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The turnover of circulating triglycerides (TG) was determined in dogs during rest, following ingestion of food that included corn oil, and in the final period of a 1-h treadmill exercise of moderate intensity (72-84 m/min). In all cases the loss of [14C]TG from the plasma followed a first-order process. The fractional removal rate constant at rest was 26.5 +/- 1.9% (SE) n = 10) of the circulating pool size per minute, and it was increased slightly to 33.8 +/- 3.6% (n = 7) per minute during exercise. The uptake of plasma TG-derived fatty acids (5 min postinjection) was increased (P less than 0.05) in working muscle, whereas the TG uptake in fat tended to decrease. Further, the percent of TG-derived fatty acids found in the muscle's acylglyceride pool was less (90.0 +/- 3.6 vs. 53.5 +/- 1.8%), while that in the muscle's free fatty acid pool was greater (12.3 +/- 36.1 +/- 4.7%) in working compared with resting muscle. Thus the fourfold greater quantity of plasma TG-derived fatty acids found in the working muscle's free fatty acid pool could account for the entire increased TG uptake caused by exercise. This suggests that, in the fed state, circulating TG could represent a potential source of fatty acids for beta-oxidation in working muscle. However, the importance of plasma TG-derived fatty acids as an energy substrate during muscle use in a postprandial state has yet to be determined quantitatively.

Despite recommendations in most countries for giving inactivated influenza vaccine to people with asthma, only a minority currently receive it. One reason for low vaccine coverage has been concern that vaccination may induce exacerbations of asthma. In this randomized trial, 291 patients between 18 and 65 years of age received either an inactivated influenza vaccine followed 14 days later by a saline placebo or placebo followed by the vaccine. Each patient received 1 dose of vaccine and 1 dose of placebo. The percentage of patients reporting at least one asthma exacerbation within 14 days after injection was similar following vaccine or placebo (28.3% and 25.5%, respectively). The combined exacerbation rate during the first 14-day interval was higher (31.5%) than that during the second 14-day interval (22.4%, P = 0.0135), indicating that the occurrence of exacerbations was not likely to be related to the sequence of injections. The percentages of individuals with solicited systemic symptoms were 56.6% and 44.8% after vaccine or placebo injection, respectively. We conclude that influenza vaccination did not increase the incidence of asthma exacerbations compared to placebo in this study and the vaccine was well tolerated. The results thus support annual influenza vaccination in patients with asthma.

It seems likely that depletion of body carbohydrates may account for the rise in the sympathetic activity during prolonged exercise, since glucose given during or before exercise reduces the increase in plasma catecholamines. The aim of the present study was to find out whether the increase in plasma noradrenaline (NA) in response to exercise can be reduced by 1. increasing of the amount of carbohydrate available for metabolism without producing hyperinsulinemia and 2. by inhibition of afferent activity from hepatic glucoreceptors. The study was performed on dogs which exercised whilst receiving either the intravenous fructose infusion (2.2 mmol/min) or a slow glucose infusion (0.25 mmol/min) which was given either via the portal or a peripheral vein. Fructose infusion reduced the muscle glycogen depletion during exercise and reduced the increase in plasma NA and glycerol concentrations without altering the blood glucose or insulin levels. The exercise-induced increases in plasma NA and glycerol concentrations were significantly smaller with intraportal than with peripheral glucose infusion but there were no differences between these two cases in the concentration of glucose in the systemic circulation. These findings indicate that the reduction of the plasma NA response to physical effort under conditions of increased carbohydrate availability cannot be attributed to the inhibitory effect of insulin on sympathetic activity and provide evidence for the participation of hepatic glucoreceptors in the control of the sympathetic activity during exercise.