Brooke J. Cull

Does Moderate Intensity Exercise Attenuate the Postprandial Lipemic and Airway Inflammatory Response to a High-Fat Meal?

We investigated whether an acute bout of moderate intensity exercise in the postprandial period attenuates the triglyceride and airway inflammatory response to a high-fat meal (HFM) compared to remaining inactive in the postprandial period. Seventeen (11 M/6 F) physically active (≥150 min/week of moderate-vigorous physical activity (MVPA)) subjects were randomly assigned to an exercise (EX; 60% VO2peak) or sedentary (CON) condition after a HFM (10 kcal/kg, 63% fat). Blood analytes and airway inflammation via exhaled nitric oxide (eNO) were measured at baseline, and 2 and 4 hours after HFM. Airway inflammation was assessed with induced sputum and cell differentials at baseline and 4 hours after HFM. Triglycerides doubled in the postprandial period (~113 ± 18%, P < 0.05), but the increase did not differ between EX and CON. Percentage of neutrophils was increased 4 hours after HFM (~17%), but the increase did not differ between EX and CON. Exhaled nitric oxide changed nonlinearly from baseline to 2 and 4 hours after HFM (P < 0.05,  η 2 = 0.36). Our findings suggest that, in active individuals, an acute bout of moderate intensity exercise does not attenuate the triglyceride or airway inflammatory response to a high-fat meal.

Postprandial lipemic and inflammatory responses to high-fat meals: a review of the roles of acute and chronic exercise

Postprandial lipemia is an independent risk factor for development of cardiovascular disease. Postprandial inflammation following the prolonged elevation of triglycerides occurring subsequent to ingestion of high-fat meals, provides a likely explanation for increased disease risk. Substantial evidence has shown that acute exercise is an effective modality for attenuation of postprandial lipemia following a high-fat meal. However, much of the evidence pertaining to exercise intensity, duration, and overall energy expenditure for reducing postprandial lipemia is inconsistent. The effects of these different exercise variables on postprandial inflammation is largely unknown. Long-term, frequent exercise, however, appears to effectively reduce systemic inflammation, especially in at-risk or diseased individuals. With regard to an acute postprandial response, without a recent bout of exercise, high levels of chronic exercise do not appear to reduce postprandial lipemia. This review summarizes the current literature on postprandial and inflammatory responses to high-fat meals, and the roles that both acute and chronic exercise play. This review may be valuable for health professionals who wish to provide evidence-based, pragmatic advice for reducing postprandial lipemia and cardiovascular disease risk for their patients. A brief review of proposed mechanisms explaining how high-fat meals may result in pro-inflammatory and pro-atherosclerotic environments is also included.

Does chronic physical activity level modify the airway inflammatory response to an acute bout of exercise in the postprandial period

Recent studies have confirmed that a single high-fat meal (HFM) leads to increased airway inflammation. However, exercise is a natural anti-inflammatory and may modify postprandial airway inflammation. The postprandial airway inflammatory response is likely to be modified by chronic physical activity (PA) level. This study investigated whether chronic PA modifies the airway inflammatory response to an acute bout of exercise in the postprandial period in both insufficiently active and active subjects. Thirty-nine nonasthmatic subjects (20 active, 13 males/7 females) who exceeded PA guidelines (≥150 min moderate-vigorous PA/week) and 19 insufficiently active (6 males/13 females) underwent an incremental treadmill test to exhaustion to determine peak oxygen uptake. Subjects were then randomized to a condition (COND), either remaining sedentary (CON) or exercising (EX) post-HFM. Exercise was performed at the heart rate corresponding to 60% peak oxygen uptake on a treadmill for 1 h post-HFM (63% fat, 10 kcal/kg body weight). Blood lipids and exhaled nitric oxide (eNO: marker of airway inflammation) were measured at baseline and 2 h and 4 h post-HFM. Sputum differential cell counts were performed at baseline and 4 h post-HFM. The mean eNO response for all groups increased at 2 h post-HFM (∼6%) and returned to baseline by 4 h (p = 0.03). There was a time × COND interaction (p = 0.04), where EX had a greater eNO response at 4 h compared with CON. Sputum neutrophils increased at 4 h post-HFM (p < 0.05). These findings suggest that airway inflammation occurs after an HFM when exercise is performed in the postprandial period, regardless of habitual activity level.

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.

Postprandial Metabolic Responses Differ by Age Group and Physical Activity Level

ObjectivesTo compare the postprandial metabolic responses to a high-fat meal in healthy adults who differ by age and physical activity level.DesignCross-sectional, quasi-experimental design.SettingPhysical Activity and Nutrition Clinical Research Consortium (PAN-CRC) at Kansas State University (Manhattan, KS, USA).ParticipantsTwenty-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).InterventionFollowing 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.MeasurementsFasting and postprandial triglycerides (TG), glucose, Total-C, and HDL-C were measured. Metabolic load index (MLI) and LDL-C were calculated.ResultsThere 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.ConclusionBoth 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.

Wellness-Promoting Practices Through Girl Scouts: A Pragmatic Superiority Randomized Controlled Trial With Additional Dissemination

Purpose: To evaluate the effectiveness of in-person versus online Girl Scout leader wellness training for implementation of wellness-promoting practices during troop meetings (phase I) and to assess training adoption and current practices across the council (phase II). Design: Pragmatic superiority trial (phase 1) followed by serial cross-sectional study (phase II). Setting: Girl Scout troop meetings in Northeast Kansas. Participants: Eighteen troop leaders from 3 counties (phase 1); 113 troop leaders from 7 counties (phase II). Intervention: Phase I: Troop leaders attended 2 wellness training sessions (first in groups, second individually), wherein leaders set wellness-promoting practice implementation goals, self-monitored progress, and received guidance and resources for implementation. Leaders received the intervention in person or online. Measures: Phase I: At baseline and postintervention, leaders completed a wellness-promoting practice implementation questionnaire assessing practices during troop meetings (max score = 11). Phase II: Leaders completed a survey about typical troop practices and interest in further training. Analysis: Phase I: Generalized linear mixed modeling. Results: Phase I: In-person training increased wellness-promoting practice implementation more than online training (in person = 2.1 ± 1.8; online = 0.2 ± 1.2; P = .022). Phase II: Fifty-six percent of leaders adopted the training. For 8 of 11 wellness categories, greater than 50% of leaders employed wellness-promoting practices. Conclusion: In-person training was superior to online training for improvements in wellness-promoting practices. Wellness training was adopted by the majority of leaders across the council.

Realistic Test-Meal Protocols Lead to Blunted Postprandial Lipemia but Similar Inflammatory Responses Compared with a Standard High-Fat Meal

Abstract Background: A substantial increase in triglycerides (TGs) after a meal is associated with an increased risk of cardiovascular disease. Most studies investigating the effects of a meal on TGs have not used meals that reflect typical consumption. Objective: The objective of this study was to compare the TG and inflammatory responses of true-to-life meals, containing moderate fat and energy contents, with a high-fat, high-energy, low-carbohydrate meal (HFM) typically used to test TG responses. Methods: Nine healthy, insufficiently active men [mean ± SD age: 25.1 ± 6.7 y; body mass index (in kg/m2): 25.8 ± 7.0; <150 min moderate- to vigorous-intensity physical activity/wk] completed 3 meal trials in random order: an HFM (17 kcal/kg, 60% fat), a moderate-fat meal (MFM; 8.5 kcal/kg, 30% fat), and a biphasic meal (BPM), in which participants consumed the full MFM at baseline and 3 h postmeal. Blood samples were collected via an indwelling catheter at baseline and hourly for 6 h. Results: Peak blood TGs were significantly greater (P = 0.003) after the HFM (285.2 ± 169.7 mg/dL) than after the MFM (156.0 ± 98.7 mg/dL), but the BPM (198.3 ± 182.8 mg/dL) was not significantly different from the HFM (P = 0.06) or the MFM (P = 0.99). Total area under the curve for TGs was greater after the HFM (1348.8 ± 783.7 mg/dL × 6 h) than after the MFM (765.8 ± 486.8 mg/dL × 6 h; P = 0.0005) and the BPM (951.8 ± 787.7 mg/dL × 6 h; P = 0.03), although the MFM and BPM were not significantly different (P = 0.72). There was a significant time-by-meal interaction for interferon γ, but not for interleukins 6, 8, or 10. Conclusion: These findings in insufficiently active, healthy young men suggest that the large TG response after HFMs in previous studies may not reflect the metabolic state of many individuals in daily life.

The Seated Inactivity Trial (SIT): Physical Activity and Dietary Outcomes Associated With 8 Weeks of Imposed Sedentary Time

BACKGROUND Sedentary time is an independent risk factor for chronic diseases and mortality. It is unknown whether active adults alter their dietary and/or physical activity behaviors in response to imposed sedentary time, possibly modifying risk. The aim of this study was to determine whether imposed sedentary time would alter typical behaviors of active adults. METHODS Sixteen physically active, young adults were randomized to the no-intervention control (CON, n = 8) group or the sedentary-intervention (SIT, n = 8) group. SIT participants attended monitored sedentary sessions (8 wk, 10 h/wk). Assessments including diet and physical activity occurred at baseline, week 4, and week 9. RESULTS There were no differences (P > .05) between CON and SIT groups for step counts or time spent in sedentary, light, moderate, or vigorous physical activity when comparing a week during imposed sedentary time (week 4) to baseline and week 9. At week 4, caloric intake was not different from baseline (P > .05) in either group. Caloric intake decreased significantly (P > .05) in SIT from baseline to week 9. CONCLUSIONS Active adults did not alter physical activity or dietary behaviors during the imposed sedentary intervention. However, SIT reduced caloric intake from baseline to week 9, indicating a possible compensatory response to imposed sitting in active adults.