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This study investigated the impact of repeated-sprint (RS) training with voluntary hypoventilation at low lung volume (VHL) on RS ability (RSA) and on performance in a 30-15 intermittent fitness test (30-15IFT). Over 4 weeks, 17 basketball players included eight sessions of straight-line running RS and RS with changes of direction into their usual training, performed either with normal breathing (CTL, n = 8) or with VHL (n = 9). Before and after the training, athletes completed a RSA test (12 × 30-m, 25-s rest) and a 30-15IFT. During the RSA test, the fastest sprint (RSAbest), time-based percentage decrement score (RSASdec), total electromyographic intensity (RMS), and spectrum frequency (MPF) of the biceps femoris and gastrocnemius muscles, and biceps femoris NIRS-derived oxygenation were assessed for every sprint. A capillary blood sample was also taken after the last sprint to analyse metabolic and ionic markers. Cohen's effect sizes (ES) were used to compare group differences. Compared with CTL, VHL did not clearly modify RSAbest, but likely lowered RSASdec (VHL: −24.5% vs. CTL: −5.9%, group difference: −19.8%, ES −0.44). VHL also lowered the maximal deoxygenation induced by sprints ([HHb]max; group difference: −2.9%, ES −0.72) and enhanced the reoxygenation during recovery periods ([HHb]min; group difference: −3.6%, ES −1.00). VHL increased RMS (group difference: 18.2%, ES 1.28) and maintained MPF toward higher frequencies (group difference: 9.8 ± 5.0%, ES 1.40). These changes were concomitant with a lower potassium (K+) concentration (group difference: −17.5%, ES −0.67), and the lowering in [K+] was largely correlated with RSASdec post-training in VHL only (r = 0.66, p < 0.05). However, VHL did not clearly alter PO2, hemoglobin, lactate and bicarbonate concentration and base excess. There was no difference between group velocity gains for the 30-15IFT (CTL: 6.9% vs. VHL: 7.5%, ES 0.07). These results indicate that RS training combined with VHL may improve RSA, which could be relevant to basketball player success. This gain may be attributed to greater muscle reoxygenation, enhanced muscle recruitment strategies, and improved K+ regulation to attenuate the development of muscle fatigue, especially in type-II muscle fibers.

The permeabilization of liposomes by melittin, an antimicrobial peptide (AMP), has been studied by an electrochemiluminescence (ECL) imaging strategy. The methodology consisted first of encapsulating ECL reagents in sealed giant asymmetrical liposomes (100 μm in diameter) made of DOPG/DOPC phospholipids (i.e., 1,2-dioleoyl-sn-glycerol-3-phospho-(1′-rac-glycerol) sodium salt/1,2-dioleolyl-sn-glycero-3-phosphocholine). Then liposomes were placed on an indium tin oxide electrode coated with poly-l-lysine to avoid any membrane poration/permeabilization through polarization of the electrode surface. Finally, the addition of melittin (from 10 μM to 100 nM in concentration) enabled the permeabilization of the lipid membrane followed by the liposome content release and subsequent light generation through the ECL reagents oxidation processes. Interestingly, at a melittin concentration of 10 μM, two successive leakages occurring on the same liposome could be imaged. Combination of ECL and photoluminescence imaging allowed comprehensive monitoring of the permeabilization and content release of a single liposome. This ECL imaging approach opens interesting perspectives to characterize the instant release of vesicle content upon permeabilization by AMPs or other membrane-active species.

The hippocampal subfields, pivotal to episodic memory, are distinct both in terms of cyto- and myeloarchitectony. Studying the structure of hippocampal subfields in vivo is crucial to understand volumetric trajectories across the lifespan, from the emergence of episodic memory during early childhood to memory impairments found in older adults. However, segmenting hippocampal subfields on conventional MRI sequences is challenging because of their small size. Furthermore, there is to date no unified segmentation protocol for the hippocampal subfields, which limits comparisons between studies. Therefore, we introduced a novel segmentation tool called HSF short for hippocampal segmentation factory, which leverages an end-to-end deep learning pipeline. First, we validated HSF against currently used tools (ASHS, HIPS, and HippUnfold). Then, we used HSF on 3,750 subjects from the HCP development, young adults, and aging datasets to study the effect of age and sex on hippocampal subfields volumes. Firstly, we showed HSF to be closer to manual segmentation than other currently used tools (p < 0.001), regarding the Dice Coefficient, Hausdorff Distance, and Volumetric Similarity. Then, we showed differential maturation and aging across subfields, with the dentate gyrus being the most affected by age. We also found faster growth and decay in men than in women for most hippocampal subfields. Thus, while we introduced a new, fast and robust end-to-end segmentation tool, our neuroanatomical results concerning the lifespan trajectories of the hippocampal subfields reconcile previous conflicting results.

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.

Breath-hold diving involves environmental challenges, such as water immersion, hydrostatic pressure, and asphyxia, that put the respiratory system under stress. While training and inherent individual factors may increase tolerance to these challenges, the limits of human respiratory physiology will be reached quickly during deep breath-hold dives. Nonetheless, world records in deep breath-hold diving of more than 214 m of seawater have considerably exceeded predictions from human physiology. Investigations of elite breath-hold divers and their achievements revised our understanding of possible physiological adaptations in humans and revealed techniques such as glossopharyngeal breathing as being essential to achieve extremes in breath-hold diving performance. These techniques allow elite athletes to increase total lung capacity and minimize residual volume, thereby reducing thoracic squeeze. However, the inability of human lungs to collapse early during descent enables respiratory gas exchange to continue at greater depths, forcing nitrogen (N2) out of the alveolar space to dissolve in body tissues. This will increase risk of N2 narcosis and decompression stress. Clinical cases of stroke-like syndromes after single deep breath-hold dives point to possible mechanisms of decompression stress, caused by N2 entering the vasculature upon ascent from these deep dives. Mechanisms of neurological injury and inert gas narcosis during deep breath-hold dives are still incompletely understood. This review addresses possible hypotheses and elucidates factors that may contribute to pathophysiology of deep freediving accidents. Awareness of the unique challenges to pulmonary physiology at depth is paramount to assess medical risks of deep breath-hold diving.

Devices that harness electron flow from photosynthetic organisms generally compromise host photosynthesis. Here, the authors show that, by redesigning the QAsite of Photosystem II, it is possible to reroute electrons to an exogenous quinone while maintaining endogenous photosynthetic electron transfer in a green alga.

Acute decompression illness (DCI) involving the brain (Cerebral DCI) is one of the most serious forms of diving-related injuries which may leave residual brain damage. Cerebral DCI occurs in compressed air and in breath-hold divers, likewise. We conducted this study to investigate whether long-term breath-hold divers who may be exposed to repeated symptomatic and asymptomatic brain injuries, show brain damage on magnetic resonance imaging (MRI).Our study subjects were 12 commercial breath-hold divers (Ama) with long histories of diving work in a district of Japan. We obtained information on their diving practices and the presence or absence of medical problems, especially DCI events. All participants were examined with MRI to determine the prevalence of brain lesions.Out of 12 Ama divers (mean age: 54.9±5.1 years), four had histories of cerebral DCI events, and 11 divers demonstrated ischemic lesions of the brain on MRI studies. The lesions were situated in the cortical and/or subcortical area (9 cases), white matters (4 cases), the basal ganglia (4 cases), and the thalamus (1 case). Subdural fluid collections were seen in 2 cases.These results suggest that commercial breath-hold divers are at a risk of clinical or subclinical brain injury which may affect the long-term neuropsychological health of divers.