56 ± 10 bpm ; p = 0.038), divers had a similar cardiovagal baroreflex gain (−1.22 ± 0.47 beats/mmHg) as controls (−1.29 ± 0.61 ; NS). Similarly, though MSNA burst frequency was slightly higher in divers at rest (16 ± 4 bursts/min vs. 10 ± 5 bursts/min, p = 0.03) there was no difference in baseline burst incidence, sympathetic baroreflex gain (−3.8 ± 2.1%/mmHg vs. −4.7 ± 1.7%/mmHg) or respiratory modulation of MSNA between groups. Resting total peripheral resistance (11.9 ± 2.6 vs. 12.3 ± 2.2 mmHg/L/min) and pulse wave velocity (5.82 ± 0.55 vs. 6.10 ± 0.51 m/s) also were similar between divers and controls, respectively. Further, the sympathetic response to asphyxic rebreathing was not different between controls and divers (−1.70 ± 1.07 vs. −1.74 ± 0.84 a.u./% desaturation). Thus, these data suggest that, unlike patients with sleep apnoea, apnoea training in otherwise healthy individuals does not produce detectable autonomic dysregulation or maladaption.

Involuntary apnea episodes in obstructive sleep apnea patients result in selective potentiation of peripheral chemoreceptor regulation of sympathetic vasomotor tone. Breath-hold diving is associated with repeated "voluntary" apnea episodes and massive arterial oxygen desaturation, which could also perturb chemoreflex function. We measured ventilation, heart rate, blood pressure, cardiac stroke volume, and muscle sympathetic nerve activity (MSNA) during isocapnic hypoxia in 11 breath-hold divers and eleven matched control subjects. The study was carried out at least 1 month after intense apnea training. Baseline MSNA frequency was 30 +/- 4 bursts/min in control subjects and 31 +/- 7 bursts/min in divers (ns). During hypoxia MSNA frequency and total activity increased similarly in both groups (30 and 66% in controls and 27 and 60% in divers, respectively). MSNA remained increased after termination of hypoxia and approached baseline measurements after 20 min. Hypoxia-induced stimulation of minute ventilation was similar in both groups, although in divers it was maintained by higher tidal volumes and lower breathing frequency compared with control subjects. In both groups, hypoxia-induced tachycardia drove an increase in cardiac output whereas total peripheral resistance decreased. Blood pressure remained unchanged. We conclude that after the end of intensive training/competition periods, apnea divers show normal peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone. Although voluntary apnea may not lead to sustained changes in sympathetic nervous system regulation, we cannot exclude the possibility that repeated sympathetic activation elicited by voluntary apnea imposes a burden on the cardiovascular system.

Introduction: Self-contained underwater breathing apparatus diving reduces cardiovascular function and increases pulmonary artery pressure (PAP) up to 3 days after a single dive. Acute antioxidants partially attenuated arterial endothelial dysfunction, whereas cardiac and PA functions were unaffected. We tested the hypothesis that acute tetrahydobiopterin (BH4), as a cofactor of endothelial nitric oxide (NO) synthase, reduces bubble grade (BG) and attenuates alteration in cardiovascular function after diving because of increased NO bioavailability. Materials and methods: Mean PAP (mPAP), PA acceleration time and right ventricle ejection time, left ventricle ejection fraction (LV-EF) and BG were measured after oral placebo (P), vitamin C (C) or a combination of vitamin C and BH4 (BH4) in a randomized, placebo controlled trial before and after field dive to 30 m of sea water for 30 min bottom time. Results: Eight recreational divers performed three dives with a 3-days period between them. Regarding the primary hypothesis, no difference was observed between postdive changes in BG (2Æ 1 ± 2Æ 2 bubbles cm)2 for P, 3Æ 4 ± 3Æ 9 for C and 3Æ 6 ± 2Æ 1 for BH4), mPAP (25Æ 6 ± 6Æ 5 mmHg for P, 25Æ 9 ± 8Æ 6 for C and 22Æ 6 ± 3Æ 5 for BH4) and LV-EF (62Æ 6 ± 4Æ 6% for P, 61Æ 4 ± 3Æ 9 for C and 61Æ 6 ± 3Æ 7 for BH4) with all three conditions. Conclusion: This suggests that co-administration of BH4 and vitamin C does not improve heart and pulmonary artery function after diving.

We tested whether breath hold divers (BHD) and obstructive sleep apnea (OSA) subjects had similar middle cerebral artery velocity (MCAV) responses to hypercapnea and hypocapnea. We analyzed changes in MCAV (cm/s) in response to hypocapnea and hyperoxic hypercapnea during placebo or after 90 min of oral indomethacin (100 mg) in BHD (N=7) and OSA (N=7). During control hypercapnea MCAV increased for 54.4% in BHD and 48.4% in OSA. Indomethacin blunted the MCAV increase in response to hypercapnea in BHD (P=0.02), but not in OSA. Indomethacin attenuated the mean arterial pressure response in BHD, but not in OSA. The blunted MCAV responses to hypercapnea with indomethacin in BHD, but not in OSA patients suggests that (a) the normal contribution of local vasodilating mechanisms to the cerebrovascular responses to hypercapnea is absent in OSA patients and (b) exposure to chronic/repeated apneas is not causal per se in limiting the contribution of vasodilating mechanisms to the cerebrovascular responses to hypercapnea in OSA.

Prospective study.To evaluate the formation of venous gas bubbles following open-sea scuba dives in persons with chronic spinal cord injury (SCI) and in able-bodied diving instructors (C) and to assess the risk for decompression sickness (DCS).Field study at the Island of Krk, Croatia.Gas bubbles were monitored with an ultrasound scanner 40 min after surfacing. The probability of DCS (P((DCS))) was estimated from the recorded depth-time profile using a decompression model.Divers completed six dives in 3 days using a modified Bühlmann decompression model, and none developed signs of DCS. Mean P((DCS)) was similar in both groups, SCI (0.51+/-0.2%) and C (0.64+/-0.27%), and was seen to increase with subsequent dives. Number of bubbles (bubbles per cm(2)) was low in both groups on all 3 days of diving.We have used the P((DCS)) as a severity index of diving exposure. Overall, the severity of exposure in SCI subjects was consistent with the range of typical recreational dives, suggesting that the diving profile used is very safe.

Introduction Most decompression procedures induce the formation of asymptomatic venous gas bubbles. They can be classified as "silent bubbles," which are asymptomatic compared to paradoxical arterialization of venous gas emboli, which can lead to serious neurologic damage. The penetration of such gas bubbles into the arterial circulation is due to pulmonary barotrauma, intrapulmonary (I-P) passage after massive bubble formation ("chokes"), or intracardiac shunting. Venous gas bubbles can be monitored and graded with echocardiographic scanning. Case We believe this is the first case to be reported of a recreational diver who, after surfacing from a dive, developed grade 5 ("white-out") venous gas bubbles in the right heart with evidence of I-P shunt at rest without any symptoms of decompression sickness. Grade 4 gas bubbles were found on the left side of the heart, indicating significant I-P shunting even at rest. Conclusion We observed venous bubbles crossing through the I-P shunt during post-dive recovery at rest in a diver who developed "white out" of venous bubbles. Previously, the maximum bubble grade 5 had been observed in experimental animals, but not in humans. Moreover, a significant bubble grade was found on the left side of the heart, indicating a need for further studies to investigate the mechanisms of post-dive changes in peripheral and central circulation.

The fact that impaired endothelial-dependent vasodilatation after scuba diving often occurs without visible changes in the endothelial layer implies its biochemical origin. Since Lewis x (CD15) and sialyl-Lewis x (CD15s) are granulocyte and monocyte carbohydrate antigens recognized as ligands by endothelial selectins, we assumed that they could be sensitive markers for impaired vasodilatation following diving. Using flow cytometry, we determined the CD15 and CD15s peripheral blood mononuclear cells of eight divers, 30 mins before and 50 mins after a single dive to 54 m for 20 mins bottom time. The number of gas bubbles in the right heart was monitored by ultrasound. Gas bubbles were seen in all eight divers, with the average number of bubbles/cm2 1.9 ± 1.9. The proportion of CD15 + monocytes increased 2-fold after the dive as well as the subpopulation of monocytes highly expressing CD15s. The absolute number of monocytes was slightly, but not significantly, increased after the dive, whereas the absolute number of granulocytes was markedly elevated (up to 61%). There were no significant correlations between bubble formation and CD15 + monocyte expression (r = − 0.56; P = 0.17), as well as with monocytes highly expressing CD15s (r = 0.43; P = 0.29). This study suggests that biochemical changes induced by scuba diving primarily activate existing monocytes rather than increase the number of monocytes at a time of acute arterial endothelial dysfunction.