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Background & Aims: Although regular and moderate exercise reduces cardiovascular risk, recent studies have shown an increase in biomarkers compatible with heart damage (e.g., cardiac troponin T after prolonged periods of exercise in healthy individuals without cardiovascular disease) (1–3). Studies show that strenuous physical activity may cause acute cardiovascular and hemodynamic stress, which can be assessed through necrosis of myocytes and myocardial infarction. Research shows that exercise is an effective factor in changing the levels of indicators Heart damage includes cardiac troponin T.Prolonged exercise is associated with an acute increase in cardiac biomarkers. Cardiac troponin T is a very specific marker of myocardial damage. Which is released from the myocardium during different periods of stress and heart damage(9). Cardiac troponin I and cardiac troponin T are proteins present in the contractile system of heart cells and are very sensitive and specific indicators of cardiac cell necrosis.As a result, these indicators are a good tool for assessing the potential damage to heart muscle cells in athletes. Prolonged exercise also leads to increased plasma free fatty acid concentrations(10). The aim of this study was to explain Effect of physical activityon cardiac troponin T and free fatty acids. Methods: 20 professional Sky Running athletes with an average age of 27-37 years from Tehran participated in this competition voluntarily and purposefully. The race was held in the valleys of Central Alborz, the total distance traveled was 21 km and 200 m, the starting point was 1650 m above sea level and the maximum altitude was 3150 m. 5 ml of blood was taken from the subjects 30 minutes before the start of the race. Immediately after the race and 1 hour later, 5 ml of blood was taken from the subjects again. To isolate serum after blood sampling, blood was poured into sterile test tubes labeled with each sample that did not contain any anticoagulants and incubated at room temperature for 60 minutes. They were then centrifuged at 2000 rpm for 20 minutes. The clear supernatant (serum) was carefully separated by a sampler 1000 so that it did not mix with the red blood cells, and the serum was kept at -80 ° C until the experiment was performed. Cardiac troponin T was injected by ELISA with a highsensitive kit with1.56 ng / L sensitivity of Zellbio brand made in Germany and free fatty acids were measured by colorimetric method with a hypersensitive kit with a sensitivity of 5 µmol/ L by Zellbio brand made in Germany. Correlated t-test at the significance level of 0.05 alpha was used to evaluate the changes in the studied variables. Results: The amount of cardiac troponin T immediately after and one hour after the end of the race increased significantly compared to before the race (P <0.05). The amount of free fatty acids immediately and one hour after the end of the race increases significantly compared to before the race (P <0.05)Conclusion: The results of this study showed that immediately and 1 hour after the end of the Sky Running competition, the amount of cardiac troponin T increased significantly. These changes identified in our study are in accordance with the results of previous studies performed in athletes completing endurance competitions. Richardson et al. reported an increase in cardiac troponin T after the marathon, stating that an increase in cardiac troponin T was related to exercise intensity associated with ventilation threshold and maximal oxygen consumption, but it has nothing to do with a person's cardiovascular fitness, training status or exercise history(16). Similarly, Dapont et al. reported that cardiac troponin I was elevated in all marathon runners(17). Lagzaras et al. showed an increase in troponin levels in all participants in the triple race (18).While Kim et al. Moreover, Park et al. Did not observe a significant increase in cardiac troponin T after prolonged exercise(19,20). Physiological mechanisms of cardiac biomarker enhancement associated with endurance activities include increased permeability of the cardiomyocyte membrane, which causes the release of cardiac troponin T in the cytosol on a concentration gradient from intracellular to extracellular. The initial peak represents the release of cardiac troponin T through the sarcolemma membrane, the level of which decreases after 24 hours and reflects the half-life and subsequent clearance of cardiac troponin T subunits. It has been suggested that mechanical or oxidative stress through Transient disorder (wounding) of sarcolemma may be responsible for this increase in membrane permeability and increase troponin secretion(21).Therefore; it seems that the increase in troponin following exercise may be a reflection of the adaptation of cellular cascades seen in exercise-induced remodeling and cardiac hypertrophy. Another result observed in the present study was a significant increase in free fatty acids immediately and 1 hour after the race compared to before the race. Which was in line with previous studies in this field. Vincent et al. 2020 showed that long-term high-intensity exercise could deplete the heart fat basin(24). Waskiwisk et al. 2011 showed that prolonged exercise significantly increased free fatty acids immediately, 12 and 24 hours after competition(35). Pak and Walk 2019 showed that cardiac troponin T did not change significantly, but free fatty acids immediately after Completion of triple and triple ultra competitions increased significantly(20). Bilt et al. 2011 showed that a 2-hour cycle of fasting cycling in 11 men untrain, tripled plasma free fatty acid concentrations while increasing cardiac lipid content, but did not impair systolic function(36). Elevated cardiac troponin T and elevated free fatty acids can indicate a degree of "cardiac fatigue." Increased free fatty acids after competition and long-term exercise appear to play an important role in reducing cardiac inotropic.Due to the multifaceted nature of heart fatigue, two main hypotheses have been proposed: A reversible process of heart damage is often referred to as “stunning “; Myocardial injury can underlie left ventricular diastolic and systolic dysfunction; transient ischemia has a mechanism similar to cardiac fatigue, and can lead to a process called stunning, stunning theory because it leads to necrosis or injury.It does not become a permanent cell, it has a transient nature.It is called cardiac beta-adrenergic receptor desensitization. A wide range of studies have identified biomarkers of increased heart damage after prolonged exercise and have linked them to functional changes(29–32). Increased catecholamine concentrations, increased plasma free fatty acids, and accumulation of oxygen free radicals may lead to decreased blood flow to the heart through increased vascular tone and endothelial dysfunction(33). Physical activity increase heart injury biomarkers in professional athletes. Elevated cardiac troponin T and elevated free fatty acids can indicate a degree of "cardiac fatigue". Increased free fatty acids after competition and longterm exercise appear to play an important role in reducing cardiac inotropic. [ABSTRACT FROM AUTHOR]

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]

Background: Echocardiographic signs of exercise-induced cardiac fatigue (EICF) have been described after strenuous endurance exercise. Nevertheless, few data are available on the effects of repeated strenuous exercise, especially when associated with other constraints as sleep deprivation or mental stress which occur during military selection boot camps. Furthermore, we aimed to study the influence of experience and training level on potential EICF signs.Methods: Two groups of trained soldiers were included, elite soldiers from the French Navy Special Forces (elite; n = 20) and non-elite officer cadets from a French military academy (non-elite; n = 38). All underwent echocardiography before and immediately after exposure to several days of uninterrupted intense exercise during their selection boot camps. Changes in myocardial morphology and function of the 4 cardiac chambers were assessed.Results: Exercise-induced decrease in right and left atrial and ventricular functions were demonstrated with 2D-strain parameters in both groups. Indeed, both atrial reservoir strain, RV and LV longitudinal strain and LV global constructive work were altered. Increase in LV mechanical dispersion assessed by 2D-strain and alteration of conventional parameters of diastolic function (increase in E/e' and decrease in e') were solely observed in the non-elite group. Conventional parameters of LV and RV systolic function (LVEF, RVFAC, TAPSE, s mitral, and tricuspid waves) were not modified.Conclusions: Alterations of myocardial functions are observed in soldiers after uninterrupted prolonged intense exercise performed during selection boot camps. These alterations occur both in elite and non-elite soldiers. 2D-strain is more sensitive to detect EICF than conventional echocardiographic parameters.

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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]

Abstract Background: Cardiac troponin T and creatine kinase are used as biological markers for cardiomyocytes and its levels in serum are used as indicators of myocardial cell injury. The purpose of this study was to compare the effects of 3 different training protocols (runing, swimming, and pedaling training) on myocardial cell injury biomarkers in young girls. Materials and Methods: In this semi-experimental study with pretest–posttest design, ten healthy young girls (aged 23.0±1.6 y) were selected in a convenience sampling way. The subjects performed three types of exercise in 7 days interval. Blood sample was assessed before and after the exercise sessions. Data were analyzed using t-test and analysis of variance. Results: Our results indicated that creatin kinase increased significantly after three types of exercise (p0.05). Conclusion: Our data suggest that intensive exercise is associated with cardiac damage in less trained girls and the type of exercise is determinants of the magnitude of myocardial injury biomarkers release.

Purpose: Moderate overtraining has been characterized by decreased exercising HR and recently decreased exercising stroke volume (SV), independent of alterations to blood volume. The aim of this study was to assess changes in arterial stiffness and central hemodynamics, and their relationship to exercising SV, after 3 wk of overload training. Methods: Twenty-six cyclists and triathletes completed 3 wk of either regular training (CON; n = 13) or overload training (OL; n = 13). Testing took place before (PRE) and after regular or overload training (POST). Resting measures included brachial blood pressure, HR, carotid–femoral pulse wave velocity (PWV) to assess arterial stiffness, and carotid pulse wave analysis to assess wave reflections and central hemodynamics. An incremental cycle test was used to assess peak power, maximal HR, and maximal lactate to assess overtraining status. Cardiac output (Q˙), SV, and HR were assessed using cardiac impedance. Results: Resting arterial stiffness was unaltered in CON but increased with OL after increased training (CON −0.1 ± 0.6 m·s−1 vs OL +0.5 ± 0.8 m·s−1, P = 0.04). Resting blood pressure and central hemodynamics, including aortic pressures, augmentation index, and subendocardial viability ratio, did not change (all P > 0.05). Maximal SV (CON +3 mL vs OL −9 mL, P = 0.04), HR (CON −2 ± 4 bpm vs OL −9 ± 3 bpm, P < 0.001), and Q˙ (CON +0.32 L·min−1 vs OL −1.75 L·min−1, P = 0.01) decreased with OL from PRE to POST. A significant inverse relationship existed between changes in PWV and maximal Q˙ (r = −0.44, P = 0.04) and changes in PWV and peak power (r = −0.48, P = 0.01), and trended for SV and PWV (r = −0.41, P = 0.055). Conclusions: Overload training results in increased resting arterial stiffness and reduced SV during exercise, with no changes to resting central hemodynamics. [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]

Background: Cardiac troponin T and creatine kinase are used as biological markers for cardiomyocytes and its levels in serum are used as indicators of myocardial cell injury. The purpose of this study was to compare the effects of 3 different training protocols (runing, swimming, and pedaling training) on myocardial cell injury biomarkers in young girls. Materials and Methods: In this semi-experimental study with pretest-posttest design, ten healthy young girls (aged 23.0±1.6 y) were selected in a convenience sampling way. The subjects performed three types of exercise in 7 days interval. Blood sample was assessed before and after the exercise sessions. Data were analyzed using t-test and analysis of variance. Results: Our results indicated that creatin kinase increased significantly after three types of exercise (p<0.05). Running exercise led to greater increase in serum creatine kinase (p<0.05). Also, troponin T levels significantly were increased after three types of exercise (p<0.05), although no significant differences were observed between exercise types (p>0.05). Conclusion: Our data suggest that intensive exercise is associated with cardiac damage in less trained girls and the type of exercise is determinants of the magnitude of myocardial injury biomarkers release. [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]

Cardiac electrical-mechanical delay ( cEMD), left ventricular ( LV) function, and cardiac troponin I ( cTnI) were assessed after 40 km cycle time trials completed at high ( HIGH) and moderate ( MOD) intensities in 12 cyclists. Echocardiograms and blood samples were collected before, 10, and 60 min after cycling. cEMD as assessed by time from QRS onset to peak systolic ( S') tissue velocity was lengthened after both bouts of cycling but was not mediated by cycling intensity ( HIGH: 174 ± 52 vs 198 ± 26 ms; MOD: 151 ± 40 vs 178 ± 52 ms, P < 0.05). Global LV systolic function was unaltered by exercise. cEMD from QRS to peak early ( E') diastolic tissue velocity was also increased post-exercise ( HIGH: 524 ± 95 vs 664 ± 68 ms; MOD: 495 ± 62 vs 604 ± 91 ms, P < 0.05). Indices of LV diastolic function was reduced after cycling but were not mediated by exercise intensity. cTnI was elevated in two participants after HIGH trial (0.06 ug/ L; 0.04 ug/ L) and one participant after MOD trial (0.02 ug/ L). While cEMD is lengthened and LV diastolic function was reduced post-cycling, altering time-trial intensity had little impact upon cEMD, LV function, and cTnI release. [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]

The Sports Medicine Research Center of Keio University was founded in April 1989 as a clinical and research institute not only for athletes, but also for people interested in health promotion. More than ten thousand candidates enroll in the center each year. In this paper, clinical research works conducted in the center, especially in the cardiovascular field, were reviewed. These included the importance of diagnosis of 'athlete heart syndrome', morphologic characteristics of the heart of Japanese professional sumo wrestlers, possibility of the occurrence of depressed left ventricular contractile function after exhaustive exercise, physiological profile of older top-class climbers, as well as questionnaires to protect against sudden cardiac death in high school students, and basic life support (BLS) in the integrated school system in Keio. [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 this study was to examine cardiac dysfunction following ultra-endurance exercise in male athletes. Fourteen athletes (mean±SD, age 39±8 years) were evaluated before and after the European Championship in Triathlon 2003 using echocardiogram (ECG), cardiac markers [cardiac troponin T (cTnT) and pro-brain natriuretic peptide (pro-BNP)] and echocardiography. Conventional echocardiography techniques and new Doppler tissue imaging (DTI) modalities were applied before and immediately after the competition. Blood samples were drawn 1 week before, immediately after and 12–24 h post-competition. CTnT significantly increased immediately, but decreased to within normal limits 12–24 h post-competition. Pro-BNP was significantly increased immediately post-race (27±21 vs 7±2 pmol/L pre-race, P≤0.007), which 12–24 h later, decreased to 19±14 pmol/L ( P=0.07 vs pre-race). During echocardiography, no significant differences were found in regional or global systolic parameters. Early diastolic peak flow velocity (9±2, P=0.04) and E/ A ratio (2±1, P=0.004) were increased pre-race and decreased significantly toward normal values. In one athlete, cTnT levels increased significantly and systolic velocities decreased, thus suggesting reversible cardiac fatigue. When using cardiac markers and echocardiographic findings, a triathlon was found to have no significant negative effects on left ventricular function or myocardial tissue in male athletes. [ABSTRACT FROM AUTHOR]

The article presents a study which summarizes the findings of studies being conducted in relation to the topic of whether prolonged exercise can lead to transient depression in left ventricular (LV) functions. It presents several research studies which utilized various techniques as evidences including echocardiographic technology, tissue Doppler imaging (TDI) and assessment on myocardial strain rate. In conclusion, it notes the growing evidence which indicates that extended exercise may cause reduction in both systolic and diastolic LV functions.

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]

The impact of prolonged exercise upon right ventricular (RV) function is poorly understood and to date no studies have utilized tissue-Doppler imaging (TDI). Thirty-five marathon runners (age range 18–50 years) volunteered for the study. Two-dimensional, pulsed Doppler, and TDI studies were performed one day before and immediately following race completion. Right and left ventricular (LV) longitudinal TDI myocardial velocities were acquired from the tricuspid annulus and mitral annulus, providing velocity data during systole (S′), early diastole (E′), and late diastole (A′). Transtricuspid and transmitral, early diastolic (E), and late diastolic (A) velocities and ratios were assessed using conventional pulsed-wave Doppler. RV and LV fractional area changes (FAC) were calculated from RV and LV end-diastolic and end-systolic areas recorded from 2D scans in a subsample (n = 23). RV myocardial velocities were unchanged pre-post race in S′ (21.1 ± 2.7 to 21.7 ± 4.5 cm s−1, P > 0.05), reduced in E′ (23.3 ± 3.5 to 19.9 ± 5.3 cm s−1, P < 0.05), increased in A′ (19.1 ± 3.6 to 23.7 ± 6.8 cm s−1, P < 0.05) with a resultant decline in E′/A′ (1.28 ± 0.36 to 0.94 ± 0.45, P < 0.05). This pattern of data was mirrored in the LV. Similarly both pulsed-Doppler tricuspid and mitral E/A ratios decreased from pre- to postrace (P < 0.05). FAC for the RV and LV were unaltered postrace (P > 0.05). The impact of differing age, finishing time (173–330 min), hemodynamic loading and heart rate upon RV and LV function pre- to postrace was negligible. In conclusion, TDI and 2D data, for both the RV and LV demonstrated little change in systolic function after a marathon race. Conversely, a reduction in diastolic function was observed in both ventricles for which a mechanism has yet to be deduced. [ABSTRACT FROM AUTHOR]

Background: Running a marathon is a stressful event for athletes. Limited research exists on the role of cardiac markers during such a strenuous event. The aim of this study was to investigate detailed changes in cardiac markers before and after a long-distance run. Methods: We studied 25 male and 2 female runners (age 34–64 years) who were running the Visé-Maastricht-Visé marathon. Blood samples were drawn just before and immediately after finishing the marathon. An additional blood sample was collected 24 h later. Results: Running the marathon led to a significant increase in cortisol. This returned to baseline values 24 h after the marathon. There was a slight increase in brain natriuretic peptide (BNP); however, this was not statistically significant. On the contrary, the N-terminal fragment of BNP (NT-pro-BNP) was significantly increased immediately after the run and was normalized 24 h later in 26 out of 27 runners (96%). The magnitude of the transient elevations in BNP and NT-pro-BNP increased with the age of the athletes. Furthermore, in 9 out of 27 runners there was a significant increase in troponin T. However, in all these runners this increase was transient and troponin-T levels returned to baseline values 24 h after the marathon. Conclusions: Running a marathon significantly increases NT-pro-BNP levels in healthy adults. This increase could be partially attributed to cardiac stress. The transient increases in BNP, NT-pro-BNP and troponin T are more likely to reflect myocardial stunning than cardiomyocyte damage. It seems that the magnitude of the increase in BNP could serve as a marker of the biological age of the myocardium. Clin Chem Lab Med 2006;44:999–1003. [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 article looks into the left ventricular function immediately following prolonged exercise. The author pointed out that evidence supporting cardiac fatigue following prolonged endurance exercise remains equivocal. The meta-analysis was aimed to quantify all data fulfilling the specified inclusion criteria, examining the short-term effect of prolonged endurance exercise on left ventricular function. Significantly, the weighted mean change in ejection fraction (EF), systolic blood pressure/end systolic volume ratio (SBP/ESV), and early-to-late diastolic filling were conducted. Finally, the decrease in EF and SBP/ESV observed indicates a reduction in systolic function, partially explained by altered cardiac loading.

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]

Background: Echocardiographic signs of exercise-induced cardiac fatigue (EICF) have been described after strenuous endurance exercise. Nevertheless, few data are available on the effects of repeated strenuous exercise, especially when associated with other constraints as sleep deprivation or mental stress which occur during military selection boot camps. Furthermore, we aimed to study the influence of experience and training level on potential EICF signs. Methods: Two groups of trained soldiers were included, elite soldiers from the French Navy Special Forces (elite; n = 20) and non-elite officer cadets from a French military academy (non-elite; n = 38). All underwent echocardiography before and immediately after exposure to several days of uninterrupted intense exercise during their selection boot camps. Changes in myocardial morphology and function of the 4 cardiac chambers were assessed. Results: Exercise-induced decrease in right and left atrial and ventricular functions were demonstrated with 2D-strain parameters in both groups. Indeed, both atrial reservoir strain, RV and LV longitudinal strain and LV global constructive work were altered. Increase in LV mechanical dispersion assessed by 2D-strain and alteration of conventional parameters of diastolic function (increase in E/e' and decrease in e') were solely observed in the non-elite group. Conventional parameters of LV and RV systolic function (LVEF, RVFAC, TAPSE, s mitral, and tricuspid waves) were not modified. Conclusions: Alterations of myocardial functions are observed in soldiers after uninterrupted prolonged intense exercise performed during selection boot camps. These alterations occur both in elite and non-elite soldiers. 2D-strain is more sensitive to detect EICF than conventional echocardiographic parameters., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Charton, Kervio, Matelot, Lachard, Galli, Donal, Carré, Le Douairon Lahaye and Schnell.)

Aim: To provide a state-of-the-art review of the last 10 years focusing on cardiac fatigue following a marathon., Methods: The PubMed, Bookshelf and Medline databases were queried during a time span of 10 years to identify studies that met the inclusion criteria. Twenty-four studies focusing only on the impact of marathons on the cardiac function and factors involved in cardiac fatigue were included in this review., Results: Sixteen studies focused on the impact of marathons on several biomarkers (e.g., C-reactive protein, cardiac troponin T). Seven studies focused on the left (LV) or right (RV) ventricular function following a marathon and employed cardiac magnetic resonance, echocardiography, myocardial speckle tracking and heart rate variability to analyze global and regional LV or RV mechanics and the impact of the autonomic nervous system on cardiac function. One study focused on serum profiling and its association with cardiac changes after a marathon., Conclusions: This review reported a negligible impact of marathons on LV and RV systolic and contractile function but a negative impact on LV diastolic function in recreational runners. These impairments are often associated with acute damage to the myocardium. Thus, the advice of the present review to athletes is to adapt their training and have a regular medical monitoring to continue to run marathons while preserving their cardiac health.

Abstract: Although the underlying mechanisms responsible for cardiac dysfunction after prolonged exercise remains to be elucidated, it has reported cardiac deterioration following exhaustive exercise in the absence of underlying cardiovascular diseases, which has been attributed to cardiac fatigue. The objective of this study was to evaluate cardiac functions, exercise capacity, and flow-mediated dilatation in overreaching syndrome. We studied 13 male marathon runners who took part in a marathon. Cardiopulmonary exercise testing, transthoracic echocardiography and endothelium-dependent vasodilatation of the brachial artery were performed at before- and after-race. Peak oxygen consumption, left ventricular tissue Doppler imaging parameters and flow-mediated dilatation were decreased after-race values compared with before-race values. Overreaching syndrome could arise involves a physio-pathological trivest, cardio-vasculo-muscular axis, which include three vicious cycles. [Copyright &y& Elsevier]

Abstract: Background: Although the underlying mechanisms responsible for cardiac dysfunction after prolonged exercise remains to be elucidated, it has reported cardiac deterioration following exhaustive exercise in the absence of underlying cardiovascular diseases, which has been attributed to cardiac fatigue. The study was designed to investigate the effects of after fatiguing exercise on oxygen kinetics. Methods: Six athletes have taken examination, firstly by echocardiography, secondly by cardiopulmonary exercise testing and then by near-infrared spectroscopy (NIRS), before 2 days (pre-race) and after 1 day (post-race) marathon competition. Results: We found decrease in left ventricular systolic and diastolic functions, and peak oxygen consumption while increasing half time of muscular oxygen delivery after race period. Conclusion: Cardiopulmonary exercise testing in conjunction with oxygen kinetics of skeletal muscle measured by NIRS may be a tool for detecting cardiac fatigue. [Copyright &y& Elsevier]