Effects of acute exercise on liver function and blood redox status in heavy drinkers

Kalliopi Georgakouli, Eirini Manthou, Ioannis G Fatouros, Chariklia K Deli, Demetrios A Spandidos, Aristidis M Tsatsakis, Demetrios Kouretas, Yiannis Koutedakis, Yannis Theodorakis, Athanasios Z Jamurtas, Kalliopi Georgakouli, Eirini Manthou, Ioannis G Fatouros, Chariklia K Deli, Demetrios A Spandidos, Aristidis M Tsatsakis, Demetrios Kouretas, Yiannis Koutedakis, Yannis Theodorakis, Athanasios Z Jamurtas

Abstract

Excessive alcohol consumption can induce oxidative stress, resulting in the development of several diseases. Exercise has been reported to prevent and/or improve a number of health issues through several mechanisms, including an improvement in redox status. It has also been previously suggested that exercise can help individuals with alcohol use disorders reduce their alcohol intake; however, research in this field is limited. The aim of the present study was to investigage the effects of acute exercise of moderate intensity on the liver function and blood redox status in heavy drinkers. For this purpose, a total of 17 heavy drinkers [age, 31.6±3.2 years; body mass index (BMI), 27.4±0.8 kg/m2; experimental group (EG)] and 17 controls [age, 33.5±1.3 years; BMI, 26.1±1.4 kg/m2; control group (CG), who did not exceed moderate alcohol consumption], underwent one trial of acute exercise of moderate intensity (50-60% of the heart rate reserve) for 30 min on a cycle ergometer, following an overnight fast, and abstaining from smoking and alcohol consumption. Blood samples were obtained before and immediately after exercise for later determination of the indices of liver function and blood redox status. The subjects in the EG had significantly higher (p<0.05) baseline γ-glutamyl transferase (γ-GT) levels compared to the subjects in the CG. Exercise thus resulted in significantly higher γ-GT levels (p<0.005) only in the EG. No significant differences in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) baseline levels were observed between the 2 groups. Following exercise, the AST levels increased significantly (p<0.001) in both groups, whereas the ALT levels increased significantly (p<0.01) only in the EG. The baseline glutathione (GSH) levels were significantly lower (p<0.05) and remained low following exercise in the EG. In addition, we observed a trend for higher (p=0.07) baseline levels of thiobarbituric acid-reactive substances (TBARS), which remained elevated post-exercise in the EG compared to the CG. Significantly increased post-exercise total antioxidant capacity (TAC; p<0.01) and uric acid (UA; p<0.05) levels were noted in the CG, whereas the TAC (p=0.06) and UA (p=0.08) levels increased and approached significance post-exercise in the EG. No significant differences in the baseline levels of total bilirubin and protein carbonyl were observed between the 2 groups, even post-exercise. Thus, the findings of the present study indicate that even though heavy drinkers may be prone to oxidative stress, their exercise-induced antioxidant response is similar to that of individuals who do not drink heavily.

Keywords: alcohol; alcoholism; antioxidants; excessive alcohol consumption; oxidative stress; training.

Figures

Figure 1.
Figure 1.
(A) γ-glutamyl transferase (γ-GT), (B) aspartate aminotransferase (AST) and (C) alanine aminotransferase (ALT) levels before and immediately after acute exercise in heavy drinkers [experimental group (EG)] and the control group (CG). **Significantly different from the pre-exercise value in the same group (p$significantly different from the pre-exercise value in the same group (p<0.05); #significantly different from CG at the same time point (p<0.05).
Figure 2.
Figure 2.
(A) Glutathione (GSH) and (B) catalase levels before and immediately after acute exercise in heavy drinkers [experimental group (EG)] and the control group (CG). $Significantly different from the pre-exercise value in the same group (p<0.07); #significantly different from the CG at the same time point (p<0.05). Hb, hemoglobin.
Figure 3.
Figure 3.
(A) Total antioxidant capacity (TAC) and (B) uric acid (UA) levels before and immediately after acute exercise in heavy drinkers [experimental group (EG)] and the control group (CG). *Significantly different from the pre-exercise value in the same group (p#significantly different from the pre-exercise value in the same group (p=0.08); $significantly different from the pre-exercise value in the same group (p<0.06).
Figure 4.
Figure 4.
Total bilirubin, thiobarbituric acid-reactive substances (TBARS) levels before and immediately after acute exercise in heavy drinkers [experimental group (EG)] and the control group (CG). #Significantly different from CG (p=0.08) at baseline; significantly different from CG (p=0.06) after exercise.

References

    1. Brien SE, Ronksley PE, Turner BJ, Mukamal KJ, Ghali WA. Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. BMJ. 2011;342:d636. doi: 10.1136/bmj.d636.
    1. Ronksley PE, Brien SE, Turner BJ, Mukamal KJ, Ghali WA. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ. 2011;342:d671. doi: 10.1136/bmj.d671.
    1. . National Institute for Alcohol Abuse and Alcoholism: Drinking Levels Defined. 2014 Jan 10; Retrieved.
    1. Greenfield TK, Ye Y, Bond J, Kerr WC, Nayak MB, Kaskutas LA, Anton RF, Litten RZ, Kranzler HR. Risks of alcohol use disorders related to drinking patterns in the U.S. general population. J Stud Alcohol Drugs. 2014;75:319–327. doi: 10.15288/jsad.2014.75.319.
    1. Sies H, Jones D. Oxidative stress. In: Fink G, editor. Encyclopedia of Stress. 2nd. Vol. 3. Amsterdam: Elsevier; 2007. pp. 45–48.
    1. Das SK, Vasudevan DM. Alcohol-induced oxidative stress. Life Sci. 2007;81:177–187. doi: 10.1016/j.lfs.2007.05.005.
    1. Zima T, Kalousová M. Oxidative stress and signal transduction pathways in alcoholic liver disease. Alcohol Clin Exp Res. 2005;29(Suppl 11):110S–115S. doi: 10.1097/01.alc.0000189288.30358.4b.
    1. Tsukamoto H, Lu SC. Current concepts in the pathogenesis of alcoholic liver injury. FASEB J. 2001;15:1335–1349. doi: 10.1096/fj.00-0650rev.
    1. Davies KJ, Quintanilha AT, Brooks GA, Packer L. Free radicals and tissue damage produced by exercise. Biochem Biophys Res Commun. 1982;107:1198–1205. doi: 10.1016/S0006-291X(82)80124-1.
    1. Finaud J, Lac G, Filaire E. Oxidative stress: relationship with exercise and training. Sports Med. 2006;36:327–358. doi: 10.2165/00007256-200636040-00004.
    1. Coffey VG, Hawley JA. The molecular bases of training adaptation. Sports Med. 2007;37:737–763. doi: 10.2165/00007256-200737090-00001.
    1. Michailidis Y, Jamurtas AZ, Nikolaidis MG, Fatouros IG, Koutedakis Y, Papassotiriou I, Kouretas D. Sampling time is crucial for measurement of aerobic exercise-induced oxidative stress. Med Sci Sports Exerc. 2007;39:1107–1113. doi: 10.1249/01.mss.0b013e318053e7ba.
    1. Steinbacher P, Eckl P. Impact of oxidative stress on exercising skeletal muscle. Biomolecules. 2015;5:356–377. doi: 10.3390/biom5020356.
    1. Read JP, Brown RA. The role of physical exercise in alcoholism treatment and recovery. Prof Psychol Res Pract. 2003;34:49–56. doi: 10.1037/0735-7028.34.1.49.
    1. Zschucke E, Heinz A, Ströhle A. Exercise and physical activity in the therapy of substance use disorders. ScientificWorldJournal. 2012;2012:901741. doi: 10.1100/2012/901741.
    1. Giesen ES, Deimel H, Bloch W. Clinical exercise interventions in alcohol use disorders: a systematic review. J Subst Abuse Treat. 2015;52:1–9. doi: 10.1016/j.jsat.2014.12.001.
    1. Jamurtas AZ, Zourbanos N, Georgakouli K, Georgoulias P, Manthou E, Fatouros IG, Goudas M, Koutedakis Y, Theodorakis Y. Beta endorphin and alcohol urge responses in alcoholic patients following an acute bout of exercise. J Addict Res Ther. 2014;5:1000194.
    1. Goldfarb AH, Jamurtas AZ. Beta-endorphin response to exercise. An update. Sports Med. 1997;24:8–16. doi: 10.2165/00007256-199724010-00002.
    1. Gianoulakis C. Endogenous opioids and addiction to alcohol and other drugs of abuse. Curr Top Med Chem. 2004;4:39–50. doi: 10.2174/1568026043451573.
    1. Moussas G, Dadouti G, Douzenis A, Poulis E, Tzelembis A, Bratis D, Christodoulou C, Lykouras L. The Alcohol Use Disorders Identification Test (AUDIT): reliability and validity of the Greek version. Ann Gen Psychiatry. 2009;8:11. doi: 10.1186/1744-859X-8-11.
    1. World Health Organization: The Alcohol Use Disorders Identification Test: Guidelines for Use in Primare Care. 2nd. Geneva: WHO Press; 2001.
    1. Janaszewska A, Bartosz G. Assay of total antioxidant capacity: comparison of four methods as applied to human blood plasma. Scand J Clin Lab Invest. 2002;62:231–236. doi: 10.1080/003655102317475498.
    1. Keles MS, Taysi S, Sen N, Aksoy H, Akçay F. Effect of corticosteroid therapy on serum and CSF malondialdehyde and antioxidant proteins in multiple sclerosis. Can J Neurol Sci. 2001;28:141–143.
    1. Patsoukis N, Zervoudakis G, Panagopoulos NT, Georgiou CD, Angelatou F, Matsokis NA. Thiol redox state (TRS) and oxidative stress in the mouse hippocampus after pentylenetetrazol-induced epileptic seizure. Neurosci Lett. 2004;357:83–86. doi: 10.1016/j.neulet.2003.10.080.
    1. Aebi H. Catalase in vitro. Methods Enzymol. 1984;105:121–126. doi: 10.1016/S0076-6879(84)05016-3.
    1. Reddy YN, Murthy SV, Krishna DR, Prabhakar M. Role of free radicals and antioxidants in tuberculosis patients. Indian J Tuberc. 2004;51:213–218.
    1. Whitehead TP, Robinson D, Allaway SL. The effects of cigarette smoking and alcohol consumption on serum liver enzyme activities: a dose-related study in men. Ann Clin Biochem. 1996;33:530–535. doi: 10.1177/000456329603300607.
    1. Banfi G, Colombini A, Lombardi G, Lubkowska A. Metabolic markers in sports medicine. Adv Clin Chem. 2012;56:1–54. doi: 10.1016/B978-0-12-394317-0.00015-7.
    1. Robinson D, Whitehead TP. Effect of body mass and other factors on serum liver enzyme levels in men attending for well population screening. Ann Clin Biochem. 1989;26:393–400. doi: 10.1177/000456328902600503.
    1. Halonen PI, Konttinen A. Effect of physical exercise on some enzymes in the serum. Nature. 1962;193:942–944. doi: 10.1038/193942a0.
    1. Parikh DJ, Ramanathan NL. Exercise induced serum enzyme changes in untrained subjects. Indian J Physiol Pharmacol. 1977;21:175–180.
    1. Fibach E, Rachmilewitz E. The role of oxidative stress in hemolytic anemia. Curr Mol Med. 2008;8:609–619. doi: 10.2174/156652408786241384.
    1. Cho J, Lee I, Kim D, Koh Y, Kong J, Lee S, Kang H. Effect of aerobic exercise training on non-alcoholic fatty liver disease induced by a high fat diet in C57BL/6 mice. J Exerc Nutrition Biochem. 2014;18:339–346. doi: 10.5717/jenb.2014.18.4.339.
    1. Keating SE, Hackett DA, Parker HM, O'Connor HT, Gerofi JA, Sainsbury A, Baker MK, Chuter VH, Caterson ID, George J, Johnson NA. Effect of aerobic exercise training dose on liver fat and visceral adiposity. J Hepatol. 2015;63:174–182. doi: 10.1016/j.jhep.2015.02.022.
    1. Tseng YM, Tsai SM, Lin CC, Jin YR, Yeh WH, Hsiao JK, Chen CF, Lan WH, Tsai LY. Oxidative stress-related enzyme polymorphisms associated with the immunological biomarkers levels in heavy drinkers in Taiwan. J Clin Lab Anal. 2013;27:494–503. doi: 10.1002/jcla.21633.
    1. Loguercio C, Blanco FD, De Girolamo V, Disalvo D, Nardi G, Parente A, Blanco CD. Ethanol consumption, amino acid and glutathione blood levels in patients with and without chronic liver disease. Alcohol Clin Exp Res. 1999;23:1780–1784. doi: 10.1111/j.1530-0277.1999.tb04073.x.
    1. Maithreyi R, Janani AV, Krishna R, Shweta A, Edwin RR, Mohan SK. Erythrocyte lipid peroxidation and antioxidants in chronic alcoholics with alcoholic liver disease. Asian J Pharm Clin Res. 2010;3:183–185.
    1. Gupta S, Pandey R, Katyal R, Aggarwal HK, Aggarwal RP, Aggarwal SK. Lipid peroxide levels and antioxidant status in alcoholic liver disease. Indian J Clin Biochem. 2005;20:67–71. doi: 10.1007/BF02893045.
    1. Meister A. Mitochondrial changes associated with glutathione deficiency. Biochim Biophys Acta. 1995;1271:35–42. doi: 10.1016/0925-4439(95)00007-Q.
    1. Viña J, Estrela JM, Guerri C, Romero FJ. Effect of ethanol on glutathione concentration in isolated hepatocytes. Biochem J. 1980;188:549–552. doi: 10.1042/bj1880549.
    1. Fernández-Checa JC, García-Ruiz C, Colell A, Morales A, Marí M, Miranda M, Ardite E. Oxidative stress: role of mitochondria and protection by glutathione. Biofactors. 1998;8:7–11. doi: 10.1002/biof.5520080102.
    1. Han D, Hanawa N, Saberi B, Kaplowitz N. Mechanisms of liver injury. III. Role of glutathione redox status in liver injury. Am J Physiol Gastrointest Liver Physiol. 2006;291:G1–G7. doi: 10.1152/ajpgi.00001.2006.
    1. Barden A, Zilkens RR, Croft K, Mori T, Burke V, Beilin LJ, Puddey IB. A reduction in alcohol consumption is associated with reduced plasma F2-isoprostanes and urinary 20-HETE excretion in men. Free Radic Biol Med. 2007;42:1730–1735. doi: 10.1016/j.freeradbiomed.2007.03.004.
    1. Lubin B, Chiu D. Properties of vitamin E-deficient erythrocytes following peroxidant injury. Pediatr Res. 1982;16:928–932. doi: 10.1203/00006450-198211000-00005.

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