Rory B Weiner1, James R DeLuca2, Francis Wang2, Jeffrey Lin2, Meagan M Wasfy2, Brant Berkstresser2, Eric Stöhr2, Rob Shave2, Gregory D Lewis2, Adolph M Hutter2, Michael H Picard2, Aaron L Baggish2. 1. From the Cardiovascular Performance Program, Massachusetts General Hospital, Boston (R.B.W., J.R.D., J.L., M.M.W., G.D.L., A.M.H., M.H.P., A.L.B.); Harvard University Health Services, Cambridge, MA (R.B.W., F.W., B.B., A.L.B.); and Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom (E.S., R.S.). rweiner@partners.org. 2. From the Cardiovascular Performance Program, Massachusetts General Hospital, Boston (R.B.W., J.R.D., J.L., M.M.W., G.D.L., A.M.H., M.H.P., A.L.B.); Harvard University Health Services, Cambridge, MA (R.B.W., F.W., B.B., A.L.B.); and Cardiff School of Sport, Cardiff Metropolitan University, Cardiff, United Kingdom (E.S., R.S.).
Abstract
BACKGROUND: Contemporary understanding of exercise-induced cardiac remodeling is based on cross-sectional data and relatively short duration longitudinal studies. Temporal progression of exercise-induced cardiac remodeling remains incompletely understood. METHODS AND RESULTS: A longitudinal repeated-measures study design using 2-dimensional and speckle-tracking echocardiography was used to examine acute augmentation phase (AAP; 90 days) and more extended chronic maintenance phase (39 months) left ventricular (LV) structural and functional adaptations to endurance exercise training among competitive male rowers (n=12; age 18.6±0.5 years). LV mass was within normal limits at baseline (93±9 g/m(2)), increased after AAP (105±7 g/m(2); P=0.001), and further increased after chronic maintenance phase (113±10 g/m(2); P<0.001 for comparison to post-AAP). AAP LV hypertrophy was driven by LV dilation (ΔLV end-diastolic volume, 9±3 mL/m(2); P=0.004) with stable LV wall thickness (ΔLV wall thickness, 0.3±0.1 mm; P=0.63). In contrast, chronic maintenance phase LV hypertrophy was attributable to LV wall thickening (Δ LV wall thickness, 1.1±0.4 mm; P=0.004) with stable LV chamber volumes (ΔLV end-diastolic volume, 1±1 mL/m(2); P=0.48). Early diastolic peak tissue velocity increased during AAP (-11.7±1.9 versus -13.6±1.3 cm/s; P<0.001) and remained similarly increased after chronic maintenance phase. CONCLUSIONS: In a small sample of competitive endurance athletes, exercise-induced cardiac remodeling follows a phasic response with increases in LV chamber size, early diastolic function, and systolic twist in an acute augmentation phase of exercise training. This is followed by a chronic phase of adaptation characterized by increasing wall thickness and regression in LV twist. Training duration is a determinant of exercise-induced cardiac remodeling and has implications for the assessment of myocardial structure and function in athletes.
BACKGROUND: Contemporary understanding of exercise-induced cardiac remodeling is based on cross-sectional data and relatively short duration longitudinal studies. Temporal progression of exercise-induced cardiac remodeling remains incompletely understood. METHODS AND RESULTS: A longitudinal repeated-measures study design using 2-dimensional and speckle-tracking echocardiography was used to examine acute augmentation phase (AAP; 90 days) and more extended chronic maintenance phase (39 months) left ventricular (LV) structural and functional adaptations to endurance exercise training among competitive male rowers (n=12; age 18.6±0.5 years). LV mass was within normal limits at baseline (93±9 g/m(2)), increased after AAP (105±7 g/m(2); P=0.001), and further increased after chronic maintenance phase (113±10 g/m(2); P<0.001 for comparison to post-AAP). AAPLV hypertrophy was driven by LV dilation (ΔLV end-diastolic volume, 9±3 mL/m(2); P=0.004) with stable LV wall thickness (ΔLV wall thickness, 0.3±0.1 mm; P=0.63). In contrast, chronic maintenance phase LV hypertrophy was attributable to LV wall thickening (Δ LV wall thickness, 1.1±0.4 mm; P=0.004) with stable LV chamber volumes (ΔLV end-diastolic volume, 1±1 mL/m(2); P=0.48). Early diastolic peak tissue velocity increased during AAP (-11.7±1.9 versus -13.6±1.3 cm/s; P<0.001) and remained similarly increased after chronic maintenance phase. CONCLUSIONS: In a small sample of competitive endurance athletes, exercise-induced cardiac remodeling follows a phasic response with increases in LV chamber size, early diastolic function, and systolic twist in an acute augmentation phase of exercise training. This is followed by a chronic phase of adaptation characterized by increasing wall thickness and regression in LV twist. Training duration is a determinant of exercise-induced cardiac remodeling and has implications for the assessment of myocardial structure and function in athletes.
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