Oxborough et al.

Echo Research & Practice (2025) 12:7 Echo Research & Practice
https://doi.org/10.1186/s44156-025-00069-0

GUIDELINE Open Access

Echocardiography in the cardiac

assessment of young athletes: a 2025 guideline
from the British Society of Echocardiography
(endorsed by Cardiac Risk in the Young)
David Oxborough1*, Keith George1, Robert Cooper1,16, Raghav Bhatia2,14, Tristan Ramcharan3, Abbas Zaidi4,
Sabiha Gati5,8, Keerthi Prakash6, Dhrubo Rakhit7, Shaun Robinson1,8, Graham Stuart9, Jan Forster10,
Melanie Ackrill11, Daniel Augustine12, Aneil Malhotra13, Michael Papadakis14, Silvia Castelletti15,
Victoria Pettemerides16, Liam Ring17, Antoinette Kenny18, Aaron Baggish19 and Sanjay Sharma14

Abstract
Sudden cardiac death in a young physically active individual or athlete is a rare but tragic event. Pre-participation
screening and follow-up investigations are utilised to reduce the risk and occurrence of these events. Echocardi-
ography plays a key role in the cardiac diagnostic pathway and aims to identify underlying inherited or congenital
structural cardiac conditions. In 2013 the British Society of Echocardiography and Cardiac Risk in the Young produced
a joint guidance document to support echocardiographers in this setting. The document was subsequently updated
in 2018, and it is now timely to provide a further update to the guideline drawing on the advances in our knowledge
alongside the developments in ultrasound technology within this nuanced area of sports cardiology.
Keywords Athlete, Echocardiography, Guideline, Sport

*Correspondence:
David Oxborough
[email protected]
Full list of author information is available at the end of the article

© The Author(s) 2025. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which
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Oxborough et al. Echo Research & Practice (2025) 12:7 Page 2 of 34

Graphical Abstract

Introduction comprehensive and systematic approach to acquisition

Echocardiography plays an important role in the cardiac and interpretation of the echocardiogram in athletes
assessment of young (typically 14–35 years old) individu- including guidance related to the added value of exer-
als who engage in greater than 3 h of structured exercise cise stress echocardiography (ESE), strain imaging and
per week [1] (termed athlete from here onwards). The 3-dimensional echocardiography (3DE) in this important
aim of echocardiography in the athlete, is to identify or field of sports cardiology.
exclude structural and functional abnormalities consist-
ent with underlying cardiac disease which may predis- Background
pose them to an acute cardiac event or sudden cardiac Sudden cardiac death in young athletes
death (SCD). This can be achieved in isolation and/or The death of a young athletic person is devastating with
in conjunction with other diagnostic investigations and the premature loss of life alongside the significant impact
hence in 2013 the British Society of Echocardiography on their family and the wider community. These tragic
(BSE) (supported and endorsed by Cardiac Risk in the events are even more difficult to comprehend when they
Young) published guidance on the standardised echo- occur in individuals who are considered healthy and
cardiographic approach to image acquisition and inter- have engaged in regular sporting activities. The preva-
pretation in sports participants which was subsequently lence and incidence of SCD in young athletes is not fully
updated in 2018. Since the 2018 update, our understand- elucidated due to challenges associated with compiling
ing in this field has advanced considerably and there data from often unreliable and incomplete sources. This
have been significant refinements in echocardiographic is compounded by a lack of structured registries and the
techniques to distinguish physiological cardiac adapta- absence of longitudinal data which may, in part, explain
tion from structural diseases implicated in SCD in the the large range of the reported prevalence of SCD in ath-
young athletic population. It is therefore timely to update letes (1 in 14,000 to 1 in 100,000) [2, 3]. Data also high-
the guidelines to reflect these advancements. The aim light that athletes have a 6–8 fold increased risk of SCD
of this iteration is to provide a working document that compared to non-athletes of the same age with male
can be used to support healthcare practitioners for a athletes and those of black ethnicity being at the greatest
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 3 of 34

risk [4, 5]. Many of these adverse events occur during symptomatic athletes (including echocardiography) may
exercise [4] in athletes who are already predisposed and help to reduce any additional risk.
harbouring pre-existing cardiac disease. This observation
is the fundamental rationale for pre-participation cardiac
screening (PPCS) to identify vulnerable athletes. The role of echocardiography
Structural cardiac conditions responsible for SCD in Pre-participation cardiac screening has been shown to
athletes are primarily inherited but can also be congeni- effectively diagnose underlying cardiac conditions and
tal and acquired. Recent data from a large UK database reduce the risk of SCD in young athletes between 14
of 748 decedents [4] who had engaged in regular sport- and 35 years old [2, 12–14]. Echocardiography provides
ing activities demonstrated that although there was a a non-invasive, easily accessible and relatively inexpen-
predominance of sudden arrhythmic death syndrome sive means of accurately assessing cardiac structure and
(SADS), 42% of males and 30% of females had condi- function in athletes, leading to its integration into various
tions that could have been detectable on echocardiog- PPCS and follow-up protocols [15]. The predictive capac-
raphy. These conditions include hypertrophic (HCM), ity, efficacy and diagnostic yield of PPCS have been dem-
dilated (DCM) and arrhythmogenic cardiomyopathy onstrated to be high with the accepted European protocol
(ACM), coronary artery anomalies (CAA), idiopathic left suggesting PPCS in athletes should be undertaken every
ventricular (LV) fibrosis, aortic dissection, valve disease 1–2 years. This includes a questionnaire (to capture
and myocarditis [5–7]. The recent global SARS-Cov-2 demographics including quantifying physical activity and
health pandemic has also provided concern regarding the exercise levels, symptoms and family history), a physical
impact of viral myocarditis in the athletic / active popula- examination and a 12-lead electrocardiogram (ECG) [15].
tion. Data from North America and Europe suggest that Figure 1 highlights normal athletic criteria on the 12-lead
cardiac abnormalities following COVID-19 infection in ECG and the abnormal criteria that should trigger follow-
these populations ranges from 0.2% to 4% [8, 9] and the up secondary investigations [16]. In this setting, echo-
established associations between myocarditis and SCD cardiography is used as a secondary investigation and as
[10, 11] mean that consideration of cardiac evaluation in such is advocated in the presence of abnormal findings.

Fig. 1 12-lead ECG criteria for onward referral to Echocardiography as per the International Guidelines for Electrocardiographic Interpretation
in Athletes (adapted from Sharma et al. 2018)
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 4 of 34

It has been suggested that up to 16% of SCD cases are an echocardiogram before returning to physical activity
related to structural heart disease with no accompany- [25]. The echocardiogram is aimed at confirming nor-
ing electrocardiographic abnormalities [17] and hence mal ventricular structure and function and excluding any
some professional sporting organisations also integrate evidence of pericardial or myocardial involvement [25].
echocardiography as a primary investigation tool and Figure 2 highlights the recommended role of echocardi-
/or a once-only echocardiogram at the athlete’s first ography in the assessment of the athlete’s heart.
assessment (often in adolescence) [18]. The added value
of echocardiography at this time point allows the exclu- The athletes heart
sion of congenital, valvular and structural heart disease Our understanding of the athlete’s heart has developed
with evidence to suggest that echocardiography provides significantly over recent years in tandem with the evo-
additional diagnostic yield in 1.2%—4.5% of adolescent lution of echocardiographic techniques and technology
athletes [2, 19]. That aside, based on the challenges of dif- [26]. The echocardiographer involved in the assessment
ferentiating physiological from pathological adaptation, of an athlete should understand 1) the physiological
echocardiography may still provide inconclusive findings adaptation of cardiac structure and function that occurs
and hence further assessment including ESE, 3DE, car- in response to regular exercise training, 2) the variabil-
diac magnetic resonance imaging (cMRI) and computed ity depending on the type and volume of training and 3)
tomography (CT) should be considered and may provide the impact of the athlete’s ethnicity, sex, age and body
additional value in these challenging cases [20, 21]. size. The following section aims to summarise these key
There are data highlighting the small risk (1–4%) of points, and we draw the reader’s attention to the narra-
(peri)myocarditis following viral infections (including tive review [26] detailing the multi-factorial aspects asso-
COVID-19) in athletic populations [22] with a higher ciated with physiological cardiac remodelling.
prevalence in symptomatic individuals or those experi- It is well established that exercise training causes adap-
encing a debilitating illness [9]. Based on this, the role of tation of the heart linked to improvements in cardio-
echocardiography in the return to play of athletes recov- respiratory fitness [27]. Hence an individual athlete’s
ering from viral infection has received appropriate atten- training volume (defined as training intensity x train-
tion [23, 24]. Although the details of the ‘return to play’ ing duration or Metabolic Equivalent Test (MET hrs/
training protocols may vary, there is a consensus that wk = MET × training duration)) should be estimated. An
an athlete with cardiac symptoms would benefit from example of a select range of sporting disciplines and their

Fig. 2 The recommended role of Echocardiography in the Assessment of the Athletes Heart
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 5 of 34

specific METS is highlighted in Table 1. In summary, low- all types of training (3–12% and 0–8% in male and female
intensity exercise is defined as corresponding to 1.8–2.9 athletes respectively [32, 33]) and although it has been
METS, moderate intensity is defined as 3–6 METS and documented more frequently in athletes of black ethnic-
high-intensity exercise as > 6 METS [28]. ity and those who are older with a lifelong exposure to
The magnitude of adaptation is greatest in those ath- exercise [32–34] there is little evidence to support previ-
letes who engage in predominantly mixed (combined ous theories of it being a primary response to resistance
dynamic and strength) or endurance exercise rather than training [27, 35]. Most studies highlight the multifactorial
pure resistance training [29–31]. Endurance/ dynamic nature of the athlete’s heart with additional factors such
activity can be defined as aerobic isotonic dynamic exer- as body size [32] also impacting the magnitude of struc-
cise at incremental workloads of 70–90% of maximum tural adaptation [26]. In view of this, scaling to body size
heart rate and includes sporting disciplines such as is mandated in athletes. Although the ideal approach is to
long- and middle-distance running, swimming or cycling scale allometrically, there is currently a lack of sufficient
as well as common team sports such as soccer and bas- population-based exponents and the associated normal
ketball. Resistance training can be defined as anaerobic athletic ranges to make this approach clinically useful
dynamic exercise at incremental workloads of > 30% max- and hence a standard ratiometric / linear scaling to body
imal voluntary contraction and includes sporting disci- surface area (BSA) or height is currently recommended.
plines such as martial arts, sumo wrestling, shot-put and Structural adaptation of the right ventricle (RV) occurs
weightlifting. It is important to note that many sporting in athletes of predominantly mixed / endurance exercise
disciplines and training regimes involve a combination of training [36, 37] with balanced adaptation of the inflow
resistance and endurance exercise (for example, boxing, and outflow [38]. These adaptations occur irrespective of
rugby, rowing, and American football). body size [39] and ethnicity [40]. Right ventricular adap-
Studies using echocardiography have highlighted the tation [40, 41] is also proportional to LV enlargement
specific type of left ventricular (LV) structural adapta- and hence an objective and subjective assessment of the
tion in athletes and have usually highlighted normal relative adaptation can provide valuable insight [42].
geometry or eccentric hypertrophy i.e. LV cavity enlarge- The atria of the heart are no exception to physiological
ment with concomitant increase in LV wall thickness enlargement with the greatest magnitude of adaptation
[32]. Left ventricular concentric hypertrophy is rare in seen in athletes of high dynamic sports [43], balanced to
both right and left atria and across athlete demograph-
ics [44, 45]. Although absolute values of all chambers
are greater in males, female athletes also demonstrate
Table 1 Sporting examples demonstrating specific MET values
proportional adaptation highlighting the independent
for determining exercise Intensity (adapted from Hermann et al.
2023)
impact of a training stimulus.
The echocardiographic assessment of LV and RV func-
Sporting discipline Metabolic tion (systolic and diastolic) is important to aid differen-
equivalent
(MET) tiation from inherited cardiomyopathies and hence a
thorough understanding of functional adaptation to exer-
Soccer 9.5 cise training is vital [26]. Generally, systolic functional
Running (6 mph) 9.3 indices, ejection fraction (EF), global longitudinal strain
Running (7.5 mph) 11.0 (GLS), RV free wall strain (RVFWS) RV fractional area
Running (8 mph) 12.0 change (RVFAC) and tissue Doppler indices are within
Cycling (Racing > 20 mph) 16.8 the published normal ranges for non-athletes [26]. How-
Cycling (Leisure < 10 mph) 5.8 ever, it is important to note that 12–17% of predomi-
Cricket 4.8 nantly male athletes may have borderline-low or reduced
Rugby 8.3 resting values of EF, GLS and RVFAC [20, 46–49]. The
Tennis (singles) 8.0 mechanism is thought to be related to the physiologically
Field Hockey 7.8 enlarged chambers requiring a lower contractile state
Netball 7.0 to deliver a sufficient stroke volume (SV) at rest along-
Boxing 12.3 side a low resting heart rate (HR) [50] secondary to high
Golf 4.5 vagal tone. It is important to note that these physiological
Rowing (competitive) 15.5 functional changes are related to structural adaptation
Swimming (leisure) 6.0 and hence it is less common to observe low resting func-
Swimming (competitive) 10.5 tional indices from normal-sized chambers such as in
Weight lifting 6.0 resistance trained athletes [27, 51, 52] There are a small
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 6 of 34

proportion of athletes with low resting function that will physiological adaptation presents with normal values of
have a genetic predisposition for dilated cardiomyopathy reservoir, conduit and booster LA and RA strain irre-
[47] and hence we encourage echocardiographers to have spective of atrial size [43].
a low threshold for recommending ESE as an additional There is evidence to suggest that the morphology of the
assessment in this setting (see Fig. 2). aortic root in young athletes remains normal [56] but is
Left ventricular diastolic function is superior in the larger when compared to non-athletes [57]. The great-
athlete, related to high training volumes and high car- est dimensions are seen in high-dynamic endurance
dio-respiratory fitness [53]. This is achieved through male athletes [57, 58] but with values above established
enhanced relaxation, faster reduction in LV pressures absolute cut-offs (40 mm in male athletes and 38mm in
and greater untwist which are likely to be more apparent female athletes) seen in only 0.2% and 0.4% respectively
during exercise when increased SV is required. At rest [57]. The diameter of the aortic root is linearly related to
the athlete will typically exhibit normal or supranormal the height of the athlete [56] and therefore it is impor-
indices of diastolic function with only 1.8% of athletes tant, as with other cardiac indices, to scale appropriately.
displaying lower values than what is considered normal It is noteworthy that these values do not apply to mas-
for non-athletes [54]. The presence of diastolic dysfunc- ter endurance athletes aged 50–70 years old of whom an
tion warrants further investigation. Atrial function is aortic root diameter exceeds 40mm in 31% males and 8%
fast becoming an important parameter in the echocar- females [41].
diographic assessment of those non-athletic individuals Table 2 and Fig. 3 have been adapted from Flanagan
with LA enlargement and diastolic dysfunction [55]. In et al. 2023 [26] and summarise the multifactorial nature
view of this, LA and RA strain may have additional diag- of the athlete’s heart.
nostic value as studies have demonstrated that athletic

Table 2 The multi-factorial nature of the athlete heart—points for considerations

Sporting type Endurance athletes often present with physiological eccentric hypertrophy of the LV; however concentric remodelling in any athlete
is rare
Endurance athletes typically present normal or decreased systolic function and normal or superior diastolic function compared
with the non-athletic population
Athletes engaging in endurance disciplines may present with bi-atrial dilatation which is strongly correlated with exercise capacity
Endurance and resistance trained athletes tend to present larger aortic root size than the non-athletic population. However, these dif-
ferences in size are not clinically significant and therefore the presence of a dilated aortic root warrants further investigation
Ethnicity There is a greater prevalence of LVH in black athletes compared to white, Asian, Arab, Pacific Islander and mixed ethnicity athletes
Mixed ethnicity athletes of black lineage have phenotypical similarities to black athletes although less pronounced and have a greater
LV wall thickness than white athletes
Male black athletes may have a RWT of up to 0.51 or 0.48 in female black athletes, but this finding should be interpreted with caution
in the presence of symptoms or a family history of SCD, or an abnormal 12-lead ECG demonstrating, for example, lateral T wave inver-
sion
RV structural adaptation is similar across ethnicities
Black athletes appear to have larger LA dimensions than white athletes but until this has been reproduced in future studies the existing
normal ranges should be applied
Body size Indexing LV end diastolic diameter and LV mass to fat free mass is most optimal compared to BSA, body mass and height and is impor-
tant in athletes displaying extreme anthropometry
Indexing all chambers to BSA with population-specific allometric b exponents, is optimal, however, until these values have been vali-
dated across cohorts it is recommended that standard linear scaling to BSA is undertaken in line with BSE guidelines for non-athletes
whilst acknowledging the limitations of this approach
Indexed aortic root dimensions should be ratiometrically scaled to height. As aortic root dimension values typically fall within estab-
lished normal limits, indexed aortic reference values may be helpful in the early detection of aortic pathologies in athletes who exceed
these limits
Sex Concentric LVH is extremely rare in female athletes and rare in male athletes
Female athletes present with smaller LV, RV and bi-atrial structural dimensions compared to male athletes
Males have larger aortic root dimensions compared to females with values of ≥ 40 mm for males and ≥ 38 mm for females being
extremely rare. Values exceeding these limits may be indicative of pathology and further assessment would prove beneficial
Age LV dimensions in adolescent athletes are larger when compared with non-athlete controls. LV cavity enlargement very rarely exceeds
60mm but in cases where it does, whilst also in the presence of an impairment of systolic or diastolic function, a diagnosis of DCM
should be considered
Adolescent athletes present bi-atrial remodelling compared to non-athlete controls. However bi-atrial function is preserved with LA
and RA EF similar between athletes and controls and thus signifies normal physiological remodelling
Aortic dilation is rare in adolescent athletes. The aortic diameter cut off values of 40mm for males and 38 mm for females may not be
appropriate for the adolescent athlete and therefore scaling to height is warranted
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 7 of 34

Fig. 3 The multi-factorial nature of the athlete’s heart—an overview

The standard echocardiographic examination RV and septal defects. In contrast, T-wave inversion in
Pre‑echocardiographic information the lateral leads, regardless of age, would warrant similar
Whether as a screening tool or a secondary investigation, scrutiny of the LV apex and broader phenotypic features
echocardiography aims to identify underlying inherited of an underlying cardiomyopathic substrate. In addition,
or congenital structural cardiac disease. Therefore, the an understanding of the athlete’s ethnicity, sex, body
echocardiographer needs to be knowledgeable about size, age, training type and volume will provide insight
these conditions and proficient in detecting or exclud- into the expected type and magnitude of athletic adapta-
ing pathology. Additionally, the echocardiographer tion (see Tables 1 and 2 and Fig. 3). The pre-echocardio-
must recognise and acknowledge uncertainties that may graphic information will contextualise and contribute to
require further tailored downstream investigations. It is the subsequent management of the athlete, and therefore,
equally important that they fully understand the com- it is recommended that, wherever possible, this informa-
plexities and nuances associated with the normal athlete’s tion is readily available before the examination.
heart. In all settings, the echocardiogram should be used The athlete should attend the examination having not
alongside a 12-lead ECG, a questionnaire (to capture trained for a minimum of 3 h prior. There is strong evi-
symptoms, family history and training volume), and, in dence demonstrating acute effects of high intensity and
some settings a physical examination [15]. The informa- endurance exercise on LV and RV systolic and diastolic
tion obtained will influence the scope and focus of the function. These effects include a transient reduction in
echocardiographic examination. For example, an athlete EF, E velocity and GLS with an increase in RV size with
aged over 16 years presenting with non-training related reduced RVFAC / RV strain [59–61]. These studies high-
12-lead ECG changes such as T-wave inversion in the light the physiological nature of this phenomenon and
anterior leads would warrant a closer assessment of the
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 8 of 34

generally demonstrate a return to baseline values within function albeit at a lower magnitude than those athletes
3 h. currently using [69].
It is apparent that the cardiac chambers will adapt dif-
ferently during a competitive season, with more marked The echocardiographic examination
physiological remodelling occurring during those periods The echocardiogram will be directed by the pre-echo-
of higher training volume [62–65]. As a result, the poten- cardiographic information but should also fully adhere
tial for a broader diagnostic grey area exists for both one- to the BSE minimum dataset [70]. The BSE minimum
off and serial assessments. Due to the inherent logistics dataset is subsequently extended to 1) include addi-
associated with sports practice it is challenging to stand- tional parasternal short axis (PSAX) images to accurately
ardise the timing of a cardiac assessment. Therefore, define LV wall thicknesses from eight myocardial regions
seasonal-linked variation in cardiac adaptation should be (basal and mid anteroseptum, inferoseptum, inferolat-
an expected phenomenon and prompt and reinforce the eral and lateral walls), 2) provide detail of the extent of
echocardiographer to establish the athlete’s past and cur- myocardial trabeculations, 3) demonstrate the origin of
rent training load and subsequently interpret accordingly. both the left and right coronary arteries and 4) include
The current use or past use of performance-enhanc- GLS where possible. The inclusion of the maximal wall
ing drugs should be noted where the athlete divulges thicknesses should replace any wall thickness measure-
this information or where there is a suspicion. In those ments made in a parasternal long-axis (PLAX) orienta-
athletes who are currently using Androgenic Anabolic tion and the anteroseptal and inferolateral values should
Steroids (AAS) it is common to find increased LV mass be used to calculate the LV mass and relative wall thick-
beyond the values that would be expected for their train- ness (RWT). A geometry classification should be offered
ing volume, type and body size [66]. This often manifests as per standard reference values for non-athletes [71]
as a balanced increase in cavity size and wall thickness (see Fig. 4) and it is important to provide absolute and
(eccentric hypertrophy) with reduced EF, GLS and left scaled chamber dimensions, volumes and areas to BSA
atrial function [67–69]. The previous use of AAS has (aortic dimensions scaled to height). In addition, the api-
been shown to have a lasting impact on cardiac size and cal views (AP4CH, AP3CH and AP2CH) should be opti-
mised to provide technically adequate images for the

Fig. 4 Defining LV Geometry using Standard 2-dimensional Echocardiography

Oxborough et al. Echo Research & Practice (2025) 12:7 Page 9 of 34

Table 3 Extended athlete’s heart echocardiographic protocol

View and Modality Explanatory Note Image

PSAX (Aortic Valve Level) (1) Identify coronary ostia. The left
and right ostia usually originate from their
respective aortic sinuses
(2) Ensure origin is at sinus level
(3) Identify proximal courses and aim
to exclude aberrant vessel, especially
malignant course between great vessels
(aorta and pulmonary artery)

PSAX (Basal LV Level) LV wall thicknesses should be measured

from the maximum dimension at end
diastole from:
(1) Anterior septum
(2) Inferior septum
(3) Posterior/Inferolateral wall
(4) Lateral/Anterolateral wall

PSAX (Mid LV Level) LV wall thicknesses should be measured

from the maximum dimension at end
diastole from:
(1) Anterior septum
(2) Inferior septum
(3) Posterior/Inferolateral wall
(4) Lateral/Anterolateral wall
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 10 of 34

Table 3 (continued)
View and Modality Explanatory Note Image

PSAX (Mid to apical LV level) (1) Excess LV trabeculation is a common

finding in athletes
(2) LV hypertrabeculation is more preva-
lent in black athletes
(3) Red-flags—thinned compacted layer
<5 mm and regional wall motion abnor-
mality in the region of excess trabecula-
tion.
Further imaging is advised to exclude LV
hypertrabeculation/cardiomyopathy

AP4CH, AP2CH and AP3CH for GLS Provide GLS where possible. Bear in mind
the technical limitations including image
quality, foreshortening and maintaining
frame-rates as high as possible up to 90
frames per second

post-processing assessment of GLS, and all functional guideline will highlight the additional echocardiographic
indices should be clearly defined including the use of insight required to aid the differentiation between physi-
Simpsons biplane or 3DE methods for LV volumes and ological and pathological adaptation.
LV EF. Table 3 highlights the extended protocol with
examples of the required images and any technical con- Image and data interpretation
siderations. Figure 5 provides an exemplar reporting tem- We have provided a consensus of echocardiographic
plate highlighting the required measurements. During ‘normal ranges’ for chamber size and function in
the examination, it may become appropriate to draw on males and females (white and black athletes where
other guidelines including but not limited to the follow- available) derived from key studies and meta-analy-
ing references [72–77]. The subsequent sections in this ses (see Table 4). These should be used as a guide and
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 11 of 34

Fig. 5 Exemplar Echocardiographic Report

Oxborough et al. Echo Research & Practice (2025) 12:7 Page 12 of 34

Table 4 Consensus of Upper / Lower Range for Chamber Structure and Function in Athletes over 18 years of Age
Parameter Male Male BA Female Female BA

Left ventricle, left atrium and aortic root

LVEDd (mm) [81–83] 63 62 56 56
LVEDd index (mm/m2) [81] 33 – 34
IVSd (mm) [81–83] 12 15 11 12
PWd (mm) [81–83] 12 15 11 12
LVM (g) [32, 81–83] 271 442 171 271
LVMi (g/m2) [33, 34] 143 153 117 116
RWT [34] 0.44 0.51 0.43 0.48
LVEDVi (ml/m2) [81] 103 – 91 –
EF (%) [81] 47 – 47 –
GLS (%) [51, 84, 85] − 16 – − 16 –
Septal E’ (cm/s) [54] 7.7 – 7.7 –
Lateral E’ (cm/s) [54] 10.6 – 10.6 –
LAVi (ml/m2) [78] 40 – 34 –
Aortic Root (SoV) (mm) [56, 57, 86] 39 – 33 –
Aortic Root index (SoV) (mm/m) [56, 58] 20 – 19 –
Right ventricle and right atrium
RVD1 (mm) [36, 37, 40] 54 55 50 46
RVD1 index (mm/m2) [36, 37, 40] 28 27 28 27
RVD2 (mm) [36, 37, 40] 46 48 43 42
RVD2 index (mm/m2) [36, 37, 40] 24 25 25 25
RVD area (mm) [36, 37, 40] 40 38 33 29
RVD area index ­(cm2/m2) [36, 37, 40] 20 19 18 17
RA area ­(cm2) [36, 37, 40] 29 27 25 21
RVOTplax (mm) [40] 40 39 38 34
RVOTplax index (mm/m2) [40] 20 19 22 20
RVOT1 (mm) [40] 43 43 41 37
RVOT1 index (mm/m2) [40] 23 21 23 22
RVOT2 (mm) [40] 34 31 29 28
RVOT2 (mm/m2) [40] 18 15 16 16
RVOT1/RVD1 [79] 1 – 1 –
RV:LV [79] 1 – 1 –
TAPSE (mm) [37] 17 – 17 –
RVFAC (%) [36, 37] 32 – 32 –
RV S’ (cm/s) [37] 10 – 10 –

interpreted within the context of the individual ath- should also be considered such that the RV:LV ratio is
lete’s training type and volume. For example, a pure infrequently greater than 0.9 [37], atrial dilatation often
resistance-trained athlete of average body size (or occurs alongside other chamber enlargement [39, 78]
one with low training volume defined by their METS and the RVOT1:RVD1 ratio rarely exceeds 1.0 [79]. It
x duration [see Table 1]) is unlikely to have chamber is also important to note that body size impacts cardiac
sizes close to the upper cut-offs, whilst an endurance size and therefore in the extremes of anthropometry,
athlete with a high training volume is more likely to absolute chamber values may fall outside of the normal
reach values close to the cut-offs. More so, an athlete range justifying the need to include scaled values [80].
with a smaller chamber size or higher heart rate is less The following two algorithms have been proposed
likely to have functional parameters close to or below to support the interpretation of the echocardiographic
the normal range. The balanced nature of physiological LV and RV data and provide recommendations for the
adaptation and our understanding of proportionality onward management of the athlete (see Figs. 6 and 7).
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 13 of 34

Fig. 6 Left Ventricular Interpretation Algorithm

Fig. 7 Right Ventricular Interpretation Algorithm

Note that entry level into the LV algorithm draws non-athlete cut-offs and our athlete consensus data
upon the BSE non-athlete cut-offs whilst entry into the reported in these guidelines and is based on abso-
RV algorithm is based on a combination of both BSE lute values only. This conservative approach is aimed
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 14 of 34

at maximising the sensitivity of the algorithms whilst The atria and aortic root
maintaining specificity (due to the heterogeneous Dilatation of both atria is frequently observed in athletes
presentation of the athlete’s heart) and hence reduc- across a range of demographics with the magnitude being
ing the risk of false negative findings. The algorithms proportional to training volume and cardiorespiratory
do not include the use of RV or LA strain due to the fitness [88, 89]. The dilatation is unlikely to be isolated
limited athlete data available however their use is not (albeit it can be) and tends to co-exist with ventricu-
discouraged and in fact, may provide added value to lar enlargement [90]. Atrial enlargement, defined by an
conventional parameters when considering referral for indexed volume, should be interpreted as ‘normal physi-
additional assessments/ investigations. ological enlargement’ when there is no evidence of sig-
nificant valve disease or ventricular diastolic dysfunction.
The left ventricle The aortic root should be measured at the sinus of Val-
The LV algorithm starts with the definition of hyper- salva, sinotubular junction and proximal ascending aorta
trophy as per standard geometry classifications or the and should be presented as an absolute value as well as
presence of an increased wall thickness/ cavity size [71]. scaled to height [71]. The value should fall within the nor-
Based on the relatively infrequent presentation of con- mal range for non-athletes, and therefore any deviation
centric hypertrophy in athletes [32], if encountered, the from these should be interpreted as abnormal [57, 91].
echocardiographer should already be considering pathol- It is important, to note effacement or relative dilatation,
ogy, whereas if the athlete presents with eccentric hyper- particularly in the presence of a bicuspid aortic valve.
trophy the echocardiographer should primarily consider
physiology. In both instances, it is important to place
The report
the findings in context by considering training type and
The echocardiographic report should follow local guide-
volume, body size and any clinical correlates. Irrespec-
lines but with the interpretation relative to the indi-
tive, a full functional assessment is important to further
vidual athlete. Left and right ventricular geometry, size
refine the likelihood of pathological or physiological
and function should be described and interpreted in the
adaptation and is aimed at providing valuable informa-
context of the athlete’s demographics. The presence or
tion into the grey area of cardiac adaptation. The pres-
absence of congenital and valve disease should be high-
ence of an LV EF ≤ 47% or GLS ≤ − 15% should raise a red
lighted, the size and morphology of the aorta should be
flag for potential pathology whereas an LV EF ≥ 55% or
described and the identification (or failure to identify) of
GLS ≥ − 17% is more likely to represent physiology. The
the coronary ostia should be stated. A conclusion should
intermediate range including reduced diastolic function
be offered stating whether the findings are consistent
and/or LV EF between 48 and 54% and GLS of −16% may
with physiological adaptation or whether further investi-
warrant additional assessment with ESE [20].
gations are recommended.

The right ventricle Differentiation from disease

The RV algorithm starts with the criteria for RV enlarge- The following section highlights the nature of the cardiac
ment at either outflow or inflow or the presence of dis- phenotype specific to the athlete in various cardiac con-
proportionate RV inflow to outflow or RV to LV ratios. ditions whilst highlighting the challenging grey area of
Where enlargement exists, it is essential to further put diagnosis. Please also refer to the relevant BSE disease-
this into the context of the athletes training type and specific guidelines.
volume and body size and to utilise an assessment of RV
function. In the presence of reduced longitudinal func-
Hypertrophic cardiomyopathy
tion (S’ ≤ 9 cm/s and/or ≤ TAPSE 16 mm) or reduced
RVFAC (≤ 31%) then additional assessment with ESE is Hypertrophic cardiomyopathy is an autosomal dominant
indicated [87]. A comprehensive subjective assessment cardiac myocyte disease characterised by LVH, diastolic
should be applied to determine the presence or absence dysfunction, dynamic LV outflow obstruction and myo-
of regional wall motion abnormalities or aneurysms. cardial ischaemia. Between 30 and 60% of patients have
This may be supported using RV strain or 3DE; however, been found to have a pathogenic variant in genes encod-
our limited understanding of normal athlete regional ing sarcomeric contractile proteins [92]. Left ventricular
values suggests that it should not be relied upon in iso- hypertrophy is required for a clinical diagnosis: ≥ 15 mm
in at least one LV myocardial segment in the absence of
lation. If wall motion abnormalities or aneurysms are
abnormal loading conditions, or ≥ 13 mm in the context
identified on examination, then it is extremely impor-
of a pathogenic variant or family history [93].
tant to initiate the cascade for further assessment.
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 15 of 34

The prevalence of clinical HCM in adult populations identified LVED < 51 mm and septal E’ ≤ 11 cm/s as the
has been reported to be 1 in 500, with the UK biobank only positive predictors for HCM. It is important to
population suggesting a general population prevalence note that based on the heterogeneous nature of both
of LVH ≥ 15 mm in 0.11% [94]. The incidence of SCD the athlete’s heart and HCM phenotypes, the external
across a large series of reported groups was 0.43% per validity of these findings is limited.
annum (95% CI 0.37–0.50%), but more pertinently this
was reported as 1.09% (95% CI 0.69–1.73%) per annum Dilated cardiomyopathy
in young adults and children [95]. In young athletes, Four chamber dilation is the hallmark of endurance ath-
HCM is recognised as a common cause of SCD [4, 5, letes but is also noted in athletes participating in sports
7]. with a high dynamic exercise component, such as soccer
Echocardiography is typically the first line imaging and rugby [103]. High cardiac output, often sustained
tool to diagnose and assess severity of HCM. Left ven- for hours during training and competition, can lead to
tricular EF is typically normal/supranormal in HCM, marked balanced dilation of both atria and ventricles
until “end stage” disease when there is a deterioration [104]. The athlete with physiologic dilation of the LV
but reduced GLS can be seen in HCM with normal should demonstrate normal or supra-normal indices of
LVEF [96]. In athletes, GLS ≤ 15% is suggestive of path- diastolic function. Normal trans-mitral pulsed wave and
ological LVH [51, 85, 97]. LV TDI in an athlete with LV dilation are consistent with
Additional anatomical/ macroscopic features sugges- physiologic remodelling [53].
tive of a HCM phenotype may include abnormal mitral Dilation of the LV is also commonly encountered in
valve (MV) and sub-valvular apparatus [98, 99] which patients with DCM. The term DCM refers to a group
can contribute to systolic anterior motion of the MV of aetiologically heterogeneous myocardial disorders
and outflow tract obstruction in 30–50% of affected defined by LV or biventricular dilation in conjunction
individuals, a feature not seen in athletic adaptation. with global or regional systolic dysfunction not other-
Individuals with HCM can demonstrate abnormal elon- wise explained by abnormal loading conditions such as
gation of the MV leaflets (anterior MV leaflet > 30 mm, hypertension, valvular pathology, or coronary artery dis-
posterior MV leaflet height > 15 mm), abnormal papil- ease [105]. Common aetiologies of DCM include genetic
lary muscles (hypertrophy and apical displacement), alterations (i.e. Titin, Lamin A/C mutations), post-infec-
and abnormalities of the chordae including direct tious sequalae, alcohol toxicity, underlying systemic
insertion onto the anterior MV leaflet and elongation immune disorders, and tachycardia-induced myopathy.
that may result in prolapse. The additional presence of There are a subset of patients with DCM that will present
LV crypts also warrants further investigation. without systolic dysfunction and hence complicating the
A minority of athletes exhibit physiological LVH that diagnostic challenge [106].
falls within the so called ‘grey zone’ (i.e. 13–15 mm). The differentiation of DCM from benign exercise-
Studies have attempted to differentiate physiologi- induced ventricular dilation requires the integration
cal LVH from mild HCM [100, 101] and identified the of exercise training/competition history, clinical pres-
main discriminators suggestive of HCM in an athlete as entation, and echocardiographic imaging data. Benign
LVED ≤ 53 mm, LA ≤ 39 mm, abnormal diastolic func- physiologic ventricular dilation often occurs among
tion, concentric LV geometry and asymmetrical LVH asymptomatic, high functioning endurance athletes
(IVS:PW ratio ≤ 1.3). It is important to acknowledge and team athletes who participate in sports with a high
that these discriminators have been based on compari- endurance component. Dilation of the LV (or RV) in
sons between healthy athletes versus sedentary HCM athletes participating in sporting disciplines with a low
patients. In comparison with sedentary HCM patients, endurance or low dynamic exercise component should
athletes with HCM demonstrate a lesser magnitude of trigger concern for DCM. Similarly, all athletes present-
LVH (often 15-16mm), larger LV cavity dimensions and ing with impaired exercise capacity, a family history of
higher diastolic indices. There is also a lower preva- cardiomyopathy, or malignant ventricular arrhythmias,
lence of outflow tract obstruction and valve disease. alongside LV (and/or RV) dilation should be considered
Athletes with HCM can demonstrate co-existent at high risk for DCM. Ventricular dimensions are neither
physiological adaptation. In a comparison between ath- sensitive nor specific for DCM [107, 108]. Although for-
letes with HCM and healthy athletes with ‘grey zone’ mal criteria for DCM include specific cut-points for LV
LVH, LA diameter was a poor discriminator, with size, there is considerable overlap between ventricular
87% of athletes with HCM demonstrating normal LA sizes in patients with DCM and highly trained endur-
dimensions. Additionally, 14% of athletes with HCM ance athletes. Ventricular dilation of a single chamber
demonstrated LVEDD > 54 mm [54, 102]. ROC analysis
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 16 of 34

in isolation should never be considered physiologic and Arrhythmogenic cardiomyopathy

should prompt concerns for DCM. Arrhythmogenic cardiomyopathy is predominantly
Inherent in the definition of DCM is reduced systolic caused by pathogenic variants in genes encoding cardiac
and diastolic function. The finding of an LV EF less than desmosomal proteins. The population prevalence is esti-
40% and/or impaired indices of diastolic function, should mated at 1:2000–1:500. The condition is characterised by
raise concern for DCM and prompt a comprehensive myocardial fibrofatty infiltration, predisposing to ven-
diagnostic evaluation. In contrast, a mildly reduced LV tricular tachyarrhythmias and is a major cause of exercise
EF (45–50%) may be identified among highly trained related SCD in young athletes [7].
endurance athletes [109]. As such, the diagnosis of DCM The 2010 Modified Task Force Criteria focused exclu-
in an otherwise healthy endurance athlete with LV dila- sively on RV parameters for diagnosis [123], however,
tion should not be based solely on a mildly reduced LV concomitant LV involvement is now recognised in most
EF in isolation. Additional features suggesting disease, cases. This has led to a change in terminology such that
include isolated enlargement of the LV, myocardial thin- ACM with predominant RV, LV, or biventricular involve-
ning and regional wall motion abnormalities. The pres- ment may be preferable to previous nomenclature
ence of impaired GLS < − 17% should also raise the (‘arrhythmogenic right ventricular cardiomyopathy’ or
suspicion of DCM albeit the overlap with reduced GLS in ‘ARVC’).
athletes further complicates the differentiation. Among The diagnosis of ACM relies primarily on data from
endurance athletes with mildly reduced LV EF and/or resting and ambulatory ECG, imaging investigations,
GLS, assessment of LV systolic function during exercise and genetic / familial evaluation, with ‘major’ and ‘minor’
to confirm normal augmentation is warranted [110] (see thresholds within each category. Typical electrocardio-
ESE section). graphic findings include T-wave inversion in the limb
or precordial leads, frequent ventricular extrasystoles
or complex ventricular arrhythmias. The 2010 criteria
Left ventricular hypertrabeculation identified echocardiographic dilatation of the RVOT
Left ventricular hypertrabeculation in adults is charac- (proximal RVOT ≥ 36 mm or ≥ 21 mm/m2), or reduc-
terised by prominent LV trabeculae, deep intertrabecular tion in RVFAC (≤ 33%), in combination with RV regional
recesses and a thin compacted epicardial layer. In some wall motion abnormalities as imaging features of ARVC.
individuals, these changes are associated with progres- Recently proposed diagnostic criteria (the ‘Padua cri-
sive LV systolic dysfunction, ventricular arrhythmias and teria’) acknowledge the biventricular nature of this dis-
thromboembolic complications [111]. The precise aeti- ease [124]. In addition to stipulating the presence of RV
ology is unclear. Retarded intrauterine morphogenesis regional wall motion abnormalities, the Padua criteria are
has been postulated, however several mutations in genes extended to include assessment of LV function (using EF
implicated in familial cardiomyopathy have also been or GLS), and inspection for LV wall motion abnormalities
reported (e.g. in the sarcomeric protein, Z-disc, cytoskel- also incorporating the detection of myocardial fibrosis
eton and nuclear envelope) [112–116]. The structural using cMRI. There is also evidence of disproportionate
phenotype may be stimulated by acquired conditions RA enlargement in athletes with AVC. Highlighting the
associated with a high cardiac preload such as severe added value of RA volume index (RAVi) as a ratio to
valvular regurgitation, anaemia, pregnancy or following LAVi (RAVi:LAVi) [125].
intensive physical exercise [117–119]. Healthy athletes frequently exhibit ventricular dilata-
Left ventricular hypertrabeculation is observed in up tion, including that of the RV, and borderline-low/ mildly
to 8% of athletes and is generally of no concern [117, reduced resting systolic function. Indeed, around half of
119–122]. Athletes with LV hypertrabeculation might be elite athletes demonstrate RVOT enlargement numeri-
suspected of having cardiomyopathy if they exhibit car- cally exceeding major diagnostic thresholds for ACM
diac symptoms, report a family history of the disease, [40]. Anterior T-wave inversion is also observed in 4% of
show abnormal repolarisation changes on the ECG (e.g. athletes, resulting in a diagnostic grey area.
T-wave inversion in the inferolateral leads), demonstrate Differentiation between ACM and athletic remodelling
LV dysfunction with an EF below 45%, possess a com- requires a multifaceted approach [126]. Sinister cardiac
pacted myocardial layer less than 5mm at end-diastole, or symptoms such as syncope, family history of cardiomyo-
exhibit diastolic dysfunction [118]. It is typically advised pathy or premature sudden death, complex ventricular
to conduct cMRI to assess for LV fibrosis or thrombi, and arrhythmias on ambulatory monitoring or stress testing,
to perform ESE to evaluate for contractile reserve and myocardial fibrosis on cMRI, or electrocardiographic
rule out exercise-induced complex arrhythmias in these patterns not considered typical in athletes [16].
athletes.
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 17 of 34

The magnitude of structural remodelling should be coronary arteries when evaluating young athletes [75,
proportionate to the athlete’s age, gender, size, and sport- 133]. However, this is a complex process that demands
ing discipline (see Fig. 3). Profound remodelling exceed- a systematic approach, adequate time, and significant
ing thresholds in Figs. 6 and 7 should prompt further expertise [75].
investigation. Echocardiography should demonstrate For the purposes of optimising image acquisition and
balanced, symmetrical cardiac remodelling (RV/LV diagnostic yield, athlete position and comfort are cru-
ratio ≤ 0.9), whilst disproportionate RV enlargement may cial. Utilise the coronary pre-set if available and ensure
suggest pathology [126]. Regional wall motion abnormal- the transducer frequency is set for the highest harmonic
ities should not be present in healthy athletes. This can frequency. From the PLAX, the origin of the right coro-
be assessed visually, although strain assessment (reduced nary artery (RCA) from the right sinus of Valsalva may
global or segmental strain, or abnormal patterns such as be appreciated. This is particularly helpful in identify-
systolic stretch or mechanical dyssynchrony) permits a ing high take off RCAs, which arise above the sinotubu-
more objective evaluation [127]. Profoundly reduced RV lar junction (STJ). Additionally, a discrete circle in the
function (RVFAC ≤ 30%) [126] and impaired RV long axis vicinity of the ascending aorta in the PLAX view, should
function (RV S’ < 10 cm/s, or RV free wall strain < 20%) raise suspicion of an interarterial or intramural course
should be considered abnormal [127]. Borderline-low between the great vessels. The optimal view for assessing
functional indices in either ventricle should augment rap- the ostial of the coronary arteries is the PSAX view. Ath-
idly during ESE, which also permits assessment for exer- letes may need to be rotated further on to their left and
tional arrhythmias or symptoms. the transducer may need to be angled gradually supe-
riorly with gradual modified sweeping motions of the
Coronary artery anomalies probe. Optimise the image by adjusting the zoom, sector
Coronary artery anomalies encompass a wide range of width, and gain. Utilise colour flow mapping, reducing
congenital variations in the origin of a coronary artery the Nyquist limit to 30 cm/s, which assists in excluding
from the ascending aorta and/or its subsequent course. pericardial folds or venous coronary structures that may
Outcomes are highly variable and include benign and cause diagnostic dilemmas. Trace the coronary arteries
incidental findings, to more malignant CAAs associated to their origins using the cine/freeze function, focusing
with exercise related SCD [4, 7, 17]. CAAs have been on one artery at a time rather than attempting to dem-
reported to account for 9% of deaths in athletic adoles- onstrate multiple arteries in one image. As a frame of
cent individuals aged between 10 and 19 years, compared reference, the RCA typically arises at a 11–12 o’ clock
to 1% of non-athletic individuals [128]. position and the left coronary artery (LCA) typically
Anomalies where the coronary artery course runs pos- arises at a 3–4 o’clock position. Clockwise probe rotation
terior to the aorta (retroaortic) or anterior to the pul- may visualise the bifurcation of the left coronary to dem-
monary artery (pre-pulmonic) are generally not prone onstrate the left anterior descending (LAD) and left cir-
to compression during exercise and thus may be consid- cumflex (LCx) arteries; and counterclockwise rotation for
ered benign after comprehensive evaluation. In contrast, the RCA. Both standardised and non-standardised views
anomalies associated with interarterial or intramural are necessary, and any uncertainty should be acknowl-
course are typically associated with coronary obstruction, edged in the final report (see Table 5). For a comprehen-
malignant ventricular arrhythmia, or myocardial ischae- sive overview of this topic, we encourage the reader to a
mia. Additionally, a slit-like orifice or acute angle take-off recently published practical guide [75].
of the coronary artery ostia and proximal course are addi- Despite these considerations, limitations and uncer-
tional high risk factors [129]. Notably, an anomalous left tainties may exist in assessing higher or lower take-off
coronary artery arising from the right sinus of Valsalva coronary arteries, mid to distal vessel course/ termina-
(ALCA) and from the pulmonary artery (ALCAPA) have tion and intracoronary pathology. In such cases, depend-
been frequently observed in autopsy studies of SCD vic- ing on the clinical scenario, other non-invasive imaging
tims, suggesting a higher risk of exercise-related sudden modalities like computed tomography coronary angi-
death [129–131]. It is noteworthy that an anomalous CA ography (CTCA), cMRI and functional assessments to
originating from the pulmonary artery (PA) (ALCAPA or assess for CV symptoms, myocardial ischaemia and ven-
ARCAPA) is rare (0.01%), [132] and 85% of cases present tricular arrhythmia may be required. Following identifi-
in early childhood, whereas, an anomalous aortic origin cation or suspicion of a CAA, management is primarily
of a coronary artery (AAOCA) is more likely to be identi- based on expert-consensus recommendations and a
fied in adolescents and adulthood. shared decision-making approach [133–135].
Given the association of CAAs with SCD in athletes,
it is essential to thoroughly assess the origins of the
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 18 of 34

Table 5 Differentiation from disease—key points

Condition Key Points Images

Hypertrophic Cardiomyopathy Echo parameters to suggest pathological LVH in ath-

letes:
  - LVH > 15mm
  - Asymmetrical LVH
  - Concentric LVH geometry
  - LVEDD < 54mm
  - GLS < 16%
  - Abnormal MV and subvalvular apparatus
  - LVOTO/SAM
  - LV crypts
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 19 of 34

Table 5 (continued)
Condition Key Points Images

Dilated Cardiomyopathy The athlete with physiologic dilation of the LV should

demonstrate normal or supra-normal indices of dias-
tolic function.
An LV EF less than 40% and/or impaired indices of dias-
tolic function, should raise concern for DCM.
Among endurance athletes with mildly reduced LV
EF, assessment of LV systolic function during exercise
to confirm normal augmentation is warranted.
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 20 of 34

Table 5 (continued)
Condition Key Points Images

Left Ventricular Hypertrabeculation Left ventricular non-compaction is now no longer

considered to be a cardiomyopathy and is identified
as an isolated phenotypic trait or occurring in com-
bination with systolic dysfunction and ventricular
arrhythmias.
Athletes with LV hypertrabeculation in the absence
of symptoms, family history of cardiomyopathy, abnor-
mal ECG, impaired LV systolic function or complex
ventricular arrhythmias can participate in sports of any
intensity.
Athletes with LV hypertrabeculation and impaired
LV systolic function that is consistent with exercise
induced cardiac remodelling should follow the recom-
mendations for athletes with dilated cardiomyopathy
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 21 of 34

Table 5 (continued)
Condition Key Points Images

Arrhythmogenic Cardiomyopathy Most commonly RV enlargement and dysfunction,

with regional wall motion abnormalities. LV or biven-
tricular involvement is increasingly recognised.
Diagnosis of ACM is complex and requires integra-
tion of data from the ECG, ambulatory monitoring,
imaging investigations, and genetics. Newer proposed
diagnostic criteria have acknowledged LV involvement,
and the utility of echocardiographic strain assessment.
Pathology should be suspected when there is pro-
found remodelling exceeding thresholds in Figs. 6
and 7, remodelling which is disproportionate
to the athlete’s demographic profile (Fig. 3), unbal-
anced remodelling, impaired long axis function (TDI
or strain), or regional wall motional abnormalities
in either ventricle.
Vigorous augmentation of cardiac function (including
the RV) should be seen during exercise echocardiogra-
phy in healthy athletes.
A period of detraining (at least 6 weeks) should result
in partial or complete resolution of training-induced
structural and function adaptations in the RV and/
or LV.
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 22 of 34

Table 5 (continued)
Condition Key Points Images
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 23 of 34

Table 5 (continued)
Condition Key Points Images

Coronary Anomalies Optimise athlete position to acquire standardised

and non-standarised views.
PLAX view may give clues to low/high take off coro-
nary arteries, intramural course.
Emphasis on modified SAX view at AV level; with angu-
lation of probe above the AV and modified sweeping
movements with gentle clockwise and anticlockwise
rotation.
Focus on optimising the image (zoom, sector width,
gain, cine/freeze function) to adequately comment
on the (a) individual ostia of the coronary arter-
ies from the ascending aorta; and (b) any potential
abnormal course of the ostia or proximal segments
of the artery.
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 24 of 34

Table 5 (continued)
Condition Key Points Images

Myocarditis (including COVID) Myocarditis is an important cause of cardiac damage

in athletes
TDI and Strain play an important role in the identifica-
tion of regional abnormalities.
Athletes diagnosed with myocarditis required evalua-
tion in expert sports cardiology centres.
Return to play protocols should be followed to avoid
cardiac complications.

Aortic Root Disease and Bicuspid Aortic Increased intensity of sport correlates with larger aortic
Valve dimensions, but they rarely exceed normal limits even
in endurance athletes.
Bicuspid aortic valve is the commonest congenital
heart defect, present in 1-2% of the population,
with one-third developing aortic stenosis, regurgita-
tion, or aortic root dilation.
Risk of SCD is related to sudden aortic dissection,
accounting for 0.8% of SCD in athletes
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 25 of 34

Table 5 (continued)

Condition Key Points Images

Mitral Valve Prolapse Arrhythmic MVP is typically associated with myxo-
matous degeneration and prolapse of both leaflets
with a degree of mitral annular disjunction (MAD).
An increase in LV end-diastolic or end-systolic dimen-
sions/volumes or reduction in LVEF within a short
time-frame and without a change in training type
or volume are more the adverse remodelling effects
of chronic significant MR in athletes with MVP.
Disproportionate dilatation of the LA is more likely
related to the degree of MR in athletes with MVP.
ateral S’ that peaks in late systole (‘Pickelhaube sign’)
and at a velocity > 16 cm/s has been proposed
as a marker of greater arrhythmic risk in MVP and MAD.
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 26 of 34

Myocarditis (including COVID‑19) When 2D images are suboptimal, contrast echocardi-

Myocarditis is a non-ischaemic inflammatory heart mus- ography or 3DE can assist in the diagnosis of myocarditis
cle disorder and may be complicated by cardiac dysfunc- by identifying subtle regional wall motion abnormalities
tion and potentially fatal arrhythmias [11]. It is reported detecting any left ventricular thrombus. In addition, 3D
to cause 2–7% of all SCDs in young athletes [7]. Viral strain is emerging as a promising tool in the diagnosis of
infection is the most common aetiology, however other patients with acute myocarditis [146].
recognised causes including illicit drugs such as cocaine Undertaking exercise during the active phase of myo-
[136] or vaccines such as influenza [137] should be carditis may exacerbate the inflammatory response and
considered. induce malignant arrhythmias. Any athlete diagnosed
The spectrum of clinical presentation of myocarditis in with myocarditis, should be advised to refrain from
athletes is variable and ranges from asymptomatic status, structured exercise in the acute phase of the illness.
self-resolving symptoms such as mild chest discomfort, When advising on the duration of abstinence from high-
dyspnoea or fatigue, to more serious clinical sequelae intensity exercise or assessing fitness for return to com-
including decompensated heart failure or cardiogenic petitive sport, affected individuals should be evaluated
shock [138]. Cardiac enzyme markers may be elevated. and closely supervised by physicians with expertise in
In addition, the ECG may demonstrate variable findings sports cardiology in conjunction with consensus guide-
such as ST segment or T waves changes, low QRS volt- lines [133].
ages, conduction abnormalities, frequent ectopic beats
and sustained arrhythmias. Aortic root disease and bicuspid aortic valve
The gold standard method to establish a diagnosis of Aortic root disease generally relates to pathologic dilation
myocarditis is with endomyocardial biopsy; however, of the aorta which needs to be differentiated from physi-
this is an invasive procedure which has low sensitivity as ological enlargement secondary to exercise. Increased
the pattern of inflammation may be patchy and suscepti- intensity of sport correlates with larger aortic dimen-
ble to sampling of non-inflamed tissue. Cardiac MRI has sions, however even in endurance athletes who have
evolved as a useful and reliable investigation to establish the largest diameters, very rarely does this enlargement
a prompt diagnosis by detection of ventricular dysfunc- fall outside of normal limits [147, 148]. A meta-analysis
tion, myocardial inflammation or scar [139]. showed the aortic root (SoV) was only 3.2 mm larger in
Two-dimensional echocardiography is the first line athletes compared to controls, but still within normal
imaging modality. Diagnostic features of acute myocar- limits [148].
ditis include regional wall motion abnormalities, LV/RV Bicuspid aortic valve (BAV) is the most common con-
systolic or diastolic dysfunction, ventricular dilatation, genital heart defect, present in 1–2% of the population
pericardial effusion and an increase in LV mass or ven- with 30–50% of individuals developing aortic stenosis,
tricular wall thickening [140]. While 2D echocardiogra- regurgitation, or aortic root dilation [149, 150].
phy may not detect wall motion abnormalities, additional Although it is often straight forward to distinguish a
techniques, such as TDI, strain imaging, contrast echo- bileaflet from trileaflet aortic valve on echocardiogra-
cardiography, or 3DE may unmask subtle cardiac func- phy, the true challenge lies in distinguishing physiologi-
tion abnormalities. cal aortic dilation from an underlying aortopathy. The
Tissue Doppler parameters may be abnormal in both risk of SCD in individuals with aortopathy is related to
athletes and non-athletes with myocarditis [141–143]. sudden aortic dissection, accounting for 0.8% of SCD in
Strain imaging may detect early ventricular dysfunction athletes [7]. Aortic dissection becomes increasingly likely
in individuals with acute myocarditis. In a study of non- with a dilated aorta due to increased shear wall stress on
athletes with acute myocarditis and preserved LVEF, a a thinned enlarged aorta, and an underlying wall abnor-
significant reduction in GLS was demonstrated when mality in the aorta. This risk of SCD will, therefore, be
compared to healthy controls [144]. Other studies have magnified for those doing high intensity or highly iso-
identified that strain measurements are more sensitive metric sports with dissection due to increased blood
than 2D echocardiography in identifying subtle regional pressure and subsequent wall stress during exercise. In
wall motion abnormalities and diagnosing acute myocar- addition, a dilated aortic root can lead to progressive aor-
ditis [144, 145]. Strain analysis can also be useful to assess tic regurgitation due to failure of coaptation of the aortic
improvements in ventricular function over time as the valve leaflets.
inflammatory process resolves. The assessment of strain Although there may be subtle clinical signs of BAV at
should therefore be routinely used in patients with sus- auscultation, this is unreliable and clinical examination
pected or recovering myocarditis. rarely forms part of many pre-participation screening
protocols. Moreover, aortic root dilation in an athlete is
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 27 of 34

impossible to detect clinically, unless there are associated between the MV annulus, the LA wall and the basal
clinical features of an underlying connective tissue disor- region of the LV myocardium [152]. While there is some
der, such as Marfan’s syndrome. guidance for the echocardiographic measurement of
Echocardiography is, therefore, an important investi- MAD length [153], with > 8.5 mm reportedly identifying
gation in PPS. Although assessment of the aortic valve 67% of patients who experienced non-sustained ventric-
and aortic root are key aspects of any echocardiographic ular tachycardia on Holter [154], care must be taken to
examination, this is particularly pertinent in the young ensure accurate measurement when the posterior leaflet
athlete. An important caveat to the use of echocardi- hinge-point becomes masked as the leaflet base becomes
ography is that the aortic root is usually symmetrical in ‘muralised’ with the LA wall in late systole.
orthogonal planes however in certain aortopathies there Lateral TDI may reflect abnormal myocardial mechan-
can be asymmetric dilation, and so the typical PLAX ics secondary to bileaflet prolapse and hence can aid in
view may underestimate the size of the aortic root. 3D identifying arrhythmic risk [155]. Lateral S’ that peaks
echocardiography may be helpful in these athletes to bet- in late systole (‘Pickelhaube sign’) and at a velocity > 16
ter quantify the size of the aorta. cm/s has been proposed as a marker of greater arrhyth-
An aortic root dimension of > 39 mm (males) and > 33 mic risk associated with fibrosis and late Gadolinium
mm (females) or scaled/height of > 20 mm/m (males) enhancement on cMRI [155]. In those with proven ven-
and > 19 mm/m (females) is likely to represent patho- tricular arrhythmia, a high ectopic burden can lead to LV
logical dilation [56–58]. A universal sex-based cutoff dilatation and impairment. In the setting of high ectopic
however is fraught with danger as it may lead to smaller burden, careful assessment of MR severity, including the
athletes with a comparatively large aortic root being duration of MR and its impact on regurgitant volume, is
passed as normal. It is important to scale the aortic root crucial to elucidate the true cause of LV dilatation and
measurement in accordance with body size and, although impairment.
body surface area has been used previously, the use of Athletic cardiac remodelling is characterised by
height alone removes inconsistencies related to weight enlargement of all cardiac chamber dimensions and
change [56]. Similarly, it is essential to use a reproducible therefore, a mild degree of functional MR is common
measurement technique for serial root measurements in athletes secondary to both LA and LV dilation. This,
and the inner-edge to inner-edge methodology in end- however, does not become haemodynamically signifi-
diastole, defined as the onset of the QRS complex is rec- cant when valve morphology is normal. The diagnostic
ommended [71]. Care must be taken in interpreting the challenge arises in athletes who present with MVP and
clinical significance of measurements in syndromic aor- moderate to severe chronic mitral regurgitation and
topathies. As we learn more about genotype/phenotype LV dilatation. Consideration of interval changes in LV
interactions the aortic size at which dissection occurs size or function are key. An increase in LV end-diastolic
may be lower in certain high-risk genotypes [151]. or end-systolic dimensions/volumes, or reduction in
LVEF within a short time-frame and without a change in
training type or volume are more likely to represent the
Mitral valve prolapse adverse remodelling effects of chronic significant MR,
Mitral valve prolapse (MVP) is defined as the systolic dis- especially when the LV diameter exceeds 60 mm [156].
placement of one or both mitral leaflets above the plane Additionally, low forward resting SV is contradictory to
of the annulus and affects 1–3% of the general population the athlete’s heart and will reflect the large regurgitant
[133]. Although it is a common cause of mitral regurgita- volume. Estimating the regurgitant fraction in conjunc-
tion (MR) it is also associated with ventricular arrhyth- tion with SV is helpful in this setting with a low SV and
mia and SCD in young individuals [arrhythmic mitral a high regurgitant fraction indicative of pathological LV
valve prolapse (AMVP)]. The incidence of SCD second- dilation secondary to significant MR.
ary to AMVP is uncertain although it has been reported The presence of severe MR will further elevate LV
to account for 2–4% of SCD in competitive and non- preload and reduce afterload and hence LV EF and GLS
competitive athletes [7]. Echocardiography can play an are often elevated in this setting, typically with values of
important role in patients with MVP by providing find- greater than 60% and − 18%. Therefore, a finding of low
ings that may raise suspicion of an increased arrhythmic LVEF or low GLS in an athlete with chronic severe MR
risk. should also raise the suspicion of impaired LV systolic
Arrhythmic MVP is typically associated with myxo- function.
matous degeneration and prolapse of both leaflets with Left atrial dilatation is common in both athletic adapta-
a degree of mitral annular disjunction (MAD). Mitral tion and MR. However, increases in LA volume second-
annular disjunction describes the distinct separation ary to athletic adaptation are likely to be accompanied
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 28 of 34

by dilatation of all cardiac chambers, including the right there is also an increased oxygen demand imposed on the
atrium. Disproportionate dilatation of the LA is more working myocardium. A healthy athletic individual with
likely related to the degree of MR in athletes with MVP. normal coronary arteries will have an enhanced supply
Similarly, an elevated resting pulmonary pressure should of blood to match the increasing demand for oxygen and,
raise the suspicion of an increased haemodynamic bur- hence, will be able to meet the required cardiac reserve.
den from the co-existing MR and MVP. Athletic individuals with inherited cardiomyopathy,
myocarditis or underlying coronary artery disease have
compromised myocardial function that may limit the
Additional assessment heart in responding to the increasing challenges of exer-
Exercise stress echocardiography cise [20, 158–160]. This can be observed as a reduced
Acute aerobic exercise poses a significant challenge to cardiac reserve from a blunted functional response and/
the cardiovascular system. The heart responds with an or direct impairment [50] and serves as the rationale for
elevation in HR and enhanced myocardial contractility/ incorporating ESE in the routine evaluation of athletes
relaxation to provide a higher SV and cardiac output. with borderline resting ventricular function. The primary
Athletic conditioning results in physiological cardiac aim of ESE is to unmask the resting grey zone of the ath-
chamber enlargement and therefore the athlete is well lete heart and enhance the accuracy of diagnosing under-
conditioned in this regard to generate the higher car- lying cardiac disease.
diac outputs required for performance. Despite showing Although there is anecdotal evidence to support bed-
excellent function and HR during intense exercise [157], side methods such as leg raises or squats, there is cur-
athletes often exhibit a lower resting LV and RV function rently no agreed consensus on the specific protocols that
(reduced EF, RVFAC and GLS) when compared to non- should be employed for undertaking ESE in an athletic
athletic individuals [20, 26, 46, 49]. population [161]. It is however sensible to suggest that
The difference between resting and maximum contrac- an athletic individual should undergo an exercise proto-
tility and HR is termed the cardiac reserve and secondary col (as opposed to a pharmacological stimulus) using a
to lower basal values, this reserve is greater in athletes dedicated supine cycle ergometer where available. This
compared to the non-athlete [110], contributing to an allows for a true physiological stress whilst enabling
enhanced cardiovascular performance. During exercise, diagnostic quality echocardiographic images. If a supine

Fig. 8 Suggested exercise echocardiography protocol

Oxborough et al. Echo Research & Practice (2025) 12:7 Page 29 of 34

cycle ergometer is unavailable, then an upright cycle or combined volume and function of both the inflow and
treadmill can be used but are associated with the addi- the outflow. This limitation is critical when evaluating
tional challenges to image quality when acquired during regional dysfunction in certain cardiomyopathies such as
exercise. The design of the protocol should be aimed at ACM. Data from cMRI highlights unique RV remodelling
pushing the athlete to a maximum HR (based on a value in endurance athletes and its correlation with exercise
obtained from previous cardiopulmonary exercise testing capacity [166], particularly dilatation towards the outflow
or using the generally accepted equation of (220-athlete of the infundibulum. This data alongside evidence of dis-
age) [162]). The maximum HR is achieved by gradually tinct 3D mechanics [21] underscores the potential added
increasing the intensity of exercise through increments value of 3DE in this setting. We, therefore, acknowledge
in workload with the magnitude of the increments being the role of 3DE as a follow-up investigation where con-
flexible and dependent on the athlete’s cardio-respira- ventional imaging is inconclusive or identifies potential
tory fitness. For example, an increase of 50 watts every maladaptation and regional dysfunction. The diagnostic
2 min would allow a very fit athlete to reach their maxi- algorithms presented here highlight the role of 3DE as a
mum HR within 10 min whereas increments of 30 watts second line investigation.
would allow a similar test duration in a less fit individual.
The protocol should always include a recovery period Conclusion
allowing the HR and contractile state to return to close Echocardiography is a fundamental tool in the assess-
to baseline levels. Echocardiographic images should be ment of the young athlete’s heart. These guidelines
acquired at baseline, throughout the protocol at each highlight the importance and the effective role of echo-
workload increment and into recovery. An alterna- cardiography in the differentiation of physiological from
tive is to acquire images at a percentage of the athlete’s pathological adaptation. The systematic approach is
HR reserve (defined as maximum HR—basal HR [162]) detailed within and includes the integration of pre-echo-
which allows for direct comparison between individuals cardiographic Information, the standardised examina-
of varying fitness. tion, and the evidence-based interpretation along with
The choice and prioritisation of echocardiographic the potential for an extended role of additional modalities
images should be focused and relative to the differential including ESE and 3DE. With adherence to these guide-
disease for assessment but should address the balance lines, the BSE and Cardiac Risk in the Young, aim for
between clinical value and time. Alongside acquiring the improved detection of cardiovascular disease in this pop-
echocardiographic images (with inherent rhythm ECG), ulation and highlight this as ‘best practice’ in the assess-
systemic blood pressure, HR and symptoms should also ment of the young athlete.
be recorded. Figure 8 provides an exemplar protocol for
ESE in an athletic individual.
Author contributions
All authors contributed to conception and design and contributed directly to
3D echocardiography sections of the guideline. All authors critically revised the manuscript and gave
Three-dimensional echocardiography enables compre- final approval.
hensive assessment of cardiac volume, providing a more Funding
accurate view of the morphological changes in the ath- No funding.
lete’s heart compared to 2D imaging. While data on 3DE
Data availability
assessment of the athlete’s heart are limited, current 3DE No datasets were generated or analysed during the current study.
studies consistently reveal ventricular enlargement and
lower resting function in athletes with high endurance Declarations
training, mirroring those obtained by 2D echocardiogra-
phy [21, 163, 164]. Noteably, 3DE LV volume assessments Competing interests
The authors declare no competing interests.
demonstrate greater concordance with cMRI [165] than
conventional echocardiography in various non-athlete Clinical Trial Number
populations and in a relatively small but well charac- Not Applicable.

terised athlete population [163]. Importantly this study Author details

highlighted the capacity to detect changes over time with 1
Research Institute for Sport and Exercise Sciences and the Liverpool Centre
analogous findings observed between modalities at a for Cardiovascular Science at Liverpool John Moores University, Tom Reilly
Building, Byrom Street, Liverpool L3 3AF, UK. 2 Hull University Teaching Hos-
2-year follow-up. These findings were reciprocated in RV pitals NHS Trust, Kingston‑Upon‑Hull, UK. 3 Heart Unit, Birmingham Women’s
volumes and EF, which highlights arguably the greatest and Children’s NHS Foundation Trust, Birmingham, UK. 4 University Hospital
benefit of 3DE. The non-uniform RV geometry constrains of Wales, Cardiff, UK. 5 Department of Cardiology, Royal Brompton & Harefield
NHS Foundation Trust, London, UK. 6 Bradford Teaching Hospitals NHS Founda-
standard 2D assessments, particularly in quantifying the tion Trust, Bradford, UK. 7 University Hospital Southampton NHS Foundation
Oxborough et al. Echo Research & Practice (2025) 12:7 Page 30 of 34

Trust, Southampton, UK. 8 Imperial College Healthcare NHS Trust, London, Cardiology of the Working Group of Cardiac Rehabilitation and. Eur
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