Consequences of aerobic resistance exercise combined with Liprimar in the treatment of Chronic obstructive pulmonary disease Liprimar and aerobic resistance exercise on lung function
Main Article Content
Keywords
aerobic resistance exercise; atorvastatin; Chronic obstructive pulmonary disease (COPD)
Abstract
Abstract. Background: Aerobic resistance exercise is fundamentally required for the patients with COPD at a stable stage, to recover their exercise function. While the patients need to be supplemented with medication as well to inhibit the production of inflammatory factors. Atorvastatin calcium (a derivative of Atorvastatin) is reported as component in Liprimar. However, there are only few studies available on the treatment of COPD by Liprimar. The current study investigates the therapeutic value of aerobic resistance exercise, combined with Liprimar, in treating COPD patients and attempts to provide a basis for the treatment of COPD. Methods: The author(s) recruited a total of 147 patients diagnosed with COPD and were hospitalized at Internal medicine department, Third Clinical Medical College, Xinjiang Medical University (Cancer Hospital) and the study period was between October 2015 and June 2019. 120 patients were selected as subjects of this experiment on a voluntary basis. Aerobic resistance exercise therapy, Liprimar and combination therapy were provided to the patients. The patients’ physical fitness indicators, levels of inflammatory cytokines and cardiopulmonary function were observed to evaluate the treatment plan. Results: The COPD patients who received aerobic and obstructive exercise treatment, in combination with Liprimar, showed improvement in the indicators related to physical fitness, decreased body fat percentage, waist-to-hip ratio, BMI, blood sugar, Hba1c content, blood lipid, low levels of inflammatory factors (such as IL-8, IL-6, TNF-α), and notable recovery in cardiopulmonary function. Conclusions: A combination of aerobic and obstructive exercises with Liprimar can treat COPD patients in a better way. It can improve the exercise function and cardiopulmonary function of the patients. However, the clinical application of this treatment plan should be verified with more sample size. Further, the clinical application should also adjust the plan appropriately, according to individual differences.
References
[2] Kikugawa K, Machida Y, Kida M, et al. study on peroxidized lipids Ⅲ: Fluorescent pigments derived from the reaction of malonaldehyde and amino acids. Chem Pharm Bull, 1981, 29 (11) :3003 -3011. [DOI:10.1248/cpb.29.3003]
[3] Wolf f A A, Hines D K, Karliner T S. Refined membrane preparations mask ischemic fall in myocardial β -receptor density. Am J physiol, 1989, 257(3 Pt 2):H1032 -1036. [PMID:2551189 DOI:10.1152/ajpheart.1989.257.3.H1032]
[4] Hwang D F, Wang L C. Effect of taurine on toxicity of cadmium in rats. Toxicology , 2001 , 167(3):173 -180 . [DOI:10.1016/S0300-483X(01)00472-3]
[5] Nieminen M L, Tuomist O L, Solatunturi E, et al. Taurine in the osmoregnlation of the Brat teboro rat. Life Sci, 1988, 42(21):2137 -2143. [DOI:10.1016/0024-3205(88)90128-2]
[6] Chronic Obstructive Pulmonary Disease Committee, Respiratory Society, Chinese Medical Association. Guidelines for the diagnosis and treatment of chronic obstructive pulmonary disease (2007 revision) [S]. Chinese Journal of Tuberculosis and Respiratory Diseases, 2007，30( 1) : 8 － 17．
[7] El Idrissi A, Messing J, Scalia J, et al. Prevent ion of epilepti cseizures by taurine. Adv Exp Med Biol, 2003, 526:515-525. [PMID:12908638 DOI:10.1007/978-1-4615-0077-3_62]
[8] El Idrissi A, Trenkner E. Taurine regulates mitochond rial calcium homeostasis. Adv Exp Med Biol, 2003, 526:527-536. [PMID:12908639 DOI:10.1007/978-1-4615-0077-3_63]
[9] Camerino D C, Tricarico D, Pierno S, et al. Taurine and skeletal muscle disorders. Neu rochem Res, 2004, 29(1):135-142. [PMID:14992272 DOI:10.1023/B:NERE.0000010442.89826.9c]
[10] Urso M L, Clarkson P M. Oxidative stress, exercise, and antioxidant supplementation. Toxicology, 2003, 189(14):41-54. [DOI:10.1016/S0300-483X(03)00151-3]
[11] Yin D Z, Chen K J. The essential mechanisms of aging: Irreparable damage accumulation of biochemical side-reactions. Experimental Gerontology, 2005, 40:455 -465. [PMID:15935593 DOI:10.1016/j.exger.2005.03.012]
[12] Dawson R Jr, Biasetti M, Messina S, et al. The cytoprotective role of taurine in exercise -induced muscle injury. Amino Acids, 2002, 22(4):309 -324. [PMID:12107759 DOI:10.1007/s007260200017]
[13] Nandhini AT, Thirunavukkarasu V, Ravichand ran MK, et al , Effect of taurine on biomarkers of oxidative stress in tissues of fructose -fed insulin-resistant rat s .Singapore Med J , 2005, 46(2):82-87.
[14] Schreuder THA, Munckhof IVD, Poelkens F, et al. Combined aerobic and resistance exercise training decreases peripheral but not central artery wall thickness in subjects with type 2 diabetes. European Journal of Applied Physiology, 2015, 115( 2) : 317 - 326. [PMID:25308877 DOI:10.1007/s00421-014-3016-5]
[14] Mohammed J, Derom E,Van OJ, et al. Evidence for aerobic exercise training on the autonomic function in patients with chronic obstructive pulmonary disease ( COPD) : a systematic review. . Physiotherapy,2017, 104 (1): 12 - 14.
[16] Sherpa CT, Leclerq SL, Singh S, et al. Validation of the St. George＇s Respiratory Questionnaire in Nepal. Chronic Obstr Pulm Dis, 2015,2 (4): 281 - 289. [PMID:28848850 DOI:10.15326/jcopdf.2.4.2014.0156]
[17] Martin S, Wolf Eichbaum D, Duinkerken G, et a1. Development of type 1 diabetes despite severe hereditary β-cell deficiency. New England Journal of Medicine,2001,315(11):1036-1010.
[PMID:11586956 DOI:10.1056/NEJMoa010465]
[18] Alidjinou EK, Sané F, Engelmann, et al. Enterovirus persistence as a mechanism in the pathogenesis of type 1 diabetes. Dicovery Medicine,2011,18(100):273-282.
[18] Schneider DA, Von Herrath MG. Potential viral pathogenic mechanism in human type 1 diabetes. Diabetologia,2011,57(10):2009-2018. [PMID:25073445 DOI:10.1007/s00125-014-3340-7]
[20] Ramakrishna V,Jailkhani R. Evaluation of oxidative stress in insulin dependent diabetes mellitus (IDDM) patients.Diagnostic Pathology,2007,2(1):22-21. [PMID:17603912 DOI:10.1186/1746-1596-2-22]
[21] Hieronymus L,Geil P.Family awareness. Monitoring diabetes risk. Diabetes selfmanagement, 2011, 31(1):22-21.
[22] Chang AM, Halter JB. Aging and insulin secretion.American Journal Physiol Endocrinol Metabolism,2003,248(1):E7-E12. [PMID:12485807 DOI:10.1152/ajpendo.00366.2002]
[23] Dillon N, Chung S, Kelly J, Malley K. Age and beta adrenoceptor-mediated function.Clinic Pharmacology Therapy,1984,27:769-772. [PMID:6247116 DOI:10.1038/clpt.1980.108]
[24] Saitoh S, Shimoda T, Hamamoto Y, et al. Correlations among obesity-associated gene polymorphisms, body composition, and physical activity in patients with type 2 diabetes mellitus.Indian Journal of Endocrinology Meatabolism, 2015,19(1):66-71. [PMID:25593829 DOI:10.4103/2230-8210.131757]
[25] Hahn V, Halle M,Schmidt TA, et al. Physical activity and metabolic syndrome in elderly German and women. Diabetes Care, 2009,32(3):511-513. [PMID:19074996 DOI:10.2337/dc08-1285]
[26] Hui SS, Hui GP, Xie YJ. Association between physical activity knowledge and levels of physical Activity in Chinese adults with type 2 diabetes. Plos One,2014,9(12):1371-1378. [PMID:25493559 DOI:10.1371/journal.pone.0115098]
[27] Paffenbarger RS Jr, Lee IM, Kamperl JB. Physical activity in the prevention of noninsulindependent diabetes mellitus.World Review of Nutrion Dietecs, 1997,82:210~218.
[PMID:9270323 DOI:10.1159/000059640]
[28] Wakabayashi. Relationship between smoking and metabolic syndrome in men with diabetes mellitus. Metabolic Syndrome and Related Disorders, 2014, 12 (1): 70-78. [PMID:24266721 DOI:10.1089/met.2013.0110]
[29] Wei XE M, Yu S. A meta-analysis of passive smoking and risk of developing type 2 diabetes mellitus.Diabetes Research and Clinical Practice,2015,107(1):9-14. [PMID:25488377 DOI:10.1016/j.diabres.2014.09.019]
[30] Choi SE, Choi KM, Yoon IH, et a1. IL-6 protects pancreatic islet beta cells from pro-inflammatory cytokines-induced cell death and functional impairment in vitro and in vivo.Trandplant Immunology,2004,13(1):43-53. [PMID:15203128 DOI:10.1016/j.trim.2004.04.001]
[31] Ezzidi I, Mtraoui N, Chaieb M, et al. Diabetic retinopathy, PAI-1 4G/5G and 844G/A polymrphisms and changes in circulating PAI-1 levels in Tunisian type 2 diabetes patients.Diabetes Metabolism,2009, 35(3):214-219. [PMID:19419896 DOI:10.1016/j.diabet.2008.12.002]
Article Sidebar
Article Details
How to Cite
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Transfer of Copyright and Permission to Reproduce Parts of Published Papers.
Authors retain the copyright for their published work. No formal permission will be required to reproduce parts (tables or illustrations) of published papers, provided the source is quoted appropriately and reproduction has no commercial intent. Reproductions with commercial intent will require written permission and payment of royalties.
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
How to Cite
