@2024 Afarand., IRAN
ISSN: 2252-0805 The Horizon of Medical Sciences 2017;23(4):279-283
ISSN: 2252-0805 The Horizon of Medical Sciences 2017;23(4):279-283
Effect of 8 Weeks Resistance Training on Some Antioxidant/Oxidative Indexes in Postmenopausal Women with Breast Cancer
ARTICLE INFO
Article Type
Original ResearchAuthors
Fathollahi Shoorabeh F. (*)Tarverdyzadeh B. (1)
Aminbaksahayesh S. (2)
(*) Sport Physiology Department, Literature & Humanities Faculty, Shahrekord University, Shahrekord, Iran
(1) Sport Physiology Department, Graduate Studies Faculty, Bushehr Branch, Islamic Azad University, Bushehr, Iran
(2) Sport Physiology Department, Physical Education & Sport Sciences Faculty, ehran Center Branch, Islamic Azad University, Tehran, Iran
Correspondence
Address: Sport Physiology Department, Literature & Humanities Faculty, Shahrekord University, Km2 Saman Road, Shahrekord, IranPhone: -
Fax: -
f.fathollahi1363@gmail.com
Article History
Received: August 7, 2016Accepted: May 3, 2016
ePublished: September 8, 2017
BRIEF TEXT
Breast cancer is the most common cancer among women. It usually begins due to the abnormal growth and division of the various breast cells [1]. Types of therapies are used to improve breast cancer, including chemotherapy, surgery, radiation therapy, and the targeted therapy with trastuzumab (Herceptin brand name) [2]. One of the most effective and used chemotherapy drugs is anthracycline doxorubicin (DOX) [3]. Despite extensive clinical application, the mechanism of action of doxorubicin has remained discussed. The damage to non-target tissue often complicates the treatment of cancer and the heart is the preferred tissue for the toxicity of doxorubicin. This drug also affects other organs, such as the brain, the kidneys and the liver [4].
… [5-10]. There is some evidence that shows that there is an inverse relationship between levels of antioxidants and the risk of breast cancer [11]. There is also evidence that exercise protects against doxorubicin-dependent cardiac malfunction. For example, endurance training may strengthen body defense against doxorubicin`s cardiovascular toxicity [12]. Researchers believe that stress from exercise can be harmful and exacerbate conditions beyond the natural range of disease [13]. Some of side effects of exercise are attributed to the production of Reactive Oxygen Species (ROS). Excessive consumption of oxygen in endurance training following the ischemic phenomenon- the loss of blood flow to tissue increases the production of ROS and leads to oxidative stress [14].
One of the common practice methods is resistance training that it has the benefits of other exercises, including less oxygen requirements. It should be noted that so far no studies have been conducted on the effect of resistance training on antioxidant/oxidative indices on women with breast cancer that have been treated with doxorubicin chemotherapy. Therefore, the aim of this study was to investigate the effect of 8 weeks resistance training on some antioxidant/oxidative indices in postmenopausal women with breast cancer.
This study is semi-experimental.
This research was conducted in 2014 among postmenopausal women with breast cancer in Khorramabad, Iran.
To conduct the study, 35 subjects were selected through convenience sampling method. The 35 subjects were randomly divided into experimental (18 subjects) and control (17 subjects) groups, of which 5 were discarded at the time of the test. Finally, data were collected from 30 subjects (16 in the experimental group and 14 in the control group). The criteria for entering the study were: the completion of chemotherapy and pharmacotherapy at the moment, having no menstrual period from the previous 12 months, no smoking from the previous 12 months, no alcohol, at least one year from the time of surgery, and no heart disease, diabetes, non-controllable hypertension, thyroid disease, mental illness, infection, hormonal or immunological malformations, weight changes of 10% or more over the past 6 months, and any problem that disturbs their participation in resistance training program.
Measuring blood indicators: the subjects were told that they would not participate in any physical activity 48 hours before blood sampling and after the test. Blood sampling were performed in two stages (48 hours before the first session and 48 hours after the last session) after 12 hours of fasting overnight. At each stage, 10 ml of blood was taken from the prostate vein of the patients. Blood samples were centrifuged at 1500 rpm for 10 minutes to isolate the serum. Then, the serum was stored in the special containers of Eppendorf to measure the indices and immediately stored in a freezer of -80 ° C. To measure the amount of GPX and SOD enzymes, ELISA kit (CAYMAN, USA) was used with a coefficient of variation of 4.5% and sensitivity of 1.95 ng/ml, and a coefficient of variation of 0.5% and sensitivity of 0.04 μg / ml, respectively. Also, the MDA value was determined using a special kit (Cusabio Italy) with a coefficient of variation of 3.7% and a sensitivity of 7 nmol/ml. All variables were measured by ELISA. Resistance training protocol: A resistance training protocol was performed for 8 weeks and 3 sessions per week. Initially, 1 Maximum Repeat (1RM) of individuals was determined using the following formula: IRM= (Displaced weight (kg))/([1.0278-(number of repletiion unit fatigue)x0.0278]) The exercise program included 10 minutes of warm up with a variety of intense and tightening movements in the upper and lower muscles under the supervision of the instructor. The main protocol of the resistance training included leg pressures, chest press, paralysis, bending of knees (back of the thigh), shoulder, back of the arm, opening the knee (forehead) and forearm. The resistance training program was carried out progressively in the way that in the first and second weeks, there was 2 sets with 12 repetitions, in the 3rd and 4th weeks there was 3 sets with 10 repetitions, in the 5th and 6th weeks there were 3 sets with 8 repetitions, and in the 7th and 8th weeks, there were 4 sets with 6 repetitions. In addition, the resistance training program reached 30% of a maximum repetition at the beginning of the training to 45-50% of a maximum repetition at the end of the eighth week. The rest between the repetitions was also considered for 2 minutes. At the end of each training session, the subjects performed the cooling exercise for 10 minutes. Meanwhile, the time for running protocol was in the evening. Data analysis: data were analyzed using SPSS 10 software. To describe the data, central descriptive data, and dispersion indices were used and to determine the meaningfulness, inferential statistics were used. For this purpose, at first, the Kolmogorov-Simonov test was used to determine the normal distribution of data. Considering the normality of data distribution, the independent t-test and the dependent t-test were used to examine the intergroup and intragroup differences in the dependent variables respectively.
The mean age in the control group and experimental groups was 58.00±6.30 and 56.01±9.90 years respectively. There was a significant difference between the serum levels of GPX, SOD, and MDA in the experimental group before and after the 8 weeks of resistance training, so that in the post-test stage, the serum levels of SOD increased by 2.9%. The serum level of GPX was increased 11.8% and the MDA serum level was decreased by 11.9%. However, the changes in the control group was not significant. In the study of intergroup changes, GPX, SOD, and MDA serum levels was not significantly different between the two groups in the pretest stage. However, there was a significant difference between the two groups in the post-test stage (Table 1).
In the current study, 8 weeks of resistance training increased the levels of SOD by 2.9 % in the experimental group in the posttest stage compared to pretest stage. The results of this study is in consistency with the results of studies by Miyazaki et al. [15], Hathao et al. [16], and Gon et al. [17]. Also, resistance exercise increased serum levels of GPX by 11.8% and MDA reduction of 11.9% in the experimental group. In the present study, contrary to SOD, there was more consistent adaptations of GPX to exercise activity. Carant and Jawartanam [18], and Marsh et al. [19] reported that exercise caused increase in the amount of GPX in rest after exercise. … [20-30]. Lipid peroxidation induced by ROS produced by doxorubicin has been confirmed. In this regard, Swami et al. stated that induction of doxorubicin resulted in damage to heart muscle by reducing antioxidants (superoxide dismutase, catalase and glutathione) and an increase in oxidative indices (lactate dehydrogenase, keratin phosphokinase, and malondialdehyde) [31]. … [32].
Women with breast cancer are recommended to perform resistance training in order to reduce oxidative stress, and use resistance training as a non-prescriptive supplement under supervision of their doctors.
The limitations of this study were the lack of diet control and the effect of different doses of drugs.
8 weeks of resistance training increases the antioxidant indices and decreases the oxidative indices in postmenopausal women with breast cancer.
We thank all the patients who helped us with this study.
There is no conflicts of interests in this study.
This study has been morally codified in accordance with code SH/473/365.
This paper is based on a master`s thesis and its funding has been provided by researchers.
TABLES and CHARTS
Show attach fileCITIATION LINKS
[1]Kazemi AR, Eisanezhad A, Koushesh A, Farahbakhsh E, Ghanbarzade M. The effects of six weeks of aerobic interval training and use of tamoxifen on the levels of IL-6 and IL-10 tumor-bearing mice tumor breast cancer. Iran J Breast Dis. 2014;7(4):15-22. [Persian]
[2]Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. Cancer J Clin. 2016;66(1):7-30.
[3]Ascensao A, Oliveira PJ, Magalhaes J. Exercise as a beneficial adjunct therapy during doxorubicin treatment-role of mitochondria in cardioprotection. Int J Cardiol. 2012;156(1):4-10.
[4]Carvalho C, Santos RX, Cardoso S, Correia S, Oliveira PJ, Santos MS, et al. Doxorubicin: The good, the bad and the ugly effect. Curr Med Chem. 2009;16(25):3267-85.
[5]Simoncikova P, Ravingerova T, Barancik M. The effect of chronic doxorubicin treatment on mitogen-activated protein kinases and heat stress proteins in rat hearts. Physiol Res. 2008;57(Suppl 2):s97-102.
[6]Ascensao A, Magalhaes J, Soares J, Ferreira R, Neuparth M, Marques F, et al. Endurance training attenuates doxorubicin-induced cardiac oxidative damage in mice. Int J Cardiol. 2005;100(3):451-60.
[7]Bayer M, Paulsen G, Ugelstad I, Hallen J, Kalhovde J, Raastad T. Relocalization and upregulation of hsp70 after muscle damaging eccentric exercise. 11th Annual Congress of the European College of Cport Science. Lausanne/ Switzerland: University of Bern, University of Lausanne, École Polytechnique Fédérale de Lausanne and the Swiss Society of Sports Medicine; 2006.
[8]Benjamin IJ, Horie S, Greenberg ML, Alpern RJ, Williams RS. Induction of stress proteins in cultured myogenic cells. Molecular signals for the activation of heat shock transcription factor during ischemia. J Clin Invest. 1992;89(5):1685-9.
[9]Ascensao A, Magalhaes J, Soares J, Oliveira J, Duarte J. Exercise and cardiac oxidative stress. Rev Port Cardiol. 2003;22(5):651-78.
[10]Atalay M, Oksala NK, Laaksonen DE, Khanna S, Nakao C, Lappalainen J, et al. Exercise training modulates heat shock protein response in diabetic rats. J Appl Physiol. 2004;97(2):605-11.
[11]Berthiaume JM, Wallace KB. Adriamycin-induced oxidative mitochondrial cardiotoxicity. Cell biol Toxicol. 2007;23(1):15-25.
[12]Hydock DS, Lien CY, Schneider CM, Hayward R. Exercise preconditioning protects against doxorubicin-induced cardiac dysfunction. Med Sci Sports Exerc. 2008;40(5):808-17.
[13]Bowles DK. Curing the cure: Utilizing exercise to limit cardiotoxicity. Med Sci Sports Exerc. 2008;40(5):806-7.
[14]Jakovljevic VLi, Zlatkovic M, Cubrilo D, Pantic I, Djuric DM. The effects of progressive exercise on cardiovascular function in elite athletes: Focus on oxidative stress. Acta Physiol Hung. 2011;98(1):51-8.
[15]Miyazaki H, Oh-ishi S, Ookawara T, Kizaki T, Toshinai K, Ha S, et al. Strenuous endurance training in humans reduces oxidative stress following exhausting exercise. Eur J Appl Physiol. 2001;84(1-2):1-6.
[16]Hatao H, Oh-ishi S, Itoh M, Leeuwenburgh C, Ohno H, Ookawara T, et al. Effects of acute exercise on lung antioxidant enzymes in young and old rats. Mech Ageing Dev. 2006;127(4):384-90.
[17]Goon JA, Aini AH, Musalmah M, Anum MY, Nazaimoon WM, Ngah WZ. Effect of Tai Chi exercise on DNA damage, antioxidant enzymes, and oxidative stress in middle-age adults. J Phys Act Health. 2009;6(1):43-54.
[18]Karanth J, Jeevaratnam K. Oxidative stress and antioxidant status in rat blood, liver and muscle: Effect of dietary lipid, carnitine and exercise. Int J Vitam Nutr Res. 2005;75(5):333-9.
[19]Marsh SA, Laursen PB, Coombes JS. Effects of antioxidant supplementation and exercise training on erythrocyte antioxidant enzymes. Int J Vitam Nutr Res. 2006;76(5):324-31.
[20]Fhathollahi Shoorabeh F, Dabidiroshan V, Sheikhsaraf B, Nuri R. Investigating the effects of regular resistance training and prostatic massage on proinflammatory markers and serum prostate-specific antigen levels in males with prostate cancer. Middle East J Rehabil Health Stud. 2016;3(1):e33651.
[21]Billingham ME, Mason JW, Bristow MR, Daniels JR. Anthracycline cardiomyopathy monitored by morphologic changes. Cancer Treat Rep. 1978;62(6):865-72.
[22]Monti E, Prosperi E, Supino R, Bottiroli G. Free radicaldependent DNA lesions are involved in the delayed cardiotoxicity induced by Adriamycin in the rat. Anticancer Res. 1995;15(1):193-7.
[23]Bristow MR, Sageman WS, Scott RH, Billingham ME, Bowden RE, Kernoff RS, et al. Acute and chronic cardiovascular effects of doxorubicin in the dog: The cardiovascular pharmacology of drug-induced histamine release. J Cardiovasc Pharmacol. 1980;2(5):487-515.
[24]Tong J, Ganguly PK, Singal PK. Myocardial adrenergic changes at two stages of heart failure due to Adriamycin treatment in rats. Am J Physiol. 1991;260(3 Pt 2):H909-16.
[25]Singal PK, Segstro RJ, Singh RP, Kutryk MJ. Changes in lysosomal morphology and enzyme activities during the development of adriamycin-induced cardiomyopathy. Can J Cardiol. 1985;1(2):139-47.
[26]Singal PK, Pierce GN. Adriamycin stimulates lowaffinity ca2+ binding and lipid peroxidation but depresses myocardial function. Am J Physiol. 1986; 250(3 Pt 2):h419-25.
[27]Adams AK, Best TM. The role of antioxidants in exercise and disease prevention. Phys Sports Med. 2002;30(5):37-44.
[28]Nohl H. A novel superoxide radical generator in heart mitochondria. FEBS let. 1987;214(2):269-73.
[29]Davies KJ, Doroshow JH. Redox cycling of anthracyclines by cardiac mitochondria: Anthracycline radical formation by NADPH dehydrogenous. J Biol Chem. 1986;261(7):3060-7.
[30]Eder AR, Arriaga EA. Capillary electrophoresis monitors enhancement in subcellular reactive oxygen species production upon treatment with doxorubicin. Chem Res Toxicol. 2006;19(9):1151-9.
[31]Swamy AV, Gulliaya S, Thippeswamy A, Basavaraj C.K, Donnahalli VM. Cardioprotective effect of curcumin against doxorubicin-induced myocardial toxicity in albino rats. Indian J pharmacol. 2012; 44(1):73–7.
[32]Ammar el-SM, Said SA, Suddek GM, El-Damarawy SL. Amelioration of doxorubicin-induced cardiotoxicity by deferiprone in rats. Can J Physiol Pharmacol. 2011;89(4):269-76.
[2]Siegel RL, Miller KD, Jemal A. Cancer statistics, 2016. Cancer J Clin. 2016;66(1):7-30.
[3]Ascensao A, Oliveira PJ, Magalhaes J. Exercise as a beneficial adjunct therapy during doxorubicin treatment-role of mitochondria in cardioprotection. Int J Cardiol. 2012;156(1):4-10.
[4]Carvalho C, Santos RX, Cardoso S, Correia S, Oliveira PJ, Santos MS, et al. Doxorubicin: The good, the bad and the ugly effect. Curr Med Chem. 2009;16(25):3267-85.
[5]Simoncikova P, Ravingerova T, Barancik M. The effect of chronic doxorubicin treatment on mitogen-activated protein kinases and heat stress proteins in rat hearts. Physiol Res. 2008;57(Suppl 2):s97-102.
[6]Ascensao A, Magalhaes J, Soares J, Ferreira R, Neuparth M, Marques F, et al. Endurance training attenuates doxorubicin-induced cardiac oxidative damage in mice. Int J Cardiol. 2005;100(3):451-60.
[7]Bayer M, Paulsen G, Ugelstad I, Hallen J, Kalhovde J, Raastad T. Relocalization and upregulation of hsp70 after muscle damaging eccentric exercise. 11th Annual Congress of the European College of Cport Science. Lausanne/ Switzerland: University of Bern, University of Lausanne, École Polytechnique Fédérale de Lausanne and the Swiss Society of Sports Medicine; 2006.
[8]Benjamin IJ, Horie S, Greenberg ML, Alpern RJ, Williams RS. Induction of stress proteins in cultured myogenic cells. Molecular signals for the activation of heat shock transcription factor during ischemia. J Clin Invest. 1992;89(5):1685-9.
[9]Ascensao A, Magalhaes J, Soares J, Oliveira J, Duarte J. Exercise and cardiac oxidative stress. Rev Port Cardiol. 2003;22(5):651-78.
[10]Atalay M, Oksala NK, Laaksonen DE, Khanna S, Nakao C, Lappalainen J, et al. Exercise training modulates heat shock protein response in diabetic rats. J Appl Physiol. 2004;97(2):605-11.
[11]Berthiaume JM, Wallace KB. Adriamycin-induced oxidative mitochondrial cardiotoxicity. Cell biol Toxicol. 2007;23(1):15-25.
[12]Hydock DS, Lien CY, Schneider CM, Hayward R. Exercise preconditioning protects against doxorubicin-induced cardiac dysfunction. Med Sci Sports Exerc. 2008;40(5):808-17.
[13]Bowles DK. Curing the cure: Utilizing exercise to limit cardiotoxicity. Med Sci Sports Exerc. 2008;40(5):806-7.
[14]Jakovljevic VLi, Zlatkovic M, Cubrilo D, Pantic I, Djuric DM. The effects of progressive exercise on cardiovascular function in elite athletes: Focus on oxidative stress. Acta Physiol Hung. 2011;98(1):51-8.
[15]Miyazaki H, Oh-ishi S, Ookawara T, Kizaki T, Toshinai K, Ha S, et al. Strenuous endurance training in humans reduces oxidative stress following exhausting exercise. Eur J Appl Physiol. 2001;84(1-2):1-6.
[16]Hatao H, Oh-ishi S, Itoh M, Leeuwenburgh C, Ohno H, Ookawara T, et al. Effects of acute exercise on lung antioxidant enzymes in young and old rats. Mech Ageing Dev. 2006;127(4):384-90.
[17]Goon JA, Aini AH, Musalmah M, Anum MY, Nazaimoon WM, Ngah WZ. Effect of Tai Chi exercise on DNA damage, antioxidant enzymes, and oxidative stress in middle-age adults. J Phys Act Health. 2009;6(1):43-54.
[18]Karanth J, Jeevaratnam K. Oxidative stress and antioxidant status in rat blood, liver and muscle: Effect of dietary lipid, carnitine and exercise. Int J Vitam Nutr Res. 2005;75(5):333-9.
[19]Marsh SA, Laursen PB, Coombes JS. Effects of antioxidant supplementation and exercise training on erythrocyte antioxidant enzymes. Int J Vitam Nutr Res. 2006;76(5):324-31.
[20]Fhathollahi Shoorabeh F, Dabidiroshan V, Sheikhsaraf B, Nuri R. Investigating the effects of regular resistance training and prostatic massage on proinflammatory markers and serum prostate-specific antigen levels in males with prostate cancer. Middle East J Rehabil Health Stud. 2016;3(1):e33651.
[21]Billingham ME, Mason JW, Bristow MR, Daniels JR. Anthracycline cardiomyopathy monitored by morphologic changes. Cancer Treat Rep. 1978;62(6):865-72.
[22]Monti E, Prosperi E, Supino R, Bottiroli G. Free radicaldependent DNA lesions are involved in the delayed cardiotoxicity induced by Adriamycin in the rat. Anticancer Res. 1995;15(1):193-7.
[23]Bristow MR, Sageman WS, Scott RH, Billingham ME, Bowden RE, Kernoff RS, et al. Acute and chronic cardiovascular effects of doxorubicin in the dog: The cardiovascular pharmacology of drug-induced histamine release. J Cardiovasc Pharmacol. 1980;2(5):487-515.
[24]Tong J, Ganguly PK, Singal PK. Myocardial adrenergic changes at two stages of heart failure due to Adriamycin treatment in rats. Am J Physiol. 1991;260(3 Pt 2):H909-16.
[25]Singal PK, Segstro RJ, Singh RP, Kutryk MJ. Changes in lysosomal morphology and enzyme activities during the development of adriamycin-induced cardiomyopathy. Can J Cardiol. 1985;1(2):139-47.
[26]Singal PK, Pierce GN. Adriamycin stimulates lowaffinity ca2+ binding and lipid peroxidation but depresses myocardial function. Am J Physiol. 1986; 250(3 Pt 2):h419-25.
[27]Adams AK, Best TM. The role of antioxidants in exercise and disease prevention. Phys Sports Med. 2002;30(5):37-44.
[28]Nohl H. A novel superoxide radical generator in heart mitochondria. FEBS let. 1987;214(2):269-73.
[29]Davies KJ, Doroshow JH. Redox cycling of anthracyclines by cardiac mitochondria: Anthracycline radical formation by NADPH dehydrogenous. J Biol Chem. 1986;261(7):3060-7.
[30]Eder AR, Arriaga EA. Capillary electrophoresis monitors enhancement in subcellular reactive oxygen species production upon treatment with doxorubicin. Chem Res Toxicol. 2006;19(9):1151-9.
[31]Swamy AV, Gulliaya S, Thippeswamy A, Basavaraj C.K, Donnahalli VM. Cardioprotective effect of curcumin against doxorubicin-induced myocardial toxicity in albino rats. Indian J pharmacol. 2012; 44(1):73–7.
[32]Ammar el-SM, Said SA, Suddek GM, El-Damarawy SL. Amelioration of doxorubicin-induced cardiotoxicity by deferiprone in rats. Can J Physiol Pharmacol. 2011;89(4):269-76.