Endurance exercise training attenuates natriuretic peptide release during maximal effort exercise: biochemical correlates of the “athlete’s heart”

Abstract

Endurance exercise training (ET) stimulates eccentric left ventricular hypertrophy (LVH) with left atrial dilation. To date, the biochemical correlates of exercise-induced cardiac remodeling (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. Midregional proatrial natriuretic peptide (MR-proANP), NH2-terminal pro B-type natriuretic peptide (NT-proBNP), and high-sensitivity troponin T were measured at rest, peak MECPET, and 60 min post-MECPET at both study time points. Endurance exercise training 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 V̇o2 = 53.0 ± 5.9 vs. 67.3 ± 8.2 ml·kg−1·min−1, P < 0.001). Left ventricular remodeling was characterized by an ~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 with chamber dilation. NEW & NOTEWORTHY Using longitudinal pre- and postendurance training natriuretic peptide measurements, we demonstrate that the development of exercise-induced cardiac remodeling results in an attenuated natriuretic peptide response to acute bouts of maximal intensity exercise. Exercise-induced cardiac remodeling was associated with a disproportionally higher ventricular wall thickening compared with chamber dilation, a pattern that reduces cardiac wall stress. These observations advance our understanding of both the structural and biochemical adaptations that underlie the cardiovascular response to endurance training.

Effects of aerobic, strength, and combined training during pregnancy in the blood pressure: A systematic review and meta-analysis

“…AT physiological effects include a cardiac output increases during exercise as the heart can pump more blood each beat delivering more blood if required, the oxygen uptake increases with AT as the blood becomes more efficient, and there is more hemoglobin in the blood to extract oxygen from the lungs ( Eriksson et al, 1975 ; Fernandes et al, 2012 ; McGee et al, 2018 ; Lee et al, 2020 ). The Hemoglobin levels increase with AT to try and get more oxygen to the muscles activity (Yuing et al, 2019); AT exercises strengthen the heart, which increases its stroke volume, which means at rest, the heart does not need to beat as often (Hagerman, 1984), AT, therefore, can promote a lower resting heart rate ( Shah et al, 2018 ). AT could lead to the increased size of slow twitch fibers and minimal change to the fast twitch fibers ( Steinacker, 1993 ).…”

Secretion of Atrial Natriuretic Peptide (Anp), Heart Reconditioning and Remolding in Elite Endurance Trained Athletes

“…6 When the heart faces a hemodynamic burden, it can do the following to compensate: (1) use the Frank-Starling mechanism to increase cross bridge formation; (2) augment muscle mass to bear the extra load; and (3) recruit neurohormonal mechanisms to increase contractility. 7 The maximum heart rate in athletes remain unchanged having protective effects on their cardiovascular health. 8 These cardiac adaptations include electrical, structural and functional alterations are generally considered benign.…”