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.

The effect of moderate intensity exercise in the postprandial period on the inflammatory response to a high-fat meal: an experimental study.

BACKGROUND: Consuming a high-fat meal (HFM) may lead to postprandial lipemia (PPL) and inflammation. Postprandial exercise has been shown to effectively attenuate PPL. However, little is known about the impact of postprandial exercise on systemic inflammation and whether PPL and inflammation are associated. The purpose of this study was to determine whether moderate intensity exercise performed 60 min following a true-to-life HFM would attenuate PPL and inflammation. METHODS: Thirty-nine young adults (18-40 year) with no known metabolic disease were randomized to either a control group (CON) who remained sedentary during the postprandial period or an exercise (EX) group who walked at 60 % VO2peak to expend ≈ 5 kcal/kgbw one-hour following the HFM. Participants consumed a HFM of 10 kcal/kgbw and blood draws were performed immediately before, 2 h and 4 h post-HFM. RESULTS: At baseline, there were no differences between EX and CON groups for any metabolic or inflammatory markers (p > 0.05). Postprandial triglycerides (TRG) increased from baseline to 4 h in the EX and CON groups (p < 0.001), with no differences between groups (p = 0.871). High density lipoprotein cholesterol (HDL-C) decreased in both groups across time (p < 0.001) with no differences between groups (p = 0.137). Interleukin-6 (IL-6) was significant as a quadratic function over time (p = 0.005), decreasing from baseline to 2 h then increasing and returning to baseline at 4 h in all participants with no difference between groups (p = 0.276). Tumor necrosis factor-alpha (TNF-α) was not different from baseline to 4 h between groups (p > 0.05). There was an increase in soluble vascular adhesion molecule (sVCAM-1) from baseline to 4 h (p = 0.027) for all participants along with a group x time interaction (p = 0.020). Changes in TRG were associated with changes in interleukin-10 (IL-10) from 0 to 2 h (p = 0.007), but were not associated with changes in any other inflammatory marker in the postprandial period (p > 0.05). CONCLUSIONS: Despite significant increases in PPL following a HFM, moderate intensity exercise in the postprandial period did not mitigate the PPL nor the inflammatory response to the HFM. These results indicate that in populations with low metabolic risk, PPL and inflammation following a HFM may not be directly related.

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.