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Captive chimpanzees (Pan troglodytes) mature earlier in body mass and have a greater growth rate compared to wild individuals. However, relatively little is known about how growth parameters compare between chimpanzees living in different captive environments. To investigate, body mass was measured in 298 African sanctuary chimpanzees and was acquired from 1030 zoological and 442 research chimpanzees, using data repositories. An analysis of covariance, adjusting for age, was performed to assess same‐sex body mass differences between adult sanctuary, zoological, and research populations. Piecewise linear regression was performed to estimate sex‐specific growth rates and the age at maturation, which were compared between sexes and across populations using extra‐sum‐of‐squares F tests. Adult body mass was greater in the zoological and resarch populations compared to the sanctuary chimpanzees, in both sexes. Male and female sanctuary chimpanzees were estimated to have a slower rate of growth compared with their zoological and research counterparts. Additionally, male sanctuary chimpanzees were estimated to have an older age at maturation for body mass compared with zoological and research males, whereas the age at maturation was similar across female populations. For both the zoological and research populations, the estimated growth rate was greater in males compared to females. Together, these data contribute to current understanding of growth and maturation in this species and suggest marked differences between the growth patterns of chimpanzees living in different captive environments. Highlights: African sanctuary chimpanzees are lighter compared with their zoological and research counterparts. Additionally, sanctuary chimpanzees have a slower growth rate compared to zoological and research populations, and male sanctuary chimpanzees have an older age at maturation.Male sanctuary chimpanzees have a slower growth rate and an older age at maturation compared to zoological and research males. [ABSTRACT FROM AUTHOR]

Pre-participation screening (PPS), using a 12-lead electrocardiogram (ECG), is recommended to identify athletes at risk of sudden cardiac death (SCD). ECG interpretation criteria have been developed to address the concern arising from high false-positives in athletes. There are limited ECG data in elite female footballers. The aims of this study were to (1) compare the ECG outcomes using three published ECG criteria (European Society of Cardiology [ESC], Seattle, International) in elite female footballers and (2) compare ECG data at three different stages of a competitive season. Eighty-one elite female footballers (21 ± 4 yr) completed a medical assessment, anthropometrics, resting blood pressure and a resting 12-lead ECG. Each 12-lead ECG was interpreted in accordance with (1) ESC; (2) Seattle; (3) International Criteria to determine training-related and non-training-related ECG changes. A subset of thirteen (26 ± 4 yr) footballers had repeated resting ECG tests at three time points across the competitive season. Eighty percent of females had training-related ECG patterns. Sinus bradycardia (65%) and early repolarization (42%) were the most common. Using the ESC Criteria 25% (20/81) of the athletes were considered to have an abnormal ECG, compared to 0% using the Seattle and International Criteria, mainly due to alterations in QT length criteria. There were no clinically significant differences in ECG data across a competitive season. The Seattle and International ECG Criteria significantly reduced the number of ECG false-positives in elite female footballers and the time point of PPS within a competitive season is unlikely to alter the PPS outcomes. Abbreviations: AMSSM: American Medical Society for Sports Medicine; ANOVA: Analysis of Variance; BSA: Body Surface Area; ECG: Electrocardiogram; ESC: European Society of Cardiology; FA: Football Association; FIFA: The Fédération Internationale de Football Association (FIFA); F-MARC: FIFA Medical Assessment and Research Centre; LAE: Left atrial enlargement; LVH: Left ventricular hypertrophy; PPS: Pre-participation screening; SCD: Sudden cardiac death [ABSTRACT FROM AUTHOR]

New Findings: What is the central question of this study?Endurance athletes demonstrate altered regional right ventricular (RV) wall mechanics, characterized by lower basal deformation, in comparison to non‐athletic control subjects at rest. We hypothesized that regional adaptations at the RV base reflect an enhanced functional reserve capacity in response to haemodynamic volume loading.What is the main finding and its importance?Free wall RV longitudinal strain is elevated in response to acute volume loading in both endurance athletes and control subjects. However, the RV basal segment longitudinal strain response to acute volume infusion is greater in endurance athletes. Our findings suggest that training‐induced cardiac remodelling might involve region‐specific adaptation in the RV functional response to volume manipulation. Eccentric remodelling of the right ventricle (RV) in response to increased blood volume and repetitive haemodynamic load during endurance exercise is well established. Structural remodelling is accompanied by decreased deformation at the base of the RV free wall, which might reflect an enhanced functional reserve capacity in response to haemodynamic perturbation. Therefore, in this study we examined the impact of acute blood volume expansion on RV wall mechanics in 16 young endurance‐trained men (aged 24 ± 3 years) and 13 non‐athletic male control subjects (aged 27 ± 5 years). Conventional echocardiographic parameters and the longitudinal strain and strain rate were quantified at the basal and apical levels of the RV free wall. Measurements were obtained at rest and after 7 ml/kg i.v. Gelofusine infusion, with and without a passive leg raise. After infusion, blood volume increased by 12 ± 4 and 14 ± 5% in endurance‐trained individuals versus control subjects, respectively (P = 0.264). Both endurance‐trained individuals (8 ± 10%) and control subjects (7 ± 9%) experienced an increase in free wall strain from baseline, which was also similar following leg raise (7 ± 10 and 6 ± 10%, respectively; P = 0.464). However, infusion evoked a greater increase in basal longitudinal strain in endurance‐trained versus control subjects (16 ± 14 vs. 6 ± 11%; P = 0.048), which persisted after leg raise (16 ± 18 vs. 3 ± 11%; P = 0.032). Apical longitudinal strain and RV free wall strain rates were not different between groups and remained unchanged after infusion across all segments. Endurance training results in a greater contribution of longitudinal myocardial deformation at the base of the RV in response to a haemodynamic volume challenge, which might reflect a greater region‐specific functional reserve capacity. [ABSTRACT FROM AUTHOR]

Background: Clinical electrocardiographic (ECG) guidelines for athlete's heart are based upon cross-sectional data. We aimed to longitudinally evaluate the influence of endurance training on the ECG and compare the prevalence of ECG abnormalities defined by contemporary criteria. Methods: A group of 66 training-naïve individuals completed a six-month training programme with resting ECGs and cardiopulmonary exercise tests performed at baseline, two and six months. Data were analysed using repeated measures analysis of variance and the prevalence of ECG abnormalities compared between proposed criteria. Results: Maximal oxygen consumption increased from 45.4 ± 7.1 to 50.3 ± 7.1 ml·kg−1·min−1 (p < 0.05) pre-to-post training. ECG changes included, bradycardia (60 ± 12 vs. 53 ± 8 beats·min−1; p < 0.05), shorter P wave duration (106 ± 10 vs. 103 ± 11 ms; p < 0.05), reduced QTc (413 ± 27 vs. 405 ± 22 ms; p < 0.05), and increased left ventricular Sokolow-Lyon index (2.45 ± 0.66 vs. 2.62 ± 0.78 mV; p < 0.05). 85% of individuals showed ≥1 'training-related' ECG finding at six months vs. 68% at baseline. Using the 2013 Seattle Criteria, 4 ECGs were 'abnormal' at baseline and 3 at month six vs. 2 at baseline and 1 at month six, using the 2017 International Consensus. Prevalence of 'borderline' findings did not increase with training (11% at baseline and six months). Conclusion: Six-months endurance training leads to a greater prevalence of 'training-related' but not 'borderline' or 'training-unrelated' ECGs. 'Borderline findings' may not necessarily represent training-related cardiac remodelling in novice athletes following a six-month training intervention. KEY MESSAGES This study aimed to assess the longitudinal ECG changes following six months of endurance training, in training-naïve individuals, and whether these ECG changes support the revisions made to the recent 2017 international consensus criteria. The prevalence of 'training-related' findings were increased with six months of endurance training, however the prevalence of the revised 'borderline' criteria, according to the 2017 international consensus, did not increase and the associated quantitative ECG data (e.g. P-wave amplitude, QRS axis and QRS duration) remained unchanged. Further clinical consideration may be warranted for individuals within the early phase of exercise engagement presenting with 'borderline' ECG abnormalities, defined by the International criteria. [ABSTRACT FROM AUTHOR]

Abstract: There is growing evidence that dilated cardiomyopathy may be a major cause of death in captive Livingstone's fruit bats (Pteropus livingstonii). Therefore, the primary aim of this prospective, exploratory study was to examine whether a systematic cardiac ultrasound protocol is feasible in this critically endangered species and to report basic measures of cardiac structure and function from a cohort of apparently healthy bats. A secondary aim was to test the effect posture (dorsal recumbency vs. roosting) has upon cardiac function in this species. Transthoracic echocardiograms, including 2D, Doppler, and tissue Doppler measures of cardiac structure and function were completed as part of routine health examinations for bats at a single center (n = 19). Bats were then grouped by age and disease status and the mean and range data reported for each group. In healthy adult bats, with the exception of a reduction in heart rate (P ≤ 0.05), right atrial systolic area (P ≤ 0.05), and right ventricular velocity during atrial contraction, there were no significant changes in cardiac structure or function in response to the roosting position. However, in the bats presenting with dilated cardiomyopathy the current data suggest that left ventricular ejection fraction is improved while roosting. Further work is required to confirm our initial findings, generate diagnostic reference intervals, and explore the causes of dilated cardiomyopathy in this species. [ABSTRACT FROM AUTHOR]

New Findings What is the central question of this study? Left ventricular (LV) twist is reduced when afterload is increased, but the meaning of this specific heart muscle response and its impact on cardiac output are not well understood., What is the main finding and its importance? This study shows that LV twist responds even when arterial haemodynamics are altered only locally, and without apparent change in metabolic (i.e. heat-induced) demand. The concurrent decline in cardiac output and LV twist during partial arterial occlusion despite the increased peripheral demand caused by heat stress suggests that LV twist may be involved in the protective sensing of heart muscle stress that can override the provision of the required cardiac output., Whether left ventricular (LV) twist and untwisting rate (LV twist mechanics) respond to localised, peripheral, non-metabolic changes in arterial haemodynamics within an individual's normal afterload range is presently unknown. Furthermore, previous studies indicate that LV twist mechanics may override the provision of cardiac output, but this hypothesis has not been examined purposefully. Therefore, we acutely altered local peripheral arterial haemodynamics in 11 healthy humans (women/men n = 3/8; age 26 ± 5 years) by bilateral arm heating (BAH). Ultrasonography was used to examine arterial haemodynamics, LV twist mechanics and the twist-to-shortening ratio (TSR). To determine the arterial function-dependent contribution of LV twist mechanics to cardiac output, partial blood flow restriction to the arms was applied during BAH (BAHBFR). Bilateral arm heating increased arm skin temperatures [change (Δ) +6.4 ± 0.9°C, P < 0.0001] but not core temperature (Δ −0.0 ± 0.1°C, P > 0.05), concomitant to increases in brachial artery blood flow (Δ 212 ± 77 ml, P < 0.0001), cardiac output (Δ 495 ± 487 l min−1, P < 0.05), LV twist (Δ 3.0 ± 3.5 deg, P < 0.05) and TSR (Δ 3.3 ± 1.3, P < 0.05) but maintained carotid artery blood flow (Δ 18 ± 147 ml, P > 0.05). Subsequently, BAHBFR reduced all parameters to preheating levels, except for TSR and heart rate, which remained at BAH levels. In conclusion, LV twist mechanics responded to local peripheral arterial haemodynamics within the normal afterload range, in part independent of TSR and heart rate. The findings suggest that LV twist mechanics may be more closely associated with intrinsic sensing of excessive pressure stress rather than being associated with the delivery of adequate cardiac output. [ABSTRACT FROM AUTHOR]

Left ventricular (LV) structural remodeling following athletic training has been evidenced through training-specific changes in wall thickness and geometry. Whether the LV response to changes in hemodynamic load also adapts in a training-specific manner is unknown. Using echocardiography, we examined LV responses of endurance-trained ( n = 15), resistance-trained ( n = 14), and nonathletic men ( n = 13) to 1 ) 20, 40, and 60% one repetition-maximum (1RM), leg-press exercise and 2 ) intravascular Gelofusine infusion (7 mL/kg) with passive leg raise. While resting heart rate was lower in endurance-trained participants versus controls ( P = 0.001), blood pressure was similar between groups. Endurance-trained individuals had lower wall thickness but greater LV mass relative to body surface area versus controls, with no difference between resistance-trained individuals and controls. Leg press evoked a similar increase in blood pressure; however, resistance-trained participants preserved stroke volume (SV; -3 ± 8%) versus controls at 60% 1RM (-15 ± 7%, P = 0.001). While the maintenance of SV was related to the change in longitudinal strain across all groups ( R = 0.537; P = 0.007), time-to-peak strain was maintained in resistance-trained but delayed in endurance-trained individuals (1 vs. 12% delay; P = 0.021). Volume infusion caused a similar increase in end-diastolic volume (EDV) and SV across groups, but leg raise further increased EDV only in endurance-trained individuals (5 ± 5 to 8 ± 5%; P = 0.018). Correlation analysis revealed a relationship between SV and longitudinal strain following infusion and leg raise ( R = 0.334, P = 0.054); however, we observed no between-group differences in longitudinal myocardial mechanics. In conclusion, resistance-trained individuals better maintained SV during pressure loading, whereas endurance-trained individuals demonstrated greater EDV reserve during volume loading. These data provide novel evidence of training-specific LV functional remodeling. NEW & NOTEWORTHY Training-specific functional remodeling of the LV in response to different loading conditions has been recently suggested, but not experimentally tested in the same group of individuals. Our data provide novel evidence of a dichotomous, training-specific LV adaptive response to hemodynamic pressure or volume loading.