INTRODUCTION: Hyperoxia causes oxidative stress. Breath-hold diving is associated with transient hyperoxia followed by hypoxia and a build-up of carbon dioxide (CO₂), chest-wall compression and significant haemodynamic changes. This study analyses variations in plasma oxidative stress markers after a series of repetitive breath-hold dives. METHODS: Thirteen breath-hold divers were asked to perform repetitive breath-hold dives to 20 metres' depth to a cumulative breath-hold time of approximately 20 minutes over an hour in the open sea. Plasma nitric oxide (NO), peroxinitrites (ONOO⁻) and thiols (R-SH) were measured before and after the dive sequence. RESULTS: Circulating NO significantly increased after successive breath-hold dives (169.1 ± 58.26% of pre-dive values; P = 0.0002). Peroxinitrites doubled after the dives (207.2 ± 78.31% of pre-dive values; P = 0.0012). Thiols were significantly reduced (69.88 ± 19.23% of pre-dive values; P = 0.0002). CONCLUSION: NO may be produced by physical effort during breath-hold diving. Physical exercise, the transient hyperoxia followed by hypoxia and CO₂ accumulation would all contribute to the increased levels of superoxide anions (O₂²⁻). Since interaction of O₂²⁻ with NO forms ONOO⁻, this reaction is favoured and the production of thiol groups is reduced. Oxidative stress is, thus, present in breath-hold diving.

OBJECTIVE: The aim of this study is to observe the effects of dark chocolate on endothelial function after a series of successive apnea dives in non-thermoneutral water...

OBJECTIVE:Scuba and breath-hold divers are compared to investigate whether endothelial response changes are similar despite different exposure(s) to hyperoxia. DESIGN:14 divers (nine scuba and five breath-holding) performed either one scuba dive (25m/25 minutes) or successive breath-hold dives at a depth of 20 meters, adding up to 25 minutes of immersion time in a diving pool. Flow-mediated dilation (FMD) was measured using echography. Peripheral post-occlusion reactive hyperemia (PORH) was assessed by digital plethysmography and plasmatic nitric oxide (NO) concentration using a nitrate/nitrite colorimetric assay kit. RESULTS:The FMD decreased in both groups. PORH was reduced in scuba divers but increased in breath-hold divers. No difference in circulating NO was observed for the scuba group. Opposingly, an increase in circulating NO was observed for the breath-hold group. CONCLUSION:Some cardiovascular effects can be explained by interaction between NO and superoxide anion during both types of diving ending to less NO availability and reducing FMD. The increased circulating NO in the breath-hold group can be caused by physical exercise. The opposite effects found between FMD and PORH in the breath-hold group can be assimilated to a greater responsiveness to circulating NO in small arteries than in large arteries.

Erythropoiesis is affected during deep saturation dives. The mechanism should be related to a downregulation of serum Erythropoietin (s-EPO) concentration or to a toxic effect of the hyperbaric hyperoxia. We evaluated s-EPO and other haematological parameters in 6 scuba divers before, during and after a 14-days guinness saturation dive (8-10 m). Athletes were breathing air at 1.8-2 ATA, under the control of a team of physicians. Serum parameters were measured before diving (T0) and: 7 days (T1), 14 days (T2) after the beginning of the dive and 2 h (T3) and 24 h (T4) after resurfacing. Hgb, and many other haematological parameters did not change whereas Ht, s-EPO, the ratio between s-EPO predicted and that observed and reticulocytes (absolute, percent) declined progressively from T0 to T3. At T4 a significant rise in s-EPO was observed. Hgb did not vary but erythropoiesis seemed to be affected as s-EPO and reticulocyte counts showed. All these changes were statistically significant. The experiment, conducted in realistic conditions of dive length, oxygen concentration and pressure, allows us to formulate some hypotheses about the role of prolonged hyperbarism on erythropoiesis. The s-EPO rise, 24 h after resurfacing, is clearly documented and related to the "Normobaric Oxygen Paradox". This evidence suggests interesting hypotheses for new clinical applications such as modulation of s-EPO production and Hgb content triggered by appropriate O₂ administration in pre-surgical patients or in some anemic disease.

Bubbles are known to form in the body after scuba dives, even those done well within the decompression model limits. These can sometimes trigger decompression sickness and the dive protocols should therefore aim to limit bubble formation and growth from hyperbaric decompression. Understanding these processes physiologically has been a challenge for decades and there are a number of questions still unanswered. The physics and historical background of this field of study is presented and the latest studies and current developments reviewed. Heterogeneous nucleation is shown to remain the prime candidate for bubble formation in this context. The two main theories to account for micronuclei stability are then to consider hydrophobicity of surfaces or tissue elasticity, both of which could also explain some physiological observations. Finally the modeling relevance of the bubble formation process is discussed, together with that of bubble growth as well as multiple bubble behavior.