The effect of long-term soccer training on left ventricular structure and function in elite male youth soccer players.

AIMS: Cardiac adaptations in elite, male adolescent youth soccer players have been demonstrated in relation to training status. The time course of these adaptations and the delineation of the influence of volatile growth phases from the training effect on these adaptations remain unclear. Consequently, the aims of the study were to evaluate the impact of 3 years of elite-level soccer training on changes in left ventricular (LV) structure and function in a group of highly trained elite youth male soccer players (SP) as they transitioned through the pre-to-adolescent phase of their growth. METHODS: Twenty-two male youth SP from the highest Level of English Premier League Academy U-12 teams were evaluated once a year for three soccer seasons as the players progressed from the U-12 to U-14 teams. Fifteen recreationally active control participants (CON) were also evaluated over the same 3-year period. Two-dimensional transthoracic echocardiography was used to quantify LV structure and function. RESULTS: After adjusting for the influence of growth and maturation, training-induced increases in Years 2 and 3 were noted for: LV end diastolic volume (LVEDV; p = 0.02) and LV end systolic volume (LVESV; p = 0.02) in the SP compared to CON. Training-induced decrements were noted for LV ejection fraction (LVEF; p = 0.006) and TDI-S' (p < 0.001). CONCLUSIONS: An increase in training volume (Years 2 and 3) were aligned with LV volumetric adaptations and decrements in systolic function in the SP that were independent from the influence of rapid somatic growth. Decrements in systolic function were suggestive of a functional reserve for exercise.

Defining left ventricular remodeling using lean body mass allometry: a UK Biobank study.

PURPOSE: The geometric patterns of ventricular remodeling are determined using indexed left ventricular mass (LVM), end-diastolic volume (LVEDV) and concentricity, most often measured using the mass-to-volume ratio (MVR). The aims of this study were to validate lean body mass (LBM)-based allometric coefficients for scaling and to determine an index of concentricity that is independent of both volume and LBM. METHODS: Participants from the UK Biobank who underwent both CMR and dual-energy X-ray absorptiometry (DXA) during 2014-2015 were considered (n = 5064). We excluded participants aged ≥ 70 years or those with cardiometabolic risk factors. We determined allometric coefficients for scaling using linear regression of the logarithmically transformed ventricular remodeling parameters. We further defined a multiplicative allometric relationship for LV concentricity (LVC) adjusting for both LVEDV and LBM. RESULTS: A total of 1638 individuals (1057 female) were included. In subjects with lower body fat percentage (< 25% in males, < 35% in females, n = 644), the LBM allometric coefficients for scaling LVM and LVEDV were 0.85 ± 0.06 and 0.85 ± 0.03 respectively (R2 = 0.61 and 0.57, P < 0.001), with no evidence of sex-allometry interaction. While the MVR was independent of LBM, it demonstrated a negative association with LVEDV in (females: r = - 0.44, P < 0.001; males: - 0.38, P < 0.001). In contrast, LVC was independent of both LVEDV and LBM [LVC = LVM/(LVEDV0.40 × LBM0.50)] leading to increased overlap between LV hypertrophy and higher concentricity. CONCLUSIONS: We validated allometric coefficients for LBM-based scaling for CMR indexed parameters relevant for classifying geometric patterns of ventricular remodeling.

Exercise-Induced Cardiac Troponin Elevations: From Underlying Mechanisms to Clinical Relevance.

Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field.

A comparison of modelled serum cTnT and cTnI kinetics after 60 min swimming.

Post-exercise elevations of cardiac troponin T (cTnT) and I (cTnI) are often used in isolation but interpreted interchangeably. Research suggests, however, that post-exercise cTn kinetic might differ with each isoform. In this cross-sectional observational study, we collected blood samples before, immediately after (5 minutes), and at 1-, 3-, 6-, 12-, and 24-hour post-exercise in a mixed cohort of 56 participants after a distance-trial of 60 min continuous swimming (age range from 14 to 22, 57.1% female). Cardiac troponin kinetics were modelled using Bayesian mixed-effects models to estimate time to peak (TTP) and peak concentration (PC) for each isoform, while controlling for participants sex, tanner stage and average relative heart rate during the test. Exercise induced an elevation of cTnT and cTnI in 93% and 75% of the participants, respectively. Cardiac troponin T peaked earlier, at 2.9 h (CI: 2.6 - 3.2 h) post-exercise, whereas cTnI peaked later, at 4.5 h (CI: 4.2 - 4.9 h). Peak concentrations for cTnT and cTnI were 2.5 ng/L, CI: 0 - 11.2 ng/L and 2.16 ng/L, CI: 0 - 22.7 ng/L, respectively. Additionally, we did not observe a systematic effect of sex and maturational status mediating cTn responses.

Effect of long-term soccer training on changes in cardiac function during exercise in elite youth soccer players.

It is unclear what the effect of long-term, high-volume soccer training has on left ventricular (LV) function during exercise in youth soccer players. This study evaluated changes in LV function during submaximal exercise in a group of highly trained male soccer players (SP) as they transitioned over a three-year period from pre-adolescent to adolescent athletes. Data were compared to age- and sex-matched recreationally active controls (CON) over the same time period. Twenty-two SP from two professional English Premier League youth soccer academies (age: 12.0 ± 0.3 years at start of the study) and 15 CON (age: 11.7 ± 0.3 years) were recruited. Two-dimensional echocardiography was used to quantify LV function during exercise at the same submaximal metabolic load (approx. 45%VO2peak ) across the 3 years. After controlling for growth and maturation, there were training-induced changes and superiority (p < 0.001) in cardiac index (QIndex) from year 1 in the SP compared to CON. SP (year 1: 6.13 ± 0.76; year 2: 6.94 ± 1.31; and year 3: 7.20 ± 1.81 L/min/m2 ) compared to CON (year 1: 5.15 ± 1.12; year 2: 4.67 ± 1.04; and year 3: 5.49 ± 1.06 L/min/m2 ). Similar training-induced increases were noted for mitral inflow velocity (E): SP (year 1: 129 ± 12; year 2: 143 ± 16; and year 3: 135 ± 18 cm/s) compared to CON (year 1: 113 ± 10; year 2: 111 ± 12; and year 3: 121 ± 9 cm/s). This study indicated that there was evidence of yearly, training-induced increases in left ventricular function during submaximal exercise independent from the influence of growth and maturation in elite youth SP.

Exercise Training Increases Serum Cardiac Troponin T Independent of Left Ventricular Mass.

The purpose of this study was to determine whether exercise training mediated cardiac troponin T (cTnT) and whether this was associated with increases in left ventricular mass (LVM). Fifty-four sedentary obese women were randomised to high-intensity interval training (HIIT, repeated 4-min cycling at 90% V̇O2max interspersed with 3-min rest), work-equivalent continuous aerobic training (CAT, continuous cycling at 60% V̇O2max) or a control group (CON). Resting serum cTnT was assessed using a high-sensitivity assay before and after 12 weeks of training. LVM was determined from 2D echocardiography at the same timepoints. Both HIIT and CAT induced a similar elevation (median 3.07 to 3.76 ng.l-1, p<0.05) in resting cTnT compared with pre-training and the CON (3.49 to 3.45 ng.l-1, p>0.05). LVM index in HIIT increased (62.2±7.8 to 73.1±14.1 g.m-2, p<0.05), but not in CAT (66.1±9.7 to 67.6±9.6 g.m-2, p>0.05) and CON (67.9±9.5 to 70.2±9.1 g.m-2, p>0.05). Training-induced changes in resting cTnT did not correlate with changes in LVM index (r=-0.025, p=0.857). These findings suggest that twelve weeks of either HIIT or CAT increased resting cTnT, but the effects were independent of any changes in LVM in sedentary obese women.

Exercise Training Induces Left- but not Right-sided Cardiac Remodelling in Olympic Rowers.

Whilst the athlete's heart has been extensively described, less work has focused on the potential for elite athletes to demonstrate further cardiac remodelling upon an increase in training volume. Moreover, little work explored potential side-specific cardiac remodelling. Therefore, we examined the impact of an increase in training volume across 9-months in elite rowers on left- and right-sided cardiac structure, function and mechanics (i. e. longitudinal, radial and circumferential strain, twist and strain-volume loops). As part of the preparations to the 2012 Olympic Games, twenty-seven elite rowers (26.4±3.7years, 19 male) underwent echocardiography prior to and post (9 months) an increase in training volume (24 to 30-35 h weekly). Training increased left ventricular structure, including wall thickness, diameter, volume, mass and LV twist (all p<0.05). Female rowers demonstrated larger adaptation in left ventricular diameter and mass compared to male rowers (both p<0.05). No changes were observed in other measures of left ventricular function in both sexes (all p>0.05). The 9-month intervention showed no change in right ventricular/atrial structure, function or mechanics (all p>0.05). In conclusion, our data revealed that 9-month increased training volume in elite rowers induced left-sided (but not right-sided) structural remodelling, concomitant with an increase in left ventricular twist, with some changes larger in women.

The influence of training status on right ventricular morphology and segmental strain in elite pre-adolescent soccer players.

Cardiac modifications to training are a product of the genetic pre-disposition for adaptation and the repetitive haemodynamic loads that are placed on the myocardium. Elite pre-adolescent athletes are exposed to high-intensity training at a young age with little understanding of the physiological and clinical consequences. It is unclear how right ventricular (RV) structure and function may respond to this type of stimulus. The aim of this study was to compare RV structure and strain across the cardiac cycle and within individual segments in elite soccer players (SP) and controls (CON). METHODS: Twenty-two highly trained, male pre-adolescent SP and 22 age-and sex-matched recreationally active individuals CON were investigated using 2D echocardiography, including myocardial speckle tracking to assess basal, mid-wall, apical and global longitudinal strain and strain rate during systole (SRS) and diastole (SRE and SRA). RESULTS: greater RV cavity size was identified in the SP compared to CON (RVD1 SP: 32.3 ± 3.1 vs. CON: 29.6 ± 2.8 (mm/m2)0.5; p = 0.005). No inter-group differences were noted for peak global RV strain (SP: - 28.6 ± 4.9 vs CON: - 30.3 ± 4.0%, p = 0.11). Lower mid-wall strain was demonstrated in the SP compared to CON (SP: - 27.9 ± 5.8 vs. CON: - 32.2 ± 4.4%, p = 0.007). CONCLUSION: Soccer training has the potential to increase RV size in pre-adolescent players. The unique segmental analyses used in this study have identified inter-group differences that were masked by global strain evaluations. The clinical and physiological implications of these findings warrant further investigation.

Exercise-Induced Cardiac Troponin I Increase and Incident Mortality and Cardiovascular Events.

BACKGROUND: Blood concentrations of cardiac troponin above the 99th percentile are a key criterion for the diagnosis of acute myocardial injury and infarction. Troponin concentrations, even below the 99th percentile, predict adverse outcomes in patients and the general population. Elevated troponin concentrations are commonly observed after endurance exercise, but the clinical significance of this increase is unknown. We examined the association between postexercise troponin I concentrations and clinical outcomes in long-distance walkers. METHODS: We measured cardiac troponin I concentrations in 725 participants (61 [54-69] yrs) before and immediately after 30 to 55 km of walking. We tested for an association between postexercise troponin I concentrations above the 99th percentile (>0.040 µg/L) and a composite end point of all-cause mortality and major adverse cardiovascular events (myocardial infarction, stroke, heart failure, revascularization, or sudden cardiac arrest). Continuous variables were reported as mean ± standard deviation when normally distributed or median [interquartile range] when not normally distributed. RESULTS: Participants walked 8.3 [7.3-9.3] hours at 68±10% of their maximum heart rate. Baseline troponin I concentrations were >0.040 µg/L in 9 participants (1%). Troponin I concentrations increased after walking (P<.001), with 63 participants (9%) demonstrating a postexercise troponin concentration >0.040 µg/L. During 43 [23-77] months of follow-up, 62 participants (9%) experienced an end point; 29 died and 33 had major adverse cardiovascular events. Compared with 7% with postexercise troponin I ≤0.040 µg/L (log-rank P<.001), 27% of participants with postexercise troponin I concentrations >0.040 µg/L experienced an end point. The hazard ratio was 2.48 (95% CI, 1.29-4.78) after adjusting for age, sex, cardiovascular risk factors (hypertension, hypercholesterolemia or diabetes mellitus), cardiovascular diseases (myocardial infarction, stroke, or heart failure), and baseline troponin I concentrations. CONCLUSIONS: Exercise-induced troponin I elevations above the 99th percentile after 30 to 55 km of walking independently predicted higher mortality and cardiovascular events in a cohort of older long-distance walkers. Exercise-induced increases in troponin may not be a benign physiological response to exercise, but an early marker of future mortality and cardiovascular events.

Acute impact of changes to hemodynamic load on the left ventricular strain-volume relationship in young and older men.

Chronic changes in left ventricular (LV) hemodynamics, such as those induced by increased afterload (i.e., hypertension), mediate changes in LV function. This study examined the proof of concept that 1) the LV longitudinal strain (ε)-volume loop is sensitive to detecting an acute increase in afterload, and 2) these effects differ between healthy young versus older men. Thirty-five healthy male volunteers were recruited, including 19 young (24 ± 2 yr) and 16 older participants (67 ± 5 yr). Tests were performed before, during, and after 10-min recovery from acute manipulation of afterload. Real-time hemodynamic data were obtained and LV longitudinal ε-volume loops were calculated from four-chamber images using two-dimensional echocardiography. Inflation of the anti-gravity (anti-G) suit resulted in an immediate increase in heart rate, blood pressure, and systemic vascular resistance and a decrease in stroke volume (all P < 0.05). This was accompanied by a decrease in LV peak ε, slower slope of the ε-volume relationship during early diastole, and an increase in uncoupling (i.e., compared with systole; little change in ε per volume decline during early diastole and large changes in ε per volume decline during late diastole) (all P < 0.05). All values returned to baseline levels after recovery (all P > 0.05). Manipulation of cardiac hemodynamics caused comparable effects in young versus older men (all P > 0.05). Acute increases in afterload immediately change the diastolic phase of the LV longitudinal ε-volume loop in young and older men. This supports the potency of the LV longitudinal ε-volume loop to provide novel insights into dynamic cardiac function in humans in vivo.

Left ventricular remodeling in elite and sub-elite road cyclists.

Marked adaptation of left ventricular (LV) structure in endurance athletes is well established. However, previous investigations of functional and mechanical adaptation have been contradictory. A lack of clarity in subjects' athletic performance level may have contributed to these disparate findings. This study aimed to describe structural, functional, and mechanical characteristics of the cyclists' LV, based on clearly defined performance levels. Male elite cyclists (EC) (n = 69), sub-elite cyclists (SEC) (n = 30), and non-athletes (NA) (n = 46) were comparatively studied using conventional and speckle tracking 2D echocardiography. Dilated eccentric hypertrophy was common in EC (34.7%), but not SEC (3.3%). Chamber concentricity was higher in EC compared to SEC (7.11 ± 1.08 vs 5.85 ± 0.98 g/(mL)2/3 , P < .001). Ejection fraction (EF) was lower in EC compared to NA (57 ± 5% vs 59 ± 4%, P < .05), and reduced EF was observed in a greater proportion of EC (11.6%) compared to SEC (6.7%). Global circumferential strain (GCε) was greater in EC (-18.4 ± 2.4%) and SEC (-19.8 ± 2.7%) compared to NA (-17.2 ± 2.6%) (P < .05 and P < .001). Early diastolic filling was lower in EC compared with SEC (0.72 ± 0.14 vs 0.88 ± 0.12 cm/s, P < .001), as were septal E' (12 ± 2 vs 15 ± 2 cm/s, P < .001) and lateral E' (18 ± 4 vs 20 ± 4 cm/s, P < .05). The magnitude of LV structural adaptation was far greater in EC compared with SEC. Increased GCε may represent a compensatory mechanism to maintain stroke volume in the presence of increased chamber volume. Decreased E and E' velocities may be indicative of a considerable functional reserve in EC.

Scaling of cardiac morphology is interrupted by birth in the developing sheep Ovis aries.

Scaling of the heart across development can reveal the degree to which variation in cardiac morphology depends on body mass. In this study, we assessed the scaling of heart mass, left and right ventricular masses, and ventricular mass ratio, as a function of eviscerated body mass across fetal and postnatal development in Horro sheep Ovis aries (~50-fold body mass range; N = 21). Whole hearts were extracted from carcasses, cleaned, dissected into chambers and weighed. We found a biphasic relationship when heart mass was scaled against body mass, with a conspicuous 'breakpoint' around the time of birth, manifest not by a change in the scaling exponent (slope), but rather a jump in the elevation. Fetal heart mass (g) increased with eviscerated body mass (Mb , kg) according to the power equation 4.90 Mb0.88 ± 0.26 (± 95%CI) , whereas postnatal heart mass increased according to 10.0 Mb0.88 ± 0.10 . While the fetal and postnatal scaling exponents are identical (0.88) and reveal a clear dependence of heart mass on body mass, only the postnatal exponent is significantly less than 1.0, indicating the postnatal heart becomes a smaller component of body mass as the body grows, which is a pattern found frequently with postnatal cardiac development among mammals. The rapid doubling in heart mass around the time of birth is independent of any increase in body mass and is consistent with the normalization of wall stress in response to abrupt changes in volume loading and pressure loading at parturition. We discuss variation in scaling patterns of heart mass across development among mammals, and suggest that the variation results from a complex interplay between hard-wired genetics and epigenetic influences.

The impact of high-intensity interval training on the cTnT response to acute exercise in sedentary obese young women.

AIMS: This study characterized (a) the cardiac troponin T (cTnT) response to three forms of acute high-intensity interval exercise (HIE), and (b) the impact of 12 weeks of HIE training on the cTnT response to acute exercise in sedentary obese young women. METHODS: Thirty-six sedentary women were randomized to traditional HIE training (repeated 4-minute cycling at 90% V ˙ O2max interspersed with 3-minute rest, 200 kJ/session), work-equivalent sprint interval exercise (SIE) training (repeated 1-minute cycling at 120% V ˙ O2max interspersed with 1.5-minute rest) or repeated-sprint exercise (RSE) training (40 × 6-second all-out sprints interspersed with 9-second rest) group. cTnT was assessed using a high-sensitivity assay before and immediately, 3 and 4 hours after the 1st (PRE), 6th (EARLY), 20th (MID), and 44th (END) training session, respectively. RESULTS: cTnT was elevated (P < 0.05) after all forms of acute interval exercise at the PRE and EARLY assessment with cTnT response higher (P < 0.05) after HIE (307%) and SIE (318%) than RSE (142%) at the PRE assessment. All forms of acute interval exercise at MID and END had no effect on the cohort cTnT concentration post-exercise (all P > 0.05). CONCLUSION: For sedentary obese young women, both HIE and SIE, matched for total work, induced a similar elevation in cTnT after acute exercise with a smaller rise observed after RSE. By the 44th training session, almost no post-exercise cTnT elevation was observed in all three groups. Such information is relevant for clinicians as it could improve medical decisionmaking.

The cTnT response to acute exercise at the onset of an endurance training program: evidence of exercise preconditioning?

PURPOSE: Exercise induces a cardioprotective effect referred to as "preconditioning". Whether the preconditioning impacts upon the cardiac troponin T (cTnT) response to subsequent exercise bouts is unclear. This study investigated the effects of an initial exercise bout, a second exercise bout 48 h later, as well as subsequent exercise every 48 h for 4 days or a single identical exercise bout after 8 days of inactivity gap on cTnT response to acute exercise. METHODS: Twenty-eight sedentary overweight young women were randomly assigned to either six bouts of exercise each separated by 48 h or three bouts of exercise with 48 h between the first two bouts and 8 days between the second and third bouts. All exercise bouts were identical (60% [Formula: see text], 200 kJ) and the total testing period (10 days) was the same for both groups. cTnT was assessed before and after the 1st, 2nd, and final exercise bouts. RESULTS: cTnT increased (129%, P < 0.05) after the first bout of exercise in both groups (peak post-exercise cTnT, median [range], ng l-1: 3.43[< 3.00-27.26]) with no between-group differences in the response. The second exercise bout had no significant (P > 0.05) effect on post-exercise cTnT (< 3.00[< 3.00-21.96]). The final exercise bout resulted in an increase (190%, P < 0.05) in cTnT (4.35[< 3.00-13.05]) in both groups. CONCLUSIONS: A single bout exercise resulted in a temporary blunting of cTnT response to acute exercise 48 h later. The effect of exercise preconditioning was not preserved, regardless of whether followed by repeated exercise every 48 h or a cessation of exercise for 8 days.

The right heart of the elite senior rugby football league athlete.

BACKGROUND: Right heart enlargement is common in the athletes' heart phenotype; however, few data exist regarding interpretation of normal athletic adaptation during Preparticipation Cardiac Screening (PCS) of Rugby Football League (RFL) athletes. Echocardiography is utilized during PCS and thus the primary aim of this study was to establish the normal right ventricular (RV) phenotype in elite RFL athletes using standard 2-D echocardiography and myocardial mechanics. The secondary aim was to describe right atrial (RA) structure and function using 2-D echocardiography. METHODS: 139 male RFL athletes underwent echocardiographic evaluation of the right heart including RV strain (ɛ) and strain rate (SR) imaging using speckle tracking echocardiography (STE). Nonathletic males were used for comparison and allometric scaling was applied for conventional echocardiographic parameters. RESULTS: Scaled RV dimensions were larger in athletes (P < 0.05) with the exception of the mid-cavity. No differences (P > 0.05) in RV fractional area change (FAC) and RV longitudinal ɛ were observed between groups. Tissue Doppler imaging (TDI)-indexed parameters and global strain rate (SR) were lower (P < 0.05) in athletes with HR and weight found to have co-variance with SR. The RA was larger in athletes (P < 0.001) with no functional difference (P > 0.05) observed by volume assessment. CONCLUSIONS: Reduction in SR and indexed TDI are partly associated with lower HR and increased body mass and are likely to represent normal physiological adaptation in RFL athletes. RA enlargement appears proportional to RV enlargement. These data may aid interpretation of normal athletic adaptation during PCS of RFL athletes.

Athletic Remodeling in Female College Athletes: The "Morganroth Hypothesis" Revisited.

BACKGROUND: There is limited data regarding ventricular remodeling in college female athletes, especially when appropriate scaling of cardiac dimensions to lean body mass (LBM) is considered. Moreover, it is not well established whether cardiac remodeling in female athletes is a balanced process with proportional increase in left ventricular (LV) mass and volume or the right and LV size. METHODS: During the preparticipation competitive screening, 72 female college athletes volunteered to undergo dual energy x-ray absorptiometry scan for quantification of LBM and comprehensive 2D echocardiography including assessment of longitudinal myocardial strain. The athletes were divided in 2 groups according to the intensity of the dynamic and static components of their sport categories, ie, a higher intensity dynamic and resistive group (n = 37 participating in rowing, water polo and lacrosse) and a lower intensity group (n = 35, participating in short distance running, sailing, synchronized swimming, and softball). In addition, we recruited a group of 31 age-matched nonathlete controls. RESULTS: The mean age of the study population was 18.7 ± 1.0 years. When scaled to body surface area, the higher intensity group had 17.1 ± 3.6% (P < 0.001) greater LV mass when compared with the lower intensity group and 21.7 ± 4.0% (P < 0.001) greater LV mass than the control group. The differences persisted after scaling to LBM with 14.2 ± 3.2% (P < 0.001) greater LV mass in the higher intensity group. By contrast, there was no difference in any of the relative remodeling indices including the LV mass to volume ratio, right to LV area ratio, or left atrial to LV volume ratio (P > 0.50 for all). In addition, no significant difference was noted among the 3 groups in LV ejection fraction (P = 0.22), LV global longitudinal strain (P = 0.55), LV systolic strain rate (P = 0.62), or right ventricular global longitudinal strain (P = 0.61). CONCLUSION: Female collegiate athletes participating in higher intensity dynamic and resistive sports have higher indexed LV mass even when scaled to LBM. The remodeling process does however appear to be a balanced process not only at the intraventricular level but also at the interventricular and atrioventricular levels.

Cardiac Biomarker Release After Exercise in Healthy Children and Adolescents: A Systematic Review and Meta-Analysis.

PURPOSE: The authors evaluated the impact of acute exercise and 24-hour recovery on serum concentration of cardiac troponins T and I (cTnT and cTnI) and N-terminal fragment of the prohormone brain natriuretic peptide (NT-proBNP) in healthy children and adolescents. The authors also determined the proportion of participants exceeding the upper reference limits and acute myocardial infarction cutoff for each assay. METHOD: Web of Science, SPORTDiscus, MEDLINE, ScienceDirect, and Scopus databases were systematically searched up to November 2017. Studies were screened and quality-assessed; the data was systematically extracted and analyzed. RESULTS: From 751 studies initially identified, 14 met the inclusion criteria for data extraction. All 3 biomarkers were increased significantly after exercise. A decrease from postexercise to 24 hours was noted in cTnT and cTnI, although this decrease was only statistically significant for cTnT. The upper reference limit was exceeded by 76% of participants for cTnT, a 51% for cTnI, and a 13% for NT-proBNP. Furthermore, the cutoff value for acute myocardial infarction was exceeded by 39% for cTnT and a 11% for cTnI. Postexercise peak values of cTnT were associated with duration and intensity (Q(3) = 28.3, P < .001) while NT-proBNP peak values were associated with duration (Q(2) = 11.9, P = .003). CONCLUSION: Exercise results in the appearance of elevated levels of cTnT, cTnI, and NT-proBNP in children and adolescents. Postexercise elevations of cTnT and NT-proBNP are associated with exercise duration and intensity.

Right ventricular function in elite male athletes meeting the structural echocardiographic task force criteria for arrhythmogenic right ventricular cardiomyopathy.

Athlete pre-participation screening is focused on detecting pathological conditions like arrhythmogenic right ventricular cardiomyopathy (ARVC). The diagnosis of ARVC is established by applying the revised 2010 ARVC Task Force Criteria (TFC) that assesses RV structure and function. Some athletes may meet structural TFC without having ARVC but we do not know the consequences for RV function. This study compared RV structural and functional indices in male athletes that meet the structural TFC (MTFC) for ARVC and those that do not (NMTFC). We recruited 214 male elite athletes. All participants underwent 2D, Doppler, tissue Doppler and strain (ε) echocardiography with a focused and comprehensive assessment of the right heart. Athletes were grouped on RV structural data: MTFC n = 34; NMTFC n = 180. Functional data were compared between groups. By selection, MTFC had larger absolute and scaled RV outflow tract (RVOT) diameter compared to NMTFC (P ˂0.05) but these athletes did not develop a proportional increase in the RV inflow dimensions. There was no difference in global conventional RV systolic function between both groups however, there was significantly lower global RV ε in athletes that MTFC which can be explained, in part, by the RVOT dimension.

Reduced left ventricular filling following blood volume extraction does not result in compensatory augmentation of cardiac mechanics.

NEW FINDINGS: What is the central question of this study? A reduction in left ventricular (LV) filling, and concomitant increase in heart rate, augments LV mechanics to maintain stroke volume (SV); however, the impact of reduced LV filling in isolation on SV and LV mechanics is currently unknown. What is the main finding and its importance? An isolated decrease in LV filling did not provoke a compensatory increase in mechanics to maintain SV; in contrast, LV mechanics and SV were reduced. These data indicate that when LV filling is reduced without changes in heart rate, LV mechanics do not compensate to maintain SV. ABSTRACT: An acute non-invasive reduction in preload has been shown to augment cardiac mechanics to maintain stroke volume and cardiac output. Such interventions induce concomitant changes in heart rate, whereas blood volume extraction reduces preload without changes in heart rate. Therefore, the purpose of this study was to determine whether a preload reduction in isolation resulted in augmented stroke volume achieved via enhanced cardiac mechanics. Nine healthy volunteers (four female, age 29 ± 11 years) underwent echocardiography for the assessment of left ventricular (LV) volumes and mechanics in a supine position at baseline and end extraction after the controlled removal of 25% of total blood volume (1062 ± 342 ml). Arterial blood pressure was monitored continuously by a pressure transducer attached to an indwelling radial artery catheter. Heart rate and total peripheral resistance were unchanged from baseline to end extraction, but systolic blood pressure was reduced (from 148 to 127 mmHg). From baseline to end extraction there were significant reductions in left ventricular end-diastolic volume (from 89 to 71 ml) and stroke volume (from 56 to 37 ml); however, there was no change in LV twist, basal or apical rotation. In contrast, LV longitudinal strain (from -20 to -17%) and basal circumferential strain (from -22 to -19%) were significantly reduced from baseline to end extraction. In conclusion, a reduction in preload during blood volume extraction does not result in compensatory changes in stroke volume or cardiac mechanics. Our data suggest that LV strain is dependent on LV filling and consequent geometry, whereas LV twist could be mediated by heart rate.

Impact of high-intensity interval training and moderate-intensity continuous training on resting and postexercise cardiac troponin T concentration.

NEW FINDINGS: What is the central question of this study? Does exercise training impact resting and postexercise cardiac troponin T (cTnT) concentration? What is the main finding and its importance? This randomized controlled intervention study demonstrated that 12 weeks of either high-intensity interval training or moderate-intensity continuous training largely abolished the exercise-induced elevation in cTnT when exercise was performed at the same absolute intensity. There was no impact of training on resting cTnT or postexercise appearance of cTnT when exercise was performed at the same relative intensity. These findings provide new information that might help clinicians with decision-making in relationship to basal and postexercise values of cTnT in individuals with different training status. ABSTRACT: We evaluated the influence of 12 weeks of high-intensity interval training [HIIT; repeated 4 min cycling at 90% of maximal oxygen uptake (V̇O2max) interspersed with 3 min rest, 200-300 kJ per session, 3 or 4 days each week] and work-equivalent moderate-intensity continuous training (MICT; continuous cycling at 60% V̇O2max) on resting cardiac troponin T (cTnT) and the appearance of exercise-induced cTnT. Forty-eight sedentary obese young women were randomly assigned to HIIT, MICT or a control group. The V̇O2max and body composition were measured before and after training. At baseline, cTnT was assessed using a high-sensitivity assay at rest and immediately, 2 and 4 h after 45 min cycling at 60% V̇O2max. After a 12 week training period, cTnT was assessed before and after 45 min cycling at the same relative and absolute intensities as before training. Training led to higher V̇O2max and lower fat mass in both HIIT and MICT groups (all P < 0.05). Before training, cTnT was significantly elevated in all three groups (by 35-118%, all P < 0.05) with acute exercise. After training, both resting and postexercise cTnT concentrations (same relative intensity) were similar to pretraining values. In contrast, postexercise cTnT (same absolute intensity, which represented a smaller exercise stimulus) was not elevated from rest in both HIIT and MICT groups. In conclusion, 12 weeks of either HIIT or MICT largely abolished the postexercise elevation of cTnT concentration when exercise was performed at the same absolute intensity. There was, however, no impact of training on resting cTnT or postexercise appearance of cTnT for exercise performed at the same relative intensity.