Abstract

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.

Highlights

  • Consuming a high-fat meal (HFM) may lead to postprandial lipemia (PPL) and inflammation

  • As cardiovascular disease (CVD) continues to be a prominent cause of mortality in Western society, the relationship between PPL, exercise, and postprandial inflammation is of great interest

  • low-density lipoprotein cholesterol (LDL-C) decreased from baseline to 4 h for all participants (F = 19.805, p < 0.001) and there were no differences between EX and control group (CON) groups (F = 0.537, p = 0.471)

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Summary

Introduction

Consuming a high-fat meal (HFM) may lead to postprandial lipemia (PPL) and inflammation. Postprandial exercise has been shown to effectively attenuate PPL. The Western diet is typically calorically dense and nutrient poor, and consumption of this type of diet is associated with high levels of circulating triglycerides (postprandial lipemia (PPL)), which is an established independent risk factor for cardiovascular disease (CVD) [2]. As with PPL, chronically elevated levels of systemic inflammation are associated with CVD and cardiac events [6, 7]. Aerobic exercise has been shown to effectively reduce lipemia in both the fasted and postprandial states, and to have both acute [8] and chronic [9] anti-inflammatory properties. Most studies examining exercise, PPL, and inflammation have used meal and/or exercise conditions that are not representative of the typical day-to-day lifestyles of modern Western Societies

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