Deep inspirations attenuate postprandial airway inflammation in college-aged adults with elevated baseline exhaled nitric oxide: A pilot study.

Airway inflammation (assessed by exhaled nitric oxide (eNO)) increases after a single high-fat meal (HFM), yet this response may be modified by airway stretch and baseline eNO level.Purpose: The purpose of this study was to investigate whether deep inspirations (DIs) would attenuate airway inflammation post-HFM and whether this is modulated by baseline eNO level.Methods: A total of sixteen healthy college-aged participants completed a randomized cross-over study with 8 lower eNO (14.8 ± 2.0 ppb: 3 M/5F; age: 22.0 ± 2.2 yrs) and 8 higher eNO (29.3 ± 11.6 ppb 5 M/3F; age: 22.5 ± 2.6 yrs) participants. All participants completed a control (CON) condition (no DIs pre-HFM) and DI condition (60 DI's to total lung capacity immediately pre-HFM) after an overnight fast. The primary outcome was eNO. Participants had 20 minutes to consume the HFM (1 g fat/1 kg body weight) and eNO was performed at 2- and 4- hours post-HFM. To determine whether baseline eNO levels impacted the effect of DI's, a median split was performed on their baseline eNO level.Results: There was a significant increase in eNO as a main effect of time (p < 0.001). However when analyzing the potential effect of baseline eNO, there was no significant increase in eNO post-HFM in the higher eNO group in the DI condition (p = 0.54). DIs modified the eNO response to a HFM in the group with a higher baseline eNO value.Conclusions: These data display a possible bronchoprotective protect of DIs against postprandial airway inflammation in participants with higher initial eNO level.

Genetic Polymorphisms in ADORA2A and CYP1A2 Influence Caffeine's Effect on Postprandial Glycaemia.

The liver enzyme cytochrome P450 1A2 (CYP1A2) is responsible for 90% of caffeine metabolism, while caffeine exerts many of its effects via antagonist binding to adenosine A2a receptors (ADORA2A). This study aimed to examine whether functional single nucleotide polymorphisms (SNPs) in 1976T > C (ADORA2A; rs5751876) and -163C > A (CYP1A2; rs762551) influence the effect of caffeine on the postprandial glucose (GLU) response to a carbohydrate meal. We report that individuals with the 1976T > C CC, but not CT/TT genotypes display elevated GLU levels after consuming caffeine and carbohydrate (CHO + CAFF) versus carbohydrate only (CHO). The GLU area under the curve (AUC) was also greater during the CHO + CAFF condition compared to the CHO condition in CC, but not the CT/TT genotypes. The -163C > A AC/CC, but not AA, genotypes displayed greater GLU concentrations 60-min post meal during CHO + CAFF versus CHO. Our data suggest that caffeine-induced impairments in postprandial glycaemia are related to 1976T > C and -163C > A SNPs.

Postprandial Metabolic Responses Differ by Age Group and Physical Activity Level.

OBJECTIVES: To compare the postprandial metabolic responses to a high-fat meal in healthy adults who differ by age and physical activity level. DESIGN: Cross-sectional, quasi-experimental design. SETTING: Physical Activity and Nutrition Clinical Research Consortium (PAN-CRC) at Kansas State University (Manhattan, KS, USA). PARTICIPANTS: Twenty-two healthy adults: 8 younger active (YA) adults (4M/4W; 25 ± 5 yr), 8 older active (OA) adults (4M/4W; 67 ± 5 yr), and 6 older inactive (OI) adults (3M/3W; 68 ± 7 yr). INTERVENTION: Following an overnight (10-hour) fast and having abstained from exercise for 2 days, participants consumed a high-fat meal (63% fat, 34% CHO; 12 kcal/kg body mass; 927 ± 154 kcal). To assess the metabolic response, blood draws were performed at baseline and each hour following the meal for 6 hours. MEASUREMENTS: Fasting and postprandial triglycerides (TG), glucose, Total-C, and HDL-C were measured. Metabolic load index (MLI) and LDL-C were calculated. RESULTS: There were significant group x time interactions for TG (p < 0.0001) and MLI (p = 0.004). The TG total area-under-the-curve (tAUC) response was significantly lower in YA (407.9 ± 115.1 mg/dL 6 hr) compared to OA (625.6 ± 169.0 mg/dL 6 hr; p = 0.02) and OI (961.2 ± 363.6 mg/dL 6 hr; p = 0.0002), while the OA group TG tAUC was lower than the OI group (p = 0.02). The TG peak was significantly lower in YA (90.5 ± 27.0 mg/dL) than OA (144.0 ± 42.2 mg/dL; p = 0.03) and OI (228.2 ± 96.1 mg/dL; p = 0.0003), and was lower in the OA group compared to the OI group (p = 0.03). Glucose was significantly lower 1 hour after the meal in YA (89.4 ± 10.1 mg/dL; p = 0.01) and OA (87.3 ± 22.3 mg/dL; p = 0.005) versus OI (110.7 ± 26.9 mg/dL). MLI tAUC was significantly lower in YA (936.8 ± 137.7 mg/dL 6 hr; p = 0.0007) and OA (1133.0 ± 207.4 mg/dL; p = 0.01) versus OI (1553.8 ± 394.3 mg/dL), with no difference (p = 0.14) between YA and OA groups. Total-C and LDL-C were generally lower in younger compared to older participants at baseline and throughout the postprandial period, while no group or time effects were evident in HDL-C. CONCLUSION: Both physical activity status and aging appear to affect the postprandial metabolic, namely TG, response to a high-fat meal. These findings point to an inherently diminished metabolic capacity with aging, but suggest that physical activity may help minimize this decrement.

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±6.9years) completed the HFM and MFM trials in a randomized crossover design. After a 10-hour fast, participants consumed either a HFM (71.13kJ/kg body mass, 60% fat, 23% CHO) or a MFM (35.56kJ/kg body mass, 30% fat, 52% CHO). Exhaled breath condensate to assess airway 8-isoprostane was collected at baseline and at 3 and 6hours postmeal. Venous blood samples were collected at baseline and hourly until 6hours postmeal to assess triglycerides, and every 3hours 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.