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.

The axillary arch (AA) is a muscular anatomical variation in the fossa axillaris that has been extensively studied in cadaveric specimens. Within these dissections, different innervations of the AA have been proposed, but this has never been explored in vivo. Knowledge of the innervation of the AA is required in order to better understand its function (e.g. predisposition for certain sports and/or activities, understanding shoulder injuries in overhead sports). Here, we report on the use of surface stimulodetection electromyography (SSEMG) to resolve the innervation of the AA in 20 subjects (12 women, eight men - mean age of 21.3 ± 2.7 years) with a uni- or bilateral AA. SSEMG of each muscle [M. latissimus dorsi (MLD) and M. pectoralis major] was performed with a four-channel electrostimulation measuring system in order to determine the innervation of the AA. The results showed co-contraction of the MLD in 85% of the subjects after AA stimulation. In the remaining subjects, no specific localized response was observed due to non-specific nerve stimulation, inherent to the proximity of the brachial plexus in these individuals. Our findings demonstrate that SSEMG exploration offers a practical and reliable tool for investigating anatomical aspects of muscle innervation in vivo. Using this approach, we conclude that the AA receives the same innervation as the MLD (the N. thoracodorsalis), and may be considered a muscular extension of the latter.

We examined whether the improvement of impaired NO-dependent vasorelaxation by exercise training could be mediated through a BH4-dependent mechanism. Male spontaneously hypertensive rats (SHR, n = 20) and Wistar-Kyoto rats (WKY, n = 20) were trained (Tr) for 9 weeks on a treadmill and compared to age-matched sedentary animals (Sed). Endothelium-dependent vasorelaxation (EDV) was assessed with acetylcholine by measuring isometric tension in rings of femoral artery precontracted with 10(-5) M phenylephrine. EDV was impaired in SHR-Sed as compared to WKY-Sed (p = 0.02). Training alone improved EDV in both WKY (p = 0.01) and SHR (p = 0.0001). Moreover, EDV was not different in trained SHR than in trained WKY (p = 0.934). Pretreatment of rings with L-NAME (50 μM) cancelled the difference in ACh-induced relaxation between all groups, suggesting that NO pathway is involved in these differences. The presence of 10(-5) M BH4 in the organ bath significantly improved EDV for sedentary SHR (p = 0.030) but not WKY group (p = 0.815). Exercise training turned the beneficial effect of BH4 on SHR to impairment of ACh-induced vasorelaxation in both SHR-Tr (p = 0.01) and WKY-Tr groups (p = 0.04). These results suggest that beneficial effect of exercise training on endothelial function is due partly to a BH4-dependent mechanism in established hypertension.

BACKGROUND: A novel approach to increasing erythropoietin (EPO) using oxygen (O2) (the 'normobaric oxygen paradox') has been reported in healthy volunteers. We investigated whether the EPO increase is sufficient to induce erythropoiesis by comparing two protocols of O2 administration. METHODS: We compared the effect of daily versus alternate days 100% O2, breathed for 30 minutes, on haemoglobin concentrations during a 12-day period. Nine subjects underwent the two protocols six weeks apart.

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.