Preceding exercise and postprandial hypertriglyceridemia: effects on lymphocyte cell DNA damage and vascular inflammation

Abstract

Background Exercise has proved effective in attenuating the unfavourable response normally associated with postprandial hypertriglyceridemia (PHTG) and accompanying oxidative stress. Yet, the acute effects of prior exercise and PHTG on DNA damage remains unknown. The purpose of this study was to examine if walking alters PHTG-induced oxidative damage and the interrelated inflammatory mechanisms. Methods Twelve apparently healthy, recreationally active, male participants (22.4 ± 4.1 years; 179.2 ± 6 cm; 84.2 ± 14.7 kg; 51.3 ± 8.6 ml·kg − 1 ·min − 1 ) completed a randomised, crossover study consisting of two trials: (1) a high-fat meal alone (resting control) or (2) a high-fat meal immediately following 1 h of moderate exercise (65% maximal heart rate). Venous blood samples were collected at baseline, immediately post-exercise or rest, as well as at 2, 4 and 6 h post-meal. Biomarkers of oxidative damage (DNA single-strand breaks, lipid peroxidation and free radical metabolism) and inflammation were determined using conventional biochemistry techniques. Results DNA damage, lipid peroxidation, free radical metabolism and triglycerides increased postprandially (main effect for time, p < 0.05), regardless of completing 1 h of preceding moderate intensity exercise. Plasma antioxidants (α-tocopherol and γ-tocopherol) also mobilised in response to the high-fat meal (main effect for time, p < 0.05), but no changes were detected for retinol-binding protein-4. Conclusion The ingestion of a high fat meal induces postprandial oxidative stress, inflammation and a rise in DNA damage that remains unaltered by one hour of preceding exercise.

Circadian Clocks, Redox Homeostasis, and Exercise: Time to Connect the Dots?

“…Yet, excessive RONS may cause widespread cellular toxicity [ 6 , 42 ]. Indeed, work from several labs, including our own, has demonstrated how RONS instigate oxidative damage by altering susceptible lipids, proteins, and DNA in human volunteers [ 43 , 44 , 45 ]. This can lead to impaired transcription and translational processes, altered protein function, and production of secondary by-products and metabolites which can further RONS production and/or cellular damage [ 46 ].…”

Exercise to Lower Postprandial Lipemia: Why, When, What and How

“…ii. the day of a high-fat meal [71,93,[95][96][97] or iii. the day of a moderate-fat meal [60,98,99].…”

“…Most of the studies that employed exercise immediately to 1 h before a high-fat meal found no effect on PPL in lean and obese men 93 94 , trained men 95 96 , hypercholesterolemic individuals 59 97 and adolescents 60 71 . This was also the case with low/moderate-fat meals in obese adults 98 99 and individuals with chronic paraplegia 100 .…”

Mechanisms of Atherosclerosis Induced by Postprandial Lipemia

“…Postprandial lipemia may be the main factor leading to inflammation and it affects endothelial function by changing the state of inflammation ( 61 , 62 ). A single feeding is thought to have the ability to produce a transient and low-intensity inflammatory response ( 63 ). The augment of postprandial TG is related to the upregulation of proinflammatory genes in endothelial cells, the increased expression of leukocyte activation markers, and the involvement of the complement system.…”