Diastolic dysfunction and intraventricular dyssynchrony are restored by low intensity exercise training in obese men.

The aim of this study was to evaluate the impact of a low-intensity training program on subclinical cardiac dysfunction and on dyssynchrony in moderately obese middle aged men. Ten obese and 14 age-matched normal-weight men (BMI: 33.6 ± 1.0 and 24.2 ± 0.5 kg/m(2)) were included. Obese men participated in an 8-week low-intensity training program without concomitant diet. Cardiac function and myocardial synchrony were assessed by echocardiography with tissue Doppler imaging (TDI) and speckle tracking echocardiography (STE). At baseline, obese men showed diastolic dysfunction on standard echocardiography, lower strain values (systolic strain: 15.9 ± 0.9 vs. 18.8 ± 0.3%, diastolic strain rate: 0.81 ± 0.09 vs. 1.05 ± 0.06 s(-1)), and significant intraventricular dyssynchrony (systolic: 13.3 ± 2.1 vs. 5.4 ± 2.1 ms, diastolic: 17.4 ± 3.2 vs. 9.1 ± 2.1 ms) (P < 0.05 vs. controls for all variables). Training improved aerobic fitness, decreased systolic blood pressure and heart rate, and reduced fat mass without weight loss. Diastolic function, strain values (systolic strain: 17.4 ± 0.9%, diastolic strain rate: 0.96 ± 0.12 s(-1)) and intraventricular dyssynchrony (systolic: 3.3 ± 1.7 ms, diastolic: 5.5 ± 3.4 ms) improved significantly after training (P < 0.05 vs. baseline values for all variables), reaching levels similar to those of normal-weight men. In conclusion, in obese men, a short and easy-to-perform low intensity training program restored diastolic function and cardiac synchrony and improved body composition without weight loss.

Kinetics of left ventricular strains and torsion during incremental exercise in healthy subjects: the key role of torsional mechanics for systolic-diastolic coupling.

BACKGROUND: The dynamics of systolic and diastolic strains and torsional mechanics of the left ventricle (LV) and their relation to diastolic filling never have been evaluated at various exercise intensities. METHODS AND RESULTS: Speckle tracking echocardiography was performed in 20 healthy sedentary subjects at rest and during a progressive submaximal exercise test at 20%, 30%, and 40% of maximal aerobic power. LV twist increased progressively with exercise intensity (10.5 ± 3.2 to 15.8 ± 4.5°; P<0.001), whereas longitudinal strain remained unchanged after the first workload, underlining the key role of torsional reserve in systolic-diastolic coupling during exercise. The increase in diastolic untwisting (-88.7 ± 34.2 to -182.9 ± 53.5 deg · s(-1); P<0.01) was correlated to enhanced systolic twist (R=0.61; P<0.001), and its magnitude of increase was significantly higher compared to diastolic longitudinal and circumferential strain rates (119 ± 64% versus 65 ± 44% and 57 ± 24%, respectively), emphasizing its contribution to diastolic filling. The timing of peak untwisting and the chronology of diastolic mechanical events were unchanged during effort. Untwisting was driven mainly by apical rotation and determined mitral opening and isovolumic relaxation time (R=0.47 and 0.61, respectively; P<0.001), whereas basal rotation and longitudinal and circumferential diastolic strain rates were major determinants of increased early diastolic filling (R=0.64, 0.79, and 0.81, respectively; P<0.001). CONCLUSIONS: The use of speckle tracking echocardiography gives new insights into physiological adaptive LV mechanics during incremental exercise in healthy subjects, underlining the key role of torsional mechanics. It might be useful to better understand the mechanisms of diastolic dysfunction and exercise intolerance in various pathological conditions.

Cardiac function during exercise in obese prepubertal boys: effect of degree of obesity.

The purpose of the study was to evaluate the dynamics of diastolic and systolic function from rest to maximal exercise using conventional echocardiography and tissue Doppler imaging (TDI) in obese prepubertal boys compared to age-matched lean controls. Eighteen obese (10 with first degree obesity and 8 with second degree obesity according to French curves, BMI: 23.3+/-1.8 and 29.0+/-2.0 kg/m2, respectively) and 17 lean controls (BMI=17.6+/-0.6 kg/m2, P<0.001), aged 10-12 years were recruited. After resting echocardiography, all children performed a maximal exercise test. Regional diastolic and systolic myocardial velocities were acquired at rest and each workload. Stroke volume and cardiac output were calculated. At rest, obese boys had greater left ventricular (LV) diameters and LV mass. Boys in the first degree group showed no diastolic or systolic dysfunction, whereas boys with second degree obesity showed subtle diastolic dysfunction. During exercise, both obese groups showed greater stroke volume and cardiac output. First degree obese boys exhibited greater systolic and diastolic tissue Doppler velocities than controls, whereas second degree obese boys had lower diastolic tissue velocities irrespective of exercise intensity and lower fractional shortening at high exercise intensities than controls. In conclusion, no impairment in diastolic or systolic function is noticed in prepubertal boys with first degree of obesity. Enhanced regional myocardial function response to exercise was also demonstrated in this population, suggesting adaptive compensatory cardiac changes in mild obesity. However, when obesity becomes more severe, impaired global and regional cardiac function at rest and during exercise can be observed.