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Letter to the Editor

Exercise-Induced Suppression of Postprandial Lipemia: A Possible Mechanism of Endothelial Protection?

Pornpat Chandrruangphen, Peter Collins
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https://doi.org/10.1161/01.ATV.0000020759.72566.77
Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1239
Originally published July 1, 2002
Pornpat Chandrruangphen
Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom
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Peter Collins
Department of Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, London, United Kingdom
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To the Editor:

We wish to propose a novel hypothesis of how exercise may beneficially modulate endothelial function. The benefit of exercise in the prevention of cardiovascular disease is undisputed, but the underlying mechanisms responsible for this beneficial effect, which are independent of traditional cardiovascular risk factors, remain poorly understood. Recently, attention has been focused on the influence of exercise on the endothelium, its functions, and its interactions with blood components.1,2⇓ Exercise training enhances NO and suppresses endothelin-1 production by the endothelium,3 thus potentially shifting the balance toward vasodilation and anti-atherosclerosis. Improved endothelium-dependent vasodilation (EDV) in both the coronary and peripheral vessels following exercise training has been demonstrated by a number of studies in human subjects of different age and risk groups.4,5⇓ In hypercholesterolemic patients, this improvement is independent of fasting lipid profile modification.6

In cell culture experiments, shear stress induces an upregulation of endothelial NO synthase with resultant increase in NO production and release. With exercise training of small muscle groups, such as a handgrip exercise, the local increase in blood flow directly enhances EDV through shear stress mechanisms.7 However, dynamic exercises that use larger muscle groups, such as bicycle ergometer training, produce a systemic enhancement of EDV.4,8⇓ In this setting, the systemic increase in shear stress is small, and it has been suggested that the systemic enhancement of EDV may be the result of metabolic or neurohormonal factors, which are modified by exercise.9 However, to date no likely candidates have been identified.

It has long been known that exercise training lowers postprandial lipemia:10 an environment which is considered to be proatherogenic.11 There is accumulating evidence that postprandial lipemia exerts its deleterious effect on the cardiovascular system by causing endothelial d ysfunction.12 There are now several studies demonstrating that postprandial lipemia induced by eating a fatty meal causes significant impairment of EDV in healthy humans and that the degree of impairment correlates with the rise in postprandial plasma triglyceride levels.13–15⇓⇓

We believe it is plausible that postprandial plasma lipid levels (and/or their composition) represent the missing systemic factor that links exercise training with the general improvement in endothelial function observed in vivo. Thus, in daily life, regular exercise suppresses postprandial lipemia, and through this, endothelial function is enhanced. This intriguing hypothesis links for the first time the effects of exercise on postprandial lipemia and endothelial function, which until now have been investigated separately. To provide support for this hypothesis, novel study protocols that investigate the effects of exercise training and fat-meal challenge in combination on the outcome measure of EDV are required. Furthermore, because a reduction in postprandial lipemia has been observed after a single exercise session,16 if the hypothesis is true, an equally rapid enhancement of EDV may also be seen with much shorter training periods than in previous studies.

Acknowledgments

Dr Chandrruangphen is supported by a junior fellowship from the British Heart Foundation.

References

  1. ↵
    Wang JS, Jen CJ, Chen HI. Effects of exercise training and deconditioning on platelet function in men. Arterioscler Thromb Vasc Biol. 1995; 15: 1668–1674.
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  2. ↵
    Smith JK, Dykes R, Douglas JE, Krishnaswamy G, Berk S. Long-term exercise and atherogenic activity of blood mononuclear cells in persons at risk of developing ischemic heart disease. JAMA. 1999; 281: 1722–1727.
    OpenUrlCrossRefPubMed
  3. ↵
    Maeda S, Miyauchi T, Kakiyama T, Sugawara J, Iemitsu M, Irukayama-Tomobe Y, Murakami H, Kumagai Y, Kuno S, Matsuda M. Effects of exercise training of 8 weeks and detraining on plasma levels of endothelium-derived factors, endothelin-1 and nitric oxide, in healthy young humans. Life Sci. 2001; 69: 1005–1016.
    OpenUrlCrossRefPubMed
  4. ↵
    Clarkson P, Montgomery HE, Mullen MJ, Donald AE, Powe AJ, Bull T, Jubb M, World M, Deanfield JE. Exercise training enhances endothelial function in young men. J Am Coll Cardiol. 1999; 33: 1379–1385.
    OpenUrlCrossRefPubMed
  5. ↵
    Hambrecht R, Wolf A, Gielen S, Linke A, Hofer J, Erbs S, Schoene N, Schuler G. Effect of exercise on coronary endothelial function in patients with coronary artery disease. N Engl J Med. 2000; 342: 454–460.
    OpenUrlCrossRefPubMed
  6. ↵
    Lewis TV, Dart AM, Chin-Dusting JP, Kingwell BA. Exercise training increases basal nitric oxide production from the forearm in hypercholesterolemic patients. Arterioscler Thromb Vasc Biol. 1999; 19: 2782–2787.
    OpenUrlAbstract/FREE Full Text
  7. ↵
    Hornig B, Maier V, Drexler H. Physical training improves endothelial function in patients with chronic heart failure. Circulation. 1996; 93: 210–214.
    OpenUrlAbstract/FREE Full Text
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    Linke A, Schoene N, Gielen S, Hofer J, Erbs S, Schuler G, Hambrecht R. Endothelial dysfunction in patients with chronic heart failure: systemic effects of lower-limb exercise training. J Am Coll Cardiol. 2001; 37: 392–397.
    OpenUrlCrossRefPubMed
  9. ↵
    Ferguson DW, Higashi Y, Sasaki S, Kurisu S, Yoshimizu A, Sasaki N, Matsuura H, Kajiyama G, Oshima T. regular aerobic exercise augments endothelium-dependent vascular relaxation in normotensive and hypertensive subjects: role of endothelium-derived nitric oxide response. Circulation. 2000; 102 (18): 119e-120.
    OpenUrlFREE Full Text
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    Hardman AE. The influence of exercise on postprandial triacylglycerol metabolism. Atherosclerosis. 1998; 141 (suppl 1): S93–S100.
  11. ↵
    Cohn JS. Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins. Can J Cardiol. 1998; 14 (suppl B): 18B–27B.
  12. ↵
    Doi H, Kugiyama K, Ohgushi M, Sugiyama S, Matsumura T, Ohta Y, Nakano T, Nakajima K, Yasue H. Remnants of chylomicron and very low density lipoprotein impair endothelium-dependent vasorelaxation. Atherosclerosis. 1998; 137: 341–349.
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    Vogel RA, Corretti MC, Plotnik GD. Effect of a single high-fat meal on endothelial function in healthy subjects. Am J Cardiol. 1997; 79: 350–354.
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    Ong PJL, Dean TS, Hayward CS, Lilla della Monica P, Sanders TAB, Collins P. Divergent effect of eating fat and carbohydrate on endothelial function. Lancet. 1999; 354: 2134.
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  15. ↵
    Gaenzer H, Sturm W, Neumayr G, Kirchmair R, Ebenbichler C, Ritsch A, Foger B, Weiss G, Patsch JR. Pronounced postprandial lipemia impairs endothelium-dependent dilation of the brachial artery in men. Cardiovasc Res. 2001; 52: 509–516.
    OpenUrlAbstract/FREE Full Text
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    Gill JM, Mees GP, Frayn KN, Hardman AE. Moderate exercise, postprandial lipaemia and triacylglycerol clearance. Eur J Clin Invest. 2001; 31: 201–207.
    OpenUrlCrossRefPubMed
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July 2002, Volume 22, Issue 7
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    Exercise-Induced Suppression of Postprandial Lipemia: A Possible Mechanism of Endothelial Protection?
    Pornpat Chandrruangphen and Peter Collins
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1239, originally published July 1, 2002
    https://doi.org/10.1161/01.ATV.0000020759.72566.77

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    Pornpat Chandrruangphen and Peter Collins
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1239, originally published July 1, 2002
    https://doi.org/10.1161/01.ATV.0000020759.72566.77
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