Hypoxia and cardiac arrhythmias in breath-hold divers during voluntary immersed breath-holds

The incidence and nature of cardiac arrhythmias during static apnea were studied by monitoring the electrocardiogram (ECG) and oxygen saturation (SaO₂) of 16 recreational breath-hold divers. All subjects completed a maximal apnea with a mean (±SD) breath-hold duration of 281 (±73) s without clinical complications. Both heart rate (HR) and SaO₂ decreased significantly with breath-hold duration. The decline in SaO₂ was inversely related to the decline in HR (r = −0.55, P < 0.05). Cardiac arrhythmias (supraventricular and ventricular premature complexes, right bundle branch block) occurred in 12/16 (77%) subjects and were related to breath-hold duration. Subjects with atrial premature complexes (n = 9) had a reduced BMI (P = 0.016) and a higher decline of the terminal SaO₂ (P = 0.01). In conclusion, ectopic arrhythmias were common during maximal static apneas for training purposes. The results indicate that the occurrence of ectopic beats is associated with individual factors such as the tolerable SaO₂ decrease.     

Facial cooling and peripheral chemoreflex mechanisms in humans

Aim: Reductions in arterial oxygen partial pressure activate the peripheral chemoreceptors which increase ventilation, and, after cessation of breathing, reduce heart rate. We tested the hypothesis that facial cooling facilitates these peripheral chemoreflex mechanisms. Methods: Chemoreflex control was assessed by the ventilatory response to hypoxia (10% O₂ in N₂) and the bradycardic response to voluntary end‐expiratory apnoeas of maximal duration in 12 young, healthy subjects. We recorded minute ventilation, haemoglobin O₂ saturation, RR interval (the time between two R waves of the QRS complex) and the standard deviation of the RR interval (SDNN), a marker of cardiac vagal activity throughout the study. Measurements were performed with the subject’s face exposed to air flow at 23 and 4 °C. Results: Cold air decreased facial temperature by 11 °C (P < 0.0001) but did not affect minute ventilation during normoxia. However, facial cooling increased the ventilatory response to hypoxia (P < 0.05). The RR interval increased by 31 ± 8% of the mean RR preceding the apnoea during the hypoxic apnoeas in the presence of cold air, compared to 17 ± 5% of the mean RR preceding the apnoea in the absence of facial cooling (P < 0.05). This increase occurred despite identical apnoea durations and reductions in oxygen saturation. Finally, facial cooling increased SDNN during normoxia and hypoxia, as well as during the apnoeas performed in hypoxic conditions (all P < 0.05). Conclusion: The larger ventilatory response to hypoxia suggests that facial cooling facilitates peripheral chemoreflex mechanisms in normal humans. Moreover, simultaneous diving reflex and peripheral chemoreflex activation enhances cardiac vagal activation, and favours further bradycardia upon cessation of breathing.     

Cardiovascular adjustments in breath-hold diving: comparison between divers and non-divers in simulated dynamic apnoea

The diving response is the sequence of cardiovascular, respiratory and metabolic adjustments produced by apnoea and further strengthened by cooling of the facial area and/or hypoxia. This study aimed at comparing the cardiovascular response to diving of trained divers with that of a control group. In this order, 14 trained divers were compared with 14 non-divers. By means of impedance cardiography and continuous monitoring of arterial pressure, hemodynamic data were collected during three different experimental sessions. Each session included a cycle-ergometer exercise against a workload of 0.5 W kg⁻¹ of body mass, pedalling in a steady-state condition. During exercise, each subject randomly accomplished 40 s of breath-hold exercise with face immersion (test A) or in air (test B). A control exercise test with normal breathing (test C) was also performed. Divers showed a faster onset of bradycardic response (ANOVA, P < 0.01) and a faster adjustment in systemic vascular resistance (P < 0.001 for divers vs. controls) than did non-divers. Moreover, cardiac output decreased only in divers during the first phase of test A (P < 0.01 for divers vs. controls). The most striking findings were that divers showed a more rapid cardiovascular adjustment with respect to controls, in particular in heart rate and systemic vascular resistance; moreover, with continued apnoea, a delayed increase in myocardial performance and stroke volume occurred and obscured the cardiovascular effects of the diving response.     

Effects of lung volume and involuntary breathing movements on the human diving response

The effects of lung volume and involuntary breathing movements on the human diving response were studied in 17 breath-hold divers. Each subject performed maximal effort apnoeas and simulated dives by apnoea and cold water face immersion, at lung volumes of 60%, 85%, and 100% of prone vital capacity (VC). Time of apnoea, blood pressure, heart rate, skin capillary blood flow, and fractions of end-expiratory CO₂ and O₂ were measured. The length of the simulated dives was the shortest at 60% of VC, probably because at this level the build up of alveolar CO₂ was fastest. Apnoeas with face immersion at 100% of VC gave a marked drop in arterial pressure during the initial 20?s, probably due to high intrathoracic pressure mechanically reducing venous return. The diving response was most pronounced at 60% of VC. We concluded that at the two larger lung volumes both mechanical factors and input from pulmonary stretch receptors influenced the bradycardia and vasoconstriction, resulting in a non-linear relationship between the breath-hold lung volume and magnitude of the diving response in the near-VC range. Furthermore, the involuntary breathing movements that appeared during the struggle phase of the apnoeas were too small to affect the diving response.     

Ventilatory function in breath-hold divers: effect of glossopharyngeal insufflation

This study was conducted to determine whether ventilatory parameters would change in breath-hold divers (BHDs) after they performed the glossopharyngeal technique for lung insufflation. Fifteen elite BHDs, 16 non-expert BHDs and 15 control subjects participated in this cross-sectional study. Volumes and expiratory flow rates were measured twice, before and after the glossopharyngeal technique performed at rest. Before the technique, greater forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV₁) and lower FEV₁/FVC were noted in the elite and non-expert BHDs compared with controls. No difference was noted regarding the other pulmonary parameters. After the technique, increases were noted in FVC, FEV₁ and maximal voluntary ventilation in the elite BHDs (P < 0.001, respectively). The FEF_25–75%/FVC ratios were lower in the BHDs both before and after the technique, indicating possible dysanapsis. The ventilatory parameters observed after the glossopharyngeal technique indicated (1) higher lung volumes in expert BHDs and (2) a correlation with BHD performance (maximal dynamic BH performance). This correlation became more significant after the technique, indicating a positive effect of glossopharyngeal insufflation on performance.     

Minimal nocturnal oxygen saturation predicts future subclinical carotid atherosclerosis: the Wisconsin sleep cohort

Previous data on the associations between nocturnal oxygen saturation parameters and carotid atherosclerosis are conflicting. We examined the prospective associations of nocturnal oxygen saturation (SaO₂) and cardiovascular disease (CVD) risk factors with carotid intima‐media thickness (IMT) and plaques. We used data on 689 Wisconsin sleep cohort participants who had baseline overnight polysomnography followed by carotid ultrasonography a mean (SD) of 7.8 (2.5) years later. Far wall common carotid IMT was measured using B‐mode ultrasound. Bilateral common, bifurcation and internal carotid artery segments were evaluated for plaque score. Participants (8) were aged 56 years (55% male); 32% had hypertension and mean body mass index (BMI) was 31 (7) kg m². Mean and minimum nocturnal SaO₂ were 95% (2) and 86% (7), respectively. Mean percentage sleep time with SaO₂ < 90% was 2% (8). Both mean (odds ratio [OR]: 0.60 lower plaque count per 5% higher mean SaO₂, 95% confidence interval [CI]: 0.38–0.96, P = 0.033) and minimum SaO₂ (OR: 0.88 lower plaque count per 5% higher minimum SaO₂, 95% CI: 0.80–0.97, P = 0.013) predicted carotid plaque score after adjusting for age, sex and BMI. Minimum SaO₂ predicted future plaque score after adding adjustment for traditional CVD risk factors (OR: 0.90 lower plaque count per 5% higher minimum SaO₂, 95% CI: 0.81–0.99, P = 0.038). Mean SaO₂ was not associated with carotid IMT after CVD risk factor adjustment. We conclude that minimum nocturnal SaO₂ is an independent predictor of future carotid plaque burden. Other nocturnal SaO₂ parameters are not associated with future carotid IMT or plaques after adjusting for traditional CVD risk factors.     

Aggravated hypoxia during breath-holds after prolonged exercise

Hyperventilation prior to breath-hold diving increases the risk of syncope as a result of hypoxia. Recently, a number of cases of near-drownings in which the swimmers did not hyperventilate before breath-hold diving have come to our attention. These individuals had engaged in prolonged exercise prior to breath-hold diving and it is known that such exercise enhances lipid metabolism relative to carbohydrate metabolism, resulting in a lower production of CO₂ per amount of O₂ consumed. Therefore, our hypothesis was that an exercise-induced increase in lipid metabolism and the associated reduction in the amount of CO₂ produced would cause the urge to breathe to develop at a lower P O₂, thereby increasing the risk of syncope due to hypoxia. Eight experienced breath-hold divers performed 5 or 6 breath-holds at rest in the supine position and then 5 or 6 additional breath-holds during intermittent light ergometer exercise with simultaneous apnoea (dynamic apnoea, DA) on two different days: control (C) and post prolonged sub-maximal exercise (PPE), when the breath-holds were performed 30 min after 2 h of sub-maximal exercise. After C and before the prolonged submaximal exercise subjects were put on a carbohydrate-free diet for 18 h to start the depletion of glycogen. The respiratory exchange ratio ( RER) and end-tidal P CO₂, P O₂, and SaO₂ values were determined and the data were presented as means (SD). The RER prior to breath-holding under control conditions was 0.83 (0.09), whereas the corresponding value after exercise was 0.70 (0.05) ( P <0.01). When the three apnoeas of the longest duration for each subject were analysed, the average duration of the dynamic apnoeas was 96 (14) s under control conditions and 96 (17) s following exercise. Both P O₂ and P CO₂ were higher during the control dynamic apnoeas than after PPE [PO₂ 6.9 (1.0) kPa vs 6.2 (1.2) kPa, P <0.01; P CO₂ 7.8 (0.5) kPa vs 6.7 (0.4) kPa, P <0.001; ANOVA testing]. A similar pattern was observed after breath-holding under resting conditions, i.e., a lower end-tidal P O₂ and P CO₂ after exercise (PPE) compared to control conditions. Our findings demonstrate that under the conditions of a relatively low RER following prolonged exercise, breath-holding is terminated at a lower P O₂ and a lower P CO₂ than under normal conditions. This suggests that elevated lipid metabolism may constitute a risk factor in connection with breath-holding during swimming and diving.     

Exercise limb blood flow response to acute and chronic hypoxia in Danish lowlanders and Aymara natives

Aim: The femoral artery blood flow response to submaximal, one‐legged, dynamic, knee‐extensor exercise was determined in acute and chronic hypoxia to investigate the hypotheses that with adaptation to chronic hypoxia blood haemoglobin increases, allowing preservation of blood flow as in normoxia. Methods: Sixteen Danish lowlanders participated, in groups of six to eight, in the experiments at sea level normoxia (FiO₂ ? 0.21) and acute hypoxia (FiO₂ ? 0.11), and chronic hypoxia after ～7 and 9–10 weeks at ～5260 m altitude breathing ambient air (FiO₂ ? 0.21) or a hyperoxic gas (FiO₂ ? 0.55). The response was compared with that in six Aymara natives. Results: The haemoglobin and haematocrit increased (P < 0.003) in the lowlanders at altitude vs. at sea level by ～39 and 27% respectively; i.e. to a similar (P = ns) level as in the natives. At rest, blood flow was the same (P = ns) in the lowlanders at sea level and altitude, as in the natives at altitude. During the onset of and incremental exercise, blood flow was the same (P = ns) in the lowlanders at sea level and altitude, as in the natives at altitude. Acute hypoxia increased (P < 0.05) blood flow by ～55% during exercise in the lowlanders at sea level. Acute hyperoxia decreased (P < 0.05) blood flow by ～22–29% during exercise in the lowlanders and natives at altitude. Conclusion: In chronic hypoxia, blood haemoglobin increases, allowing normalization of the elevated exercise blood flow response in acute hypoxia, and preservation of the kinetics and steady‐state exercise blood flow as in normoxia, being similar as in the natives at altitude.     

Autonomic markers of arousal during sleep in patients undergoing investigation for obstructive sleep apnoea, their relationship to EEG arousals, respiratory events and subjective sleepiness

Estimating the degree of sleep fragmentation is an important part of a respiratory sleep study and is conventionally measured using EEG micro arousals or is inferred indirectly from respiratory abnormalities such as apnoeas and desaturations. There is a need for less labour-intensive measures of sleep fragmentation, and transient rises in blood pressure and heart rate may fulfil this role. Forty unselected sleep clinic referrals undergoing investigation for possible obstructive sleep apnoea (OSA) were studied with one night of polysomnography. Three conventional indices of sleep fragmentation (EEG micro arousals, apnoea/hypopnoea index (AHI) and oxygen saturation dip rate (SaO₂ dips)) and two autonomic indices (heart rate and blood pressure rises) have been compared. Correlations between these five indices ranged from r=0.38 to r=0.73. Of the two autonomic indices, the correlations for blood pressure rises with SaO₂ dips and EEG micro arousals were stronger (r=0.71 and r=0.65, respectively) than those for heart rate rises (0.55 and 0.51). All indices of sleep fragmentation, apart from heart rate rises, were similar in their correlation with subjective sleepiness (r-values 0.21–0.36). Arousals implied from blood pressure rises (using pulse transit time) can be measured easily, are objective, and appear no worse at predicting subjective sleepiness than either EEG micro arousals or AHI. They may therefore provide a useful alternative to manual scoring of micro arousals from the EEG as an index of sleep fragmentation in sleep clinic patients undergoing investigation for possible OSA.     

Cerebral oxygenation and cerebral oxygen extraction in the preterm infant: the impact of respiratory distress syndrome

Haemodynamic factors play an important role in the etiology of cerebral lesions in preterm infants. Respiratory distress syndrome (RDS), a common problem in preterms, is strongly related with low and fluctuating arterial blood pressure. This study investigated the relation between mean arterial blood pressure (MABP), fractional cerebral oxygen saturation (ScO₂) and fractional (cerebral) tissue oxygen extraction (FTOE), a measure of oxygen utilisation of the brain, during the first 72 h of life. Thirty-eight infants (gestational age < 32 week) were included, 18 with and 20 without RDS. Arterial oxygen saturation (SaO₂), MABP and near infrared spectroscopy-determined ScO₂ were continuously measured. FTOE was calculated as a ratio: (SaO₂–ScO₂)/SaO₂. Gestational age and birth weight did not differ between groups, but assisted ventilation and use of inotropic drugs were more common in RDS infants (P<0.01). MABP was lower in RDS patients (P<0.05 from 12 up to 36 h after birth), but increased in both groups over time. ScO₂ and FTOE were not different between groups over time, but in RDS infants ScO₂ and FTOE had substantial larger variance (P<0.05 at all time points except at 36–48 h for ScO₂ and P<0.05 at 12–18, 18–24, 36–48 and 48–60 h for FTOE). During the first 72 h of life, RDS infants showed more periods of positive correlation between MABP and ScO₂ (P<0.05 at 18–24, 24–36 36–48 48–60 h) and negative correlation between MABP and FTOE (P<0.05 at 18–24, 36–48 h). Although we found that the patterns of cerebral oxygenation and extraction in RDS infants were not different as compared to infants without RDS, we suggest that the frequent periods with possible lack of cerebral autoregulation in RDS infants may make these infants more vulnerable to cerebral damage.     

Extreme human breath-hold diving

In this paper, the respiratory, circulatory and metabolic adjustments to human extreme breath-hold diving are reviewed. A survey of the literature reveals that in extreme divers, adaptive mechanisms take place that allow prolongation of apnoea beyond the limits attained by non-diving subjects, and preservation of oxygen stores during the dives. The occurrence of a diving response, including peripheral vasoconstriction, increased arterial blood pressure, bradycardia and lowered cardiac output, is strongly implicated. Some peripheral regions may be excluded from perfusion, with consequent reliance on anaerobic metabolism. In addition, extreme breath-hold divers show a blunted ventilatory response to carbon dioxide breathing, possibly as a consequence of frequent exposure to high carbon dioxide partial pressures during the dives. These mechanisms allow the attainment of particularly low alveolar oxygen (<30 mmHg) and high alveolar carbon dioxide (>50 mmHg) partial pressures at the end of maximal dry breath-holds, and reduce oxygen consumption during the dive at the expense of increased anaerobic glycolysis (rate of blood lactate accumulation >0.04 mM·s^–1). The current absolute world record for depth in breath-hold diving is 150 m. Its further improvement depends upon how far the equilibrium between starting oxygen stores, the overall rate of energy expenditure, the fraction of energy provided by anaerobic metabolism and the diving speed can be pushed, with consciousness upon emersion. The ultimate limit to breath-hold diving records may indeed be imposed by an energetic constraint. Electronic Publication     

Role of adenosine in exercise‐induced human skeletal muscle vasodilatation

The role of adenosine in exercise‐induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline‐induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one‐legged, knee‐extensor exercise at ～48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (F_aBF) by ～20%, i.e. from 3.6 ± 0.5 to 2.9 ± 0.5 L min^?1, and leg vascular conductance (VC) from 33.4 ± 9.1 to 27.7 ± 8.5 mL min^?1 mmHg^?1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) F_aBF from 0.3 ± 0.03 L min^?1 to a 15‐fold peak elevation (P < 0.05) at 4.1 ± 0.5 L min^?1. Continuous infusion of adenosine at rest and during one‐legged exercise at ～62% of peak power output increased (P < 0.05) F_aBF dose‐dependently to level off (P = ns) at 8.3 ± 1.0 and 8.2 ± 1.4 L min^?1, respectively. One‐legged exercise alone increased (P < 0.05) F_aBF to 4.7 ± 1.7 L min^?1. Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least ～20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

Blood flow in the carotid artery during breath-holding in relation to diving bradycardia

The present study investigated the mechanism of diving bradycardia. A group of 14 healthy untrained male subjects were examined during breath-holding either out of the water (30–33°C), in head-out immersion, or in whole-body submersion (27–29°C) in a diving pool. Blood velocity, blood volume flow in the carotid artery, diastolic blood pressure and electrocardiogram were measured and recorded during the experiments. The peak blood velocity increased by 13.6% (P?P? in the carotid artery increased significantly during breath-holding, e.g. increased from 0.20 (SD 0.02) m?·?s^?1 at rest to 0.33 (SD 0.04) m?·?s^?1 (P?P?P?P? and diastolic blood pressure increased significantly more and faster during breath-holding in submersion than out of the water. There was a good negative correlation with the heart rate: the root mean square correlation coefficient r was 0.73 (P?相似文献   

Dual endothelin receptor blockade with tezosentan markedly attenuates hypoxia-induced pulmonary vasoconstriction in a porcine model

Aim: Our aim was to test the hypothesis that dual endothelin receptor blockade with tezosentan attenuates hypoxia‐induced pulmonary vasoconstriction. Methods: Fourteen anaesthetized, ventilated pigs, with a mean ± SEM weight of 30.5 ± 0.6 kg, were studied, in normoxia (FiO₂ 0.21) and with tezosentan (5 mg kg^?1) infusion during (n = 7) or before (n = 7) hypoxia (FiO₂ 0.10). Results: Compared to normoxia, hypoxia increased (P < 0.05) pulmonary vascular resistance (PVR) by 3.4 ± 0.7 WU, mean pulmonary artery pressure by 13.7 ± 1.3 mmHg, mean right atrial pressure by 1.9 ± 0.4 mmHg and decreased (P < 0.02) systemic vascular resistance (SVR) by 5.2 ± 2.1 WU. Pulmonary capillary wedge pressure (PCWP), mean aortic blood pressure, heart rate, cardiac output, stroke volume and blood‐O₂‐consumption were unaltered (P = ns). Tezosentan infused during hypoxia, normalized PVR, decreased (P < 0.05) maximally mean pulmonary artery pressure by 7.5 ± 0.8 mmHg, SVR by 5.8 ± 0.7 WU, mean aortic blood pressure by 10.8 ± 3.0 mmHg and increased (P < 0.04) stroke volume by 8.5 ± 1.8 mL. Mean right atrial pressure, PCWP, heart rate, cardiac output and blood‐O₂‐consumption were unaltered (P = ns). Tezosentan infused before hypoxia additionally attenuated approx. 70% of the initial mean pulmonary artery pressure increase and abolished the PVR increase, without additionally affecting the other parameters. Conclusion: Dual endothelin receptor blockade during hypoxia attenuates the ‘sustained’ acute pulmonary vasoconstrictor response by reducing the mean pulmonary artery pressure increase by approx. 62% and by normalizing PVR. Pre‐treatment with tezosentan before hypoxia, additionally attenuates the initial hypoxia‐induced mean pulmonary artery pressure rise by approx. 70% and abolishes the PVR increase, during stable circulatory conditions, without affecting oxygenation.     

Phenotyping interindividual variability in obstructive sleep apnoea response to temazepam using ventilatory chemoreflexes during wakefulness

Centrally active agents have a variable impact in patients with obstructive sleep apnoea (OSA) that is unexplained. How to phenotype the individual OSA response is clinically important, as it may help to identify who will be at risk of respiratory depression and who will benefit from a centrally active agent. Based on loop gain theory, we hypothesized that OSA patients with higher central chemosensitivity have higher breathing instability following the use of a hypnosedative, temazepam. In 20 men with OSA in a double‐blind, placebo‐controlled cross‐over trial we tested the polysomnographically (PSG) measured effects of temazepam 10 mg versus placebo on sleep apnoea. Treatment nights were at least 1 week apart. Ventilatory chemoreflexes were also measured during wakefulness in each subject. The patients (mean ± standard deviation; 44 ± 12 years) had predominantly mild‐to‐moderate OSA [baseline apnoea–hypopnoea index (AHI) = 16.8 ± 14.1]. Patients’ baseline awake central chemosensitivity correlated significantly with both the change of SpO₂ nadir between temazepam and placebo (r = ?0.468, P = 0.038) and oxygen desaturation index (ODI; r = 0.485, P = 0.03), but not with the change of AHI (r = 0.18, P = 0.44). Peripheral chemosensitivity and ventilatory recruitment threshold were not correlated with the change of SpO₂ nadir, ODI or AHI (all P > 0.05). Mild–moderate OSA patients with higher awake central chemosensitivity had greater respiratory impairment during sleep with temazepam. Relatively simple daytime tests of respiratory control may provide a method of determining the effect of sedative–hypnotic medication on breathing during sleep in OSA patients.     

Ventilatory responses to hypercapnia in divers and non-divers: effects of posture and immersion

The aim of this study was to determine the effects on respiratory drive of two factors, one mechanical (lung volume) and one chemical (sensitivity to hypercapnia), that are involved in determining the breath-hold duration (BHD). Functional residual capacity was measured by helium dilution with the subject seated in air, seated in water and in the prone position in water. Hyperoxic hypercapnia rebreathing (Read's method) was carried out under identical environmental conditions to assess the effects of CO₂ pressure on respiratory centre output by measuring ventilation, mean inspiratory flow and occlusion pressure. Sixteen healthy volunteers were tested, 8 trained divers and 8 non-divers. Functional residual capacity decreased for the postures seated in water (30.8%–34.8%) and for prone position in water (20.3%–20.9%) when compared to the posture seated in air (P<0.0001), all subjects pooled. No difference was found between groups. The slopes of the linear regression, which characterised the sensitivity to CO₂ and were determined with the rebreathing tests, revealed differences between the two populations (ventilation: P<0.0001; mean inspiratory flow: P<0.05). No difference was found for occlusion pressure or between the different postures. These results confirmed a lower sensitivity to CO₂ for trained divers. This adaptation was shown to decrease respiratory centre activity at the origin of the breath-hold breaking point. The immersion, did not influence respiratory drive, despite a decrease in lung volumes. The authors suggest that these findings may be explained by a specific apnoea training and a pronounced bradycardia in immersion. Electronic Publication     

Hemodynamic adjustments during breath-holding in trained divers

Purpose

Voluntary breath-holding (BH) elicits several hemodynamic changes, but little is known about maximal static immersed-body BH. We hypothesized that the diving reflex would be strengthened with body immersion and would spare more oxygen than maximal dry static BH, resulting in a longer BH duration.

Methods

Eleven trained breath-hold divers (BHDs) performed a maximal dry-body BH and a maximal immersed-body BH. Cardiac output (CO), stroke volume (SV), heart rate (HR), left ventricular end-diastolic volume (LVEDV), contractility index (CTI), and ventricular ejection time (VET) were continuously recorded by bio-impedancemetry (PhysioFlow PF-05). Arterial oxygen saturation (SaO₂) was assessed with a finger probe oximeter.

Results

In both conditions, BHDs presented a bi-phasic kinetic for CO and a tri-phasic kinetic for SV and HR. In the first phase of immersed-body BH and dry-body BH, results (mean ± SD) expressed as percentage changes from starting values showed decreased CO (55.9 ± 10.4 vs. 39.3 ± 16.8 %, respectively; p < 0.01 between conditions), due to drops in both SV (24.9 ± 16.2 vs. 9.0 ± 8.5 %, respectively; p < 0.05 between conditions) and HR (39.7 ± 16.7 vs. 33.6 ± 17.0 %, respectively; p < 0.01 between conditions). The second phase was marked by an overall stabilization of hemodynamic variables. In the third one, CO kept stabilizing due to increased SV (17.0 ± 20.2 vs. 10.9 ± 13.8 %, respectively; p < 0.05 between conditions) associated with a second HR drop (14.0 ± 10.0 vs. 12.7 ± 8.9 %, respectively; p < 0.01 between conditions).

Conclusion

This study highlights similar time-course patterns for cardiodynamic variables during dry-body and immersed-body BH, although the phenomenon was more pronounced in the latter condition.     

Morphological Changes in the Chicken Ductus Arteriosi During Closure at Hatching

The chicken embryo has two functioning ductus arteriosi (DA) during development. These blood vessels connect the pulmonary arteries to the descending aorta providing a right‐to‐left shunt of blood away from the nonrespiring lungs and to the systemic circuit and chorioallanotic membrane. The DA consists of two distinct tissue types along its length, a muscular proximal portion and an elastic distal portion. During hatching, the DA must close for proper separation of systemic and pulmonary circulation. We examined the morphological changes of the chicken DA before, during, and after hatching. Occlusion of the proximal DA began during external pipping and was complete at hatching. Anatomical remodeling began as early as external pipping with fragmentation of the internal elastic lamina and smooth muscle actin appearing in the neointimal zone. By day 2 posthatch, the proximal DA lumen was fully occluded by endothelial cells and smooth muscle actin positive cells. In contrast, the distal DA was not fully occluded by day 2 posthatch. Increases in Po₂ of the blood serves as the main stimulus for closure of the mammalian DA. The responsiveness of the chicken proximal DA to oxygen increased during hatching, peaking during external pipping. This peak correlated with an increase in blood gas Po₂ and the initial occlusion of the vessel. The distal portion remained unresponsive to oxygen throughout hatching. In conclusion, the chicken DA begins to close during external pipping when arterial Po₂ increases and vessel tone is most sensitive to oxygen. Anat Rec, 291:1007–1015, 2008. © 2008 Wiley‐Liss, Inc.     

Gender differences in patients with obesity hypoventilation syndrome

The role of gender and menopause in obstructive sleep apnoea is well known; however, no study has reported the impact of gender on the clinical presentation and the nocturnal respiratory events in patients with obesity hypoventilation syndrome. Therefore, this study prospectively evaluated differences in the clinical characteristics of women and men with obesity hypoventilation syndrome in a large cohort of patients with obstructive sleep apnoea. During the study period, a total of 1973 patients were referred to the sleep clinic with clinical suspicion of obstructive sleep apnoea. All patients underwent overnight polysomnography, during which time spirometry, arterial blood samples and thyroid tests were routinely obtained. Among 1973 consecutive patients, 1693 (617 women) were diagnosed with obstructive sleep apnoea, among whom 144 suffered from obesity hypoventilation syndrome (96 women). The prevalence of obesity hypoventilation syndrome among women and men was 15.6% and 4.5%, respectively (P < 0.001). Women with obesity hypoventilation syndrome were significantly older than men with obesity hypoventilation syndrome (61.5 ± 11.9 years versus 49.1 ± 12.5 years, P < 0.001). Although there were no significant differences between genders regarding symptoms, body mass index, spirometric data or daytime PaCO₂, women with obesity hypoventilation syndrome suffered significantly more from hypertension, diabetes and hypothyroidism. The prevalence of obesity hypoventilation syndrome was higher in post‐menopausal (21%) compared with pre‐menopausal (5.3%) women (P < 0001). HCO₃ and duration of SpO₂ <90% were the only independent predictors of obesity hypoventilation syndrome. In conclusion, this study reported that among subjects referred to the sleep disorders clinic for evaluation of obstructive sleep apnoea, obesity hypoventilation syndrome is more prevalent in women than men, and that women with obesity hypoventilation syndrome suffer from significantly more co‐morbidities. Post‐menopausal women with obstructive sleep apnoea have the highest prevalence of obesity hypoventilation syndrome.     

One-legged endurance training: leg blood flow and oxygen extraction during cycling exercise

Aim: As a consequence of enhanced local vascular conductance, perfusion of muscles increases with exercise intensity to suffice the oxygen demand. However, when maximal oxygen uptake (VO₂max) and cardiac output are approached, the increase in conductance is blunted. Endurance training increases muscle metabolic capacity, but to what extent that affects the regulation of muscle vascular conductance during exercise is unknown. Methods: Seven weeks of one‐legged endurance training was carried out by twelve subjects. Pulmonary VO₂ during cycling and one‐legged cycling was tested before and after training, while VO₂ of the trained leg (TL) and control leg (CL) during cycling was determined after training. Results: VO₂max for cycling was unaffected by training, although one‐legged VO₂max became 6.7 (2.3)% (mean ± SE) larger with TL than with CL. Also TL citrate synthase activity was higher [30 (12)%; P < 0.05]. With the two legs working at precisely the same power during cycling at high intensity (n = 8), leg oxygen uptake was 21 (8)% larger for TL than for CL (P < 0.05) with oxygen extraction being 3.5 (1.1)% higher (P < 0.05) and leg blood flow tended to be higher by 16.0 (7.0)% (P = 0.06). Conclusion: That enhanced VO₂max for the trained leg had no implication for cycling VO₂max supports that there is a central limitation to VO₂max during whole‐body exercise. However, the metabolic balance between the legs was changed during high‐intensity exercise as oxygen delivery and oxygen extraction were higher in the trained leg, suggesting that endurance training ameliorates blunting of leg blood flow and oxygen uptake during whole‐body exercise.