Post-prandial systemic 8-isoprostane increases after consumption of moderate and high-fat meals in insufficiently active males

A single high-fat meal (HFM) leads to an increase in triglycerides and oxidative stress. Oxidative stress can be assessed via 8-isoprostane generation, which is associated with the development of asthma and cardiovascular disease. No previous research has investigated whether airway and systemic 8-isoprostane increases postprandially in nonasthmatic participants according to the energy and fat content of a meal. Our purpose was to assess airway and systemic 8-isoprostane after a HFM and a true-to-life moderate-fat meal (MFM). We hypothesized that airway and systemic 8-isoprostane would increase after a HFM and a MFM, with the greatest increase in the HFM condition. Eight nonasthmatic men (25.8 ± 6.9 years) completed the HFM and MFM trials in a randomized crossover design. After a 10-hour fast, participants consumed either a HFM (71.13 kJ/kg body mass, 60% fat, 23% CHO) or a MFM (35.56 kJ/kg body mass, 30% fat, 52% CHO). Exhaled breath condensate to assess airway 8-isoprostane was collected at baseline and at 3 and 6 hours postmeal. Venous blood samples were collected at baseline and hourly until 6 hours postmeal to assess triglycerides, and every 3 hours for systemic 8-isoprostane. Airway 8-isoprostane responses were not significant as a main effect of time (P = .072), between conditions (P = .365), or between time and condition (P = .319) postmeal. Systemic 8-isoprostane increased over time (P < .001), but not between conditions (P = .124) or between time and condition (P = .649) postmeal. Triglyceride incremental area under the curve was different in the HFM compared to the MFM condition (P = .013). After a HFM and a MFM, 8-isoprostane increases systemically; however, airway 8-isoprostane does not change.