Eight different asymptotic models, of which some are entirely new while others are revised versions, are compared with respect to their goodness of fit for the description of the longitudinal growth of stature in 27 healthy children from the French Auxological Survey. Some growth models are based on total age, defined as measured from the time of fertilization, and may be particularly suitable if prenatal data are to be included in the analysis or if prenatal extrapolations are desired. Other models are based on postnatal age (age after birth), and some of these are the most accurate, but they would not be suitable for prenatal data or extrapolations. More general models, such as the polynomial logistic or the triple logistic, can be used but are not the most accurate among those included in the present study. Two new models are proposed which possess an improved goodness of fit. © 1992 Wiley-Liss, Inc.

A new seven-parameter asymptotic growth curve has been applied to longitudinal data on the height of 13 boys and 14 girls from 1 month to 19 years of age. The residual sums of squares with this new curve were 7.5 times lower on the average than with the currently-used five-parameter curve No. 1 of Preece and Baines (1978, Annals of Human Biology 5, 1-24) and 2.4 times lower than with the recent six-parameter curve of Shohoji and Sasaki (1987, Growth 51, 432-450). The new curve is expressed with respect to total age, passes through the origin, and fits infants as satisfactorily as older children.

There appears to be a reduction in endothelium-dependent and endothelium-independent, macro- and microvascular function associated with diving. Our results suggest that in the process of vascular dysfunction during diving, functional changes in the vessel wall may not be limited to the endothelium and may be mediated by alterations in vascular smooth muscle.

Pre-dive oral hydration decreases circulatory bubbles, thus offering a relatively easy means of reducing decompression sickness risk. The prehydration condition allowed attenuation of dehydration and prevention of hypovolaemia induced by the diving session. Hydration and diving did not change plasma surface tension in this study.

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G ERMONPRE P, PONTIER J-M, GEMPP E, BLATTEAU J-E, DENEWETH S, LAFÉRE P, MARRONIIntroduction: The preconditioning of divers to reduce post-dive decompression sickness (DCS) has gained increased interest in diving medical research over the last few years. The benefi cial effects of physical exercise, oxygen breathing, hyperbaric exposure, heat exposure, hyperhydration, or nitroglycerin administration before the dive are only a few examples of ongoing research. In this work, we investigated the effects of pre-dive whole-body vibration on post-dive bubble formation. Methods: Following French Navy standard dive procedures, 14 healthy male military divers performed 2 identical dives 1 wk apart to 30 m of seawater (msw) for 30 min. One of the dives was randomly preceded by a 30-min whole-body vibration session (frequencies 35-40 Hz) 1 h before the dive. Post-dive bubbles were measured precordially 30, 60, and 90 min after the dive and were graded according to the Kissman Integrated Severity Score (KISS) protocol, with and without knee fl exing. Arterial endothelial function was measured before and after vibration using fl ow mediated dilation (FMD) measurement. Results: A signifi cant reduction in bubble scores was observed after the " vibration " dive. Conclusion: As there was no observed change in FMD after vibration, we do not believe a nitric oxide mediated mechanism is involved; rather, a mechanical dislodgement or enhanced lymphatic elimination of gas nuclei is hypothesized.

Previous studies have highlighted that bubble-induced platelet aggregation is a predictor index of decompression sickness (DCS) severity in animals and bubble formation after a single air dive in humans. The present study attempted to investigate plasmatic indexes of the coagulation system and platelet activation in our rat model of DCS. Male Sprague-Dawley rats were assigned to one experimental group with a hyperbaric exposure and one control group maintained at atmospheric pressure. Rats were compressed to 1,000 kPa (90 m saltwater) for 45 min while breathing air. The onset of death time and DCS symptoms were recorded during a 30-min observed period after rats had surfaced. Plasmatic indexes were platelet factor 4 (PF4) for platelet activation, soluble glycoprotein V (sGPV) for thrombin generation, and thrombin-antithrombin complexes for the coagulation system. Blood samples for a platelet count and markers were taken 3 wk before the experimental protocol and within the 30 min after rats had surfaced. We confirmed a correlation between the percent fall in platelet count and DCS severity. Plasmatic levels of sGPV and PF4 were significantly increased after the hyperbaric exposure, with no change in the control group. The present study confirms platelet consumption as a potential index for evaluating decompression stress and DCS severity. The results point to the participation of thrombin generation in the coagulation cascade and platelet activation in bubble-induced platelet aggregation. In our animal model of DCS, the results cannot prejudge the mechanisms of platelet activation between bubble-induced vessel wall injury and bubble-blood component interactions.

Objectives: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. Participants and methods: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. Results: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. Conclusion: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.