Key result
Endurance exercise training in competitive male rowers increased left ventricular mass from 93 g/m2 at baseline to 105 g/m2 at 90 days and 113 g/m2 at 39 months (P<0.001).
Why the study?
Does endurance exercise training alter left ventricular structure and function over time in competitive male rowers?
Observational (n=12)
Does endurance exercise training alter left ventricular structure and function over time in competitive male rowers?
p-value: p=<0.001
Exercise-induced cardiac remodeling follows a phasic response, with initial LV dilation followed by chronic wall thickening, which has implications for assessing myocardial structure in athletes.
May warrant adjusted LV mass norms in endurance athletes; extends phasic remodeling evidence but leaves open outcome relevance.
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.
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Weiner et al. (2015) conducted an observational in Competitive athletes (n=12). Endurance exercise training vs. Baseline was evaluated on Left ventricular mass (p=<0.001). Endurance exercise training in competitive male rowers increased left ventricular mass from 93 g/m2 at baseline to 105 g/m2 at 90 days and 113 g/m2 at 39 months (P<0.001).
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