Frédéric Lemaître

This single-blind, crossover study aimed to measure and evaluate the short-term metabolic responses to continuous and intermittent hypoxic patterns in individuals with obesity. Indirect calorimetry was used to quantify changes in resting metabolic rate (RMR), carbohydrate (CHOox, %CHO), and fat oxidation (FAT(ox), %FAT) in nine individuals with obesity pre and post: 1) breathing normoxic air [normoxic sham control (NS-control)], 2) breathing continuous hypoxia (CH), or 3) breathing intermittent hypoxia (IH). A mean peripheral oxygen saturation ([Formula: see text]) of 80-85% was achieved over a total of 45 min of hypoxia. Throughout each intervention, pulmonary gas exchanges, oxygen consumption (Vo(2)) carbon dioxide production (Vco(2)), and deoxyhemoglobin concentration (Delta[HHb]) in the vastus lateralis were measured. Both RMR and CHOox measured pre- and postinterventions were unchanged following each treatment: NS-control, CH, or IH (all P > 0.05). Conversely, a significant increase in FAT(ox) was evident between pre- and post-IH (+44%, P = 0.048). Although the mean Delta[HHb] values significantly increased during both IH and CH (P < 0.05), the greatest zenith of Delta[HHb] was achieved in IH compared with CH (P = 0.002). Furthermore, there was a positive correlation between Delta[HHb] and the shift in FAT(ox) measured pre- and postintervention. It is suggested that during IH, the increased bouts of muscle hypoxia, revealed by elevated Delta[HHb], coupled with cyclic periods of excess posthypoxia oxygen consumption (EPHOC, inherent to the intermittent pattern) played a significant role in driving the increase in FAT(ox) post-IH.

PurposeThe hippocampus is organized in subfields (HSF) involved in learning and memory processes and widely implicated in pathologies at different ages of life, from neonatal hypoxia to temporal lobe epilepsy or Alzheimer’s disease. Getting a highly accurate and robust delineation of sub-millimetric regions such as HSF to investigate anatomo-functional hypotheses is a challenge. One of the main difficulties encountered by those methodologies is related to the small size and anatomical variability of HSF, resulting in the scarcity of manual data labeling. Recently introduced, capsule networks solve analogous problems in medical imaging, providing deep learning architectures with rotational equivariance. Nonetheless, capsule networks are still two-dimensional and unassessed for the segmentation of HSF.ApproachWe released a public 3D Capsule Network (3D-AGSCaps, https://github.com/clementpoiret/3D-AGSCaps) and compared it to equivalent architectures using classical convolutions on the automatic segmentation of HSF on small and atypical datasets (incomplete hippocampal inversion, IHI). We tested 3D-AGSCaps on three datasets with manually labeled hippocampi.ResultsOur main results were: (1) 3D-AGSCaps produced segmentations with a better Dice Coefficient compared to CNNs on rotated hippocampi (p=0.004, cohen’s d=0.179); (2) on typical subjects, 3D-AGSCaps produced segmentations with a Dice coefficient similar to CNNs while having 15 times fewer parameters (2.285M versus 35.069M). This may greatly facilitate the study of atypical subjects, including healthy and pathological cases like those presenting an IHI.ConclusionWe expect our newly introduced 3D-AGSCaps to allow a more accurate and fully automated segmentation on atypical populations, small datasets, as well as on and large cohorts where manual segmentations are nearly intractable.

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.

Editorial: Physiology and Physiopathology of Breath-Holding Activity

Nitrogen (N₂) accumulation in the blood and tissues can occur due to breath-hold (BH) diving. Post-dive venous gas emboli have been documented in commercial BH divers (Ama) after repetitive dives with short surface intervals. Hence, BH diving can theoretically cause decompression illness (DCI). “Taravana,” the diving syndrome described in Polynesian pearl divers by Cross in the 1960s, is likely DCI. It manifests mainly with cerebral involvements, especially stroke-like brain attacks with the spinal cord spared. Neuroradiological studies on Ama divers showed symptomatic and asymptomatic ischemic lesions in the cerebral cortex, subcortex, basal ganglia, brainstem, and cerebellum. These lesions localized in the external watershed areas and deep perforating arteries are compatible with cerebral arterial gas embolism. The underlying mechanisms remain to be elucidated. We consider that the most plausible mechanisms are arterialized venous gas bubbles passing through the lungs, bubbles mixed with thrombi occlude cerebral arteries and then expand from N₂ influx from the occluded arteries and the brain. The first aid normobaric oxygen appears beneficial. DCI prevention strategy includes avoiding long-lasting repetitive dives for more than several hours, prolonging the surface intervals. This article provides an overview of clinical manifestations of DCI following repetitive BH dives and discusses possible mechanisms based on clinical and neuroimaging studies.

The aim of this study was to investigate the impact of breath-hold diving strategies regarding loss of consciousness (LOC). Three international competitions were examined through video in constant weight diving with (CWT) or without (CNF) fins. We analysed three breath-hold parameters (time, speed, and movements count) for the following phases: active descent, passive descent, turning, and ascent. Divers who had LOC during CNF were slower in the active descent phase, faster in the passive descent phase with a longer turn, and slower in the ascent phase than divers who did not have LOC. They also had lower amplitude and higher frequency. Men were deeper (72.9 m vs. 56.3 m) for a longer dive time (181.1 s vs. 154.6 s), faster, with a greater amplitude than women. In CWT, divers with an LOC had longer dive times (197 s vs. 167 s) with a faster active descent phase. Men had lower amplitude and greater frequency than women. This is the first study showing that breath-hold divers undergoing an LOC event shown differences in efficiency during CWT and CNF regarding velocities, amplitudes, and frequencies. In conclusion, our results suggest that the speed parameter during active descent phase influence the LOC.

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 (SpO₂) 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 SpO₂ 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.

This short review focuses on pulmonary injury in breath-hold (BH) divers. When practicing their extreme leisure sport, they are exposed to increased pressure on pulmonary gas volumes, hypoxia, and increased partial gas pressures. Increasing ambient pressures do present a serious problem to BH deep divers, because the semi-rigid thorax prevents the deformation required by the Boyle-Mariotte law. As a result, a negative-pressure barotrauma (lung squeeze) with acute hemoptysis is not uncommon. Respiratory maneuvers such as glossopharyngeal insufflation (GI) and glossopharyngeal exsufflation (GE) are practiced to prevent lung squeeze and to permit equalizing the paranasal sinuses and the middle ear. GI not only impairs venous return, thereby provoking hypotension and even fainting, but also produces intrathoracic pressures likely to induce pulmonary barotrauma that is speculated to induce long-term injury. GE, in turn, further increases the already negative intrapulmonary pressure, thereby favoring alveolar collapse (atelectasis). Finally, hypoxia seemingly not only induces brain injury but initiates the opening of intrapulmonary shunts. These pathways are large enough to permit transpulmonary passage of venous N₂ bubbles, making stroke-like phenomena in deep BH divers possible.

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.