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Several obesity related factors are reported to exacerbate premature arterial stiffening, including inactivity and metabolic disarray. The aim of the current study was to investigate the relationship between physical activity, arterial stiffness and adiposity using objective methods. To further explore the role of adiposity in this complex process, obesity associated anthropometric and humoral biomarkers were measured.
Seventy-nine healthy, lifelong nonsmoking subjects were recruited. Habitual physical activity was measured using accelerometry. Arterial stiffness [augmentation index (AIx) and pulse wave velocity (PWV)] was measured using tonometry. Body composition was estimated using bioimpedence. Adipose associated biomarkers, leptin and adiponectin, were also measured.
Sedentary time was significantly associated with AIx (r = 0.38, P < .001), PWV (r = 0.33, P < .01), body fat composition (r = 0.40, P < .001) and age (r = 0.30, P < .01). Moderate-to-vigorous physical activity (MVPA) was inversely correlated with AIx (r = –0.28, P < .05), body fat composition (r = –0.30, P < .01), postprandial insulin (r = –0.35, P < .01), and leptin/adiponectin ratio (r = –0.28, P < .05). MVPA, body fat composition, and postprandial insulin remained independent predictors of AIx but not PWV.
The more time healthy individuals spend being sedentary, the greater their body fat and arterial stiffness. Conversely higher activity levels are associated with reduced body fat and less arterial stiffness.
Mac Ananey (email@example.com) is with the School of Biological Sciences, Dublin Institute of Technology, Dublin, Ireland. Mac Ananey, L Maher, and V Maher are with the Dept of Cardiology, Tallaght Hospital, Dublin, Ireland. McLoughlin, Leonard, Gaffney, and Boran are with the Dept of Chemical Pathology, Tallaght Hospital, Dublin, Ireland.