Effect of a Single Session of Acute Aerobic Exercise on the Activities of High Density Lipoprotein Enzymes

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  • Division of Nutrition, St John's Research Institute ,IN
  • Department of Biochemistry, St. John's Medical College and Hospital, Bangalore ,IN
  • Division of Nutrition, St John's Research Institute, ,IN
  • Division of Nutrition, St John's Research Institute ,IN
  • Division of Nutrition, St John's Research Institute ,IN




Acute exercise, antioxidant enzymes, CETP, HDL-C, PON1
Food Science and Technology


High Density Lipoprotein (HDL) is considered to be an anti-atherogenic molecule and its beneficial function is driven by a number of enzymes such as LCAT (Lecithin Cholesterol Acyl Transferase), PON1 (Paraoxonase 1), PAF-AH (Platelet-Activating Factor Acetyl Hydrolase) and CETP (Cholesteryl Ester Transfer Protein). Low HDL-C level is the most prevalent dyslipidemia seen in India and exercise is one reliable way to improve its levels. While acute exercise is known to increase HDL-C levels, not much is known about its effects on HDL functions. This study was aimed at assessing the effect of a single bout of acute aerobic exercise on key HDL functions. Ten healthy adult male volunteers (20-35 years) were made to exercise at 65-80% VO2 max to expend 200 Kcal using a modified Bruce protocol. Plasma samples were collected at different time points (before exercise, 15 min, 1 hour, 2 hours, 4 hours, 24 hours, 48 hours post-exercise) for analysis of HDL anti-inflammatory function and its related enzyme activities. Friedman ANOVA followed by post-hoc Wilcoxon matched pair test, showed that PON1 activity increased immediately but reached significance 48 hours post-exercise (Z = -2.666, p = 0.008). CETP and LCAT activities were decreased significantly at the 4th hour post-exercise and continued to be low even up to 48 hours (Z = -2.666, p = 0.008), whereas HDL-C levels, MPO activity and HDL-II did not vary significantly at different time points. Enhanced activity of the antioxidant enzyme PON1, in combination with decreased activities of pro-atherogenic enzymes CETP and LCAT suggest that even a single bout of acute exercise could be effective in eliciting athero-protective changes in HDL function independent of HDL-C levels.


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How to Cite

Bannikoppa, P. S., Uthappa, S., Thomas, T., Kurpad, A. V., & Mani, I. (2018). Effect of a Single Session of Acute Aerobic Exercise on the Activities of High Density Lipoprotein Enzymes. The Indian Journal of Nutrition and Dietetics, 55(1), 18–28. https://doi.org/10.21048/ijnd.2018.55.1.17878



Original Articles
Received 2017-08-10
Accepted 2017-10-25
Published 2018-01-12



Guptha, S., Gupta, R., Deedwania, P., Bhansali, A., Maheshwari, A., Gupta A., et al.Cholesterol lipoproteins and prevalence of dyslipidemias in urban Asian Indians: A cross sectional study. Ind. Heart. J., 2014, 66, 280-8.

Briel, M., Ferreira-Gonzalez, I., You, J.J., Karanicolas, P.J., Akl, E.A., et al. Association between change in high density lipoprotein cholesterol and cardiovascular disease morbidity and mortality: systematic review and meta-regression analysis. BMJ., 2009, 338, b92.

Dodani, S., Grice, D.G. and Joshi, S. Is HDL function as important as HDL quantity in the coronary artery disease risk assessment? J. Clin. Lipidol., 2009, 3, 70–77.

Navab, M., Reddy, S.T., Van Lenten, B.J. and Fogelman, A.M. HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms. Nat. Rev. Cardiol., 2011, 8, 222– 232.

Eren, E., Yilmaz, N. and Aydin, O. High density lipoprotein and its dysfunction. Open.Biochem. J., 2012, 6, 78–93.

Despres, J.P. and Lamarche, B. Low-intensity endurance exercise training, plasma lipoproteins and the risk of coronary heart disease. J. Intern. Med., 1994, 236, 7–22.

Durstine, J.L. and Haskell, W.L. Effects of exercise training on plasma lipids and lipoproteins. In: Exercise and Sport Sciences Reviews, edited by J.O. Holloszy. Baltimore, MD: Williams & Wilkins, 1994, 477–521.

Thompson, P.D., Cullinane, E.M., Sady, S.P., Flynn, M.M., Bernier, D.N., Kantor, M.A., et al. Modest changes in high-density lipoprotein concentration and metabolism with prolonged exercise training. Circulation., 1988, 78, 25–34.

Wood, P.D., Stefanick, M.L., Dreon, D.M., Frey-Hewitt, B., Garay, S.C., Williams, P.T., et al. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N. Engl. J. Med., 1988, 319, 1173–1179.

Gomez-Cabrera, M.C., Domenech, E. and Viña, J. Moderate exercise is an antioxidant: Upregulation of antioxidant genes by training. Free. Radic. Biol. Med., 2008, 44, 126–131.

Tseng, M.L., Ho, C.C., Chen, S.C., Huang, Y.C., Lai, C.H. and Liaw, Y.P. A simple method for increasing levels of high-density lipoprotein cholesterol: A pilot study of combination aerobic and resistance-exercise training. Int. J. Sport. Nutr. Exerc. Metab., 2013, 23, 271-81.

Sharma, M., Rao, M., Jacob, S. and Jacob, C.K. Validation of 24-hour dietary recall: A study in hemodialysis patients. J. Ren. Nutr., 1998, 8, 199-202.

Bharathi, A.V., Sandhya, N. and Vaz, M. The development and characteristics of a physical activity questionnaire for epi-demiological studies in urban middle class Indians. J. Med.Res., 2000, 111, 95-102.

Bruce, R.A., Kusumi, F. and Hosmer, D. Maximal oxygen intake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am. Heart. J., 1973, 85, 546–562.

Navab, M., Hama, S.Y., Hough, G.P., Subbanagounder, G., Reddy, S.T. and Fogelman, A.M. A cell-free assay for detecting HDL that is dysfunctional in preventing the formation of or inactivating oxidized phospholipids. J. Lipid. Res., 2001, 42, 1308-1317.

Burlina, A., Michielin, E. and Galzigna, L. Characteristics and behavior of arylesterase in human serum and liver. Eur. J. Clin. Invest., 1977, 7, 17-20.17. Krueger, A.J., Yang, J.J., Roy, T.A., Robbins, D.J. and Mackerer, C.R. An automated myeloperoxidase assay. Clin. Chem., 1990, 36, 158.

Fisher-Wellman, K. and Bloomer, R.J. Acute exercise and oxidative stress: A 30 year history. Dyn Med., 2009, 8, 1.

Mackness, M.I., Arrol, S., Abbott, C.A. and Durrington, P.N. Protection of low density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. Atherosclerosis, 1993, 104, 129–135.

Aviram, M., Rosenblat, M., Bisgaier, C.L., Newton, R.S., Primo-Parmo, S.L. and La Du, B.N.

Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions.A possible peroxidative role for paraoxonase. J. Clin. Invest., 1998, 101, 1581–1590.

Taylor, J.K., Esco, M.R., Qian, L., Dugan, K. and Jones, K. A single session of aerobic exercise influences paraoxonase 1 activity and concentration. Retos., 2015, 27, 222-225.

Otocka-Kmiecik, A., Lewandowski, M., Szkudlarek, U., Nowak, D. and OrlowskaMajdak, M. Aerobic training modulates the effects of exercise-induced oxidative stress on PON1 activity: A preliminary study. Sc. World Jr., 2014, doi:10.1155/2014/230271.

Toma´s, M., Elosua, R., Senti, M., Molina, L., Vila, J., Anglada, R., et al. Paraoxonase1192 polymorphism modulates the effects of regular and acute exercise on paraoxonase1 activity. J. Lipid. Res., 2002, 43, 713e20.

Nalcakan, G.R., Varol, S.R., Turgay, F., Nalcakan, M., Ozkol, M.Z. and Karamizrak, S.O.

Effects of aerobic training on serum paraoxonase activity and its relationship with PON1192 phenotypes in women. J. Sport and Health Sci., 2015, http://dx.doi.org/10.1016/ j.jshs.2015.01.010.

Iborra, R.T., Ribeiro, I.C., Neves, M.Q., Charf, A.M., Lottenberg, S.A., Negrí£o, C.E., et al.

Aerobic exercise training improves the role of high-density lipoprotein antioxidant and reduces plasma lipid peroxidation in type 2 diabetes mellitus. Scand. J. Med. Sci. Sports., 2008, 18, 742-750.

Zahabi, G., Barari, A.R., Farzanegi, P. and Ahmadi, M. Effect of concurrent training on the serum paraoxonase-1(PON-1) activity and lipid profile in obese men. Intl. Res. J. Appl. Basic.

Sci., 2014, 8, 1434-1437.

Tsopanakis, C., Kotsarellis, D. and Tsopanakis, A. Plasma lecithin: cholesterol acyltransferase activity in elite athletes from selected sports. Eur. J. Appl. Physiol., 1988, 58, 262-265.

Dullaart, R.P., Perton, F., van der Klauw, M.M., Hillege, H.L. and Sluiter, W.J., PREVEND Study Group. High plasma lecithin: cholesterol acyltransferase activity does not predict low incidence of cardiovascular events: possible attenuation of cardioprotection associated with high HDL cholesterol. Atherosclerosis, 2010, 208, 537–542.

Holleboom, A.G., Kuivenhoven, J.A., Vergeer, M., Hovingh, G.K., van Miert, J.N., Wareham, N.J., et al. Plasma levels of lecithin: cholesterol acyltransferase and risk of future coronary artery disease in apparently healthy men and women: a prospective case-control analysis nested in the EPIC-Norfolk population study. J. Lipid. Res., 2010, 51, 416–21.

McPherson, P.A., Young, I.S. and McEneny, J.A. Dual role for lecithin: cholesterol acyltransferase (EC 2.3. 1.43) in lipoprotein oxidation. Free. Radic. Biol. Med., 2007, 43,

Dullaart, R.P., Perton, F., Sluiter, W.J., de Vries, R. and van Tol, A. Plasma lecithin:cholesterol acyltransferase activity is elevated in metabolic syndrome and is an independent marker of increased carotid artery intima media thickness. J. Clin. Endocrinol.Metab., 2008, 93, 4860–4866.

Gruppen, E.G., Connelly, M.A., Otvos, J.D., Bakker, S.J. and Dullaart, R.P. A novel protein glycan biomarker and LCAT activity in metabolic syndrome. Eur. J. Clin. Invest., 2015, 45, 850-859. doi: 10.1111/eci.12481.

Ng, D.S. Lecithin cholesterol acyltransferase deficiency protects from diet-induced insulin resistance and obesity-novel insights from mouse models. Vitam. Horm., 2013, 91, 259-70.doi: 10.1016/B978-0-12-407766-9.

Takanami, Y., Iwane, H., Kawai, Y., Katsumura, T. and Shimomitsu, T. Influence of strenuous endurance exercise on cholesteryl transfer protein and HDL metabolism in serum (Abstract).Med. Sci. Sports. Exerc., 1996, 28, S29.

Grandjean, P.W., Crouse, S.F. and Rohack, J.J. Influence of cholesterol status on blood lipid and lipoprotein enzyme responses to aerobic exercise. J. Appl. Physiol., 2000, 89, 472–480.

Seip, R.L., Moulin, P., Cocke, T., Tall, A., Kohrt, W.M. and Mankowitz, K. Exercise training decreases plasma cholesteryl ester transfer protein. Arterioscler. Thromb., 1993, 13, 9.

Foger, B., Wohlfarter, T., Ritsch, A., Lechleitner, M., Miller, C.H. and Dienstl, A. Kinetics of lipids, apolipoproteins, and cholesteryl ester transfer protein in plasma after a bicycle marathon. Metab., 1994, 43, 633-639.

Pownall, H.J., Rosales, C., Gillard, B.K. and Ferrari, M. Native and Reconstituted Plasma lipoproteins in nanomedicine: physicochemical determinants of nanoparticle structure, stability and metabolism. Methodist. Debakey. Cardiovasc. J., 2016, 12, 146–150.

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