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

Colby S Teeman, Stephanie P Kurti, Brooke J Cull, Sam R Emerson, Mark D Haub, Sara K Rosenkranz, Colby S Teeman, Stephanie P Kurti, Brooke J Cull, Sam R Emerson, Mark D Haub, Sara K Rosenkranz

Abstract

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.

Keywords: Aerobic exercise; High-fat meal; Inflammation; Physical activity; Postprandial lipemia.

Figures

Fig. 1
Fig. 1
The proposed pro-inflammatory pathway following ingestion of a HFM. Triglycerides (TRG), Triglyceride Rich Lipoproteins (TRL), Postprandial lipemia (PPL), High-density lipoprotein cholesterol (HDL), Low Density Lipoprotein cholesterol (LDL), Nuclear Factor Kappa B (NF-κB), Interleukin 1β (IL-1β), Interleukin-6 (IL-6), Tumor Necrosis Factor-α (TNF-α). Increased TRG in circulation leads to increase HDL clearance from circulation and an increase in small dense LDL particles. This process increases subendothelial retention of lipoproteins, leads to oxidized LDL, and activation of the vascular endothelium. The activated endothelium increases the recruitment of immune cells, mainly monocytes, to the vascular surface to scavenge oxidized LDL molecules. Accumulation of lipid inside monocytes leads to formation of macrophages and secretion of several pro-inflammatory cytokines. Macrophages accumulate enough lipid to form foam cells that result in fatty streaks within the vascular endothelium
Fig. 2
Fig. 2
The proposed anti-inflammatory effect of acute aerobic exercise. Triglyceride rich lipoproteins (TRL), High-density lipoprotein cholesterol (HDL), Low-density lipoprotein cholesterol (LDL), Very-low density lipoprotein cholesterol (VLDL), Interleukin-1 (IL-1), Interleukin-6 (IL-6), Interleukin-10 (IL-10), Tumor Necrosis Factor- α (TNF- α). Acute aerobic exercise decreases circulating triglycerides through increased TRL clearance from circulation, decreased TRL appearance from the small intestine, decreased VLDL secretion from the liver, and increased lipolysis and fat oxidation. Each of these processes contributes to lower PPL, increased HDL, decreased TRL resident time in circulation, and decreased LDL oxidation. These processes combine to create a less inflammatory environment within the vasculature. Muscle contractions during aerobic exercise release the anti-inflammatory cytokines IL-6 and IL-10. These cytokines inhibit production of pro-inflammatory cytokines TNF- α and IL-1 leading to lower inflammation within the vasculature

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