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

Research output: Contribution to journalArticle

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 PHTGinduced 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.
LanguageEnglish
Article number125 (2019)
Pages1-12
Number of pages12
JournalLipids in Health and Disease
Volume18
Issue number1
DOIs
Publication statusPublished - 29 May 2019

Fingerprint

Lymphocytes
Hypertriglyceridemia
DNA Damage
Blood Vessels
Meals
Fats
Inflammation
Oxidative stress
DNA
Lipid Peroxidation
gamma-Tocopherol
Lipids
Oxidative Stress
Retinol-Binding Proteins
Biochemistry
alpha-Tocopherol
Biomarkers
Single-Stranded DNA Breaks
Metabolism
Free Radicals

Keywords

  • Exercise
  • Postprandial hypertriglyceridemia
  • Oxidative stress
  • DNA
  • Inflammation

Cite this

@article{7a1a24f5939f4cfb84f9b37446c1f4a0,
title = "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 PHTGinduced 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.",
keywords = "Exercise, Postprandial hypertriglyceridemia, Oxidative stress, DNA, Inflammation",
author = "Malcolm Brown and CM McClean and Gareth Davison and John Brown and Murphy, {Marie H}",
note = "1. O'Keefe JH, Bell DS. Postprandial hyperglycaemia/hyperlipidaemia (postprandial dysmetabolism) is a cardiovascular risk factor. Am J Cardiol. 2007;100(5):899–904. 2. Chan DC, Pang J, Romic G, Watts GF. Postprandial hypertriglyceridemia and cardiovascular disease: current and future therapies. Current Atheroscler Reports. 2013;15(3):309. 3. Rebolledo OR, Actis Dato SM. Postprandial hyperglycaemia and hyperlipidaemia-generated glycoxidative stress: its contribution to the pathogenesis of diabetes complications. Eur Rev Med Pharmacol Sci. 2005; 9(4):191–208. 4. Bae JH, Bassenge E, Kim KB, Kim YN, Kim KS, Lee HJ, et al. Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress. Atherosclerosis. 2001;155(2):517–23. 5. Jackson MJ, Pye D, Palomero J. The production of reactive oxygen and nitrogen species by skeletal muscle. J Appl Physiol. 2007;102(4):1664–70. 6. Roberts AC, Porter KE. Cellular and molecular mechanisms of endothelial dysfunction in diabetes. Diabetes Vasc Dis Res. 2013;10(6):472–82. 7. Szab{\'o} C, Ischiropoulos H, Radi R. Peroxynitrite: biochemistry, pathophysiology and development of therapeutics. Nat Rev - Drug Discov. 2007;6(8):662–80. 8. McClean CM, Mc Laughlin J, Burke G, Murphy MH, Trinick T, Duly E, et al. The effect of acute aerobic exercise on pulse wave velocity and oxidative stress following postprandial hypertriglyceridemia in healthy men. Eur J Appl Physiol. 2007;100(2):225–34. 9. Padilla J, Harris RA, Fly AD, Rink LD, Wallace JP. The effect of acute exercise on endothelial function following a high-fat meal. Eur J Appl Physiol. 2006; 98(3):256–62. 10. Davison GW. Exercise and oxidative damage in nucleoid DNA quantified using single cell gel electrophoresis: present and future applications. Front Physiol. 2016;7:249. 11. Mahmoudi M, Mercer J, Bennett M. DNA damage and repair in atherosclerosis. Cardiovasc Res. 2006;71(2):259–68. 12. Cooke MS, Olinski R, Loft S. European standards committee on urinary (DNA) lesion analysis. Measurement and meaning of oxidatively modified DNA lesions in urine. Cancer Epidemiol Biomark Prev. 2008;17(1):3–14. 13. Fogarty MC, Hughes CM, Burke G, Brown JC, Trinick TR, Duly E, et al. Exercise-induced lipid peroxidation: implications for deoxyribonucleic acid damage and systemic free radical generation. Environ Mol Mutagen. 2011; 52(1):35–42. 14. Nappo F, Esposito K, Cioffi M, Giugliano G, Molinari AM, Paolisso G, et al. Postprandial endothelial activation in healthy subjects and in type 2 diabetic patients: role of fat and carbohydrate meals. J Am Coll Cardiol. 2002;39(7):1145–50. 15. Sallam N, Laher I. Exercise modulates oxidative stress and inflammation in aging and cardiovascular diseases. Oxidative Med Cell Longev. 2016;32. 16. Norata GD, Grigore L, Raselli S, Redaelli L, Hamsten A, Maggi F, et al. Postprandial endothelial dysfunction in hypertriglyceridemic subjects: molecular mechanisms and gene expression studies. Atherosclerosis. 2007;193(2):321– 7. 17. Fowler AJ, Richer AL, Bremner RM, Inge LJ. A high-fat diet is associated with altered adipokine production and a more aggressive esophageal adenocarcinoma phenotype in vivo. J Thorac Cardiovasc Surg. 2015;149(4): 1185–91. 18. Yang Q, Graham TE, Mody N, Preitner F, Peroni OD, Zabolotny JM, et al. Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes. Nature. 2005;436(7049):356–62. 19. Gill JM, Hardman AE. Exercise and postprandial lipid metabolism: an update on potential mechanisms and interactions with high-carbohydrate diets (review). J Nut Biochem. 2003;14(3):122–32. 20. Katsanos CS. Prescribing aerobic exercise for the regulation of postprandial lipid metabolism: current research and recommendations. Sports Med. 2006; 36(7):547–60. 21. Peddie MC, Rehrer NJ, Perry TL. Physical activity and postprandial lipidemia: are energy expenditure and lipoprotein lipase activity the real modulators of the positive effect? Prog Lipid Res. 2012;51(1):11–22. 22. Freese EC, Gist NH, Cureton KJ. Effect of prior exercise on postprandial lipaemia: an updated quantitative review. J Appl Physiol. 2014;116(1):67–75. 23. Burns SF, Miyashita M, Stensel DJ. High-intensity interval exercise and postprandial triacylglycerol. Sports Med. 2015;45(7):957–68. 24. Altena TS, Michaelson JL, Ball SD, Thomas TR. Single sessions of intermittent and continuous exercise and postprandial lipaemia. Med Sci Sports Exerc. 2004;36(8):1364–71. 25. Petridou A, Gerkos N, Kolifa M, Nikolaidis MG, Simos D, Mougios V. Effect of exercise performed immediately before a meal of moderate fat content on postprandial lipaemia. Br J Nutr. 2004;91(5):683–7. 26. MacInnis MJ, Gibala MJ. Physiological adaptations to interval training and the role of exercise intensity. J Physiol. 2017;595(9):2915–30. 27. Cooke MS, Evans MD, Dizdaroglu M, Lunec J. Oxidative DNA damage: mechanisms, mutation, and disease. FASEB J. 2003;17(10):1195–214. 28. McClean C, Harris RA, Brown M, Brown JC, Davison GW. Effects of exercise intensity on post-exercise endothelial function and oxidative stress. Oxidative Med Cell Longev 2015; 8 pages. 29. Collins AR, Oscoz AA, Brunborg G, Gaivao I, Giovannelli L, Kruszewski M, et al. The comet assay: topical issues. Mutagenesis. 2008;23(3):143–51. 30. Sies H, Stahl W, Sevanian A. Nutritional, dietary and postprandial oxidative stress. J Nutr. 2005;135(5):969–72. 31. Van Oostrom AJ, Sijmonsma TP, Verseyden C, Jansen EH, de Koning EJ, Rabelink TJ, et al. Postprandial recruitment of neutrophils may contribute to endothelial dysfunction. J Lipid Res. 2003;44(3):576–83. 32. Alipour A, van Oostrom AJ, Izraeljan A, Verseyden C, Collins JM, Frayn KN, et al. Leukocyte activation by triglyceride-rich lipoproteins. Arterioscler Thromb Vasc Biol. 2008;28(4):792–7. 33. Bedard K, Krause KH. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol Rev. 2007;87(1):245–313. 34. Klop B, Proctor SD, Mamo JC, Botham KM, Castro Cabezas M. Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases. Int J Vasc Med. 2012;11. 35. Dizdaroglu M, Jaruga P. Mechanisms of free radical-induced damage to DNA. Free Radic Res. 2012;46(4):382–419. 36. Jenkins NT, Landers RQ, Thakkar SR, Fan X, Brown MD, Prior SJ, et al. Prior endurance exercise prevents postprandial lipaemia-induced increases in reactive oxygen species in circulating CD31+ cells. J Physiol. 2011;589(22): 5539–53. 37. Radak Z, Ishihara K, Tekus E, Varga C, Posa A, Balogh L, et al. Exercise, oxidants, and antioxidants change the shape of the bell-shaped hormesis curve. Redox Biol. 2017;12:285–90. 38. Imlay JA. Cellular defences against superoxide and hydrogen peroxide. Annu Rev Biochem. 2008;77:755–76. 39. David SS, O'Shea VL, Kundu S. Base-excision repair of oxidative DNA damage. Nature. 2007;447(7147):941–50. 40. Azqueta A, Slyskova J, Langie SA, Gaivao IO, Collins A. Comet assay to measure DNA repair: approach and applications. Front Genet. 2014;5:8. 41. Clegg M, McClean C, Davison G, Murphy MH, Trinick T, Duly E, et al. Exercise and postprandial lipaemia: effects on peripheral vascular function, oxidative stress and gastrointestinal transit. Lipids Health Dis. 2007;6:30. 42. Ayala A, Munoz MF, Arguelles S. Lipid peroxidation: production, metabolism, and signalling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal. Oxidative Med Cell Longev. 2014;31. 43. Spickett CM, Wiswedel I, Siems W, Zarkovic K, Zarkovic N. Advances in methods for the determination of biologically relevant lipid peroxidation products. Free Radic Res. 2010;44(10):1172–202. 44. Young IS, Woodside JV. Antioxidants in health and disease. J Clin Pathol. 2001;54(3):176–86. 45. Fogarty MC, Hughes CM, Burke G, Brown JC, Davison GW. Acute and chronic watercress supplementation attenuates exercise-induced peripheral mononuclear cell DNA damage and lipid peroxidation. Br J Nutr. 2013;109:293–301. 46. Herieka M, Erridge C. High-fat meal induced postprandial inflammation. Mol Nutr Food Res. 2014;58(1):136–46. 47. Brandauer J, Landers-Ramos RQ, Jenkins NT, Spangenburg EE, Hagberg JM, Prior SJ. Effects of prior acute exercise on circulating cytokine concentration responses to a high-fat meal. Physiol Reports. 2013;1(3). 48. Teeman CS, Kurti SP, Cull BJ, Emerson SR, Haub MD, Rosenkranz SK. The effect of moderate intensity exercise in the postprandial period on the inflammatory response to a high-fat meal: an experimental study. Nutr J. 2016;15:24. 49. Fuller KNZ, Summers CM, Valentine RJ. Effect of a single bout of aerobic exercise on high-fat meal-induced inflammation. Metab Clin Exp. 2017;71: 144–52. 50. Zabetian-Targhi F, Mahmoudi MJ, Rezaei N, Mahmoudi M. Retinol binding protein 4 in relation to diet, inflammation, immunity, and cardiovascular diseases. Adv Nutr. 2015;6(6):748–62. 51. Canale RE, Farney TM, McCarthy CG, Bloomer RJ. Influence of acute exercise of varying intensity and duration on postprandial oxidative stress. Eur J Appl Physiol. 2014;114:1913–24. 52. Katsanos CS, Grandjean PW, Moffatt RJ. Effects of low and moderate exercise intensity on postprandial lipaemia and postheparin plasma lipoprotein lipase activity in physically active men. J Appl Physiol. 2004;96(1): 181–8. 53. Kashiwabara K, Kidokoro T, Yanaoka T, Burns SF, Stensel DJ, Miyashita M. Different patterns of walking and postprandial triglycerides in older women. Med Sci Sports Exerc. 2018;50(1):79–87. 54. Ghafouri K, Cooney J, Bedford DK, Wilson J, Caslake MJ, Gill JM. Moderate exercise increases affinity of large very low-density lipoproteins for hydrolysis by lipoprotein lipase. J Clin Endocrinol Metab. 2015;100(6):2205– 13. 55. Tsekouras YE, Magkos F, Kellas Y, Basioukas KN, Kavouras SA, Sidossis LS. High-intensity interval aerobic training reduces hepatic very low-density lipoprotein-triglyceride secretion rate in men. Am J Physiol - Endocrinol Metab. 2008;295(4):E851–8. 56. Gabriel B, Ratkevicius A, Gray P, Frenneaux MP, Gray SR. High-intensity exercise attenuates postprandial lipaemia and markers of oxidative stress. Clin Sci. 2012;123(5):313–21. 57. Yang TJ, Wu CL, Chiu CH. High-intensity intermittent exercise increases fat oxidation rate and reduces postprandial triglyceride concentrations. Nutrition. 2018;10:492. 58. Lee CL, Kuo YH, Cheng CF. Acute high-intensity interval cycling improves postprandial lipid metabolism. Med Sci Sports Exerc. 2018;50(8):1687–96. 59. Tucker WJ, Sawyer BJ, Jarrett CL, Bhammar DM, Ryder JR, Angadi SS, et al. High-intensity interval exercise attenuates but does not eliminate endothelial dysfunction after a fast food meal. Am J Physiol Heart Circ Physiol. 2018;314(2):H188–94. 60. Lopes Kr{\"u}ger R, Costa Teixeira B, Boufleur Farinha J, Cauduro Oliveira Macedo R, Pinto Boeno F, Rech A, et al. Effect of exercise intensity on postprandial lipaemia, markers of oxidative stress, and endothelial function after a high-fat meal. Appl Physiol Nutr Metab. 2016;41(12):1278–84.",
year = "2019",
month = "5",
day = "29",
doi = "10.1186/s12944-019-1071-y",
language = "English",
volume = "18",
pages = "1--12",
journal = "Lipids in Health and Disease",
issn = "1476-511X",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Preceding exercise and postprandial hypertriglyceridemia: effects on lymphocyte cell DNA damage and vascular inflammation

AU - Brown, Malcolm

AU - McClean, CM

AU - Davison, Gareth

AU - Brown, John

AU - Murphy, Marie H

N1 - 1. O'Keefe JH, Bell DS. Postprandial hyperglycaemia/hyperlipidaemia (postprandial dysmetabolism) is a cardiovascular risk factor. Am J Cardiol. 2007;100(5):899–904. 2. Chan DC, Pang J, Romic G, Watts GF. Postprandial hypertriglyceridemia and cardiovascular disease: current and future therapies. Current Atheroscler Reports. 2013;15(3):309. 3. Rebolledo OR, Actis Dato SM. Postprandial hyperglycaemia and hyperlipidaemia-generated glycoxidative stress: its contribution to the pathogenesis of diabetes complications. Eur Rev Med Pharmacol Sci. 2005; 9(4):191–208. 4. Bae JH, Bassenge E, Kim KB, Kim YN, Kim KS, Lee HJ, et al. Postprandial hypertriglyceridemia impairs endothelial function by enhanced oxidant stress. Atherosclerosis. 2001;155(2):517–23. 5. Jackson MJ, Pye D, Palomero J. The production of reactive oxygen and nitrogen species by skeletal muscle. J Appl Physiol. 2007;102(4):1664–70. 6. Roberts AC, Porter KE. Cellular and molecular mechanisms of endothelial dysfunction in diabetes. Diabetes Vasc Dis Res. 2013;10(6):472–82. 7. Szabó C, Ischiropoulos H, Radi R. Peroxynitrite: biochemistry, pathophysiology and development of therapeutics. Nat Rev - Drug Discov. 2007;6(8):662–80. 8. McClean CM, Mc Laughlin J, Burke G, Murphy MH, Trinick T, Duly E, et al. The effect of acute aerobic exercise on pulse wave velocity and oxidative stress following postprandial hypertriglyceridemia in healthy men. Eur J Appl Physiol. 2007;100(2):225–34. 9. Padilla J, Harris RA, Fly AD, Rink LD, Wallace JP. The effect of acute exercise on endothelial function following a high-fat meal. Eur J Appl Physiol. 2006; 98(3):256–62. 10. Davison GW. Exercise and oxidative damage in nucleoid DNA quantified using single cell gel electrophoresis: present and future applications. Front Physiol. 2016;7:249. 11. Mahmoudi M, Mercer J, Bennett M. DNA damage and repair in atherosclerosis. Cardiovasc Res. 2006;71(2):259–68. 12. Cooke MS, Olinski R, Loft S. European standards committee on urinary (DNA) lesion analysis. Measurement and meaning of oxidatively modified DNA lesions in urine. Cancer Epidemiol Biomark Prev. 2008;17(1):3–14. 13. Fogarty MC, Hughes CM, Burke G, Brown JC, Trinick TR, Duly E, et al. Exercise-induced lipid peroxidation: implications for deoxyribonucleic acid damage and systemic free radical generation. Environ Mol Mutagen. 2011; 52(1):35–42. 14. Nappo F, Esposito K, Cioffi M, Giugliano G, Molinari AM, Paolisso G, et al. Postprandial endothelial activation in healthy subjects and in type 2 diabetic patients: role of fat and carbohydrate meals. J Am Coll Cardiol. 2002;39(7):1145–50. 15. Sallam N, Laher I. Exercise modulates oxidative stress and inflammation in aging and cardiovascular diseases. Oxidative Med Cell Longev. 2016;32. 16. Norata GD, Grigore L, Raselli S, Redaelli L, Hamsten A, Maggi F, et al. Postprandial endothelial dysfunction in hypertriglyceridemic subjects: molecular mechanisms and gene expression studies. Atherosclerosis. 2007;193(2):321– 7. 17. Fowler AJ, Richer AL, Bremner RM, Inge LJ. A high-fat diet is associated with altered adipokine production and a more aggressive esophageal adenocarcinoma phenotype in vivo. J Thorac Cardiovasc Surg. 2015;149(4): 1185–91. 18. Yang Q, Graham TE, Mody N, Preitner F, Peroni OD, Zabolotny JM, et al. Serum retinol binding protein 4 contributes to insulin resistance in obesity and type 2 diabetes. Nature. 2005;436(7049):356–62. 19. Gill JM, Hardman AE. Exercise and postprandial lipid metabolism: an update on potential mechanisms and interactions with high-carbohydrate diets (review). J Nut Biochem. 2003;14(3):122–32. 20. Katsanos CS. Prescribing aerobic exercise for the regulation of postprandial lipid metabolism: current research and recommendations. Sports Med. 2006; 36(7):547–60. 21. Peddie MC, Rehrer NJ, Perry TL. Physical activity and postprandial lipidemia: are energy expenditure and lipoprotein lipase activity the real modulators of the positive effect? Prog Lipid Res. 2012;51(1):11–22. 22. Freese EC, Gist NH, Cureton KJ. Effect of prior exercise on postprandial lipaemia: an updated quantitative review. J Appl Physiol. 2014;116(1):67–75. 23. Burns SF, Miyashita M, Stensel DJ. High-intensity interval exercise and postprandial triacylglycerol. Sports Med. 2015;45(7):957–68. 24. Altena TS, Michaelson JL, Ball SD, Thomas TR. Single sessions of intermittent and continuous exercise and postprandial lipaemia. Med Sci Sports Exerc. 2004;36(8):1364–71. 25. Petridou A, Gerkos N, Kolifa M, Nikolaidis MG, Simos D, Mougios V. Effect of exercise performed immediately before a meal of moderate fat content on postprandial lipaemia. Br J Nutr. 2004;91(5):683–7. 26. MacInnis MJ, Gibala MJ. Physiological adaptations to interval training and the role of exercise intensity. J Physiol. 2017;595(9):2915–30. 27. Cooke MS, Evans MD, Dizdaroglu M, Lunec J. Oxidative DNA damage: mechanisms, mutation, and disease. FASEB J. 2003;17(10):1195–214. 28. McClean C, Harris RA, Brown M, Brown JC, Davison GW. Effects of exercise intensity on post-exercise endothelial function and oxidative stress. Oxidative Med Cell Longev 2015; 8 pages. 29. Collins AR, Oscoz AA, Brunborg G, Gaivao I, Giovannelli L, Kruszewski M, et al. The comet assay: topical issues. Mutagenesis. 2008;23(3):143–51. 30. Sies H, Stahl W, Sevanian A. Nutritional, dietary and postprandial oxidative stress. J Nutr. 2005;135(5):969–72. 31. Van Oostrom AJ, Sijmonsma TP, Verseyden C, Jansen EH, de Koning EJ, Rabelink TJ, et al. Postprandial recruitment of neutrophils may contribute to endothelial dysfunction. J Lipid Res. 2003;44(3):576–83. 32. Alipour A, van Oostrom AJ, Izraeljan A, Verseyden C, Collins JM, Frayn KN, et al. Leukocyte activation by triglyceride-rich lipoproteins. Arterioscler Thromb Vasc Biol. 2008;28(4):792–7. 33. Bedard K, Krause KH. The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology. Physiol Rev. 2007;87(1):245–313. 34. Klop B, Proctor SD, Mamo JC, Botham KM, Castro Cabezas M. Understanding postprandial inflammation and its relationship to lifestyle behaviour and metabolic diseases. Int J Vasc Med. 2012;11. 35. Dizdaroglu M, Jaruga P. Mechanisms of free radical-induced damage to DNA. Free Radic Res. 2012;46(4):382–419. 36. Jenkins NT, Landers RQ, Thakkar SR, Fan X, Brown MD, Prior SJ, et al. Prior endurance exercise prevents postprandial lipaemia-induced increases in reactive oxygen species in circulating CD31+ cells. J Physiol. 2011;589(22): 5539–53. 37. Radak Z, Ishihara K, Tekus E, Varga C, Posa A, Balogh L, et al. Exercise, oxidants, and antioxidants change the shape of the bell-shaped hormesis curve. Redox Biol. 2017;12:285–90. 38. Imlay JA. Cellular defences against superoxide and hydrogen peroxide. Annu Rev Biochem. 2008;77:755–76. 39. David SS, O'Shea VL, Kundu S. Base-excision repair of oxidative DNA damage. Nature. 2007;447(7147):941–50. 40. Azqueta A, Slyskova J, Langie SA, Gaivao IO, Collins A. Comet assay to measure DNA repair: approach and applications. Front Genet. 2014;5:8. 41. Clegg M, McClean C, Davison G, Murphy MH, Trinick T, Duly E, et al. Exercise and postprandial lipaemia: effects on peripheral vascular function, oxidative stress and gastrointestinal transit. Lipids Health Dis. 2007;6:30. 42. Ayala A, Munoz MF, Arguelles S. Lipid peroxidation: production, metabolism, and signalling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal. Oxidative Med Cell Longev. 2014;31. 43. Spickett CM, Wiswedel I, Siems W, Zarkovic K, Zarkovic N. Advances in methods for the determination of biologically relevant lipid peroxidation products. Free Radic Res. 2010;44(10):1172–202. 44. Young IS, Woodside JV. Antioxidants in health and disease. J Clin Pathol. 2001;54(3):176–86. 45. Fogarty MC, Hughes CM, Burke G, Brown JC, Davison GW. Acute and chronic watercress supplementation attenuates exercise-induced peripheral mononuclear cell DNA damage and lipid peroxidation. Br J Nutr. 2013;109:293–301. 46. Herieka M, Erridge C. High-fat meal induced postprandial inflammation. Mol Nutr Food Res. 2014;58(1):136–46. 47. Brandauer J, Landers-Ramos RQ, Jenkins NT, Spangenburg EE, Hagberg JM, Prior SJ. Effects of prior acute exercise on circulating cytokine concentration responses to a high-fat meal. Physiol Reports. 2013;1(3). 48. Teeman CS, Kurti SP, Cull BJ, Emerson SR, Haub MD, Rosenkranz SK. The effect of moderate intensity exercise in the postprandial period on the inflammatory response to a high-fat meal: an experimental study. Nutr J. 2016;15:24. 49. Fuller KNZ, Summers CM, Valentine RJ. Effect of a single bout of aerobic exercise on high-fat meal-induced inflammation. Metab Clin Exp. 2017;71: 144–52. 50. Zabetian-Targhi F, Mahmoudi MJ, Rezaei N, Mahmoudi M. Retinol binding protein 4 in relation to diet, inflammation, immunity, and cardiovascular diseases. Adv Nutr. 2015;6(6):748–62. 51. Canale RE, Farney TM, McCarthy CG, Bloomer RJ. Influence of acute exercise of varying intensity and duration on postprandial oxidative stress. Eur J Appl Physiol. 2014;114:1913–24. 52. Katsanos CS, Grandjean PW, Moffatt RJ. Effects of low and moderate exercise intensity on postprandial lipaemia and postheparin plasma lipoprotein lipase activity in physically active men. J Appl Physiol. 2004;96(1): 181–8. 53. Kashiwabara K, Kidokoro T, Yanaoka T, Burns SF, Stensel DJ, Miyashita M. Different patterns of walking and postprandial triglycerides in older women. Med Sci Sports Exerc. 2018;50(1):79–87. 54. Ghafouri K, Cooney J, Bedford DK, Wilson J, Caslake MJ, Gill JM. Moderate exercise increases affinity of large very low-density lipoproteins for hydrolysis by lipoprotein lipase. J Clin Endocrinol Metab. 2015;100(6):2205– 13. 55. Tsekouras YE, Magkos F, Kellas Y, Basioukas KN, Kavouras SA, Sidossis LS. High-intensity interval aerobic training reduces hepatic very low-density lipoprotein-triglyceride secretion rate in men. Am J Physiol - Endocrinol Metab. 2008;295(4):E851–8. 56. Gabriel B, Ratkevicius A, Gray P, Frenneaux MP, Gray SR. High-intensity exercise attenuates postprandial lipaemia and markers of oxidative stress. Clin Sci. 2012;123(5):313–21. 57. Yang TJ, Wu CL, Chiu CH. High-intensity intermittent exercise increases fat oxidation rate and reduces postprandial triglyceride concentrations. Nutrition. 2018;10:492. 58. Lee CL, Kuo YH, Cheng CF. Acute high-intensity interval cycling improves postprandial lipid metabolism. Med Sci Sports Exerc. 2018;50(8):1687–96. 59. Tucker WJ, Sawyer BJ, Jarrett CL, Bhammar DM, Ryder JR, Angadi SS, et al. High-intensity interval exercise attenuates but does not eliminate endothelial dysfunction after a fast food meal. Am J Physiol Heart Circ Physiol. 2018;314(2):H188–94. 60. Lopes Krüger R, Costa Teixeira B, Boufleur Farinha J, Cauduro Oliveira Macedo R, Pinto Boeno F, Rech A, et al. Effect of exercise intensity on postprandial lipaemia, markers of oxidative stress, and endothelial function after a high-fat meal. Appl Physiol Nutr Metab. 2016;41(12):1278–84.

PY - 2019/5/29

Y1 - 2019/5/29

N2 - 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 PHTGinduced 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.

AB - 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 PHTGinduced 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.

KW - Exercise

KW - Postprandial hypertriglyceridemia

KW - Oxidative stress

KW - DNA

KW - Inflammation

UR - http://www.scopus.com/inward/record.url?scp=85066395858&partnerID=8YFLogxK

U2 - 10.1186/s12944-019-1071-y

DO - 10.1186/s12944-019-1071-y

M3 - Article

VL - 18

SP - 1

EP - 12

JO - Lipids in Health and Disease

T2 - Lipids in Health and Disease

JF - Lipids in Health and Disease

SN - 1476-511X

IS - 1

M1 - 125 (2019)

ER -