Cardiac Remodeling in Response to 1 Year of Intensive Endurance Training

Abstract

Background It is unclear whether, and to what extent, the striking cardiac morphological manifestations of endurance athletes are a result of exercise training or a genetically determined characteristic of talented athletes. We hypothesized that prolonged and intensive endurance training in previously sedentary healthy young individuals could induce cardiac remodeling similar to that observed cross-sectionally in elite endurance athletes. Methods and Results Twelve previously sedentary subjects (aged 29±6 years; 7 men and 5 women) trained progressively and intensively for 12 months such that they could compete in a marathon. Magnetic resonance images for assessment of right and left ventricular mass and volumes were obtained at baseline and after 3, 6, 9, and 12 months of training. Maximum oxygen uptake (V̇o2 max) and cardiac output at rest and during exercise (C2H2 rebreathing) were measured at the same time periods. Pulmonary artery catheterization was performed before and after 1 year of training, and pressure-volume and Starling curves were constructed during decreases (lower body negative pressure) and increases (saline infusion) in cardiac volume. Mean V̇o2 max rose from 40.3±1.6 to 48.7±2.5 mL/kg per minute after 1 year (P<0.00001), associated with an increase in both maximal cardiac output and stroke volume. Left and right ventricular mass increased progressively with training duration and intensity and reached levels similar to those observed in elite endurance athletes. In contrast, left ventricular volume did not change significantly until 6 months of training, although right ventricular volume increased progressively from the outset; Starling and pressure-volume curves approached but did not match those of elite athletes. Conclusions One year of prolonged and intensive endurance training leads to cardiac morphological adaptations in previously sedentary young subjects similar to those observed in elite endurance athletes; however, it is not sufficient to achieve similar levels of cardiac compliance and performance. Contrary to conventional thinking, the left ventricle responds to exercise with initial concentric but not eccentric remodeling during the first 6 to 9 months after commencement of endurance training depending on the duration and intensity of exercise. Thereafter, the left ventricle dilates and restores the baseline mass-to-volume ratio. In contrast, the right ventricle responds to endurance training with eccentric remodeling at all levels of training.

Global and regional cardiac function in lifelong endurance athletes with and without myocardial fibrosis

“…Alternatively, athletes with MF may be more prone to cardiac remodelling. Several cross sectional (George et al, 2011;Pelliccia, Maron, Spataro, Proschan, & Spirito, 1991) and longitudinal studies (Arbab-Zadeh et al, 2014; 10 ± 1 12 ± 2 PWd (mm) 9 ± 1 11 ± 1 Diastolic function (Echo) E (cm/s) 65 ± 6 62 ± 10 A (cm/s) 60 ± 11 58 ± 5 E/A ratio 1.1 ± 0.3 1.1 ± 0.2 Septal E (cm/s) 10 ± 2 10 ± 2 A (cm/s) 11 ± 2 11 ± 1 Lateral E (cm/s) 11 ± 1 14 ± 3 A (cm/s) 11 ± 2 11 ± 1 Average E (cm/s) 11 ± 1 12 ± 2 A (cm/s) 11 ± 2 11 ± 1 E/E 6 ± 1 5 ± 2 Longitudinal strain (Echo) 2CH (%) −22.7 ± 1.9 −21.9 ± 4.4 4CH (%) −21.7 ± 2.9 −22.6 ± 3. 2CH: apical two chamber view; 4CH: apical four chamber view; APLAX: apical parasternal long axis view; E: early diastolic filling (E-wave); A: late diastolic filling (A-wave); E (cm/s): early diastolic velocity of mitral annulus; A (cm/s): late diastolic velocity of mitral annulus; S (l/s): systolic strain rate; E (l/s): early diastolic strain rate; A (l/s): late diastolic strain rate.…”

Maternal Cardiovascular Function in Normal Pregnancy

“…[20][21][22] Likewise, it is often present in elite athletes in the absence of cardiovascular disease. 20,21 This increase in volume load triggers a remodeling response, which consists mainly of LV geometric changes and spherical dilatation along the LV short axis. This remodeling response increases myocardial contractility, as demonstrated by an increase in SV, heart rate, and cardiac output.…”

“…The constellation of findings at term-reduced SV index, diastolic dysfunction, and eccentric remodeling-have been described in other volume overload states as maladaptation occurs, such as mitral regurgitation. 21 One year was chosen as the appropriate postpregnancy time point for assessment given the previous finding of persistent postpartum cardiac findings in preeclampsia.2 At 1 year postpartum in the study participants, all geometric and hemodynamic indices returned to baseline. Septal Em/Am 2.0 (1.6-2.8) 2.1 (1.8-2.8) 2.1 (1.6-2.8) 1.6 (1.2-2.0)* † § 1.3 (1.1-1.9)* † §║ 2.1 (1.6-3.0) ‡║ <0.001…”

Stroke work progressively increased until maximal exercise in long distance runners, but plateaued at submaximal exercise in sprinters

“…CWI at rest was not significantly different in long-distance runners and sprinters. CWI at 50 W, 100 W, and 150 W was lower in long-distance runners than in sprinters (at 50 W, long-distance runners: 1.02 ± 0.07 vs. sprinters: 1.21 ± 0.06 W · m -2 , p < 0.05, 1-β = 0.45; at 100 W, long-distance runners: 1.46 ± 0.06 vs. sprinters: 1.96 ± 0.14 W · m -2 , p < 0.05, 1-β = 0.77; at 150 W, long-distance runners: 2.11 ± 0.07 vs. sprinters: 2.87 ± 0.18 W · m -2 , p < 0.01, 1-β = 0.91), but CWI at maximal exercise was not significantly different between the two groups (long-distance runners: distensible ventricles which enable a steeper slope of the Frank-Starling curve 3) and lower left ventricular filling pressure to stroke volume during exercise 4) . In endurancetrained athletes, an enhanced diastolic function allows for a more complete filling during the later stages of vigorous exercise 5) .…”

“…Endurance sports athletes, such as long-distance runners, have been reported to have an increased heart volume and superior cardiac function compared to healthy controls [1][2][3][4] . Although several previous studies measured cardiac output and/or stroke volume during exercise in long-distance runners [5][6][7][8][9] , there has only been one study which measured cardiac output during exercise in both long-distance runners and sprinters 7) .…”