The right ventricle following ultra-endurance exercise: insights from novel echocardiography and 12-lead electrocardiography (original) (raw)
Related papers
Echocardiography, 2006
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. (ECHOCARDIOGRAPHY, Volume 23, September 2006) tissue Doppler, diastolic function, cardiac fatigue While data has been presented for a postexercise decline in left ventricular (LV) systolic function and/or diastolic filling 1,2 we understand less about the potential impact of prolonged exercise on the right ventricle (RV). This is partially due to the difficulties in obtaining reliable and accurate data, especially in noninvasive imaging studies. To date only three studies have assessed RV function after prolonged exercise (see ). There is some suggestion from these studies that the RV may show earlier or more pronounced signs of "exercise-induced cardiac fatigue" in welltrained ultra-endurance athletes after competition. 3-5 This could be due to the fact that RV stroke work increases more, relatively, than LV stroke work with the imposition of exercise. The postulated reason for this is a greater relative increase in arterial pressure and a smaller relative decrease in peripheral resistance in the pulmonary compared to the systemic circulation. It is unclear what the consequences of shorter bouts of exercise (such as a marathon), in a more heterogenous group of athletes in terms of age and fitness level, are on postexercise RV function.
Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography, 2018
It has been proposed that chronic exposure to prolonged strenuous exercise may result in maladaptation of the right ventricle (RV). The aim of this study was to establish RV structure and function, including septal insertion points, using conventional echocardiography and myocardial strain (ε) imaging in a veteran population of ultramarathon runners (UR) and age- and sex-matched controls. A retrospective study design provided 40 UR (>35 years old; mean ± SD training experience, 18 ± 12 years) and 24 sedentary controls who had previously undergone conventional two-dimensional, tissue Doppler and speckle-tracking echocardiography to measure RV size and function. Peak RV ε and strain rate (SR) were assessed from the base, mid, and apical lateral wall. SR were assessed during systole (SRs'), early diastole (SRe') and late diastole (SRa'). Regional assessment of RV insertion points was made at the basal inferoseptum and apical septum using left ventricular (LV) longitudina...
Alterations in Cardiac Function Following Endurance Exercise Are Not Duration Dependent
Frontiers in Physiology, 2020
Cardiac function has been shown to transiently decrease following prolonged exercise, with greater durations related to increased impairment. However, the prospective assessment of exercise duration on cardiac performance is rare, and the influence of relative exercise intensity is typically not assessed in relation to these changes. The aim of this study was to determine whether progressively longer running distances over the same course would elicit greater cardiac impairment. The present investigation examined cardiac alterations in 49 athletes, following trail-running races of 25, 50, 80, and 160 km, performed on the same course on the same day. Echocardiography, including conventional and speckle tracking imaging, was performed with legs-raised to 60 • to mitigate alterations in preload both pre-and post-race. Race-intensities were monitored via heart rate (HR). Following the races, mean arterial pressure (−11 ± 7 mmHg, P < 0.0001), and HR (19 ± 14 bpm, P < 0.0001) were altered independent of race distance. Both left and right ventricular (LV and RV) diastolic function were reduced (LV E/A −0.54 ± 0.49, P < 0.0001; RV A' + 0.02 ± 0.04 m/s, P = 0.01) and RV systolic function decreased (TAPSE −0.25 ± 0.9 cm, P = 0.01), independent of race distance. Cardiac impairment was not apparent using speckle tracking analysis with cubic spline interpolation. While race duration was unrelated to cardiac alterations, increased racing HR was related to greater RV base dilation (r = −0.37, P = 0.03). Increased time spent at higher exercise intensities was related to reduced LV ejection fraction following 25 km (r = −0.81, P = 0.03), LV systolic strain rate following 50 km (r = 0.59, P = 0.04), and TAPSE (r = −0.81, P = 0.03) following 80 km races. Increased running duration did not affect the extent of exercise-induced cardiac fatigue, however, intensity may be a greater driver of cardiac alterations.
Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes
European Heart Journal, 2012
Endurance training may be associated with arrhythmogenic cardiac remodelling of the right ventricle (RV). We examined whether myocardial dysfunction following intense endurance exercise affects the RV more than the left ventricle (LV) and whether cumulative exposure to endurance competition influences cardiac remodelling (including fibrosis) in well-trained athletes.
Current Cardiology Reports, 2013
To go too far is as bad as to fall short."Confucius (BC 551-BC 479) Chinese philosopher Echocardiography has contributed most to our current understanding and indeed our current dilemma regarding the heart of the endurance athlete. Echocardiography assesses and characterizes nicely the effects of Endurance exercise training. It allows us to assess both systolic and diastolic cardiac variables as they change with structure and function associated with intense sporting activity. Much research work using echocardiography has characterized the left and right ventricle of the endurance athlete over the last year. Indeed evidence suggests that intense prolonged exercise may result in myocardial dysfunction which predominantly affects the RV, and that chronic RV remodelling may represent a substrate for ventricular arrhythmias in athletes. This has been the source of many debates and articles over the last 12 months. The reasons underlying the predilection towards RV dysfunction with intense prolonged exercise and the variation between individuals in its occurrence are still under dispute. This article seeks to describe the recent literature over the last year which outlines the different areas research has focused on when we assess the heart of the endurance athletes using echocardiography. Ultimately the goal of all research on the heart of the endurance athletes is to search for the holy grail of when enough is enough and therefore recognize and embrace the delicate balance of endurance intensity, in other words the border line when endurance exercise is no longer beneficial but slumps and slides into the realms of induced cardiac pathology.
European journal of echocardiography : the journal of the Working Group on Echocardiography of the European Society of Cardiology, 2009
Assessment of the left ventricular responses to prolonged exercise has been limited by technology available to assess cardiac tissue movement. Recently developed strain and strain rate imaging provide the unique opportunity to assess tissue deformation in all planes of motion. Nineteen runners (mean+/-SD age; 41+/-9 years) were assessed prior to and within 60 min (34+/-10 min) of race finish (Comrades Marathon, 89 km). Standard echocardiography assessed ejection fraction and the ratio of early to atrial (E/A) peak transmitral blood flow velocities. Myocardial speckle tracking determined segmental strain as well as systolic and diastolic strain rates in radial, circumferential, and longitudinal planes. Cardiac troponin T (cTnT) assessed cardiomyocyte insult. Ejection fraction (71+/-5 to 64+/-6%) and E/A (1.47+/-0.35 to 1.25+/-0.30) were reduced (P<0.05). Peak strain and peak systolic and diastolic strain rates were altered post-race in circumferential (e.g. peak strain reduced fro...
Persistent and reversible cardiac dysfunction among amateur marathon runners
2000
Aims Transient systolic and diastolic abnormalities in ventricular function have previously been docu- mented during endurance sports. However, these described alterations may be limited by the tech- niques applied. We sought, using less load-dependent methods, to characterize both the extent and the chronology of the cardiac changes associated with endurance events. Methods and results Transthoracic echocardiography (TTE) was performed prior
Impact of marathon running on cardiac structure and function in recreational runners
Clinical Science, 2005
The present study examined the relationship between LV (left ventricular) function, markers of cardiac-specific damage and markers of oxidative stress in recreational runners following a marathon. Runners (n = 52; 43 male and nine female; age, 35 + − 10 years; height, 1.74 + − 0.08 m; body mass, 75.9 + − 8.9 kg) were assessed pre-and immediately post-marathon. LV function was assessed using standard M-mode two-dimensional Doppler echocardiography and TDI (tissue-Doppler imaging) echocardiography. Serum was analysed for cTnT (cardiac troponin-T), TEAC (Trolox equivalent antioxidant capacity; a measure of total antioxidant capacity), MDA (malondealdehyde) and 4-HNE (4-hydroxynonenal). A strong relationship was observed between standard and TDI echocardiography for all functional measures. Diastolic function was altered postmarathon characterized by a reduction in E (peak early diastolic filling: 0.79 + − 0.11 compared with 0.64 + − 0.16 cm/s; P < 0.001), an increase in A (peak late diastolic filling: 0.48 + − 0.11 compared with 0.60 + − 0.12 cm/s; P < 0.001) and a resultant decrease in E/A (ratio of E to A; 1.71 + − 0.48 compared with 1.10 + − 0.31; P < 0.001). Ejection fraction remained unchanged post-marathon. Thirtytwo runners presented with cTnT values above the lower limit of detection for the assay (0.01 µg/l), and 20 runners presented post-marathon with cTnT values above the acute myocardial infarction cut-off value (0.05 µg/l). No significant correlations were observed between cTnT and any functional measurements. MDA (2.90 + − 1.58 compared with 3.59 + − 1.47 µmol/l) and TEAC (1.80 + − 0.12 compared with 1.89 + − 0.21 mmol/l) were significantly increased post-marathon, but were unrelated to changes in function or cTnT. In conclusion, the present study demonstrated a reduction in diastolic function and widespread evidence of minimal cardiac damage following a marathon in recreational runners. The mechanism(s) underpinning the altered function and appearance of cTnT appear unrelated to reactive oxygen species.
Heart, 2008
Background: There is evidence that ultra-endurance exercise causes myocardial injury. The extent and duration of these changes remains unresolved. Recent reports have speculated that structural adaptations to exercise, particularly of the right ventricle, may predispose to tachyarrhythmias and sudden cardiac death. Objective: To quantify the extent and duration of postexercise cardiac injury with particular attention to right ventricular (RV) dysfunction. Methods: 27 athletes (20 male, 7 female) were tested 1 week before, immediately after and 1 week after an ultra-endurance triathlon. Tests included cardiac troponin I (cTnI), B-type natriuretic peptide (BNP) and comprehensive echocardiographic assessment. Results: 26 athletes completed the race and testing procedures. Post-race, cTnI was raised in 15 athletes (58%) and the mean value for the entire cohort increased (0.17 vs 0.49 mg/l, p,0.01). BNP rose in every athlete and the mean increased significantly (12.2 vs 42.5 ng/l, p,0.001). Left ventricular ejection fraction (LVEF) was unchanged (60.4% vs 57.5%, p = 0.09), but integrated systolic strain decreased (16.9% vs 15.1%, p,0.01). New regional wall motion abnormalities developed in seven athletes (27%) and LVEF was reduced in this subgroup (57.8% vs 45.9%, p,0.001). RV function was reduced in the entire cohort with decreases in fractional area change (0.47 vs 0.39, p,0.01) and tricuspid annular plane systolic excursion (21.8 vs 19.1 mm, p,0.01). At follow-up, all variables returned to baseline except in one athlete where RV dysfunction persisted. Conclusion: Myocardial damage occurs during intense ultra-endurance exercise and, in particular, there is a significant reduction in RV function. Almost all abnormalities resolve within 1 week.