Search

Purpose: Both prolonged exercise and acute high-altitude exposure are known to induce cardiac changes. We sought to describe the cardiac responses to speed climbing at high-altitude, including left ventricular (LV) performance assessment using the myocardial work index (MWI), a new index derived from 2D speckle tracking echocardiography (STE). Methods: Eleven elite alpinists (9 males, age: 26 ± 4 years) were evaluated before and immediately after a speed ascent of the Mont-Blanc (4808 m) by echocardiography using conventional measurements as well as STE and MWI computation with derivate parameters as global work efficiency (GWE) or global wasted work (GWW). Results: Athletes performed a long-duration (8 h 58 min ± 60 min) and intense (78 ± 4% of maximal heart rate) ascent under gradual hypoxic conditions (minimal SpO2 at 4808 m: 71 ± 4%). Hypoxic exercise-induced cardiac fatigue was observed post-ascent with a change in right ventricular (RV) and LV systolic function (RV fractional area change: – 20 ± 23%, p = 0.01; LV global longitudinal strain change: – 8 ± 9%, p = 0.02), as well as LV geometry and RV–LV interaction alterations with emergence of a D-shape septum in 5/11 (46%) participants associated with RV pressure overload (mean pulmonary arterial pressure change: + 55 ± 20%, p < 0.001). Both MWI and GWE were reduced post-ascent (– 21 ± 16%, p = 0.004 and – 4 ± 4%, p = 0.007, respectively). Relative decrease in MWI and GWE were inversely correlated with increase in GWW (r = – 0.86, p = 0.003 and r = -0.97, p < 0.001, respectively). Conclusions: Prolonged high-altitude speed climbing in elite climbers is associated with RV and LV function changes with a major interaction alteration. MWI, assessing the myocardial performance, could be a new tool for evaluating LV exercise-induced cardiac fatigue. [ABSTRACT FROM AUTHOR]

Strenuous exercise results in transient but minor alterations in left ventricular diastolic function (LVDF). The aim of this study is to describe and interpret the kinetics of the well-established 2D parameters of diastolic function and the novel and very sensitive 3D parameters before/after a marathon race. LVDF was evaluated by transthoracic echocardiography (TEE) in 212 healthy male [aged 42 (36–49) years)] marathon runners (all Be-MaGIC-study) in the week prior to (V1), immediately after (V2), 24 h after (V3) and 72 h after (V4) a marathon race. Real time three-dimensional echocardiography (RT3DE) included maximal and minimal left atrium (LA) volume, total LA ejection fraction (Total-EF), total LA stroke volume (Total-SV), true ejection fraction (True-EF) and atrial stroke volume (ASV). After adjustment for possible confounders (heart rate and systolic blood pressure), 2D Parameters of left ventricular inflow (E/A-ratio) decreased from pre- to immediately post-race (− 0.3 ± 0.06, p < 0.001) and returned to baseline within 24 h. E / e ′ mean -ratio remained unchanged directly post-race, but was significantly increased during follow-up of 24 and 72 h. 3D LA Vmin was increased immediately postrace and in the 24 h follow-up, LA Vmax was increased immediately post-race and in the follow-up of 24 and 72 h. During follow-up of 72 h, but not immediately postrace, TrueEF and ASV were significantly increased. Both techniques revealed acute and prolonged alterations of diastolic LV function. Considering all parameters, the recovery of diastolic LV after a marathon seems to take longer than previously assumed. Trial registration ClinicalTrials.gov ID: NCT00933218 [ABSTRACT FROM AUTHOR]

Remote ischemic preconditioning ( RIPC; repeated short reversible periods of ischemia) protects the heart against subsequent ischemic injury. We explored whether RIPC can attenuate post-exercise changes in cardiac troponin T (cTnT) and cardiac function in healthy individuals. In a randomized, crossover design, 14 participants completed 1-h cycling time trials ( TT) on two separate visits; preceded by RIPC (arms/legs, 4 × 5-min 220 mmHg), or SHAM- RIPC (20 mmHg). Venous blood was sampled before and 0-, 1-, and 3-h post-exercise to assess high sensitivity (hs-)cTnT and brain natriuretic peptide ( NT-pro BNP). Echocardiograms were performed at the same time points to assess left and right ventricular systolic (ejection fraction; EF and right ventricular fractional area change; RVFAC, respectively) and diastolic (early transmitral flow velocities; E) function. Baseline hs-cTnT was not different between RIPC and SHAM. Post-exercise hs-cTnT levels were consistently lower following RIPC (18 ± 3 vs 21 ± 3; 19 ± 3 vs 23 ± 3; and 20 ± 2 vs 25 ± 2 ng/L at 0, 1 and 3-h post-exercise, respectively; P < 0.05). There was no main effect of time, trial, or interaction for NT-pro BNP and left ventricular EF or RVFAC (all P < 0.05). A main effect of time was evident for E which transiently declined immediately after exercise to a similar level in both trials (0.85 ± 0.04 vs 0.74 ± 0.04 m/s, respectively; P < 0.05). In summary, RIPC was associated with lower hs-cTnT levels after exercise but there was no independent effect of RIPC for NT-pro BNP or LV systolic and diastolic function. The lower hs-cTnT levels after RIPC suggests that further research should evaluate the role of ischemia in exercise-induced elevation in hs-cTnT. [ABSTRACT FROM AUTHOR]

Objective: To evaluate sex differences in left ventricular (LV) function after an ultramarathon, and the association of vascular and training indices with the magnitude of exercise-induced cardiac fatigue. Design: Descriptive field study. Setting: Fat Dog 100 Ultramarathon Trail Race, Canada. Participants: Thirty-four (13 women) recreational runners (aged 28-56 years). Interventions: A 100-km or 160-km mountain marathon. Main Outcome Measures: Baseline baroreceptor sensitivity, heart rate variability, and arterial compliance; Pre-exercise and postexercise echocardiographic evaluations of LV dimensions, volumes, Doppler flow velocities, tissue velocities, strain, and strain rate. Results: Finishers represented 17 men (44.8 ± 6.6 years) and 8 women (45.9 ± 10.2 years; P = 0.758). After ultraendurance exercise, significant reductions (P < 0.05) in fractional shortening (men: 40.9 ± 6.9 to 34.1 ± 7.6%; women: 42.5 ± 6.5 to 34.6 ± 7.9%) diastolic filling (E/A, men: 1.28 ± 0.68 to 1.26 ± 0.33; women: 1.55 ± 0.51 to 1.30 ± 0.27), septal and lateral tissue velocities (E'), and longitudinal strain (men: 221.02 ± 1.98 to 218.44 ± 0.34; women: 220.28 ± 1.90 to 218.44 ± 2.34) were observed. Sex differences were found for baseline cardiac structure and global function, peak late transmitral flow velocity, and estimates of LV filling pressures (P < 0.05). Regression analysis found that higher baseline arterial compliance was associated with lower reductions in cardiac function postexercise, to which sex was a significant factor for E' of the lateral wall. Faster race pace and greater lifetime ultramarathons were associated with lower reductions in LV longitudinal strain (P < 0.05). Conclusions: Cardiac responses after an ultramarathon were similar between men and women. Greater evidence of exercise-induced cardiac fatigue was found to be associated with lower baseline arterial compliance and training status/experience. Clinical Relevance: These findings suggest that vascular health is an important contributor to the degree of cardiovascular strain incurred as the result of an acute bout of prolonged strenuous exercise. [ABSTRACT FROM AUTHOR]

This study examined standard echocardiographic measures of cardiac size and performance in response to a 3-h firefighting training exercise. Forty experienced male personnel completed a standardized 3 h live firefighting exercise. Before and after the firefighting activities, participants were weighed, height, heart rate, blood pressure and blood samples were obtained, and echocardiographic measurements were made. Firefighting produced significant decreases in left ventricular diastolic dimension, stroke volume, fractional shortening, and mitral E velocity, tachycardia, a rise in core temperature, and a reduction in calculated plasma volume. On tissue Doppler imaging, there were no changes in systolic contractile function, but a decreased lateral wall diastolic velocity was observed. These findings show that 3 h of live firefighting produced cardiac changes consistent with cardiac fatigue, coupled with a decrease in systemic arterial compliance. These data show that live firefighting produces significant cardiovascular changes and future work is needed to evaluate if these changes are related to the increase in cardiovascular risk during live firefighting. [ABSTRACT FROM AUTHOR]

We assessed myocardial deformation in sub-endocardial and sub-epicardial layers of the left ventricle (LV) wall before and after running a marathon. Echocardiography scans were performed on 14 male, non-elite runners (mean +/- SD; age 32 +/- 10 years) who completed the 42.2-km London marathon. Para-sternal short axis and apical four-chamber views were recorded for off-line analysis. Peak longitudinal, radial and circumferential strains, peak systolic and early diastolic strain rates were recorded. Circumferential rotation in basal and apical LV scans was used to calculate torsion. Pre-race strain and strain rates were generally greater in the sub-endocardial layer of the LV wall. After race completion, a mixed pattern of change was observed with a reduction in sub-epicardial radial strain (32.6 +/- 12.5 to 20.3 +/- 9.6%; P < 0.01) and sub-endocardial circumferential strain (-26.9 +/- 3.6 to -23.7 +/- 4.1%; P < 0.01) at the apex. Rotation was not altered at either the apical or basal levels and thus torsion was not changed in either the sub-endocardium (6.72 +/- 3.46 degrees to 5.67 +/- 4.98 degrees) or the sub-epicardium (3.48 +/- 2.68 degrees to 3.01 +/- 3.23 degrees). Strain rates and rotation rates were only sporadically altered post-race. There are differences in deformation characteristics between the sub-endocardium and sub-epicardium at baseline, and the limited changes observed post-race were not specific to any region or depth of the LV wall. [ABSTRACT FROM AUTHOR]

We assessed the time delay from the onset of QRS (Q) to peak systolic (S') and diastolic (E') tissue velocities in the left (LV) and right ventricle (RV) before and after prolonged exercise. Nineteen well-trained runners (mean +/- SD age, 41 +/- 9 years) had tissue-Doppler echocardiography performed before and after an 89 km ultra-marathon race. Longitudinal tissue motion was analysed in LV basal and mid-wall segments and RV free wall. Electromechanical coupling was assessed by the delay between Q and S' as well as E' tissue velocities. Average data for all segments were adjusted for the R-R interval. Comparisons were made by paired t-tests. An increase in electro-mechanical delay (EMD) was reported post-exercise in systole (Q-S' LV: 131 +/- 20 vs. 175 +/- 27 ms; RV: 171 +/- 34 vs. 258 +/- 35 ms; P < 0.05) and diastole (Q-E' LV: 486 +/- 51 vs. 647 +/- 44 ms; RV: 500 +/- 80 vs. 690 +/- 75 ms; P < 0.05). Further, post-race peak tissue velocities in basal LV and RV wall segments were reduced (P < 0.05). Recovery from prolonged running was associated with an increased "EMD", and reduced peak tissue velocities, in both ventricles. [ABSTRACT FROM AUTHOR]

We examined the effect of intensity during prolonged exercise (PE) on left (LV) and right ventricular (RV) function. Subjects included 18 individuals (mean ± SE: age = 28.1 ± 1.1 yr, maximal aerobic power = 55.1 ± 1.6 ml · kg-1 · min-1), who performed 150 mm of exercise at 60 and 80% maximal aerobic power on two separate occasions. Transthoracic echocardiography assessed systolic and diastolic performance, and blood sampling assessed hydration status and noradrenaline levels before (pre), during (15 and 150 mm), and 60 mm following (post) PE. β-Adrenergic sensitivity pre- and post-PE was assessed by dobutamine stress. High-intensity PE (15 vs. 150 mm) induced reductions in LV ejection fraction (69.3 ± 1.3 vs. 63.5 ± 1.3%, P = 0.000), LV strain (-23.5 ± 0.6 vs. -22.3 ± 0.6%, P = 0.034), and RV strain (-26.3 ± 0.6 vs. -23.0 ± 0.6%, P < 0.01). Both exercise intensities induced diastolic reductions (pre vs. post) in the ratio of septal early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (2.15 ± 0.15 vs. 1.62 ± 0.09; 2.21 ± 0.15 vs. 1.48 ± 0.10), ratio of lateral early wave of annular tissue velocities to late/atrial wave of annular tissue velocities (3.84 ± 0.42 vs. 2.49 ± 0.20; 3.56 ± 0.32 vs. 2.08 ± 0.18), ratio of early to late LV strain rate (2.42, ± 0.16 vs. 1.97 ± 0.13; 2.30 ± 0.15 vs. 1.81 ± 0.11), and ratio of early to late RV strain rate (2.03 ± 0.17 vs. 1.51 ± 0.09; 2.16 ± 0.16 vs. 1.44 ± 0.11) (P < 0.001). Evidence of 3-adrenergic sensitivity was supported by a decreased strain, strain rate, ejection fraction, and systolic pressure-volume ratio response to dobutamine (P < 0.05) with elevated noradrenaline (P < 0.01). PE-induced reductions in LV and RV systolic function were related to exercise intensity and β-adrenergic desensitization. The clinical significance of exercise-induced cardiac fatigue warrants further research. [ABSTRACT FROM AUTHOR]

Left ventricular (LV) function is characterized by contraction in the longitudinal, radial, and circumferential planes. Previous studies of postexercise changes in LV function have assessed global indices of LV function. The purpose of this study was to use 2-dimensional (2D) strain analysis to examine LV function following marathon running in the circumferential, radial, and longitudinal planes, and to compare these data with other global and regional indices of function. Fifteen (mean ± SD: age, 32 ± 7 years; stature, 1.76 ± 0.08 m; body mass, 77.8 ± 8.2 kg) competitors in the London Marathon were echocardiographically assessed pre- and postrace. 2D strain (ejection fraction (EF), Doppler (early (E) and late (A) trans-mitral filling), tissue Doppler imaging (TDI) (systolic (S′) and early diastolic (E′) wall-motion velocities); TDI-derived longitudinal strain (εTDI), and systolic and diastolic strain rate (SRTDI); and 2D-derived peak circumferential, radial, and longitudinal strain (ε2D), and systolic and diastolic strain rate (SR2D) were examined. Differences pre- and postrace completion were assessed using paired t tests, with alpha set at 0.01. All participants completed the marathon in a mean time of 213 ± 41 min. A varied response was observed for measures of LV systolic and diastolic function following completion of the marathon (mean ± SD): EF, 63 ± 6 vs. 63 ± 7% (p > 0.01); E:A, 1.70 ± 0.37 vs. 1.17 ± 0.37; E′:A′, 2.36 ± 0.79 vs. 1.60 ± 0.57 (p < 0.01); mean longitudinal εTDI, 19.1 ± 5.1 vs. 17.5 ± 4.2% (p < 0.01); mean longitudinal diastolic SRTDI, 1.81 ± 0.54 vs. 1.58 ± 0.51·s-1 (p < 0.01); mean longitudinal systolic SR2D, 0.73 ± 0.21 vs. 0.97 ± 0.22·s-1 (p < 0.01); mean longitudinal diastolic SR2D, 0.94 ± 0.34 vs. 1.01 ± 0.23·s-1 (p > 0.01); mean radial systolic SR2D, 1.20 ± 0.15 vs. 1.45 ± 0.32·s-1 (p < 0.01); mean radial diastolic SR2D, 1.19 ± 0.25 vs. 1.29 ± 0.41·s-1 (p > 0.01); mean circumferential systolic SR2D, -1.09 ± 0.16 vs. -1.24 ± 0.18·s-1 (p < 0.01); and mean circumferential diastolic SR2D, -1.27 ± 0.28 vs. -1.22 ± 0.31·s-1 (p > 0.01). Marathon running promotes a varied echocardiographic response, with some functional parameters showing no change, some increasing, and some decreasing postexercise. This varied response likely reflects the complexities of cardiac function and highlights the need to adopt a multimodality approach when assessing cardiac function following exercise. [ABSTRACT FROM AUTHOR]

The aim of the study was to examine the impact of prolonged exercise leading to physical exhaustion on left ventricular (LV) systolic and diastolic function in untrained healthy subjects, and to examine cardiovascular determinants of exercise performance. Twenty-four nonathletic healthy adults (14 males, 10 females; mean age 42 ± 11 years) were exercised on a treadmill at 70% of maximal oxygen consumption until physical exhaustion occurred after an average of 84 ± 39 minutes. Two-dimensional and Doppler echocardiography was performed before and 15 minutes after exercise to assess LV function and geometry, and right ventricular (RV) systolic function. After prolonged exercise, LV ejection fraction and geometry were unchanged, but LV end-diastolic volume, end-systolic volume, and stroke volume decreased. However, due to a higher heart rate (HR), cardiac output increased at 15 minutes post exercise. RV fractional shortening was unchanged. LV peak early to atrial filling velocity ratio decreased post exercise, with an increase in percent atrial contribution. However, less preload-dependent variables of LV diastolic function such as deceleration time, LV inflow propagation rate, mitral annular tissue Doppler and myocardial performance index were unchanged. Preexercise stroke volume and HR were the only predictors (r = 0.86, P < 0.01) of exercise duration. However, age, resting blood pressure, indices of systolic and diastolic function, and LV geometry were not predictors. Prolonged exercise leading to physical exhaustion is not associated with systolic or diastolic dysfunction. Reduced early LV diastolic filling and the relative increase in left atrial contribution seen with prolonged exercise are likely due to preload reduction rather than true diastolic dysfunction. [ABSTRACT FROM AUTHOR]

We assessed segmental and global left ventricular (LV) systolic function using tissue Doppler imaging (TDI) in 30 subjects (age: 18-62 y) before and after a marathon race. Longitudinal plane systolic (S') TDI velocities were assessed at 5 sites on the mitral annulus and radial plane S' velocities were assessed at the LV septal and free wall in a subsample (n = 9). Heart rate (HR) and LV diastolic internal dimension were also assessed before (pre) and immediately after (post) the race. Pre-post changes in all variables were analysed by repeated measures analysis of variance (ANOVA). Delta scores for TDI data were correlated with alterations in indices of LV loading, as well as with age and finishing time. Segmental longitudinal and radial TDI velocities were not significantly different pre to post race (p > 0.05), which resulted in no change in mean S' velocities (longitudinal: pre 17.0 ± 3.4 cms-1, post 17.4 ± 4.0 cms-1; radial: pre 13.0 ± 5.4 cms-1, post 14.2 ± 7.1 cms-1; p > 0.05). Any pre-post changes in TDI data were not related to an elevated post race HR (r = 0.15, p > 0.05), a decreased post race LV internal dimension in diastole (r = 0.10, p > 0.05), age (r = -0.25, p > 0.05), or finishing time (r = -0.13, p > 0.05). Our data suggest that marathon running does not induce any segmental or global depression in LV systolic function. [ABSTRACT FROM AUTHOR]

The purpose of this study was to assess left ventricular (LV) function and biochemical markers of myocyte after prolonged weightlifting activity. Seventeen male subjects (age range 20–34 years) performed a 90-min bout of weightlifting exercise consisting of three sets of 8–10 repetitions at 70% one-repetition maximum. Body mass, heart rate, systolic blood pressure (SBP) and echocardiographically determined indices of LV loading (LV internal diameter during diastole, LV meridonial wall stress), systolic function (stroke volume (SV), ejection fraction (EF), end-systolic pressure volume relationship; SBP/ESV) and diastolic filling (ratio of early to late; E:A) were obtained pre-exercise, immediately after and 24 h post-exercise. A 5-ml venous blood sample was obtained for the assessment of cardiac troponin T (cTnT) via third generation electrochemiluminescence assay. Data were assessed via one-way ANOVA and Pearson's correlation. Although SV declined (80.9 ± 18.3 vs. 66.9 ± 17.2, p 0.05). The E:A ratio was significantly decreased following exercise (1.78 ± 0.41 vs. 1.33 ± 0.37, p 2 = 0.05 to 0.24). All values returned to baseline 24 h post-exercise. No cTnT was reported in any of the blood samples. In conclusion, there was no significant evidence of any LV contractile depression and no cTnT was observed post exercise. The small reduction in diastolic filling could not be explained by changes in haemodynamic loading or the post-exercise elevation in heart rate. [ABSTRACT FROM AUTHOR]