Effects of High-Intensity Training of Professional Runners on Myocardial Hypertrophy and Subclinical Atherosclerosis
Data
2016
Autores
Bittencourt, Celia Regina de Olivera 
Izar, Maria Cristina de Oliveira
Schwerz, Valdir Lauro
Póvoa, Rui Manuel dos Santos
Fonseca, Henrique Andrade Rodrigues da
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To evaluate the effects of long-term exposure to high-intensity training among professional runners on cardiac hypertrophy and subclinical atherosclerosis. Prospective study included runners of both sexes (n = 52) and age and gender matched controls (n = 57), without classical cardiovascular risk factors. Ventricular hypertrophy was quantified by echocardiography by linear method and carotid intima-media thickness (cIMT) by 2-D images obtained by ultrasonography. Endothelial function was evaluated by flowmediated dilation (FMD). Steroid hormones were quantified by HPLC followed by LC-MS/MS. Higher left ventricular (LV) mass index was found in male athletes (p< 0.0001 vs. other groups). When adjusted for gender, the degree of left ventricular mass index classified as mildly, moderately or severely abnormal was obtained in 26%, 35%, and 30%, respectively, of female athletes, and in 39%, 14%, and 21%, respectively, of male athletes. Higher ratio of the early (E) to late (A) ventricular filling velocities was found in athletes of both genders. Male athletes presented lower cIMT in the right (p = 0.012 vs. male controls) and left (p< 0.0001 vs. male controls) common carotid arteries, without differences in cIMT between female athletes and controls. FMD results were similar among groups. Higher serum testosterone levels were found in male athletes (p< 0.0001 vs. other groups) and they were correlated with LV mass (r = 0.50, p< 0.0001). The chronic exposure of high-intensity training among professional runners of both genders was associated with increased ventricular mass and adaptive remodeling. Less subclinical atherosclerosis was found in male athletes. Differences in steroid hormones may account in part for these findings.
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Plos One. San Francisco, v. 11, n. 11, p. -, 2016.