fitness healthy

Poor physical fitness is a cardiovascular disease (CVD) risk factor (1–3). Given that physically fit, habitually active persons are at lower risk of obesity and weight gain (4), the protective effects of fitness may be partly mediated through adiposity, although this issue remains controversial. Previous epidemiologic studies have suggested that fitness is an independent predictor of CVD risk (5–7), which suggests that persons who are obese yet fit may have a lower risk of CVD than do those who are obese and unfit. However, contrasting studies suggest that obesity is a stronger risk factor, independently from fitness (8, 9). The mechanisms for the potential protective effects of fitness in obesity are incompletely understood, although specific risk markers such as inflammation have gained attention (10).

Several population studies have shown inverse associations between fitness and inflammatory markers independently of fatness (11–13), although others have suggested that obesity is a risk factor regardless of fitness (14–16). In addition, randomized controlled trials are equivocal. For example, in 152 female smokers, no changes were observed in C-reactive protein (CRP) or fibrinogen after a 12-wk exercise program that improved physical fitness, although body weight remained stable (16). In 193 sedentary, mildly obese men and women, 6-mo exercise training did not alter concentrations of CRP despite improvements in fitness and in visceral and subcutaneous adiposity (17). In contrast, significant reductions in inflammatory markers were observed after 3–6-mo exercise training without changes in body mass index (BMI; in kg/m2) or body fat in elderly participants (18, 19). In another trial that lasted for 18 mo, a dietary weight-loss intervention resulted in significant reductions in CRP, interleukin-6 (IL-6), and tumor necrosis factor- compared with the control group, although no effects were observed for an exercise intervention group (20). A number of reasons may explain these equivocal findings, including disparity in the Participants were drawn from the Whitehall II epidemiologic cohort (21) for a substudy in 1999–2000, which served as the baseline assessment for the present study. Participants were invited for a follow-up assessment 3 y later. The criteria for entry into the study included no history or objective signs of coronary heart disease and no previous diagnosis or treatment of hypertension, inflammatory diseases, or allergies. Volunteers were of white European origin, were aged 45–59 y, lived in the London area, and were employed full-time, which was dictated by the overall characteristics of the main cohort. Selection was stratified by grade of employment to include participants of higher and lower socioeconomic status. The participation rate was high, approximately 92%. Participants declining invitation to take part were generally from lower work grades. Participants were prohibited from using any antihistamine or antiinflammatory medication 24 h before testing and were rescheduled if they reported colds or other infections on the day of testing. At baseline there were 214 participants, although follow-up data were unavailable in 38, leaving 176 volunteers in the final analysis (98 men, 78 women). Participants excluded did not differ significantly from those included in the final analyses. Participants gave full informed consent to participate in the study, and ethical approval was obtained from the University College London Hospital committee on the Ethics of Human Reseaexercise interventions, poor adherence levels, differences between characteristics of participants, and variable follow-up times. Indeed, the typical duration of most intervention studies is 3–6 mo, which may not be long enough to observe significant effects. We are unaware of any work to date that has studied the joint influence of fitness and adiposity on inflammatory markers with the use of a prospective design. The aim of the present study was therefore to examine the association between fitness, adiposity, and inflammatory markers prospectively over 3 y. We hypothesized that baseline fitness and adiposity would be independently related to inflammatory marker concentrations at follow-up.