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 (10.5Ϯ3.2 to 15.8Ϯ4.5°; PϽ0.001), 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 (Ϫ88.7Ϯ34.2 to Ϫ182.9Ϯ53.5 deg ⅐ s Ϫ1 ; PϽ0.01) was correlated to enhanced systolic twist (Rϭ0.61; PϽ0.001), and its magnitude of increase was significantly higher compared to diastolic longitudinal and circumferential strain rates (119Ϯ64% versus 65Ϯ44% and 57Ϯ24%, 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 (Rϭ0.47 and 0.61, respectively; PϽ0.001), whereas basal rotation and longitudinal and circumferential diastolic strain rates were major determinants of increased early diastolic filling (Rϭ0.64, 0.79, and 0.81, respectively; PϽ0.001). 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. (Circ Cardiovasc Imaging. 2010;3:586-594.)
The contraction of cardiomyocytes induces a systolic increase in left ventricular (LV) normal (radial, circumferential and longitudinal) and shear strains, whose functional consequences have not been evaluated, so far, in athletes. We used 2D ultrasound speckle tracking imaging (STI) to evaluate LV regional strain in high-level cyclists compared to sedentary controls. Sixteen male elite cyclists and 23 sedentary controls underwent conventional, tissue Doppler, and STI echocardiography at rest. We assessed LV long and short axis normal strains and shear strains. We evaluated circumferential-longitudinal shear strain from LV torsion, and circumferential-radial shear strain from the difference between subendocardial and subepicardial torsion. Apical radial strain (42.7 ± 10.5% versus 52.2 ± 14.3%, P < 0.05) and LV torsion (6.0 ± 1.8 deg versus 9.2 ± 3.2 deg, P < 0.01) were lower in cyclists than in controls, respectively. Rotations and torsion were higher in the subendocardial than in the subepicardial region in sedentary controls, but not in cyclists. Haemodynamic and tissue Doppler based indexes of global LV diastolic and systolic functions were not different between cyclists and controls. Athlete's heart is associated with specific LV adaptation including lower apical strain and lower myocardial shear strains, with no change in global LV diastolic and systolic function. These mechanical alterations could improve the cardiovascular adjustments to exercise by increasing the radial strain and torsional (and thus untwisting) response to exercise, a key element of diastolic filling and thus of cardiac performance in athletes.
Whatever gender, aerobic training increases VO2max in children, mediated by an improvement in SVmax only. Similar mechanisms, including loading conditions and cardiac morphology, seem to be involved in both genders in order to explain such an improvement.
Background-Numerous studies have reported evidence of cardiac injury associated with transient left ventricular (LV) systolic and diastolic dysfunction after prolonged and strenuous exercise. We used 2D ultrasound speckle tracking imaging to evaluate the effect of an ultralong-duration exercise on LV regional strains and torsion. We speculated that systolic dysfunction after exercise is associated with depressed LV strains and torsion, and diastolic dysfunction results from decreased and delayed untwisting, a key factor of LV suction and early filling. Methods and Results-Twenty-three triathletes underwent conventional and speckle tracking imaging echocardiography at rest before and immediately after an ultralong distance triathlon. Measurements included LV longitudinal, circumferential and radial strains, LV rotations, and LV torsion. After the race, LV systolic dysfunction was characterized by a decrease in LV longitudinal, radial, and circumferential strains, especially for apical radial strains (44.6Ϯ15.1% versus 31.1Ϯ13.8%, PϽ0.001). Peak torsion was slightly decreased (8.3Ϯ5.1°versus 6.4Ϯ3.9°, respectively, Pϭ0.09) and significantly delayed (91Ϯ18% versus 128Ϯ31% of systolic duration, PϽ0.001) beside end-ejection. Peak untwisting was also depressed and delayed beside isovolumic relaxation. Conclusions-This study documented major alterations in cardiac strains and torsion after an ultralong distance triathlon.LV systolic strains were depressed but not delayed, whereas twisting was decreased and delayed. This altered pattern hampered the rapid untwisting during isovolumic relaxation phase, reducing LV diastolic suction and early filling.
The purpose of this study was to observe the effect of high intermittent exercise training on children's heart rate variability (HRV). Thirty-eight children (age 9.6 +/- 1.2 years) were divided into an intermittent (IT, n = 22) and a control group (CON, n = 16). At baseline and after a 7-week training period, HRV parameters, peak oxygen consumption (VO(2peak)) and maximal aerobic velocity (MAV) were assessed. Training consisted of three 30-min sessions composed by short maximal and supramaximal runs at velocities ranging from 100 up to 190% of MAV. HRV was computed in time and frequency domains. Training resulted in a significant increase in MAV and VO(2peak) in IT (P < 0.05) only without any significant change in HRV parameters for the two groups. Thus, 7 weeks of high intermittent exercise training allows to improve aerobic fitness. However, this modality of training was not sufficient enough to underline a possible effect on the heart rate autonomic regulation in children.
High-altitude exposure impaired LV diastolic function with the greatest effect observed at D2, concomitantly with the occurrence of AMS. The LV early filling impairments resulted from an increased RV afterload, a decrease in LV filling pressure and a delayed LV untwist. However, the increased LV twist probably acted as a compensatory mechanism to maintain cardiac performance during high-altitude hypoxia.
Stroke volume (SV) response to exercise depends on changes in cardiac filling, intrinsic myocardial contractility and left ventricular afterload. The aim of the present study was to identify whether these variables are influenced by endurance training in pre-pubertal children during a maximal cycle test. SV, cardiac output (Doppler echocardiography), left ventricular dimensions (time-movement echocardiography) as well as arterial pressure and systemic vascular resistances were assessed in 10 child cyclists (VO2max: 58.5 +/- 4.4 mL min-1 kg-1) and 13 untrained children (UTC) (VO2max: 45.9 +/- 6.7 mL min-1 kg-1). All variables were measured at the end of the resting period, during the final minute of each workload and during the last minute of the progressive maximal aerobic test. At rest and during exercise, stroke index was significantly higher in the child cyclists than in UTC. However, the SV patterns were strictly similar for both groups. Moreover, the patterns of diastolic and systolic left ventricular dimensions, and the pattern of systemic vascular resistance of the child cyclists mimicked those of the UTC. SV patterns, as well as their underlying mechanisms, were not altered by endurance training in children. This result implied that the higher maximal SV obtained in child cyclists depended on factors influencing resting SV, such as cardiac hypertrophy, augmented myocardium relaxation properties or expanded blood volume.
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