Impairment of muscle energy metabolism has been demonstrated in normal subjects with chronic hypoxaemia (altitude chronic respiratory failure). The purpose of this study was to verify the hypothesis that a comparable condition could develop in patients with sleep apnoea syndrome (SAS), considering that they are exposed to prolonged and repeated hypoxaemia periods. Muscle metabolism was assessed in 11 patients with SAS performing a maximal effort on cycloergometer. In comparison with normal subjects, SAS patients reached lower maximal loads [144 +/- 7 vs. 182 +/- 10 W (P < 0.005)] and lower peak oxygen uptakes [26.4 +/- 1.2 vs 33.2 +/- 1.4 ml kg-1 min-1 (P < 0.005)]. Abnormal metabolic features were found: maximal blood lactate concentration was significantly lower than in normal subjects [0.034 +/- 0.004 vs. 0.044 +/- 0.002 mmol l-1 W-1 (P < 0.05)]; and lactate elimination rate, calculated during a 30-min recovery period, was reduced [0.127 +/- 0.017 vs, 0.175 +/- 0.014 mmol l-1 min-1 (P < 0.025)]. The extent of these anomalies correlated with the severity of SAS. The patients also showed higher maximal diastolic blood pressures than normal subjects [104 +/- 5 vs. 92 +/- 4 mmHg (P < 0.05)]. These results can be interpreted as indications of an impairment of muscle energy metabolism in patients with SAS. Decrease in maximum blood lactate concentration suggests an impairment of glycolytic metabolism, while decrease in the rate of lactate elimination indicates a defect in oxidative metabolism. Since no respiratory pathology apart from SAS was found in this group of patients, it seems legitimate to link the genesis of these impairments to repeated bouts of nocturnal hypoxaemia.

Decompression sickness in diving is recognized as a multifactorial phenomenon, depending on several factors, such as decompression rate and individual susceptibility. The Doppler ultrasonic detection of circulating venous bubbles after diving is considered a useful index for the safety of decompression because of the relationship between bubbles and decompression sickness risk. The aim of this study was to assess the effects of ascent rate, age, maximal oxygen uptake (VO(2 max)), and percent body fat on the production of bubbles after diving. Fifty male recreational divers performed two dives at 35 m during 25 min and then ascended in one case at 9 m/min and in the other case at 17 m/min. They performed the same decompression stops in the two cases. Twenty-eight divers were Doppler monitored at 10-min intervals, until 60 min after surfacing, and the data were analyzed by Wilcoxon signed-rank test to compare the effect of ascent rate on the kinetics of bubbles. Twenty-two divers were monitored 60 min after surfacing. The effect on bubble production 60 min after surfacing of the four variables was studied in 47 divers. The data were analyzed by multinomial log-linear model. The analysis showed that the 17 m/min ascent produced more elevated grades of bubbles than the 9 m/min ascent (P < 0.05), except at the 40-min interval, and showed relationships between grades of bubbles and ascent rate and age and interaction terms between VO(2 max) and age, as well as VO(2 max) and percent body fat. Younger, slimmer, or aerobically fitter divers produced fewer bubbles compared with older, fatter, or poorly physically fit divers. These findings and the conclusions of previous studies performed on animals and humans led us to support that ascent rate, age, aerobic fitness, and adiposity are factors of susceptibility for bubble formation after diving.

Decompression sickness (DCS) is recognized as a multifactorial phenomenon depending on several individual factors, such as age, adiposity, and level of fitness. The detection of circulating venous bubbles is considered as a useful index for the safety of a decompression, because of the relationship between bubbles and DCS probability. The aim of this work was to study the effects of individual variables which can be assessed non invasively, on the grades of bubbles detected 60 min, after diving by means of Doppler monitoring, in a sample of 40 male recreational scuba divers. The variables investigated were: age, weight, maximal oxygen uptake (VO2max) and percentage of body fat (%BF). Bubble signals were graded according to the code of Spencer. The relationships between the bubble grades (BG) and the variables investigated were studied using two methods: the differences between the average values of each variable at each BG were analyzed by the Scheffe test. Then we performed the non-parametric Spearman correlation analysis. Significant differences (P < 0.05) were found (Scheffe test) between average values of the variables at grade 0 and 3 (age: P = 0.0323; weight: P = 0.0420; VO2max: P = 0.0484), except for %BF (P = 0.1697). Relationships with P < 0.01 were found (Spearman correlation) between BG and the variables: age: p = 0.486, P = 0.0024; weight: p = 0.463, P = 0.0039; VO2max: p = -0.481, P = 0.0027; except for %BF: p = 0.362, P = 0.0237. This work showed that bubble production after hyperbaric exposures depends on several individual factors. The effects of age, weight and VO2max are more significant than the effect of %BF. We concluded that to take into account such variables in decompression tables and diving computer programs should allow to adapt the decompression procedures to individual risk factors and reduce the DCS probability.

We studied the action of urea on the spin-spin relaxation rate of 2,3-diphosphoglycerate (2,3-DPG) phosphorus atoms in normal and uremic erythrocytes. At concentrations from 10 to 60 mM, urea increased the relaxation rates of 2,3-DPG P-3 phosphorus atoms. This evidenced a stronger binding of 2,3-DPG to hemoglobin (Hb), suggesting that the deoxyform of Hb was stabilized. This hypothesis was confirmed by measurements of the association constant of oxygen to hemoglobin (K) in normal erythrocytes in presence of urea concentrations in the range of those observed in uremic patients (30 mM). Indeed, the observed decrease in K suggests that the T structure of hemoglobin is stabilized. By contrast, with higher urea concentrations (120 mM), measurements of P50 showed an increase in the hemoglobin affinity for oxygen (decrease in P50). Moreover, the relaxation rates of 2,3-DPG P-3 phosphorus atoms were not modified, which is consistent with the simultaneous increase of K. This may be attributed to the formation of carbamylated hemoglobin in presence of urea. These results suggest two opposite effects of urea on Hb-O2 affinity: the first reinforces 2,3-DPG-Hb binding and leads to a decrease in O2 affinity; the second, mediated by carbamylation of Hb, hinders the binding of 2,3-DPG and increases the O2 affinity. These findings are consistent with the fact that, despite the presence of carbamylated hemoglobin, uremic patients do not present increased Hb-O2 affinity.

This study, intended to evaluate the role of ammonia (NH3) as a ventilatory stimulus, was conducted in three groups of subjects: 14 sedentary individuals, 12 triathletes, 5 patients with a glycolytic deficiency (Mc Ardle disease). All subjects performed maximal exercise tests on a cycle ergometer. Ventilation measured at maximal oxygen consumption (VE 100%) was correlated with lactatemia (lactate 100%) and ammonemia (NH3 100%) in the sedentary group, but only with ammonemia in triathletes, although NH3 100% and lactate 100% were correlated in both groups, which suggests that correlation between VE 100% and NH3 100% is not a false correlation. In patients with Mc Ardle disease, unable to produce lactate during exercise, VE 100% was correlated with NH3 100%. NH3 may act indirectly by increasing the production of lactate in cereberal tissue. Another hypothesis rests on the fact that the catabolism of ammonia leads to an increase in intracerebral glutamate which may act as a ventilatory stimulus.