Plasma Apelin Unchanged With Acute Exercise Insulin Sensitization.

Blood glucose and insulin responses to aerobic exercise are well defined yet the mechanisms effecting post-exercise insulin sensitization remain incomplete. Apelin has been reported to enhance glucose uptake and insulin sensitivity in vivo, but its role as a regulator of insulin sensitivity following acute aerobic exercise has not been investigated. Therefore, the purpose of this study was to investigate apelin's response to acute bouts of maximal and submaximal aerobic exercise and to elucidate apelin's influence on insulin sensitivity. Twelve (22.8 ± 2.9 yrs) healthy male (n = 7) and female (n = 5) subjects completed a graded to maximal (VO2max) and submaximal (70-75% VO2max) treadmill running bouts, as well as a 50g glucose challenge (GC). Blood was obtained at four time points (pre, post, 1hr post and 24hrs post) and assessed for glucose, insulin and apelin. Hepatic insulin sensitivity was assessed at rest and at 1hr and 24hrs via HOMA-IR and QUICKI indices. Results demonstrated that plasma apelin did not significantly change by condition (p = 0.324) or time (p = 0.633). Blood glucose and plasma insulin were significantly elevated immediately after VO2max and GC, but remained stable after submaximal exercise. Insulin sensitivity was significantly improved 1hr post-submaximal exercise, per HOMA-IR (p = 0.034) and QUICKI (p = 0.018) indices. Plasma apelin was significantly correlated with plasma insulin (r = 0.699, p = 0.011), HOMA-IR (r = 0.626, p = 0.029) and QUICKI (r = 0.660, p = 0.019) at rest. We conclude that, although hepatic insulin sensitivity was improved 1hr post-submaximal exercise, this exercise-induced insulin sensitization occurred independent of plasma apelin changes.

Effects of stimulation technique, anatomical region, and time on human sweat lipid mediator profiles.

Few studies compare sampling protocol effect on sweat composition. Here we evaluate the impact of sweat stimulation mode and site of collection on lipid mediator composition. Sweat from healthy males (n=7) was collected weekly for three weeks from the volar forearm following either pilocarpine iontophoresis or exercise, and from the forearm, back and thigh following pilocarpine iontophoresis only. Sweat content of over 150 lipid mediators were measured by liquid chromatography-tandem mass spectrometry. Seventy lipid mediators were routinely detected, including prostanoids, alcohols, diols, epoxides, ketones, nitrolipids, N-acylethanolamides, monoacylglycerols, and ceramides. Detected lipid mediators appeared unaffected by sampling site, though the forearm was the most consistent source of sweat. Pilocarpine-induced sweat showed increased concentrations of most detected compounds. Moreover, lipid mediator concentrations and profiles were temporally stable over the study duration. Sweat therefore appears to be a consistent and anatomically-stable source of lipid mediators, but care must be taken in comparing results obtained from different stimulation techniques.