Fabrice Joulia

Reduced oxidative stress and blood lactic acidosis in trained breath-hold human divers

We hypothesized that the repetition of brief epochs of hypoxemia in elite human breath-hold divers could induce an adaptation of their metabolic responses, resulting in reduced blood acidosis and oxidative stress. Trained divers who had a 7-10 year experience in breath-hold diving, and were able to sustain apnea up to 440 sec at rest, were compared to control individuals who sustained apnea for 145 sec at the most. The subjects sustained apnea at rest (static apnea), and then, performed two 1-min dynamic forearm exercises whether they breathed (control exercise) or sustained apnea (dynamic apnea). We measured arterial blood gases, venous blood pH, and venous blood concentrations of lactic acid, thiobarbituric acid reactive substances (TBARS), and two endogenous anti-oxidants (reduced glutathione, GSH, and reduced ascorbic acid, RAA). In control subjects, the three experimental conditions elicited an increase in blood lactic acid concentration and an oxidative stress (increased TBARS, decreased GSH and RAA concentrations). In divers, the changes in lactic acid, TBARS, RAA, and GSH concentrations were markedly reduced after static and dynamic apnea, as well as after control exercise. Thus, human subjects involved in a long duration training programme of breath-hold diving have reduced post-apnea as well as post-exercise blood acidosis and oxidative stress, mimicking the responses of diving animals.

Circulatory effects of apnoea in elite breath-hold divers

Aim:  Voluntary apnoea induces several physiological adaptations, including bradycardia, arterial hypertension and redistribution of regional blood flows. Elite breath‐hold divers (BHDs) are able to maintain very long apnoea, inducing severe hypoxaemia without brain injury or black‐out. It has thus been hypothesized that they develop protection mechanisms against hypoxia, as well as a decrease in overall oxygen uptake.

Static apnea effect on heart rate and its variability in elite breath-hold divers

BACKGROUND The diving response includes cardiovascular adjustments known to decrease oxygen uptake and thus prolong apnea duration. As this diving response is in part characterized by a pronounced decrease in heart rate (HR), it is thought to be vagally mediated. METHODS In five professional breath-hold divers (BHDs) and five less-trained controls (CTL), we investigated whether the diving response is in fact associated with an increase in the root mean square successive difference of the R-R intervals (RMSSD), a time-domain heart rate variability (HRV) index. HR behavior and arterial oxygen saturation (SaO2) were continuously recorded during one maximal apnea. Short-term changes in SaO2, HR, and RMSSD were calculated over the complete apnea duration. RESULTS BHDs presented bi-phasic HR kinetics, with two HR decreases (32 +/- 17% and 20 +/- 10% of initial HR). The second HR decrease, which was concomitant to the pronounced SaO2 decrease, was also simultaneous to a marked increase in RMSSD. CTL showed only one HR decrease (50 +/- 10% of initial HR), which appeared before the concomitant SaO2 and RMSSD changes. When all subject data were combined, arterial desaturation was positively correlated with total apnea time (r = 0.87, P < 0.01). CONCLUSION This study indicates that baroreflex stimulation and hypoxia may be involved in the bi-phasic HR response of BHDs and thus in their longer apnea duration.

Apnea: A new training method in sport?

The physiological responses to apnea training exhibited by elite breath-hold divers may contribute to improving sports performance. Breath-hold divers have shown reduced blood acidosis, oxidative stress and basal metabolic rate, and increased hematocrit, erythropoietin concentration, hemoglobin mass and lung volumes. We hypothesise that these adaptations contributed to long apnea durations and improve performance. These results suggest that apnea training may be an effective alternative to hypobaric or normobaric hypoxia to increase aerobic and/or anaerobic performance.

Activation of human inspiratory muscles in an upside-down posture.

During quiet breathing, activation of obligatory inspiratory muscles differs in timing and magnitude. To test the hypothesis that this coordinated activation can be modified, we determined the effect of the upside-down posture compared with standing and lying supine. Subjects (n=14) breathed through a pneumotachometer with calibrated inductance bands around the chest wall and abdomen. Surface electromyographic activity (EMG) was recorded from the scalene muscles. Crural diaphragmatic EMG and oesophageal and gastric pressures were measured in a subset of six subjects. Quiet breathing and standard lung function manoeuvres were performed. The upside-down posture reduced end-expiratory lung volume. During quiet breathing, for the same inspiratory airflow and tidal volume, ribcage contribution decreased, abdominal contribution increased and transdiaphragmatic pressure swing doubled in the upside-down posture compared to standing (p<0.05). Despite this, crural diaphragm EMG was unchanged, whereas scalene muscle EMG was reduced by ∼half (p<0.05). Thus, the mechanical effect of an upside-down posture differentially affects inspiratory muscle activation.

Plasma adenosine release is associated with bradycardia and transient loss of consciousness during experimental breath-hold diving

Plasma adenosine release is associated with bradycardia and transient loss of consciousness during experimental breath-hold diving Fabrice Joulia , Mathieu Coulange , Frederic Lemaitre , Guillaume Costalat , Frederic Franceschi , Vlad Gariboldi , Laetitia Nee , Julien Fromonot , Laurie Bruzzese , Gilles Gravier , Nathalie Kipson , Yves Jammes , Alain Boussuges , Michele Brignole , Jean Claude Deharo , Regis Guieu a,g,⁎

The oxygen-conserving potential of the diving response: A kinetic-based analysis

ABSTRACT We investigated the oxygen-conserving potential of the human diving response by comparing trained breath-hold divers (BHDs) to non-divers (NDs) during simulated dynamic breath-holding (BH). Changes in haemodynamics [heart rate (HR), stroke volume (SV), cardiac output (CO)] and peripheral muscle oxygenation [oxyhaemoglobin ([HbO2]), deoxyhaemoglobin ([HHb]), total haemoglobin ([tHb]), tissue saturation index (TSI)] and peripheral oxygen saturation (SpO2) were continuously recorded during simulated dynamic BH. BHDs showed a breaking point in HR kinetics at mid-BH immediately preceding a more pronounced drop in HR (−0.86 bpm.%−1) while HR kinetics in NDs steadily decreased throughout BH (−0.47 bpm.%−1). By contrast, SV remained unchanged during BH in both groups (all P > 0.05). Near-infrared spectroscopy (NIRS) results (mean ± SD) expressed as percentage changes from the initial values showed a lower [HHb] increase for BHDs than for NDs at the cessation of BH (+24.0 ± 10.1 vs. +39.2 ± 9.6%, respectively; P < 0.05). As a result, BHDs showed a [tHb] drop that NDs did not at the end of BH (−7.3 ± 3.2 vs. −3.0 ± 4.7%, respectively; P < 0.05). The most striking finding of the present study was that BHDs presented an increase in oxygen-conserving efficiency due to substantial shifts in both cardiac and peripheral haemodynamics during simulated BH. In addition, the kinetic-based approach we used provides further credence to the concept of an “oxygen-conserving breaking point” in the human diving response.

Ischaemia-modified albumin during experimental apnoea

Ischaemia-modified albumin (IMA) is a marker of the release of reactive oxygen species (ROS) during hypoxaemia. In elite divers, breath-hold induces ROS production. Our aim was to evaluate the kinetics of IMA serum levels during apnea. Twenty breath-hold divers were instructed to perform a submaximal static breath-hold. Twenty non-diver subjects served as controls. Blood samples were collected at rest, every minute, at the end of breath-hold, and 10 min after recovery. The IMA level increased after 1 min of breath-hold (p < 0.003) and remained high until recovery. Divers were separated into 2 groups: subjects who held their breath for less than 4 min (G-4) and those who held it for more than 4 min (G+4). After 3 min of apnoea, the increase of IMA was higher in the G-4 group than in the G+4 group (p < 0.008). However, at the end of apnoea, the IMA level did not differ between groups. If IMA level was globally correlated with the apnoea duration, it is interesting to note that the higher IMA level was not found in the best divers. Similarly, if arterial blood oxygen saturation (SpO2) was globally inversely correlated with apnoea duration, the lowest SpO2 at the end of breath-hold was not found in the divers that performed the best apnoea. We concluded that these divers save their oxygen. The IMA level provides a useful measure of resistance to hypoxaemia.

Endogenous adenosine release is involved in the control of heart rate in rats

Intravenous (i.v.) injections of adenosine exert marked effects on heart rate (HR) and arterial blood pressure (BP), but the role of an endogenous adenosine release by vagal stimulation has not been evaluated. In anaesthetized rats, we examined HR and BP changes induced by 1 min electrical vagal stimulation in the control condition, and then after i.v. injections of (i) atropine, (ii) propranolol, (iii) caffeine, (iv) 8 cyclopentyl-1,3-dipropylxanthine (DPCPX), or (v) dipyridamole to increase the plasma concentration of adenosine (APC). APC was measured by chromatography in the arterial blood before and at the end of vagal stimulation. The decrease in HR in the controls during vagal stimulation was markedly attenuated, but persisted after i.v. injections of atropine and propranolol. When first administered, DPCPX modestly but significantly reduced the HR response to vagal stimulation, but this disappeared after i.v. caffeine administration. Both the HR and BP responses were significantly accentuated after i.v. injection of dipyridamole. Vagal stimulation induced a significant increase in APC, proportional to the magnitude of HR decrease. Our data suggest that the inhibitory effects of electrical vagal stimulations on HR and BP were partly mediated through the activation of A1 and A2 receptors by an endogenous adenosine release. Our experimental data could help to understand the effects of ischemic preconditioning, which are partially mediated by adenosine.

Electrocardiogram changes during positive pressure breathing in rabbits

Positive pressure breathing produced by mechanical ventilation with an expiratory threshold load (ETL) may modify electrocardiogram (ECG) complexes independently of any recording artefact due to lung volume changes. Anaesthetized, paralyzed rabbits were treated for about 2 h, then killed. In intact then vagotomized animals two situations were studied successively. Firstly, positive inspiratory pressure breathing, and secondly, positive inspiratory plus expiratory pressure breathing by adding ETL to mechanical ventilation. Arterial blood gases were measured and held constant throughout the challenge. Oesophageal pressure, giving indirect measurement of intrathoracic pressure, arterial blood pressure, blood flows in abdominal aorta and inferior vena cava and standard ECG recordings were made at baseline condition during mechanical ventilation, then at the end of a 10-min period of ETL breathing. The ETL breathing decreased arterial blood pressure significantly and reduced arterial and venous blood flows in the same proportion. No change in the duration of ECG complexes was noticed. However, ETL markedly reduced the amplitude of P- and T0waves, but not that of R-wave, an effect significantly accentuated after vagotomy. The ETL breathing increased the T-vector angle, with no associated change in QRS vector angle. The present animal investigations revealed that positive pressure breathing modifies the ECG independently of the consequences of ETL-induced lung volume changes. We speculate that the changes in P- and T-wave amplitude may have resulted from a reduced transmural pressure gradient between the epicardium and endocardium.