Breath-hold diving is both a recreational activity, performed by thousands of enthusiasts in Europe, and a high-performance competitive sport. Several 'disciplines' exist, of which the 'no-limits' category is the most spectacular: using a specially designed heavy 'sled,' divers descend to extreme depths on a cable, and then reascend using an inflatable balloon, on a single breath. The current world record for un-assisted descent stands at more than 200 m of depth. Equalising air pressure in the paranasal sinuses and middle-ear cavities is a necessity during descent to avoid barotraumas. However, this requires active insufflations of precious air, which is thus unavailable in the pulmonary system. The authors describe a diver who, by training, is capable of allowing passive flooding of the sinuses and middle ear with (sea) water during descent, by suppressing protective (parasympathetic) reflexes during this process. Using this technique, he performed a series of extreme-depth breath-hold dives in June 2005, descending to 209 m of sea water on one breath of air.

The purpose of the study was to analyze the ultrasound lung comets (ULCs) variation, which are a sign of extra-vascular lung water. Forty-two healthy individuals performed breath-hold diving in different conditions: dynamic surface apnea; deep variable-weight apnea and shallow, face immersed without effort (static maximal and non-maximal). The number of ULCs was evaluated by means of an ultrasound scan of the chest, before and after breath-hold diving sessions. The ULC score increased significantly from baseline after dynamic surface apnea (p = 0.0068), after deep breath-hold sessions (p = 0.0018), and after static maximal apnea (p = 0.031). There was no statistically significant difference between the average increase of ULC scores after dynamic surface apnea and deep breath-hold diving. We, therefore, postulate that extravascular lung water accumulation may be due to other factors than (deep) immersion alone, because it occurs during dynamic surface apnea as well. Three mechanisms may be responsible for this. First, the immersion-induced hydrostatic pressure gradient applied on the body causes a shift of peripheral venous blood towards the thorax. Second, the blood pooling effect found during the diving response Redistributes blood to the pulmonary vascular bed. Third, it is possible that the intense involuntary diaphragmatic contractions occurring during the "struggle phase" of the breath-hold can also produce a blood shift from the pulmonary capillaries to the pulmonary alveoli. A combination of these factors may explain the observed increase in ULC scores in deep, shallow maximal and shallow dynamic apneas, whereas shallow non-maximal apneas seem to be not "ULC provoking".

ecreational divers are introducing "deep stops" at half the depth (HD-DS) to reduce the risk of spinal DCS with only Doppler evidence to support it. Therefore this research was designed to show the effect of an HD-DS on spinal DCS manifestations by evaluating whether: (1) air diving-induced spinal DCS could be produced in awake, freely moving rats at 3.5-6.0 atm abs (350-600 kPa); and (2) whether the introduction of an HD-DS reduced spinal DCS in such a model. Fifty-one female, Wistar rats (221 to 450 g) underwent one-hour compression at 350 to 600 kPa with seven minutes of decompression with/without a five-minute DS (HD-DS / No-DS). Animals were observed for three hours. Outcomes were classified as: (1) asymptomatic; (2) breathing difficulties; (3) paralysis/weakness; (4) immobility; or (5) death. Eight animals, exposed to 385 kPa air breathing for 60 minutes followed by a three-staged decompression of 7.5 minutes, remained asymptomatic. The profile is known to produce spinal DCS in anesthetized rats. Eleven animals were then used to determine the threshold for DCS: 500 kPa. A total of 14 animals were compressed to 550 kPa (Group 1). Group 1-A (n = 8) No-DS; Group 1-B (n = 6) HD-DS; 18 were compressed to 600 kPa (Group 2). Group 2-A (n = 8) No-DS; Group 2-B (n = 10) HD-DS.

INTRODUCTION: The aim of this study was to evaluate the effect of a single, shallow, swimming pool scuba dive on pulmonary function in divers with asthma as compared to controls. Opinions concerning the risks of diving with asthma are still contradictory and inconclusive in the diving community.

INTRODUCTION: After repetitive deep dives, breath-hold divers are often affected by a syndrome characterized by typical symptoms such as cough, sensation of chest constriction, blood-striated expectorate (hemoptysis) and, rarely, an overt acute pulmonary edema syndrome, often together with various degrees of dyspnea. The aim of this work is an epidemiological investigation to evaluate the prevalence of acute respiratory symptoms (ARS) in breath-hold divers (BHDs) in practicing breath-hold diving.