Exercise training is not associated with improved levels of C-reactive protein or adiponectin Taylor J. Marcell a,b, * , Kirsten A. McAuley c , Tinna Traustado ´ ttir b , Peter D. Reaven d a School of Human Performance and Recreation, University of Southern Mississippi, Hattiesburg, MS 39406-001, USA b KLRI, Phoenix, AZ 85016, USA c Edgar National Centre for Diabetes Research, Otago University, Dunedin 9021, New Zealand d Carl T. Hayden Veteran’s Administration, Phoenix, AZ 85012, USA Received 16 June 2004; revised 12 October 2004; accepted 3 November 2004 Abstract The purpose of this study was to determine the effect of exercise training on the levels of C-reactive protein (CRP) and adiponectin, and to assess whether exercise-induced changes in insulin resistance could be explained in part by changes in these inflammation markers. Study participants included 51 middle-aged (45.3 F 8.3 years; mean F SD), overweight (33.7 F 4.8 BMI), insulin-resistant, nondiabetic individuals. Subjects had their insulin sensitivity, body fat, CRP, and adiponectin levels measured, and their predicted maximal fitness calculated before and after 16 weeks of moderate, intense, or no exercise training. Modest improvements in fitness, body composition, and insulin sensitivity were observed, but these changes were not associated with decreased CRP or increased adiponectin levels, even when subjects were stratified by their change in fitness or obesity. Regression analysis demonstrated that the change in percentage of body fat was significantly related to changes in insulin sensitivity, whereas changes in VO 2 MAX, CRP, and adiponectin were not. Participation in moderate to intense exercise was not associated with improved measures of chronic inflammation markers, as measured by CRP and adiponectin. Moreover, improvements in insulin sensitivity resulting from exercise or modest weight loss did not appear to be related to changes in these markers. D 2005 Elsevier Inc. All rights reserved. 1. Introduction With the recognition that atherosclerosis is in fact an inflammatory condition [1], there has been greater appreci- ation for the importance of the many sources, consequences, and regulators of pro- and anti-inflammatory factors. An association between plasma C-reactive protein (CRP) concentrations, an excellent marker of inflammation, and cardiovascular disease (CVD) has been noted in both men and women [2,3]. Additional studies have outlined numer- ous mechanisms by which CRP may directly contribute to vascular inflammation and atherosclerosis [4-6]. Several lines of investigation also suggest the possibility that local and systemic inflammation may be important mediators in the development of insulin resistance and type 2 diabetes in many individuals [7,8]. In support of this notion, epidemiologic studies have demonstrated that several well- accepted markers of inflammation, such as interleukin 6 (IL- 6) and CRP, are independent predictors of incident diabetes [7,9]. It is now recognized that adipocytes, particularly those located within the visceral fat, are major secretors of both pro- and anti-inflammatory factors, often referred to as adipokines [10]. Although IL-6 is produced by several tissues, it has been estimated that as much as 30% may be secreted from adipocytes [11]. As IL-6 is the predominant stimulator of hepatic production of CRP, it is clear that fat tissue may be an important direct, as well as indirect, source of cytokines and inflammatory mediators [12]. An association between various adipokines and insulin resistance has been noted in both diabetic and nondiabetic states [13,14]. Of particular interest have been the recent studies demonstrating that adiponectin may play a direct role in mediating insulin-stimulated glucose uptake [15,16]. 0026-0495/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.metabol.2004.11.008 * Corresponding author. School of Human Performance and Recrea- tion, University of Southern Mississippi, Hattiesburg, MS 39406-001, USA. Tel.: +1 601 266 5599. E-mail address: taylor.marcell@usm.edu (T.J. Marcell). Metabolism Clinical and Experimental 54 (2005) 533 – 541 www.elsevier.com/locate/metabol