Aerobic training program is associated with improved systemic inflammation in smokers

Paper Details

Research Paper 01/04/2013
Views (248) Download (6)
current_issue_feature_image
publication_file

Aerobic training program is associated with improved systemic inflammation in smokers

Behbudi Laleh, Rohani Aliakbar, Jafari Rafat, Kaboli Mohamadzaman
Int. J. Biosci.3( 4), 222-227, April 2013.
Certificate: IJB 2013 [Generate Certificate]

Abstract

It was reported that smoker individuals are more prone to systemic inflammation than non-smokers. The objective of this study was to determine serum TNF-α response to a long term aerobic training in smoker men. For this purpose, thirty middle-aged healthy smokers selected for participate in this study and were divided into control and exercise groups by randomly. All subjects in exercise group were completed three months aerobic exercise training for 3 times weekly and the subjects of control group were banned on any regular training in this period. Anthropometrical and serum TNF-α were measured before and after this program in two groups. Student’s t-tests for paired samples were performed to determine whether there were significant within-group changes in the outcomes. At baseline there were no differences in the anthropometrical and biochemical parameters between the two groups. Compared to pre-training, the TNF-α level decreased significantly after aerobic program in exercise group, but not in control group. Anthropometrics variables decreased significantly after exercise intervention in exercise groups. Based on these finding, we can say that regular exercise training is associated with improved systemic inflammation in smoker men

VIEWS 1

Barbieri SS, Weksler BB. 2007. Tobacco smoke cooperates with interleukin-1 β to alter β-catenin trafficking in vascular endothelium resulting in increased permeability and induction of cyclooxygenase-2 expression in vitro and in vivo. Federation of American Societies for Experimental Biology 21, 1831-43.

Bermudez EA, Rafai N, Buring JE. 2002. Relation between markers of systemic vascular inflammation and smoking in women. American Journal of Cardiology 89, 1117–1119.

Charles P. Lambert, Nicole R. Wright, Brian N. Finck, and Dennis T. Villareal. 2008. Exercise but not diet-induced weight loss decreases skeletal muscle inflammatory gene expression in frail obese elderly persons. Journal of Applied Physiology 105, 473–478.

Chung KF. 2001. Cytokines in chronic obstructive pulmonary disease. European Respiratory Journal 34, 50-59.

Frohlich M, Sund M, Frolich M. 2003. Independent association of various smoking characteristics with markers of systemic inflammation in men: results from a representative sample of the general population (MONICA Augsburg Survey 1994/95). European Heart Journal 24, 1365– 1372.

Greiwe JS, Cheng B, Rubin DC, Yarasheski KE, Semenkovich CF. 2001. Resistance exercise decreases skeletal muscle tumor necrosis factor alpha in frail elderly humans. Federation of American Societies for Experimental Biology 15, 475–482.

Helmersson J, Larsson A, Vessby B. 2005. Active smoking and a history of smoking are associated with enhanced prostagladin F (2α) interleukin-6 and F2-isoprostane formation in elderly men. Atherosclerosis 181, 201–207.

Jovinge S, Hamsten A, Torvall P, Proudler A, Bavenholm P, Ericsson CG, Godland I, de farire Y. 1998. Evidence for a role of tumor necrosis factor alpha in disturbances of triglyceride and glucose metabolism predisposing to coronary heart disease. Metabolism 47, 113–8.

Lang CH, Frost RA, Nairn AC, MacLean DA, Vary TC. 2002. TNF-alpha impairs heart and skeletal muscle protein synthesis by altering translation initiation. American Journal of Physiology – Endocrinology and Metabolism 282, 336–347.

Lang CH, Frost RA. 2007. Sepsis-induced suppression of skeletal muscle translation initiation mediated by tumor necrosis factor alpha. Metabolism 49, 56-57.

Merghani TH, Saeed A, Alawad A. 2012. Changes in plasma IL4, TNFá and CRP in response to regular passive smoking at home among healthy school children in Khartoum, Sudan. African Health Sciences 12(1), 41-47.

Miller GD, Nicklas DJ, Loeser RF. 2008. Inflammatory biomarkers and physical function in older, obese adults with knee pain and self-reported osteoarthritis after intensive weight-loss therapy. Journal of the American Geriatrics Society 644, 51-56.

Naoya W, Mitsuo F, Ataru T, Takahide O, Yoshio N, Fusanori N, Sae A. 2011. Smoking, white blood cell counts, and TNF system activity in Japanese male subjects with normal glucose tolerance. Tobacco Induced Diseases 9(12), 2-6.

Pang B, Wang C, Weng X, Tang X, Zhang H, Niu S, Mao Y, Xin P and Huang X. 2000. Lung injury caused by passive smoking and its effects on cytokines in rats. Zhonghhua Yu Fang Yi Xue Za Zhi 34(2), 104-105.

Pessina GP, Paulesu L, Corradeschi F, Luzzi E, Tanzini M, Aldinucci C, Stefano AD, Bocci V. 1993. Chronic cigarette smoking enhances spontaneous release of tumour necrosis factor-á from alveolar macrophages of rats. Mediators of Inflammation 2(6), 423 –428.

Puglisi MJ, Fernandez ML. 2008. Modulation of C-reactive protein, tumor necrosis factor-alpha, and adiponectin by diet, exercise, and weight loss. Journal of Nutrition 138(12), 2293-6.

Puglisi MJ, Vaishnav U, Shrestha S, Torres-Gonzalez M, Wood RJ, Volek JS, Fernandez ML. 2008. Raisins and additional walking have distinct effects on plasma lipids and inflammatory cytokines. Lipids in Health and Disease 7, 14.

Qin B,  Anderson RA,  Adeli  K.  2008.  Tumor necrosis factor-a directly stimulates the overproduction of hepatic apolipoprotein B100-containing VLDL via impairment of hepatic insulin signaling. American Journal of Physiology: Gastrointestinal and Liver Physiology 294, 1120–9.

Sharman MJ, Volek JS. 2004. Weight loss leads to reductions in inflammatory biomarkers after a very-low-carbohydrate diet and a low-fat diet in overweight men. Clinical Science 107, 365–9.

Williamson  DL,  Kimball  SR,  Jefferson  LS. 2005. Acute treatment with TNF-alpha attenuates insulin-stimulated protein synthesis in cultures of C2C12 myotubes through a MEK1-sensitive mechanism. American Journal of Physiology – Endocrinology and Metabolism 289, 95–104.