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.

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.

With this study we tested the hypothesis that 6 wk of endurance training increases maximal cardiac output (Qmax) relatively more by elevating blood volume (BV) than by inducing structural and functional changes within the heart. Nine healthy but untrained volunteers (Vo2max 47 ± 5 ml·min(-1)·kg(-1)) underwent supervised training (60 min; 4 times weekly at 65% Vo2max for 6 wk), and Qmax was determined by inert gas rebreathing during cycle ergometer exercise before and after the training period. After the training period, blood volume (determined in duplicates by CO rebreathing) was reestablished to pretraining values by phlebotomy and Qmax was quantified again. Resting echography revealed no structural heart adaptations as a consequence of the training intervention. After the training period, plasma volume (PV), red blood cell volume (RBCV), and BV increased (P< 0.05) by 147 ± 168 (5 ± 5%), 235 ± 64 (10 ± 3%), and 382 ± 204 ml (7 ± 4%), respectively. Vo2max was augmented (P < 0.05) by 10 ± 7% after the training period and decreased (P < 0.05) by 8 ± 7% with phlebotomy. Concomitantly, Qmax was increased (P < 0.05) from 18.9 ± 2.1 to 20.4 ± 2.3 l/min (9 ± 6%) as a consequence of the training intervention, and after normalization of BV by phlebotomy Qmax returned to pretraining values (18.1 ± 2.5 l/min; 12 ± 5% reversal). Thus the exercise training-induced increase in BV is the main mechanism increasing Qmax after 6 wk of endurance training in previously untrained subjects.

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.

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PurposeThe aim of this study was to investigate the impact of exercise-induced hypoxaemia (EIH) developed at sea-level on exercise responses at moderate acute altitude.MethodsTwenty three subjects divided in three groups of individuals: highly trained with EIH (n = 7); highly trained without EIH (n = 8) and untrained participants (n = 8) performed two maximal incremental tests at sea-level and at 2,150 m. Haemoglobin O2 saturation (SpO2), heart rate, oxygen uptake (VO2) and several ventilatory parameters were measured continuously during the tests.ResultsEIH athletes had a drop in SpO2 from 99 ± 0.8% to 91 ± 1.2% from rest to maximal exercise at sea-level, while the other groups did not exhibit a similar decrease. EIH athletes had a greater decrease in VO2max at altitude compared to non-EIH and untrained groups (-22 ± 7.9%, -16 ± 5.3% and -13 ± 9.4%, respectively). At altitude, non-EIH athletes had a similar drop in SpO2 as EIH athletes (13 ± 0.8%) but greater than untrained participants (6 ± 1.0%). EIH athletes showed greater decrease in maximal heart rate than non-EIH athletes at altitude (8 ± 3.3 bpm and 5 ± 2.9 bpm, respectively).ConclusionEIH athletes demonstrated specific cardiorespiratory response to exercise at moderate altitude compared to non-EIH athletes with a higher decrease in VO2max certainly due to the lower ventilator and HRmax responses. Thus EIH phenomenon developed at sea-level negatively impact performance and cardiorespiratory responses at acute moderate altitude despite no potentiated O2 desaturation.

Aerobic exercise capacity is similarly modulated by pulmonary vascular reserve at moderate altitude and at sea level. Decreased aerobic exercise capacity at moderate altitude is mainly explained by exercise-induced decrease in arterial oxygenation.