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The impact of obesity on cardiac troponin levels after prolonged exercise in humans

By Thijs M. H. Eijsvogels, Matthijs T. W. Veltmeijer, Keith George, Maria T. E. Hopman and Dick H. J. Thijssen


Elevated cardiac troponin I (cTnI), a marker for cardiac damage, has been reported after high-intensity exercise in healthy subjects. Currently, little is known about the impact of prolonged moderate-intensity exercise on cTnI release, but also the impact of obesity on this response. 97 volunteers (55 men and 42 women), stratified for BMI, performed a single bout of walking exercise (30–50 km). We examined cTnI-levels before and immediately after the exercise bout in lean (BMI < 25 kg/m2, n = 30, 57 ± 19 years), overweight (25 ≤ BMI < 30 kg/m2, n = 29, 56 ± 11 years), and obese subjects (BMI ≥ 30 kg/m2, n = 28, 53 ± 9 years). Walking was performed at a self-selected pace. cTnI was assessed using a high-sensitive cTnI-assay (Centaur; clinical cut-off value ≥0.04 μg/L). We recorded subject characteristics (body weight, blood pressure, presence of cardiovascular risk) and examined exercise intensity by recording heart rate. Mean cTnI-levels increased significantly from 0.010 ± 0.006 to 0.024 ± 0.046 μg/L (P < 0.001). The exercise-induced increase in cTnI was not different between lean, overweight and obese subjects (two-way ANOVA interaction; P = 0.27). In 11 participants, cTnI was elevated above the clinical cut-off value for myocardial infarction. Logistic regression analysis identified exercise intensity (P < 0.001), but not BMI, body fat percentage or waist circumference to significantly relate to positive troponin tests. In conclusion, prolonged, moderate-intensity exercise results in a comparable increase in cTnI-levels in lean, overweight and obese subjects. Therefore, measures of obesity unlikely relate to the magnitude of the post-exercise elevation in cTnI

Topics: Original Article
Publisher: Springer-Verlag
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Provided by: PubMed Central

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