BRIEF REPORTS

Plasma brain natriuretic peptide in athletes

Brain natriuretic peptide (NT-pro-BNP) is used as marker of cardiac and pulmonary diseases. However, the predictive value of circulating NT-pro-BNP for cardiac and pulmonary performance is unclear in physiological conditions. Standard echocardiography, tissue Doppler and forced spirometry at rest were used to assess cardiac parameters and forced vital capacity (FVC) in two groups of athletes (16 elite male wrestlers (W), 21 water polo player (WP)), as different stress adaptation models, and 20 sedentary subjects (C) matched for age. Cardiopulmonary test on treadmill (CPET), as acute stress model, was used to measure peak oxygen consumption (peak VO2), maximal heart rate (HRmax) and peak oxygen pulse (peak VO2/HR). NT-pro-BNP was measured by immunoassey sandwich technique 10 min before the test – at rest, at the beginning of the test, at maximal effort, at third minute of recovery. FVC was higher in athletes and the highest in W (WP 5.60 ± 0.29 l; W 6.57 ± 1.00 l; C 5.41 ± 0.29 l; p < 0.01). Peak VO2 and peak VO2/HR were higher in athletes and the highest in WP. HRmax was not different among groups. In all groups, NT-pro-BNP decreased from rest to the beginning phase, increased in maximal effort and stayed unchanged in recovery. NT-pro-BNP was higher in C than W in all phases; WP had similar values as W and C. On multiple regression analysis, in all three groups together, ΔNT-pro-BNP from rest to the beginning phase independently predicted both peak VO2 and peak VO2/HR (r = 0.38, 0.35; B = 37.40, 0.19; p = 0.007, 0.000, respectively). NT-pro-BNP at rest predicted HRmax (r = −0.32, B = −0.22, p = 0.02). Maximal NT-pro-BNP predicted FVC (r = −0.22, B = −0.07, p = 0.02). These results show noticeable predictive value of NT-pro-BNP for both cardiac and pulmonary performance in physiological conditions suggesting that NT-pro-BNP could be a common regulatory factor coordinating adaptation of heart and lungs to stress condition.

Brain natriuretic peptide (NT-pro-BNP) was implicated in the regulation of hypothalamic–pituitary–adrenocortical (HPA) responses to psychological stressors. However, HPA axis activation in different physical stress models and its interface with NT-pro-BNP in the prediction of cardiopulmonary performance is unclear. Cardiopulmonary test on a treadmill was used to assess cardiopulmonary parameters in 16 elite male wrestlers (W), 21 water polo player (WP) and 20 sedentary age-matched subjects (C). Plasma levels of NT-pro-BNP, cortisol and adrenocorticotropic hormone (ACTH) were measured using immunoassay sandwich technique, radioimmunoassay and radioimmunometric techniques, respectively, 10 min before test (1), at beginning (2), at maximal effort (3), at 3rd min of recovery (4). In all groups, NT-pro-BNP decreased between 1 and 2; increased from 2 to 3; and remained unchanged until 4. ACTH increased from 1 to 4, whereas cortisol increased from 1 to 3 and stayed elevated at 4. In all groups together, ΔNT-pro-BNP2/1 predicted peak oxygen consumption (B = 37.40, r = 0.38, p = 0.007); cortisol at 3 predicted heart rate increase between 2 and 3 (r = −0.38,B = −0.06, p = 0.005); cortisol at 2 predicted peak carbon-dioxide output (B = 2.27, r = 0.35, p < 0.001); ΔACTH3/2 predicted peak ventilatory equivalent for carbon-dioxide (B = 0.03, r = 0.33, p = 0.003). The relation of cortisol at 1 with NT-pro-BNP at 1 and 3 was demonstrated using logistic function in all the participants together (for 1/cortisol at 1 B = 63.40, 58.52; r = 0.41, 0.34; p = 0.003, 0.013, respectively). ΔNT-pro-BNP2/1 linearly correlated with ΔACTH4/3 in WP and W (r = −0.45, −0.48; p = 0.04, 0.04, respectively). These results demonstrate for the first time that HPA axis and NT-pro-BNP interface in physical stress probably contribute to integrative regulation of cardiopulmonary performance.

Distinguishing physiological hypertrophy from hypertrophic cardiomyopathy in athletes remains difficult, but vital in view of the risk of sudden death under effort. NT-proBNP was previously reported to be usually normal in healthy athletes, but often elevated in case of hypertrophic cardiomyopathy.

o assess the interest of NT-proBNP in differential diagnosis of left ventricular hypertrophy in athletes.

NT-proBNP levels were measured at rest and after effort in trained athletes referred for suspectedly abnormal (≥ 13 mm) left ventricular hypertrophy.

17 patients were included, 10 of whom were diagnosed with hypertrophic cardiomyopathy (group I) while the other 7 presented typical signs of athlete’s heart (group II). NT-proBNP levels did not significantly differ between groups, whether at rest or after effort. NT-proBNP levels were, however, significantly elevated in 3 subjects in group I, while being consistently normal in group II.

In active athletes presenting with ambiguous left ventricular hypertrophy, abnormal NT-proBNP levels indicate hypertrophic cardiomyopathy, whereas normal values are inconclusive.

Brain natriuretic peptide (BNP), a peptide hormone secreted chiefly by ventricular myocytes, plays a key role in volume homeostasis. The plasma concentration of BNP is raised in various pathological states, especially heart failure. Many studies suggest that measurement of plasma BNP has clinical utility for excluding a diagnosis of heart failure in patients with dyspnea or fluid retention and for providing prognostic information in those with heart failure or other cardiac disease. It may also be of value in identifying patients after myocardial infarction in whom further assessment of cardiac function is likely to be worthwhile. Preliminary evidence suggests that measuring the plasma concentration of BNP may be useful in fine tuning therapy for heart failure. Artificially raising the circulating levels of BNP shows considerable promise as a treatment for heart failure. With simpler assay methods now available, it is likely that many physicians will measure plasma BNP to aid them in the diagnosis, risk stratification, and monitoring of their patients with heart failure or other cardiac dysfunction. Copyright 2002, Elsevier Science (USA). All rights reserved.