Background: Many volatile organic compounds are present in exhaled breath and may represent by-products of endogenous biological processes. Ethanol is produced via alcoholic fermentation of glucose by gut bacteria and yeast, while acetone derives from oxidations of free fatty acids, influenced by glucose metabolism. We hypothesized that the integrated analysis of breath ethanol and acetone would provide a good approximation of the blood glucose profile during a glucose load.Methods: We collected simultaneous exhaled breath gas, ambient air, and serum glucose and insulin samples from 10 healthy volunteers at baseline and during an oral glucose tolerance test (OGTT) (ingestion of 75 g of glucose followed by 120 min of sampling). Gas samples were analyzed by gas chromatography/mass spectrometry.Results: Mean glucose values displayed a typical OGTT pattern (rapid increase, peak values at 30-60 min, and gradual return to near baseline by 120 min). Breath ethanol displayed a similar pattern early in the test, with peak values at 30 min; this was followed by a fast return to basal levels by 60 min. Breath acetone decreased progressively below basal levels, with lowest readings obtained at 120 min. A multiple regression analysis of glucose, ethanol, and acetone was used to estimate glucose profiles that correlated with measured glucose values with an average individual correlation coefficient of 0.70, and not lower than 0.41 in any subject.Conclusion: The integrated analysis of multiple exhaled gases may serve as a marker of blood glucose levels. Further studies are needed to assess the usefulness of this method in different populations.

Children do not typically appear to move with the same skill and dexterity as adults, although they can still improve their motor performance in specific tasks with practice. One possible explanation is that their motor performance is limited by an inherently higher level of movement variability, but that their motor adaptive ability is robust to this variability. To test this hypothesis, we examined motor adaptation of 43 children (ages 6-17) and 12 adults as they reached while holding the tip of a lightweight robot. The robot applied either a predictable, velocity-dependent field (the "mean field") or a similar field that incorporated stochastic variation (the "noise field"), thereby further enhancing the variability of the subjects' movements. We found that children exhibited greater initial trial-to-trial variability in their unperturbed movements but were still able to adapt comparably to adults in both the mean and noise fields. Furthermore, the youngest children (ages 6-8) were able to reduce their variability with practice to levels comparable to the remaining children groups although not as low as adults. These results indicate that children as young as age 6 possess adult-like neural systems for motor adaptation and internal model formation that allow them to adapt to novel dynamic environments as well as adults on average despite increased neuromotor or environmental noise. Performance after adaptation is still more variable than adults, however, indicating that movement inconsistency, not motor adaptation inability, ultimately limits motor performance by children and may thus account for their appearance of incoordination and more frequent motor accidents (e.g., spilling, tripping). The results of this study also suggest that movement variability in young children may arise from two sources--a relatively constant, intrinsic source related to fundamental physiological constraints of the developing motor system and a more rapidly modifiable source that is modulated depending on the current motor context.

Circulating IGF-I is correlated with fitness, but results of prospective exercise training studies have been inconsistent, showing both increases and decreases in IGF-I. We hypothesized that energy balance, often not accounted for, is a regulating variable such that training plus an energy intake deficit would cause a reduction in IGF-I, whereas training plus energy intake excess would lead to an increased IGF-I. To test this, 19 young, healthy men completed a 7-day strenuous exercise program in which they were randomly assigned to either a positive energy balance [overfed (OF), n = 10] or negative energy balance [underfed (UF), n = 9] group. IGF-I (free and total), insulin, and IGF-binding protein-1 were measured before, during, and 1 wk after the training. Weight decreased in the UF subjects and increased in the OF subjects. Free and total IGF-I decreased substantially in the UF group (P < 0.0005 for both), but, in the OF group, IGF-I remained unchanged. The UF group also demonstrated an increase in IGF-binding protein-1 (P < 0.027), whereas glucose levels decreased (P < 0.0005). In contrast, insulin was reduced in both the OF and UF exercise-training groups (P < 0.044). Finally, within 7 days of the cessation of the diet and training regimen, IGF-I and IGF-binding protein-1 in the UF group returned to preintervention levels. We conclude that energy balance during periods of exercise training influences circulating IGF-I and related growth mediators. Exercise-associated mechanisms may inhibit increases in IGF-I early in the course of a training protocol, even in overfed subjects.

These data demonstrate that an intense "real-life" exercise bout in adolescent females leads to profound increases in inflammatory cytokines and reductions in anabolic mediators with substantial alterations in white blood cell subpopulations and adhesion molecules. The role of these frequent, almost daily immune and cytokine changes on growth and development have yet to be determined.

Exhaled nitric oxide (NO) remains a promising noninvasive index for monitoring inflammatory lung diseases; however, the plateau concentration (C NO,plat ) is nonspecific and requires a constant exhalation flow rate. We utilized a new technique that employs a variable flow rate to estimate key flow-independent parameters characteristic of NO exchange in a group (n ϭ 9) of 10 to 14 yr-old healthy children and children with cystic fibrosis (CF): maximum flux of NO from the airways (J NO,max , pl s