It has been proposed that relative changes of oxygen availability, rather than steady-state hypoxic or hyperoxic conditions, play an important role in hypoxia-inducible factor (HIF) transcriptional effects. According to this hypothesis describing the "normobaric oxygen paradox", normoxia following a hyperoxic event is sensed by tissues as an oxygen shortage, upregulating HIF-1 activity. With the aim of confirming, at cellular and at functional level, that normoxia following a hyperoxic event is "interpreted" as a hypoxic event, we report a combination of experiments addressing the effects of an intermittent increase of oxygen concentration on HIF-1 levels and the activity level of specific oxygen-modulated proteins in cultured human umbilical vein endothelial cells and the effects of hemoglobin levels after intermittent breathing of normobaric high (100%) and low (15%) oxygen in vivo in humans. Our experiments confirm that, during recovery after hyperoxia, an increase of HIF expression occurs in human umbilical vein endothelial cells, associated with an increase of matrix metalloproteinases activity. These data suggest that endothelial cells "interpret" the return to normoxia after hyperoxia as a hypoxic stimulus. At functional level, our data show that breathing both 15 and 100% oxygen 30 min every other day for a period of 10 days induces an increase of hemoglobin levels in humans. This effect was enhanced after the cessation of the oxygen breathing. These results indicate that a sudden decrease in tissue oxygen tension after hyperoxia may act as a trigger for erythropoietin synthesis, thus corroborating the hypothesis that "relative" hypoxia is a potent stimulator of HIF-mediated gene expressions.

Decompression sickness (DCS) in divers is caused by bubbles of inert gas. When DCS occurs, most bubbles can be found in the venous circulation: venous gas emboli (VGE). Bubbles are thought to be stabilized by low molecular weight surfactant reducing the plasma-air surface tension (γ)...

INTRODUCTION: The main limiting factors determining apnea time are generally considered to be related to blood and cerebrospinal fluid chemistry. Several physiological (adaptive) mechanisms and some psychologic parameters, such as motivation, are also known to increase apnea time. AIM:We wished to study the link between peripheral muscle fatigue, the concomitant alteration of long latency (transcortical) reflexes and respiratory control. METHODS: Fatigue was induced in a small hand muscle (abductor pollicis brevis) (n = 11). This muscle is sufficiently small that its fatigue and the resulting production of metabolites are unlikely to alter whole-blood biochemistry. The Hoffmann reflex, an involuntary reaction to electrical stimulation of muscle afferent sensory fibreswas studied, as was the long latency reflex (LLR) using the Dueschl method in which electrical stimulation is superimposed on a slight voluntary contraction, Different fatiguing protocols were performed, and respiratory rate continuously recorded.

Nutritional antioxidants have been proposed as an expedient strategy to counter the potentially deleterious effects of scuba diving on endothelial function, flow-mediated dilation (FMD) and heart function. Sixteen volunteers performing a single standard dive (20 min at 33 m) according to US Navy diving procedures were randomly assigned to two groups: one was administered with two doses of 200 mg of an anthocyanins (AC)-rich extract from red oranges, 12 and 4 h before diving. Anthocyanins supplementation significantly modulated the effects of diving on haematocrit, body water distribution and FMD.

BACKGROUND: The risk of developing decompression illness (DCI) in divers with a patent foramen ovale (PFO) has not been directly determined so far; neither has it been assessed in relation to the PFO's size. METHODS :In 230 scuba divers (age 39+/-8 years), contrast trans-oesophageal echocardiography (TEE) was performed for the detection and size grading (0-3) of PFO. Prior to TEE, the study individuals answered a detailed questionnaire about their health status and about their diving habits and accidents. For inclusion into the study, > or =200 dives and strict adherence to decompression tables were required. RESULTS: Sixty-three divers (27%) had a PFO. Overall, the absolute risk of suffering a DCI event was 2.5 per 10(4) dives. There were 18 divers (29%) with, and 10 divers (6%) without, PFO who had experienced > or =1 major DCI events P=0.016. In the group with PFO, the incidence per 10(4) dives of a major DCI, a DCI lasting longer than 24 h and of being treated in a decompression chamber amounted to 5.1 (median 0, interquartile range [IQR] 0-10.0), 1.9 (median 0, IQR 0-4.0) and 3.6 (median 0, IQR 0-9.8), respectively and was 4.8-12.9-fold higher than in the group without PFO (P<0.001). The risk of suffering a major DCI, of a DCI lasting longer than 24 h and of being treated by recompression increased with rising PFO size. CONCLUSION: The presence of a PFO is related to a low absolute risk of suffering five major DCI events per 10(4) dives, the odds of which is five times as high as in divers without PFO. The risk of suffering a major DCI parallels PFO size.