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.

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.

BackgroundConsuming 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.MethodsThirty-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.ResultsAt 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).ConclusionsDespite 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.

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.

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.

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 post-prandial airway inflammation. The post-prandial airway inflammatory response is likely to be modified by chronic physical activity (PA) level. Purpose To investigate whether chronic PA modifies the airway inflammatory response to an acute bout of exercise in the post-prandial period in both insufficiently active and active subjects. Methods Thirty-nine non-asthmatic subjects (twenty active (ACT), 13M/7F) who exceeded PA guidelines (≥150 min moderate-vigorous PA/week) and (nineteen insufficiently active (IN), 6M/13F) underwent an incremental treadmill test to exhaustion to determine VO2peak. 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% VO2peak on a treadmill one-hour post-HFM (63% fat, 10kcal/kgbw). Blood lipids and exhaled nitric oxide (eNO: marker of airway inflammation) were measured at baseline, 2 h and 4 h post-HFM. Sputum differential cell counts were performed at baseline and 4 h post-HFM. Results 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 hours compared to CON. Sputum neutrophils increased at 4 hours post-HFM (p<0.05). Conclusion These findings suggest that airway inflammation occurs after a HFM when exercise is performed in the postprandial period, regardless of habitual activity level.

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.

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