To investigate whether the intensity and duration of a sustained contraction influences reflex regulation, we compared sustained fatiguing contractions at 25 % and 50 % of maximal voluntary contraction (MVC) force in the human abductor pollicis brevis (APB) muscle. Because the activation of motoneurones during fatigue may be reflexively controlled by the metabolic status of the muscle, we also compared reflex activities during sustained and intermittent (6 s contraction, 4 s rest) contractions at 25 % MVC for an identical duration. The short‐latency Hoffmann(H) reflex and the long‐latency reflex (LLR) were recorded during voluntary contractions, before, during and after the fatigue tests, with each response normalised to the compound muscle action potential (M‐wave). The results showed that fatigue during sustained contractions was inversely related to the intensity, and hence the duration, of the effort. The MVC force and associated surface electromyogram (EMG) declined by 26.2 % and 35.2 %, respectively, after the sustained contraction at 50 % MVC, and by 34.2 % and 44.2 % after the sustained contraction at 25 % MVC. Although the average EMG increased progressively with time during the two sustained fatiguing contractions, the amplitudes of the H and LLR reflexes decreased significantly. Combined with previous data (Duchateau & Hainaut, 1993), the results show that the effect on the H reflex is independent of the intensity of the sustained contraction, whereas the decline in the LLR is closely related to the duration of the contraction. Because there were no changes in the intermittent test at 25 % MVC, the results indicate that the net excitatory spinal and supraspinal reflex‐mediated input to the motoneurone pool is reduced. This decline in excitation to the motoneurones, however, can be temporarily compensated by an enhancement of the central drive.

Patency of the foramen ovale (PFO) may be a cause of unexplained decompression sickness (DCS) in sports divers. To assess the relationship between PFO and DCS, a case-control study was undertaken in a population of Belgian sports divers. Thirty-seven divers who suffered from neurological DCS were compared with matched control divers who never had DCS. All divers were investigated with transesophageal contrast echocardiography for the presence of PFO. PFO size was semiquantified on the basis of the amount of contrast passage. Divers with DCS with lesions localized in the high cervical spinal cord, cerebellum, inner ear organs, or cerebrum had a significantly higher prevalence of PFO than divers with DCS localizations in the lower spinal cord. For unexplained DCS (DCS without commission of any diving procedural errors), this difference was significant for large PFOs only. We conclude that PFO plays a significant role in the occurrence of unexplained cerebral DCS, but not of spinal DCS. We further stress the importance of standardization and semiquantification of future PFO studies that use transesophageal contrast echocardiography.

Renal (peritubular) tissue hypoxia is a well-known physiological trigger for erythropoietin (EPO) production. We investigated the effect of rebound relative hypoxia after hyperoxia obtained under normo- and hyperbaric oxygen breathing conditions. A group of 16 healthy volunteers were investigated before and after a period of breathing 100% normobaric oxygen for 2 h and a period of breathing 100% oxygen at 2.5 ATA for 90 min (hyperbaric oxygen). Serum EPO concentration was measured using a radioimmunoassay at various time points during 24–36 h. A 60% increase ( P < 0.001) in serum EPO was observed 36 h after normobaric oxygen. In contrast, a 53% decrease in serum EPO was observed at 24 h after hyperbaric oxygen. Those changes were not related to the circadian rhythm of serum EPO of the subjects. These results indicate that a sudden and sustained decrease in tissue oxygen tension, even above hypoxia thresholds (e.g., after a period of normobaric oxygen breathing), may act as a trigger for EPO serum level. This EPO trigger, the “normobaric oxygen paradox,” does not appear to be present after hyperbaric oxygen breathing.

Decompression sickness (DCS) is a systemic disorder, assumed due to gas bubbles, but additional factors are likely to play a role. Circulating microparticles (MPs)—vesicular structures with diameters of 0.1-1.0 μm—have been implicated, but data in human divers have been lacking. We hypothesized that the number of blood-borne, Annexin V-positive MPs and neutrophil activation, assessed as surface MPO staining, would differ between self-contained underwater breathing-apparatus divers suffering from DCS vs. asymptomatic divers. Blood was analyzed from 280 divers who had been exposed to maximum depths from 7 to 105 meters; 185 were control/asymptomatic divers, and 90 were diagnosed with DCS. Elevations of MPs and neutrophil activation occurred in all divers but normalized within 24 h in those who were asymptomatic. MPs, bearing the following proteins: CD66b, CD41, CD31, CD142, CD235, and von Willebrand factor, were between 2.4- and 11.7-fold higher in blood from divers with DCS vs. asymptomatic divers, matched for time of sample acquisition, maximum diving depth, and breathing gas. Multiple logistic regression analysis documented significant associations (P < 0.001) between DCS and MPs and for neutrophil MPO staining. Effect estimates were not altered by gender, body mass index, use of nonsteroidal anti-inflammatory agents, or emergency oxygen treatment and were modestly influenced by divers' age, choice of breathing gas during diving, maximum diving depth, and whether repetitive diving had been performed. There were no significant associations between DCS and number of MPs without surface proteins listed above. We conclude that MP production and neutrophil activation exhibit strong associations with DCS.

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.

The current practice of mechanical ventilation comprises the use of the least inspiratory O₂ fraction associated with an arterial O₂ tension of 55 to 80 mm Hg or an arterial hemoglobin O₂ saturation of 88% to 95%. Early goal-directed therapy for septic shock, however, attempts to balance O₂ delivery and demand by optimizing cardiac function and hemoglobin concentration, without making use of hyperoxia. Clearly, it has been well-established for more than a century that long-term exposure to pure O₂ results in pulmonary and, under hyperbaric conditions, central nervous O₂ toxicity. Nevertheless, several arguments support the use of ventilation with 100% O₂ as a supportive measure during the first 12 to 24 hrs of septic shock. In contrast to patients without lung disease undergoing anesthesia, ventilation with 100% O₂ does not worsen intrapulmonary shunt under conditions of hyperinflammation, particularly when low tidal volume–high positive end-expiratory pressure ventilation is used. In healthy volunteers and experimental animals, exposure to hyperoxia may cause pulmonary inflammation, enhanced oxidative stress, and tissue apoptosis. This, however, requires long-term exposure or injurious tidal volumes. In contrast, within the timeframe of a perioperative administration, direct O₂ toxicity only plays a negligible role. Pure O₂ ventilation induces peripheral vasoconstriction and thus may counteract shock-induced hypotension and reduce vasopressor requirements. Furthermore, in experimental animals, a redistribution of cardiac output toward the kidney and the hepato-splanchnic organs was observed. Hyperoxia not only reverses the anesthesia-related impairment of the host defense but also is an antibiotic. In fact, perioperative hyperoxia significantly reduced wound infections, and this effect was directly related to the tissue O₂ tension. Therefore, we advocate mechanical ventilation with 100% O₂ during the first 12 to 24 hrs of septic shock. However, controlled clinical trials are mandatory to test the safety and efficacy of this approach.