Regular concurrent training had not significant effect on CRP Level in obese middle-aged men

Journal of Physical Activity and Hormones

مقاله 1، دوره 2، شماره 1 - شماره پیاپی 5، اردیبهشت 2018، صفحه 1-12   

نوع مقاله: Original Article

نویسندگان

Zahra Momen nasab^* ؛ Mohadeseh Nematollahzadeh

MS in exercise physiology, The General Department of Fars Province Education

چکیده

Introduction: C-reactive protein (CRP) is a marker of chronic systemic inflammation frequently used in cardiovascular disease risk assessment. The effect of concurrent training on this protein is not well known. Thus, this study was conducted to determine the effects of 8 weeks concurrent training on CRP level in obese middle-aged men.
Material & Methods: Twenty three sedentary obese middle-aged men participated in this study as the subject. The subjects were randomly assigned to concurrent training group (n=12) or control group (n=11). The subjects in concurrent training group performed endurance and resistance training on the same days, 3 days a week for 8 weeks.
Results: Body mass, body mass index (BMI) and waist hip ratio (WHR) were decreased (P<0.05) after 8 weeks concurrent training compared to the control group. For CRP level no significant changes were observed after the intervention.
Conclusion: Although concurrent training is the useful strategy for reduce obesity; CRP level was not affected by 8-week concurrent training in obese middle-aged men.

کلیدواژه‌ها

Concurrent training؛ CRP؛ Inflammation؛ Obesity

اصل مقاله

Introduction

C-reactive protein (CRP), a marker of systemic inflammation, is an independent predictor of cardiovascular disease (CVD) in both women and men (1,2). CRP levels are influenced by sex (3-5), smoking (3,6,7), obesity (5,8), alcohol intake (9) and regular exercise (10). CRP levels measured using the high-sensitivity assay may be useful in the assessment of cardiovascular health (11-18).

Numerous cross-sectional reports have observed an inverse relation between physical activity and CRP (19,20) while exercise intervention studies have had conflicting results. Previous studies had reported that CRP not effected (21), decreased (22) and/or increased (23,24) in response to the exercise. In addition, it has been suggested that weight loss, concurrent with exercise, may be responsible for the reduction in CRP, not exercise training per se (19). The primary limitation of existing studies of the CRP response to exercise training is that they were not designed specifically with CRP as an outcome. In addition, these studies were unable to control for potential confounding variables, were underpowered to examine changes in markers of inflammation, and included populations with normal CRP levels. Finally, there may be misclassification of the exercise intervention because exercise was not tightly controlled to account for the dose administered (21). Generally, physical fitness has been reported to be associated with CRP levels, independent of other traditional cardiovascular risk factors (25,26). These findings suggest that the beneficial effects of exercise on cardiovascular health may be mediated partially by a decrease in inflammatory status in individuals with or without cardiovascular disease. However, the effect of concurrent training on CRP level is not well known. Thus, this study was conducted to determine the effects of 8 weeks concurrent training on CRP level in obese middle-aged men.

Material & methods

Subjects

Twenty three sedentary obese middle-aged men with a mean ( ± SD) body mass index of 32.9 ± 2.4 kg/m², volunteered to participate in a 8 weeks concurrent study. All the subjects were asked to complete a personal health and medical history questionnaire, which served as a screening tool. All the subjects were completely inactive at least 6 month before the study and they were non-smokers and free from unstable chronic condition, including dementia, retinal haemorrhage and detachment; and they have no history of myocardial infarction, stroke, cancer, dialysis, restraining orthopaedic or neuromuscular diseases. Informed consent was given to all subjects and prior the study. The study was approved by the Marvdasht branch, Islamic Azad University Ethics Committee. The subjects were randomly assigned to one of the concurrent training group (n=12) or control group (n=11).

 

Exercise protocol

The concurrent training group performed 20-30 min endurance exercise at an intensity corresponding to 70-85% individual maximum heart rate and then performed circuit weight training per day. Resistance training was circularly performed in 8 stations and included 2-4 sets with 8-12 maximal repetitions at 65-80% of 1-RM in each station. Each circuit and set was separated by 2-3 min and 30 s rest respectively. The intervention was performed 3 days a week for 8 weeks.

 

Anthropometric and body composition measurements

Height was measured with a fixed stadiometer (Seca, Germany) and weight was measured with a regularly calibrated electronic scale (Seca, Germany). Body mass index (BMI) was calculated by dividing weight (kg) by height (m²). Waist circumference was determined by obtaining the minimum circumference (narrowest part of the torso, above the umbilicus) and the maximum hip circumference while standing with their heels together. The waist to hip ratio (WHR) was calculated by dividing waist by hip circumference (cm).

 

Blood sampling and analyses

Fasting blood samples (5 ml) were collected from the antecubital vein at the same time before and 48 h after 8 weeks intervention. Serum obtained was frozen at -22 ^oC for subsequent analysis. CRP level was determined in duplicate via an enzyme-linked immunosorbent assay (ELISA) kits (Diagnostics Biochem Canada, Inc). The intra and inter-assay coefficients of variation for CRP were <5.7% and a sensitivity of 10 ng/ml.

 

Statistical analysis

Descriptive statistics were computed and and distributions of all variables were assessed for normality. Paired t-test was used to compute mean (± SD) changes in the variables in control and concurrent training group pre and after the intervention. Differences among groups were assessed by using independent- samples t-test. The level of significance in all statistical analyses was set at P

 

Results

Physical characteristics of the subjects are presented in Table 1. Before the intervention, there were no significant differences in body mass index, BMI and WHR among the groups. Body mass, BMI and WHR were decreased (P<0.05) after 8 weeks concurrent training compared to the control group.

 

Table 1. Anthropometric characteristics (mean ± SD) of the subjects before and after the training

	Control (mean ± SD)			Concurrent training (mean ± SD)
	Pretraining	Posttraining		Pretraining	Posttraining
Body mass (Kg)	106.6 ± 4.7	106.5 ± 7.6		98.08 ± 6.9	94.5 ± 7.4*†
BMI (Kg/m2)	34.1 ± 2.5	34.1 ± 3.3		31.8 ± 1.7	30.6 ± 1.4*†
WHR	0.95 ± 0.03	0.95 ± 0.04		0.96 ± 0.04	0.94 ± 0.04*†

*:P

†:P<0.05, pretraining vs. posttraining values.

 

The results also showed that CRP had no significant change after the intervention (Figure 1). No significant relationship was observed between CRP with body mass, BMI and WHR.

 

Figure 1. Change of CRP before and after the intervention

Discussion

Inflammation is considered an important pathogenic mechanism in both the initiation and progression of cardiovascular diseases (CVD) (27). One of the most commonly measured markers of inflammation in clinical settings is CRP (28,29). Plasma levels of CRP have been reported to be a strong independent predictor of risk of future myocardial infarction, stroke, peripheral arterial disease, and vascular death among individuals without known CVD (28).

On the other hand, obesity has been associated with elevated levels of CRP (30). In a study involving 892 middle-age subjects, CRP levels were inversely correlated with exercise capacity (31) as well as in 1660 subjects with metabolic syndrome (32). Physical activity and exercise reduces CRP levels by multiple mechanisms, including a decrease in cytokine production by adipose tissue, improved endothelial function and insulin sensitivity, and possibly an antioxidant effect (33), among other factors. Chronic inflammation may be modulated by metabolic variables, such as BMI (34,35) and lipid profile (36), which may also be influenced by regular exercise (37). Also, the impact of exercise on inflammation in populations with excess weight is controversial and how exercise training reduces inflammation and decreases CRP levels is not well defined. While various studies show that exercise reduces inflammation, specifically CRP (38,39), other studies found no change in this parameter (40,41). We hypnotized that exercise would reduce the body mass and BMI and decrease CRP in obese men. Our results demonstrated that although body mass, BMI and WHR were decreased (P<0.05) after the intervention, CRP levels had no significant changes after 8 weeks training. On the other hand, no significant relationship was observed between CRP level change with body mass, BMI and WHR after the intervention. The relationship between the changes of CRP level with body composition is not well defined. In line with our results, Kelley and Kelley (2006) reported that aerobic exercise does not reduce CRP levels in adults, but does improve measures of body composition and physical fitness (37). However, other researchers noted that engaging in exercise training is associated with a decrease in CRP levels regardless of the decrease in BMI and body fat percent (22,42). Behind the improvement on body composition, the other mechanisms might contribute on CRP reduction after the regular exercise. Exercise can reduce the release of cytokines such as IL-6 and TNF-α by adipocyte tissue, downregulating the sympathetic tonus (43). Exercise training and physical fitness have been associated with endothelial function by increased release of endothelium-derived nitric oxide (44). The increased production of nitric oxide by endothelial cells may reduce the effects of proinflammatory cytokines and decrease CRP levels (45).

We had some limitations in this study. We didn’t measure the other inflammatory markers and cytokines and indeed we didn’t measure nitric oxide in the present study. Additional research is needed to examine the mechanisms that effect on CRP regulation after the exercise.

 

Conclusion

In conclusion, although concurrent training is the useful strategy for reduce obesity; CRP level was not affected by 8-week concurrent training in obese middle-aged men.

 

Acknowledgment

We wish to thanks all subjects whom cooperated in this study.

 

Conflict of interests: No conflict of interests amongst authors.

 

 

 

مراجع

References

1. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation 2001: 103: 1813-1818.

2. Ridker PM, Rifai N, Rose L, Buring JE, Cook NR. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med 2002; 347: 1557-1565.

3. Araujo F, Pereira AC, Latorre R, Krieger JE, Mansur AJ. High-sensitivity C-reactive protein concentration in a healthy Brazilian population. Int J Cardiol 2004; 97: 433438.

4. Khera A, McGuire DK, Murphy SA, Stanek HG, Das SR, Vongpatanasin W, et al. Race and gender differences in C-reactive protein levels. J Am Coll Cardiol 2005; 46: 464-469.

5. Ishii S, Karlamangla AS, Bote M, Irwin MR, Jacobs DR Jr, Cho HJ, et al. Gender, obesity and repeated elevation of C-reactive protein: Data from the CARDIA cohort. PLoS One 2012; 7:e36062.

6. Madsen C, Nafstad P, Eikvar L, Schwarze PE, Rønningen KS, Haaheim LL. Association between tobacco smoke exposure and levels of C-reactive protein in the Oslo II Study. Eur J Epidemiol 2007; 22: 311-317.

7. Sauriasari R, Sakano N, Wang DH, Takaki J, Takemoto K, Wang B, et al. C-reactive protein is associated with cigarette smoking-induced hyperfiltration and proteinuria in an apparently healthy population. Hypertens Res 2010; 33: 1129-1136.

8. Williams MJ, Williams SM, Milne BJ, Hancox RJ, Poulton R. Association between C-reactive protein, metabolic cardiovascular risk factors, obesity and oral contraceptive use in young adults. Int J Obes Relat Metab Disord 2004; 28: 998.

9. Albert MA, Glynn RJ, Ridker PM. Alcohol consumption and plasma concentration of C-reactive protein. Circulation 2003; 107: 443-447.

10. Rimm EB. Lifestyle predictors of C-reactive protein. In: Ridker PM, Rifai N, editors. C-reactive protein and cardiovascular disease. MediEdition; Canada: 2006; 8: 307-322.

11. Koenig W, Sund M, Fröhlich M, Fischer HG, Löwel H, Döring A, et al. C- reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: Results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992. Circulation 1999; 99: 237-242.

12. Danesh J, Whincup P, Walker M, Lennon L, Thomson A, Appleby P, et al. Low grade inflammation and coronary heart disease: Prospective study and updated meta-analyses. BMJ 2000; 321: 199-204.

13. Koenig W, Löwel H, Baumert J, Meisinger C. C-reactive protein modulates risk prediction based on the Framingham Score implications for future risk assessment: Results from a large cohort study in southern Germany. Circulation 2004; 109: 1349-1353.

14. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336: 973-939.

15. Ridker PM, Buring JE, Shih J, Matias M, Hennekens CH. Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women. Circulation 1998; 98: 731-733.

16. Cushman M, Arnold AM, Psaty BM, Manolio TA, Kuller LH, Burke GL, et al. C-reactive protein and the 10-year incidence of coronary heart disease in older men and women: The cardiovascular health study. Circulation 2005; 112: 25-31.

17. Ridker PM, Rifai N. C-reactive protein and cardiovascular disease.C-reactive protein in the primary prevention of myocardial infarction and stroke; MediEdition; Canada 2006; 9: 1-23.

18. Ridker PM, Buring JE, Rifai N, Cook NR. Development and validation of improved algorithms for the assessment of global cardiovascular risk in women: The Reynolds Risk Score. JAMA 2007; 297: 611-619.

19. Hamer M. The relative influences of fitness and fatness on inflammatory factors. Prev Med 2007; 44: 3-11.

20. Kasapis C, Thompson PD. The effects of physical activity on serum C-reactive protein and inflammatory markers: a systematic review. J Am Coll Cardiol 2005; 45: 1563-1569.

21. Church TS, Earnest CP, Thompson AM, Priest EL, Rodarte RQ, Saunders T, et al. Exercise without weight loss does not reduce C-reactive protein: the INFLAME study. Med Sci Sports Exerc 2010; 42: 708-716.

22. Fedewa MV, Hathaway ED, Ward-Ritacco CL. Effect of exercise training on C reactive protein: a systematic review and meta-analysis of randomised and non-randomised controlled trials. Br J Sports Med 2017; 51: 670-676.

23. Wakshlag JJ, Stokol T, Geske SM, Greger CE, Angle CT, Gillette RL. Evaluation of exercise-induced changes in concentrations of C-reactive protein and serum biochemical values in sled dogs completing a long-distance endurance race. Am J Vet Res 2010; 71: 1207-1213.

24. Mouridsen MR1, Nielsen OW1, Carlsen CM1, Mattsson N1, Ruwald MH2, Binici Z, et al. High-sensitivity C-reactive protein and exercise-induced changes in subjects suspected of coronary artery disease. J Inflamm Res 2014; 7: 45-55.

25. Kohli P, Gulati M. Exercise stress testing in women: Going back to the basics. Circulation 2010; 122: 2570-2580.

26. Kullo IJ, Khaleghi M, Hensrud DD. Markers of inflammation are inversely associated with VO2 max in asymptomatic men. J Appl Physiol 2007; 102: 1374-1379.

27. Tam CS, Clément K, Baur LA, Tordjman J. Obesity and low-grade inflammation: a paediatric perspective. Obes Rev 2010; 11: 118-126.

28. Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation 2003; 107: 363-369.

29. Danesh J, Collins R, Appleby P, Peto R. Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease. JAMA 1998; 279: 1477-1482.

30. Choi J, Joseph L, Pilote L. Obesity and C-reactive protein in various populations: a systematic review and meta-analysis. Obes Rev 2013; 14: 232-244.

31. Myers J, Prakash M, Froelicher V, Do D, Partington S, Atwood JE. Exercise capacity and mortality among men referred for exercise testing. N Engl J Med 2002; 346: 793-801.

32. Jouven X, Empana JP, Schwartz PJ, Desnos M, Courbon D, Ducimetière P. Heart-rate profile during exercise as a predictor of sudden death. N Engl J Med 2005; 352: 1951-1958.

33. Kasapis C, Thompson PD. The effects of physical activity on serum C-reactive protein and inflammatory markers: a systematic review. J Am Coll Cardiol 2005; 45: 1563-1569.

34. Festa A, D’Agostino R, Jr, Williams K, Karter AJ, Mayer-Davis EJ, Tracy RP, et al. The relation of body fat mass and distribution to markers of chronic inflammation. Int J Obes Relat Metab Disord 2001; 25: 1407-1415.

35. Rawson ES, Freedson PS, Osganian SK, Matthews CE, Reed G, Ockene IS. Body mass index, but not physical activity, is associated with C-reactive protein. Med Sci Sports Exerc 2003; 35: 1160-1166.

36. Kazumi T, Kawaguchi A, Hirano T, Yoshino G. C-reactive protein in young, apparently healthy men: Associations with serum leptin, QTc interval, and high-density lipoprotein-cholesterol. Metabolism 2003; 52: 1113-1116.

37. Kelley GA, Kelley KS. Effects of aerobic exercise on C-reactive protein, body composition, and maximum oxygen consumption in adults: A meta-analysis of randomized controlled trials. Metabolism 2006; 55: 1500-1507.

38. Reinehr T, Stoffel-Wagner B, Roth CL, Andler W. High-sensitive C-reactive protein, tumor necrosis factor alpha, and cardiovascular risk factors before and after weight loss in obese children. Metabolism 2005; 54: 1155-1161.

39. Tsang TW, Kohn M, Chow CM, Singh MF. A randomized controlled trial of Kung Fu training for metabolic health in overweight/obese adolescents: the “martial fitness” study. J Pediatr Endocrinol Metab 2009; 22: 595-607.

40. Nassis GP, Papantakou K, Skenderi K, Triandafillopoulou M, Kavouras SA, Yannakoulia M, et al. Aerobic exercise training improves insulin sensitivity without changes in body weight, body fat, adiponectin, and inflammatory markers in overweight and obese girls. Metabolism 2005; 54: 1472-1479.

41. Barbeau P, Litaker MS, Woods KF, Lemmon CR, Humphries MC, Owens S, et al. Hemostatic and inflammatory markers in obese youths: effects of exercise and adiposity. J Pediatr 2002; 141: 415-420.

42. García-Hermoso A, Sánchez-López M, Escalante Y, Saavedra JM, Martínez-Vizcaíno V. Exercise-based interventions and C-reactive protein in overweight and obese youths: a meta-analysis of randomized controlled trials. Pediatr Res 2016; 79: 522-527.

43. Mohamed-Ali V, Bulmer K, Clarke D, Goodrick S, Coppack SW, Pinkney JH. β-Adrenergic regulation of proinflammatory cytokines in humans. Int J Obes Relat Metab Disord 2000; 2: S154-S155.

44. Green DJ, Maiorana A, O’Driscoll G, Taylor R. Effect of exercise training on endothelium-derived nitric oxide function in humans. J Physiol 2004; 561: 1-25.

45. Nunes RA1, Araújo F, Correia GF, da Silva GT, Mansur AJ. High-sensitivity C-reactive protein levels and treadmill exercise test responses in men and women without overt heart disease. Exp Clin Cardiol 2013; 18:124-128.