Search

During deep-sea freediving, many freedivers describe symptoms fairly similar to what has been related to inert gas narcosis in scuba divers. This manuscript aims to present the potential mechanisms underlying these symptoms. First, known mechanisms of narcosis are summarized while scuba diving. Then, potential underlying mechanisms involving the toxicity of gases (nitrogen, carbon dioxide and oxygen) are presented in freedivers. As the symptoms are felt during ascent, nitrogen is likely not the only gas involved. Since freedivers are frequently exposed to hypercapnic hypoxia toward the end of the dive, it is proposed that carbon dioxide and oxygen gases both play a major role. Finally, a new "hemodynamic hypothesis" based on the diving reflex is proposed in freedivers. The underlying mechanisms are undoubtedly multifactorial and therefore require further research and a new descriptive name. We propose a new term for these types of symptoms: freediving transient cognitive impairment., Competing Interests: The authors of this paper declare no conflicts of interest exist with this submission., (Copyright© Undersea and Hyperbaric Medical Society.)

Abstract Breath-hold divers are known to develop cardiac autonomic changes and brady-arrthymias during prolonged breath-holding (BH). The effects of BH-induced hypoxemia were investigated upon both cardiac autonomic status and arrhythmogenesis by comparing breath-hold divers (BHDs) to non-divers (NDs). Eighteen participants (9 BHDs, 9 NDs) performed a maximal voluntary BH with face immersion. BHDs were asked to perform an additional BH at water surface to increase the degree of hypoxemia. Beat-to-beat changes in heart rate (HR), short-term fractal scaling exponent (DFAα1), the number of arrhythmic events [premature ventricular contractions (PVCs), premature atrial contractions (PACs)] and peripheral oxygen saturation (SpO 2 ) were recorded during and immediately following BH. The corrected QT-intervals (QTc) were analyzed pre- and post-acute BH. A regression-based model was used to split BH into a normoxic (NX) and a hypoxemic phase (HX). During the HX phase of BH, BHDs showed a progressive decrease in DFAα1 during BH with face immersion ( p  < 0.01) and BH with whole-body immersion ( p  < 0.01) whereas NDs did not ( p  > 0.05). In addition, BHDs had more arrhythmic events during the HX of BH with whole-body immersion when compared to the corresponding NX phase (5.9 ± 6.7 vs 0.4 ± 1.3; p  < 0.05; respectively). The number of PVCs was negatively correlated with SpO 2 during BH with whole-body immersion ( r  = -0.72; p  < 0.05). The hypoxemic stage of voluntary BH is concomitant with significant cardiac autonomic changes toward a synergistic sympathetic and parasympathetic stimulation. Co-activation led ultimately to increased bradycardic response and cardiac electrophysiological disturbances.

Repeated apneas are associated with severe hypoxemia that may ultimately lead to loss of consciousness in some breath-hold divers. Despite increasing number of practitioners, the relationship between apnea-induced hypoxia and neurocognitive functions is still poorly understood in the sport of free diving. To shed light onto this phenomenon, we examined the impact of long-term breath-hold diving training on attentional processing, short-term memory, and long-term mnesic and executive functions. Thirty-six men matched for age, height, and weight were separated into the following 3 groups: (i) 12 elite breath-hold divers (EBHD), mean static apnea best time 371 s, 105 months mean apnea experience; (ii) 12 novice breath-hold divers, mean best time 243 s, 8.75 months mean apnea experience; and (iii) 12 physical education students with no breath-hold diving experience; all of these participants performed varied written and computerized neuropsychological tasks. Compared with the 2 other groups, the EBHD group was slower to complete the interference card during a Stroop test (F [1,33] = 4.70, p < 0.05), and presented more errors on the interference card (F [1,33] = 2.96, p < 0.05) and a lower total interference score (F [1,33] = 5.64, p < 0.05). The time to complete the interference card test was positively correlated with maximal static apnea duration (r = 0.73, p < 0.05) and the number of years of breath-hold diving training (r = 0.79, p < 0.001). These findings suggest that breath-hold diving training over several years may cause mild, but persistent, short-term memory impairments.

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 ([HbO 2 ]), deoxyhaemoglobin ([HHb]), total haemoglobin ([tHb]), tissue saturation index (TSI)] and peripheral oxygen saturation (SpO 2 ) 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.

Purpose: Although it has been demonstrated that the exponential decay model fits the heart rate (HR) kinetics in short static breath holding (BH), this model might be inaccurate when BH is maintained for several minutes. The aim of this study was to build a new meaningful model to quantify HR kinetics during prolonged static BH., Methods: Nonlinear regression analysis was used to build a model able to quantify the beat-to-beat HR reduction kinetics observed in prolonged static BH performed both in air and in immersed condition by 11 trained breath-hold divers. Dynamic changes in cardiac autonomic regulation through heart rate variability indices [root mean square of successive difference of R-R intervals (RMSSD); short-term fractal scaling exponent: (DFAα1)] and peripheral oxygen saturation (SpO2) were also analyzed to strengthen the model., Results: The tri-phasic model showed a sharp exponential drop in HR immediately followed by a slight linear rise up until a breaking point preceding a linear drop in HR. The breaking points had similar level of SpO2 whether in air or in immersed condition (95.1 ± 2.1 vs. 95.2 ± 3.0 %, respectively; P = 0.49), and the subsequent linear drop in HR was concomitant with a shift in cardiac autonomic regulation in air (RMSSD: +109.0 ± 47.8 %; P < 0.001; DFAα1: -18.0 ± 17.4 %; P < 0.05) and in immersion (RMSSD: +112.6 ± 55.8 %; P < 0.001; DFAα1: -26.0 ± 12 %; P < 0.001)., Conclusion: In addition to accurately fitting the HR kinetics, the most striking finding is an "oxygen-conserving breaking point" highlighted by the model, which might be interpreted as unique adaptive feature against hypoxic damages in the human diving bradycardia.

Objective: Symptoms consistent with neurological decompression sickness (DCS) in commercial breath-hold (Ama) divers has been reported from a few districts of Japan. The aim of this study was to detect circulating intravascular bubbles after repetitive breath-hold diving in a local area where DCS has been reported in Ama divers., Methods: The participants were 12 partially assisted (descent using weights) male Ama divers. The equipment (AQUALAB system) consisted of continuous-wave Doppler with a 5-MHz frequency, and the Doppler probe was placed in the precordial site with the ultrasonic wave directed into the pulmonary infundibulum. We carried out continuous monitoring for 10 minutes at the end of the series of repetitive dives, and the recordings were made on numerical tracks and graded in a blind manner by 2 experienced investigators, according to the Spencer Doppler code., Results: Depths and number of dives were 8 to 20 m and 75 to 131 times. Mean diving duration and surface interval were 64 ± 12 seconds and 48 ± 8 seconds, respectively (mean ± SD). We detected the lowest grade of intravascular bubbles (Spencer's grade I) in an Ama diver whose mean surface interval was only 35.2 ± 6.2 seconds. His mean descending, bottom, and ascending times were 10.4 ± 1.6 seconds, 39.2 ± 8 seconds, and 18.2 ± 3.0 seconds, respectively, over the course of 99 dives., Conclusions: Intravascular bubbles may be formed after repetitive breath-hold dives with short surface intervals or after a long breath-holding session in Ama divers. Symptoms consistent with neurological accidents in repetitive breath-hold diving may be caused in part by the intravascular presence of bubbles, indicating the need for safety procedures., (Copyright © 2014 Wilderness Medical Society. Published by Elsevier Inc. All rights reserved.)

Trained breath-hold divers (BHDs) are exposed to repeated bouts of intermittent hypoxia and hypercapnia during prolonged breath-holding. It has thus been hypothesized that their specific training may develop enhanced chemo-responsiveness to hypoxia associated with reduced ventilatory response to hypercapnia. Hypercapnic ventilatory responses (HCVR) and hypoxic ventilatory responses at rest (HVRr) and exercise (HVRe) were assessed in BHDs (n=7) and a control group of non-divers (NDs=7). Cardiac output (CO), stroke volume (SV) and heart rate (HR) were also recorded. BHDs presented carbon dioxide sensitivity similar to that of NDs (2.85±1.41 vs. 1.85±0.93Lmin(-1)mmHg(-1), p>0.05, respectively). However, both HVRr (+68%) and HVRe (+31%) were increased in BHDs. CO and HR reached lower values in BHDs than NDs during the hypoxic exercise test. These results suggest that the exposure to repeated bouts of hypoxia/hypercapnia frequently experienced by trained breath-hold divers only enhances their chemo-responsiveness to poikilocapnic hypoxia, without altering HCVR., (Copyright © 2013 Elsevier B.V. All rights reserved.)

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.

The cardiac diving response, 12-lead electrocardiogram (ECG) and the prevalence, time of onset, and possible associations of cardiac arrhythmias were examined during deep breath-hold (BH) dives. Nine elite BH divers (33.2 +/- 3.6 years; mean +/- SD) performed one constant-weight dive of at least 75% of their best personal performance (70 +/- 7 meters for 141 +/- 22 seconds) wearing a 12-lead ECG Holter monitor. Diving parameters (depth and time), oxygen saturation (SaO2), blood lactate concentration and ventilatory parameters were also recorded. Bradycardia during these dives was pronounced (52.2 +/- 12.2%), with heart rates dropping to 46 +/- 10 beats/minute. The diving reflex was strong, overriding the stimulus of muscular exercise during the ascent phase of the dive for all divers. Classical arrhythmias occurred, mainly after surfacing, and some conduction alterations were detected at the bottom of the dives. The BH divers did not show any right shift of the QRS electrical axis during their dives.