A multi-method exploration of a cardiac rehabilitation service delivered by registered Clinical Exercise Physiologists in the UK: key learnings for current and new services.

BACKGROUND: Cardiac rehabilitation has been identified as having the most homogenous clinical exercise service structure in the United Kingdom (UK), but inconsistencies are evident in staff roles and qualifications within and across services. The recognition of Clinical Exercise Physiologists (CEPs) as a registered health professional in 2021 in the UK, provides a potential solution to standardise the cardiac rehabilitation workforce. This case study examined, in a purposefully selected cardiac exercise service that employed registered CEPs, (i) how staff knowledge, skills and competencies contribute to the provision of the service, (ii) how these components assist in creating effective service teams, and (iii) the existing challenges from staff and patient perspectives. METHODS: A multi-method qualitative approach (inc., semi-structured interviews, observations, field notes and researcher reflections) was employed with the researcher immersed for 12-weeks within the service. The Consolidated Framework for Implementation Research was used as an overarching guide for data collection. Data derived from registered CEPs (n = 5), clinical nurse specialists (n = 2), dietitians (n = 1), service managers/leads (n = 2) and patients (n = 7) were thematically analysed. RESULTS: Registered CEPs delivered innovative exercise prescription based on their training, continued professional development (CPD), academic qualifications and involvement in research studies as part of the service. Exposure to a wide multidisciplinary team (MDT) allowed skill and competency transfer in areas such as clinical assessments. Developing an effective behaviour change strategy was challenging with delivery of lifestyle information more effective during less formal conversations compared to timetabled education sessions. CONCLUSIONS: Registered CEPs have the specialist knowledge and skills to undertake and implement the latest evidence-based exercise prescription in a cardiac rehabilitation setting. An MDT service structure enables a more effective team upskilling through shared peer experiences, observations and collaborative working between healthcare professionals.

Allometric scaling for left ventricular mass and geometry in male and female athletes of mixed and endurance sports.

BACKGROUND: The athlete's heart (AH) defines the phenotypical changes that occur in response to chronic exercise training. Echocardiographic assessment of the AH is used to calculate LV mass (LVM) and determine chamber geometry. This is, however, interpreted using standard linear (ratiometric) scaling to body surface area (BSA) whereas allometric scaling is now widely recommended. This study (1) determined whether ratiometric scaling of LVM to BSA (LVMiratio) provides a size-independent index in young and veteran athletes of mixed and endurance sports (MES), and (2) calculated size-independent beta exponents for allometrically derived (LVMiallo) to BSA and (3) describes the physiological range of LVMiallo and the classifications of LV geometry. METHODS: 1373 MES athletes consisting of young (< 35 years old) (males n = 699 and females n = 127) and veteran (> 35 years old) (males n = 327 and females n = 220) were included in the study. LVMiratio was calculated as per standard scaling and sex-specific LVMiallo were derived from the population. Cut-offs were defined and geometry was classified according to the new exponents and relative wall thickness. RESULTS: LVMiratio did not produce a size independent index. When tested across the age range the following indexes LVMi/BSA0.7663 and LVMi/BSA0.52, for males and females respectively, were size independent (r = 0.012; P = 0.7 and r = 0.003; P = 0.920). Physiological cut-offs for LVMiallo were 135 g/(m2)0.7663 in male athletes and 121 g/(m2)0.52 in female athletes. Concentric remodelling / hypertrophy was present in 3% and 0% of young male and female athletes and 24% and 17% of veteran male and female athletes, respectively. Eccentric hypertrophy was observed in 8% and 6% of young male and female athletes and 9% and 11% of veteran male and female athletes, respectively. CONCLUSION: In a large cohort of young and veteran male and female MES athletes, LVMiratio to BSA is not size independent. Sex-specific LVMiallo to BSA with LVMi/BSA0.77 and LVMi/BSA0.52 for male and female athletes respectively can be applied across the age-range. Population-based cut-offs of LVMiallo provided a physiological range demonstrating a predominance for normal geometry in all athlete groups with a greater percentage of concentric remodelling/hypertrophy occurring in veteran male and female athletes.

The impact of image and performance enhancing drugs on atrial structure and function in resistance trained individuals.

BACKGROUND: Image and performance enhancing drugs (IPEDs) are commonly used in resistance trained (RT) individuals and negatively impact left ventricular (LV) structure and function. Few studies have investigated the impact of IPEDs on atrial structure and function with no previous studies investigating bi-atrial strain. Additionally, the impact of current use vs. past use of IPEDs is unclear. METHODS: Utilising a cross-sectional design, male (n = 81) and female (n = 15) RT individuals were grouped based on IPED user status: current (n = 57), past (n = 19) and non-users (n = 20). Participants completed IPED questionnaires, anthropometrical measurements, electrocardiography, and transthoracic echocardiography with strain imaging. Structural cardiac data was allometrically scaled to body surface area (BSA) according to laws of geometric similarity. RESULTS: Body mass and BSA were greater in current users than past and non-users of IPEDs (p < 0.01). Absolute left atrial (LA) volume (60 ± 17 vs 46 ± 12, p = 0.001) and right atrial (RA) area (19 ± 4 vs 15 ± 3, p < 0.001) were greater in current users than non-users but this difference was lost following scaling (p > 0.05). Left atrial reservoir (p = 0.008, p < 0.001) and conduit (p < 0.001, p < 0.001) strain were lower in current users than past and non-users (conduit: current = 22 ± 6, past = 29 ± 9 and non-users = 31 ± 7 and reservoir: current = 33 ± 8, past = 39 ± 8, non-users = 42 ± 8). Right atrial reservoir (p = 0.015) and conduit (p = 0.007) strain were lower in current than non-users (conduit: current = 25 ± 8, non-users = 33 ± 10 and reservoir: current = 36 ± 10, non-users = 44 ± 13). Current users showed reduced LV diastolic function (A wave: p = 0.022, p = 0.049 and E/A ratio: p = 0.039, p < 0.001) and higher LA stiffness (p = 0.001, p < 0.001) than past and non-users (A wave: current = 0.54 ± 0.1, past = 0.46 ± 0.1, non-users = 0.47 ± 0.09 and E/A ratio: current = 1.5 ± 0.5, past = 1.8 ± 0.4, non-users = 1.9 ± 0.4, LA stiffness: current = 0.21 ± 0.7, past = 0.15 ± 0.04, non-users = 0.15 ± 0.07). CONCLUSION: Resistance trained individuals using IPEDs have bi-atrial enlargement that normalises with allometric scaling, suggesting that increased size is, in part, associated with increased body size. The lower LA and RA reservoir and conduit strain and greater absolute bi-atrial structural parameters in current than non-users of IPEDs suggests pathological adaptation with IPED use, although the similarity in these parameters between past and non-users suggests reversibility of pathological changes with withdrawal.

The athlete's heart: insights from echocardiography.

The manifestations of the athlete's heart can create diagnostic challenges during an echocardiographic assessment. The classifications of the morphological and functional changes induced by sport participation are often beyond 'normal limits' making it imperative to identify any overlap between pathology and normal physiology. The phenotype of the athlete's heart is not exclusive to one chamber or function. Therefore, in this narrative review, we consider the effects of sporting discipline and training volume on the holistic athlete's heart, as well as demographic factors including ethnicity, body size, sex, and age.

Insights and recommendations into service model structure, staff roles and qualifications in a UK cancer specific clinical exercise service: a multi-method qualitative study.

PURPOSE: Clinical exercise delivery in the United Kingdom is disparate in terms of service structure, staff roles and qualifications, therefore it is difficult to evaluate and compare across services. Our aim was to explore, in a purposely selected cancer exercise service that was recognised as effective; (i) how staff knowledge, skills and competencies contribute to the provision of the service, (ii) how these components assist in creating effective services, and (iii) to identify existing challenges from staff and service user perspectives. METHODS: The Consolidated Framework for Implementation Research was used as an overarching guide to review the Prehab4Cancer service. Exercise specialists and service user perspectives were explored using a multi-method approach (online semi-structured interviews, online focus group and in-person observation) and data triangulation. RESULTS: Exercise specialists were educated to a minimum of undergraduate degree level with extensive cancer-specific knowledge and skills, equivalent to that of a Registration Council for Exercise Physiologist (RCCP) Clinical Exercise Physiologist. Workplace experience was essential for exercise specialist development in behaviour change and communications skills. CONCLUSIONS: Staff should be educated to a level comparable with the standards for registered RCCP Clinical Exercise Physiologists, which includes workplace experience to develop knowledge, skills and competencies in real-world settings.

Cancer servicesClinical exercise staff should attain extensive cancer-specific knowledge, skills and competencies, underpinned by undergraduate degrees in sport and exercise science-related subjects or higher and equivalent to that of Registration Council for Exercise Physiologist -registered Clinical ExerciseWorkplace experience is vital for exercise specialists to develop their knowledge, skills and competencies in real-world settings.Behaviour change and communication skills, specifically empathy and listening skills, should be incorporated into clinical exercise practitioner training.

A New Tool to Aid the Differential Diagnosis of Physiological Remodelling from Cardiac Pathology When Assessing Left Ventricle, Left Atrial and Aortic Structure and Function in Male Arab and Black Paediatric Athletes.

Aim: To determine if published Z-scores for left ventricular (LV), left atrial (LA) and aortic structure as well as indices of LV function (Doppler and TDI) in paediatric athletes and non-athletes are appropriate for application in male Arab and black paediatric athletes. If inappropriate, we aim to provide new nomograms and Z-scores for clinical application. Methods: 417 (297 Arab, 120 black) male paediatric (11-18 years) athletes, were evaluated by 2D echocardiography as per British Society of Echocardiography recommendations, and biological age (by radiological X-ray) assessment. Z-scores were tested by residual and correlation analysis together with visual inspection. New Z-scores involved allometric (a*BSA(b+c*chronological age)) and second-order polynomial (y=a*chronological age2+b*chronological age+c) equations for measures of cardiac size and indices of LV function, respectively. Results: Residual linear regression, correlation analysis and visual inspection revealed published z-scores in white peri-pubertal footballers and paediatric non-athletes to be inappropriate for application in male Arab and black paediatric athletes. Residual linear regression revealed new Z-scores for measures of LV, LA and aortic root size to be independent of BSA, ethnicity, chronological and biological age. Residual linear regression revealed new Z-scores for measures of function to be independent of chronological age. Conclusion: Our new z-scores may aid differential diagnosis of suspected pathology versus physiology remodelling, in cardiac screening of the Arab and black paediatric athlete. Nomograms are provided to assist the tracking of the paediatric athlete necessitating annual follow-up and Excel z-score calculation to facilitate use in day-to-day practice.

Charter to establish clinical exercise physiology as a recognised allied health profession in the UK: a call to action.

The UK population is growing, ageing and becoming increasingly inactive and unfit. Personalised and targeted exercise interventions are beneficial for ageing and the management of chronic and complex conditions. Increasing the uptake of effective exercise and physical activity (PA) interventions is vital to support a healthier society and decrease healthcare costs. Current strategies for exercise and PA at a population level mostly involve self-directed exercise pathways, delivered largely via the fitness industry. Even for those who opt-in and manage to achieve the current recommendations regarding minimum PA, this generic 'one-size-fits-all' approach often fails to demonstrate meaningful physiological and health benefits. Personalised exercise prescription and appropriate exercise testing, monitoring and progression of interventions for individuals with chronic disease should be provided by appropriately trained and recognised exercise healthcare professionals, educated in the cognate disciplines of exercise science (eg, physiology, biomechanics, motor control, psychology). This workforce has operated for >20 years in the Australian public and private healthcare systems. Accredited exercise physiologists (AEPs) are recognised allied health professionals, with demonstrable health and economic benefits. AEPs have knowledge of the risks and benefits of distinct forms of exercise, skills in the personalised prescription and optimal delivery of exercise, and competencies to support sustained PA behavioural change, based on the established scientific evidence. In this charter, we propose a road map for the training, accreditation and promotion of a clinical exercise physiology profession in the UK.

Acute exercise-induced changes in cardiac function relates to right ventricular remodeling following 12-wk hypoxic exercise training.

Repeated ventricular exposure to alterations in workload may relate to subsequent cardiac remodeling. We examined whether baseline acute changes in right (RV) and left ventricular (LV) function relate to chronic cardiac adaptation to 12-wk exercise training. Twenty-one healthy individuals performed 12-wk high-intensity endurance running training under hypoxia (fraction of inspired oxygen: 14.5%). Resting transthoracic echocardiography was performed before and after the training program to assess ventricular structure, function, and mechanics (including strain-area/volume loops). In addition, we examined systolic cardiac function during recumbent exercise under hypoxia at baseline (heart rate of 110-120 beats/min, "stress echocardiography"). Fifteen individuals completed training (22.0 ± 2.4 yr, 10 males). Hypoxic exercise training increased RV size, including diameter and area (all P < 0.05). With exception of an increase in RV fractional area change (P = 0.03), RV function did not change post-training (all P > 0.05). Regarding the RV strain-area loop, lower systolic and diastolic slopes were found post-training (P < 0.05). No adaptation in LV structure, function, or mechanics was observed (all P > 0.05). To answer our primary aim, we found that a greater increase in RV fractional area change during baseline stress echocardiography (r = -0.67, P = 0.01) inversely correlated with adaptation in RV basal diameter following 12-wk training. In conclusion, 12-wk high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline increase in RV fractional area change to acute exercise. These data suggest that acute cardiac responses to exercise may relate to subsequent RV remodeling after exercise training in healthy individuals.NEW & NOTEWORTHY During exercise, the right ventricle is exposed to a disproportionally higher wall stress than the left ventricle, which is further exaggerated under hypoxia. In this study, we showed that 12-wk high-intensity running hypoxic exercise training induced right-sided structural remodeling, which was, in part, related to baseline cardiac increase in RV fractional area change to acute exercise. These data suggest that acute RV responses to exercise are related to subsequent right ventricular remodeling in healthy individuals upon hypoxic training.

Exercise-Induced Cardiac Fatigue after a 45-Minute Bout of High-Intensity Running Exercise Is Not Altered under Hypoxia.

BACKGROUND: Acute exercise promotes transient exercise-induced cardiac fatigue, which affects the right ventricle and to a lesser extent the left ventricle. Hypoxic exposure induces an additional increase in right ventricular (RV) afterload. Therefore, exercise in hypoxia may differently affect both ventricles. The aim of this study was to investigate the acute effects of a bout of high-intensity exercise under hypoxia versus normoxia in healthy individuals on right- and left-sided cardiac function and mechanics. METHODS: Twenty-one healthy individuals (mean age, 22.2 ± 0.6 years; 14 men) performed 45-min high-intensity running exercise under hypoxia (fraction of inspired oxygen 14.5%) and normoxia (fraction of inspired oxygen 20.9%) in a randomized order. Pre- and post-exercise echocardiography, at rest and during low-to-moderate intensity recumbent exercise ("stress"), was performed to assess RV and left ventricular (LV) cardiac function and mechanics. RV structure, function, and mechanics were assessed using conventional two-dimensional, Doppler, tissue Doppler, speckle-tracking echocardiographic, and novel strain-area loops. RESULTS: Indices of RV systolic function (RV fractional area change, Tricuspid annular plane systolic excursion, RV s', and RV free wall strain) and LV function (LV ejection fraction and LV global longitudinal strain) were significantly reduced after high-intensity running exercise (P < .01). These exercise-induced changes were more pronounced when echocardiography was examined during stress compared with baseline. These responses in RV and LV indices were not altered under hypoxia (P > .05). CONCLUSIONS: There was no impact of hypoxia on the magnitude of exercise-induced cardiac fatigue in the right and left ventricles after a 45-min bout of high-intensity exercise. This finding suggests that any potential increase in loading conditions does not automatically exacerbate exercise-induced cardiac fatigue in this setting.

5-Year prognostic value of the right ventricular strain-area loop in patients with pulmonary hypertension.

AIMS: Patients with pre-capillary pulmonary hypertension (PH) show poor survival, often related to right ventricular (RV) dysfunction. In this study, we assessed the 5-year prognostic value of a novel echocardiographic measure that examines RV function through the temporal relation between RV strain (ϵ) and area (i.e. RV ϵ-area loop) for all-cause mortality in PH patients. METHODS AND RESULTS: Echocardiographic assessments were performed in 143 PH patients (confirmed by right heart catheterization). Transthoracic echocardiography was utilized to assess RV ϵ-area loop. Using receiver operating characteristic curve-derived cut-off values, we stratified patients in low- vs. high-risk groups for all-cause mortality. Kaplan-Meier survival curves and uni-/multivariable cox-regression models were used to assess RV ϵ-area loop's prognostic value (independent of established predictors: age, sex, N-terminal pro B-type natriuretic peptide, 6-min walking distance). During follow-up 45 (31%) patients died, who demonstrated lower systolic slope, peak ϵ, and late diastolic slope (all P < 0.05) at baseline. Univariate cox-regression analyses identified early systolic slope, systolic slope, peak ϵ, early diastolic uncoupling, and early/late diastolic slope to predict all-cause mortality (all P < 0.05), whilst peak ϵ possessed independent prognostic value (P < 0.05). High RV loop-score (i.e. based on number of abnormal characteristics) showed poorer survival compared to low RV loop-score (Kaplan-Meier: P < 0.01). RV loop-score improved risk stratification in high-risk patients when added to established predictors. CONCLUSION: Our data demonstrate the potential for RV ϵ-area loops to independently predict all-cause mortality in patients with pre-capillary PH. The non-invasive nature and simplicity of measuring the RV ϵ-area loop, support the potential clinical relevance of (repeated) echocardiography assessment of PH patients.

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.

Exercise-induced release of troponin.

It is well established that regular physical activity reduces cardiovascular disease risk; however, numerous studies have demonstrated postexercise elevations in cardiac troponin (cTn), indicative of cardiac injury in apparently healthy individuals. The prevalence of these findings in different exercise settings and population groups, as well as potential underlying mechanisms and clinical significance of exercise-induced cTn release are not yet quite determined. The present review will discuss the cTn response to exercise in light of developing cTn assays and the correlation between postexercise cTn release and cardiac function. Additionally, recent data regarding the potential link between strenuous endurance exercise and its relationship with unfavorable cardiac effects in athletes, as well as the management of patients presenting at emergency care after sport events will be briefly reviewed.

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.

Changes in dynamic left ventricular function, assessed by the strain-volume loop, relate to reverse remodeling after aortic valve replacement.

Aortic valve replacement (AVR) leads to remodeling of the left ventricle (LV). Adopting a novel technique to examine dynamic LV function, our study explored whether post-AVR changes in dynamic LV function and/or changes in aortic valve characteristics are associated with LV mass regression during follow-up. We retrospectively analyzed 30 participants with severe aortic stenosis who underwent standard transthoracic echocardiographic assessment before AVR [88 (IQR or interquartile range: 22-143) days], post-AVR [13 (6-22) days], and during follow-up [455 (226-907) days]. We assessed standard measures of LV structure, function, and aortic valve characteristics. Novel insight into dynamic LV function was provided through a four-chamber image by examination of the temporal relation between LV longitudinal strain (ε) and volume (ε-volume loops), representing the contribution of LV mechanics to volume change. AVR resulted in immediate changes in structural valve characteristics, alongside a reduced LV longitudinal peak ε and improved coherence between the diastolic and systolic part of the ε-volume loop (all P < 0.05). Follow-up revealed a decrease in LV mass (P < 0.05) and improvements in LV ejection fraction and LV longitudinal peak ε (P < 0.05). A significant relationship was present between decline in LV mass during follow-up and post-AVR improvement in coherence of the ε-volume loops (r = 0.439, P = 0.03), but not with post-AVR changes in aortic valve characteristics or LV function (all P > 0.05). We found that post-AVR improvements in dynamic LV function are related to long-term remodeling of the LV. This highlights the potential importance of assessing dynamic LV function for cardiac adaptations in vivo.NEW & NOTEWORTHY Combining temporal measures of left ventricular longitudinal strain and volume (strain-volume loop) provides novel insights in dynamic cardiac function. In patients with aortic stenosis who underwent aortic valve replacement, postsurgical changes in the strain-volume loop are associated with regression of left ventricular mass during follow-up. This provides novel insight into the relation between postsurgery changes in cardiac hemodynamics and long-term structural remodeling, but also supports the potential utility of the assessment of dynamic cardiac function.

Scaling to produce size-independent indices of echocardiographic derived aortic root dimensions in elite Rugby Football League players.

The assessment of aortic root dimensions is important in cardiac pre-participation screening. Scaling of cardiac dimensions removes the impact of body size allowing meaningful inter/intra group comparisons. Developing appropriate scaling approaches, scaling variables and extending the application to major vessels is warranted so underlying pathology can be detected and managed appropriately. The study aims to define relationships between aortic root dimensions and body surface area/height. Two hundred and twenty elite Rugby Football League athletes were recruited. All participants completed anthropometric assessments, a 12-lead ECG and echocardiogram. Aortic root was measured at the aortic annulus, sinus of valsalva, sinotubular junction and the proximal ascending aorta. Linear and allometric scaling were performed on the relationship between aortic measurements and body surface area/height. Absolute aortic root measurements fell within normal population data (mean ± standard deviation (range): aortic annulus: 22 ± 2 (17-28) mm, sinus of valsalva: 28 ± 3 (20-38) mm, sinotubular junction: 22 ± 3 (14-33) mm, proximal ascending aorta: 22 ± 3 (15-31) mm). Linear scaling to height produced size-independent indices at all aortic measurement sites (P < 0.05). Conversely, linear scaling using body surface area did not produce size-independent indices at any site (P > 0.05). Allometric scaling, using both body surface area and height, produced size-independent indices at all sites (P < 0.05). We recommend linearly scaling aortic root dimensions to height in elite Rugby Football League athletes and discourage the use of body surface area as a linear scaling quantity. Allometric scaling is also effective when using both body surface area and height.

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.

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.

Impact of 24 weeks of supervised endurance versus resistance exercise training on left ventricular mechanics in healthy untrained humans.

In addition to the well-known cardiac structural adaptation to exercise training, little work has examined changes in left ventricle (LV) mechanics. With new regional and global indexes available we sought to determine the effect of 24-wk endurance versus resistance training on LV mechanics. Twenty-three male subjects were randomly allocated to a 24-wk endurance or resistance training program. Pre- and posttraining two-dimensional echocardiographic images were acquired. Global LV mechanics [strain (ε)] were recorded in longitudinal, circumferential, and radial planes. Rotation was assessed at apical and basal levels. In addition, longitudinal ε-volume loops, across the cardiac cycle, were constructed from simultaneous LV ε (longitudinal and transverse strain) and volume measurements across the cardiac cycle as a novel measure of LV mechanics. Marginal differences in ε and rotation data were found between groups. After training, we found no change in global peak ε data. Peak basal rotation significantly increased after training, with changes in the endurance group (-2.2 ± 1.9° to -4.5 ± 3.3°) and the resistance group (-2.9 ± 3.0° to -3.4 ± 2.9°). LV ε-volume loops revealed a modest rightward shift in both groups. Although most global and regional indexes of LV mechanics were not significantly altered, 24 wk of intense supervised exercise training increased basal rotation. Further studies that assess LV mechanics in larger cohorts of subjects and those with cardiovascular disease and risk factors may reveal important training impacts. NEW & NOTEWORTHY This study builds on previous work by our group and presents a comprehensive assessment of cardiac mechanics after dichotomous exercise training programs. We highlight novel findings in addition to the inclusion of strain-volume loops, which shed light on subtle differences in longitudinal and transverse contribution to volume change throughout the cardiac cycle. Our findings suggest that training has an impact on basal rotation and possibly strain-volume loops.

Exercise-induced Changes in Soluble ST2 Concentrations in Marathon Runners.

PURPOSE: Previous studies have suggested that extreme endurance exercise may induce cardiac microdamage that could lead to subsequent myocardial fibrosis. Soluble suppression of tumorigenicity 2 (sST2) is a cardiac biomarker for assessment of myocardial fibrosis, inflammation, and strain. We evaluated baseline and exercise-induced sST2 concentrations in a heterogeneous cohort of marathon runners to identify predictors for sST2 concentrations. METHODS: Ninety-two runners supplied demographic data, health status, physical activity levels, and marathon experience. Before (baseline) and immediately after (finish) the marathon, blood was collected for analysis of sST2 and cardiac troponin I (cTnI). RESULTS: Eighty-two participants (45 ± 8 yr, 79% male) finished the race in 227 ± 28 min at 92% (88%-94%) of their predicted maximum heart rate (exercise intensity). sST2 concentrations increased in all runners, from 34 (25-46) ng·mL to 70 (53-87) ng·mL (P < 0.001), and cTnI increased from 9 (5-21) ng·L to 60 (34-102) ng·L (P < 0.001). sST2 concentrations were higher in the fastest marathon runners. Sex and marathon personal best time were associated with baseline sST2 (R = 0.27); baseline sST2, weight loss, and exercise intensity during marathon were associated with finish sST2 (R = 0.54); baseline sST2, height, sex, and weekly training hours were associated with the exercise-induced increase in sST2 (R = 0.47). We observed no association between sST2 and cTnI concentrations. CONCLUSION: An exercise-induced increase in sST2 was observed in all marathon runners with sST2 concentrations exceeding cutoff values both at baseline (48%) and finish (94%). Faster runners had higher sST2 concentrations. Our data suggest complex variables determine sST2 concentrations in marathon runners.