Endurance Exercise Training Attenuates Natriuretic Peptide Release During Maximal Effort Exercise: Biochemical Correlates of the "Athlete's Heart"
Journal of applied physiology: respiratory, environmental and exercise physiology
Endurance exercise training (ET) stimulates eccentric left ventricular hypertrophy (LVH) with left atrial dilation. To date, the biochemical correlates of exercise-induced cardiac remodelling (EICR) remain incompletely understood. Collegiate male rowers (n = 9) were studied with echocardiography and maximal-effort cardiopulmonary exercise testing (MECPET) before and after 90 days of ET intensification. Mid-regional pro-atrial natriuretic peptide (MR-proANP), N-terminal pro B-type natriuretic
... type natriuretic peptide (NT-proBNP), and high-sensitivity troponin T (hscTn) were measured at rest, peak MECPET, and 60 minutes post-MECPET at both study time points. ET resulted in eccentric LVH (LV mass = 102 ± 8 vs. 110 ± 11 g/m2, p=0.001; relative wall thickness = 0.36 ± 0.04 vs. 0.37 ± 0.04, p=0.103), left atrial dilation (74 ± 18 vs. 84 ± 15 mL, p<0.001), and increased exercise capacity (peak VO2 = 53.0 ± 5.9 vs. 67.3 ± 8.2 ml/kg/min, p<0.001). LV remodelling was characterized by an approximate 7% increase in LV wall thickness but only a 3% increase in LV chamber radius. The magnitude of natriuretic peptide release, examined as percent change from rest to peak exercise, was significantly lower for both MR-proANP (115 [95, 127]% vs. 78 [59, 87]%, p=0.04) and NT-proBNP (46 [31, 70]% vs. 27 [25, 37]%, p=0.02) after ET. Rowing-based ET and corollary EICR appear to result in an attenuated natriuretic peptide response to maximal effort exercise. This may occur as a function of decreased cardiac wall stress after ET as seen by disproportionally higher ventricular wall thickening compared to chamber dilation.