Impact of Myocardial Fibrosis in Endurance Athletes: A Systematic Review

Abstract

Regular physical exercise is undoubtedly associated with cardiovascular health benefit, increased longevity, and improved endurance performance. Competitive endurance athletes exceed the recommended exercise dose, which lead to pathologic cardiac remodeling such as myocardial fibrosis. This review examines the impact of myocardial fibrosis on atrial and ventricular structures and functions in endurance athletes. A systematic literature search identified eight trials that enrolled 470 athletes. The prevalence of myocardial fibrosis ranged from 13% to 48%, which was commonly of a focal nonischemic pattern. The included studies did not find consistent results on the impact of myocardial fibrosis on ventricular function and volume parameters. Moreover, the prognostic implications of myocardial fibrosis on patient clinical outcomes, such as arrhythmias and mortality, were not reported as there was no long-term follow-up. There is a clear unmet need to encourage larger studies on myocardial fibrosis phenotypes to shed more light on the underlying mechanism, clinical consequences, and prognosis.

INTRODUCTION

Regular exercise or training has an overall and cardiovascular health benefits,[1,2] decreases disability rates, and may prolong life expectancy. However, there are safe limits for training above which harm (e.g., metabolic derangements, cardiovascular stress, and musculoskeletal injury) may overweigh benefits. Endurance athletes who train for competitions, usually perform strenuous exercises for hours on a daily basis with an accumulated workload of 200–300 metabolic equivalents hours in a week, which exceeds the standard exercise training dose, recommended for preventing coronary heart disease, by 5 to 10 folds.[2] Cardiac remodeling, a known physiologic adaptation, caused by endurance exercise[2,3] comprises enlarged dimensions of left and right ventricles,[1,2,3] increased size of left atrial cavity,[2,3] increased thickness of left ventricular wall and myocardial mass,[1,2] and development of left ventricular hypertrophy.[1] Strenuous exercise is accompanied by a rise in catecholamine release, heart rate, cardiac biomarkers (e.g., cardiac troponin, creatinine kinase-MB, NT-pro brain natriuretic peptide) level, oxygen demand, fatty acid metabolism,[1] and inflammatory markers level.[4]

Several studies reported increased myocardial fibrosis rate with prolonged and intensive training in asymptomatic athletes[1,3,4] in comparison with age-matched inactive general population. The presence of myocardial fibrosis is a negative prognostic factor for cardiac events.[5] Cardiac magnetic resonance imaging (CMR) has advantages over other imaging modalities (i.e., echocardiography and cardiac computed tomography) in detecting myocardial fibrosis by providing a comprehensive cardiac evaluation due to its multiparametric abilities.[5] CMR visualizes myocardial fibrosis by the late gadolinium enhancement (LGE) technique[4] that differentiates the focal myocardial fibrosis areas from the normal myocardium.[5] Myocardial fibrosis pattern can be broadly categorized into ischemic and nonischemic fibrosis. The ischemic type appears as an infarct and involves the sub-endocardium, which is usually territorial or sometime transmural. In the nonischemic type, myocardial fibrosis may be focal or diffuse (i.e., patchy), located in the mid-wall (i.e., mid-myocardium) or subepicardially,[4,6] as observed in myocarditis and various cardiomyopathies.[4] Endurance athletes, who are asymptomatic with a normal electrocardiogram, demonstrate various myocardial fibrosis patterns, which are usually of nonischemic type.[7] The currently published systematic reviews focused on the prevalence and the characterization of myocardial fibrosis in athletes,[1,3,8] without adequate data on the impact of myocardial fibrosis on cardiac structure and function as well as its clinical implications in endurance athletes. Herein, this review examines the impact of myocardial fibrosis on atrial and ventricular structures and functions in endurance athletes.

METHODS

Search strategy

A systematic literature search using MEDLINE and EMBASE was conducted on February 5, 2023 and updated on February 1, 2025. The electronic search aimed to identify the studies that described or examined myocardial fibrosis in endurance athletes. The key terms that were used are “endurance training,” “physical endurance,” “exhaustive,” “intensive,” “extreme,” “strenuous,” “athlete,” “athletes,” “myocardium,” “fibrosis,” “myocardial fibrosis,” “magnetic resonance imaging,” “gadolinium enhancement,” “LGE,” and “gadolinium.” The terms were combined with Boolean operators “AND” and “OR” to refine the literature search. There were no limits used in this electronic search. A manual search of the references of the identified articles was performed to find additional studies.

Study selection

The literature record was screened at the title and abstract levels. Ineligible articles were excluded, and potential abstracts were retrieved in full texts. Case reports, conference posters, proceedings, abstracts, and studies in nonadult participants were excluded. Reviews were also excluded but were used in the manual search. Eligible studies investigated the impact of myocardial fibrosis in endurance athletes by comparing relevant outcomes between athletes with or without myocardial fibrosis. Myocardial fibrosis should be assessed by CMR and defined as LGE positive (i.e., the sign of myocardial fibrosis). In addition to the presence or absence of myocardial LGE, its extent was quantified as size in percentage of the total left ventricular mass and/or as mass in grams.[9] The studies should enroll asymptomatic adult endurance athletes in any sport discipline without known cardiovascular diseases such as arrhythmogenic or hypertrophic cardiomyopathy. Endurance athletes as study participants were defined according to the individual study in terms of competition experience, training history or exposure, and training load or intensity. Outcomes measures of interest included CMR measurements related to ventricular and atrial functions and volumes such as left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left atrial end-diastolic volume index (LAEDVi), left atrial end-systolic volume index (LAESVi), left atrial ejection fraction (LAEF), right atrial end-diastolic volume, right atrial end-systolic volume, right ventricular end-diastolic volume (RVEDV), right ventricular end-systolic volume (RVESV), and so forth.

RESULTS

Study screening

A total of 431 records were screened on the title and abstract levels. Among the 383 identified records after removing duplicates, 43 articles were retrieved in full texts [Figure 1]. Out of 43 retrieved full-text articles, eight studies were included in the qualitative synthesis of the review.[10,11,12,13,14,15,16,17] The studies investigated the impact of myocardial fibrosis on competitive athletes’ performance,[15] left ventricular function,[16] cardiac dysfunction and myocardial injury occurrence,[17] left ventricular diastolic filling,[10] or cardiac structure and function.[12]

Figure 1.

PRISMA flow chart of literature search

Study characteristics

The eight observational studies enrolling 470 asymptomatic endurance athletes were conducted in three European countries (Germany, Spain, and the United Kingdom) between 2014 and 2019. The number of athletes in each study ranged from 9 to 101, excluding the participants in the nonathlete control groups [Table 1]. Two studies did not include control groups.[12,16]

Table 1.

Baseline athletes’ characteristics in included studies

Author Size	Main country	Recruitment period	Age (years)	Male gender (%)	BSA (m2) and/or BMI (kg/m2)	Training inclusion criteria description
Chen et al., 2023[10] n=101	Germany	2014–2019	43±11	100	1.99±0.13 m2	Inclusion: Endurance training for minimum of 10 h/week and participation in competitions in last 3 years Type: triathlon
Domenech-Ximenos et al., 2020[11] n=93	Spain	2015–2017	35.7±5.8	52.7	1.78±0.18 m2	Inclusion: Highly-trained endurance athletes (20–45 years) with minimum of 12 h/week in previous 5 years Type: Not specified Exposure: 13.7±7.7 year Load: 7619±2837 METs × min/week
Eijsvogels et al., 2017[12] n=9*	United Kingdom	-	58±5	100	24.1±2.5 kg/m2	Participant: Lifelong veteran endurance athletes Type: Running, rowing, and triathlon Exposure: 43±5 years
Farooq et al., 2023[13] n=50	United Kingdom	August–December 2018	56 (53–64)	100	24.0 kg/m2 (calculated)	Inclusion: >10 h/week for >15 years and competed regularly Type: Cycling and triathlon Exposure: 15 years
Ragab et al., 2023[14] n=55**	Germany	2014–2016	44±8	100**	LGE+: 1.85±0.15# LGE−: 1.97±0.14 m2, P<0.05 LGE+: 21.7±1.9# LGE−: 23.3±1.8 kg/m2, P<0.05	Inclusion: At least 10 h/week of regular training and a history of at least 1 completed marathon race Type: Running Exposure: LGE+: 12±9 versus LGE−: 11±6 years, P=0.678
Tahir et al., 2018[15] n=54	Germany	2014–2016	44±10	100	1.98±0.1 m2 23.6±2.3 kg/m2	Inclusion: Minimum training of 10 h/week and regular participation in competition at various distances in the previous 3 years Type: Triathlon Exposure: LGE+: 15±7 versus LGE−: 13±8 years, P=0.40 Maximal power: 409±110 W Exercise time: 12±3 min Ramp load: 31±5 W/min
Tahir et al., 2019[16] n=78	Germany	2014–2017	43±11	100	1.98±0.13 m2 23.7±2.3 kg/m2	Inclusion: Training ≥10 h/week and regular participation in competitions of various distances in the past 3 years Type: Triathlon Exposure: LGE+: 15±7 versus LGE−: 13±8 years, P=0.329 load: LGE+: 11.0±3 versus LGE−: 11.0±4 h/week, P=0.933
Tahir et al., 2020[17] n=30	Germany	-	LGE+: 49±8# LGE−: 42±10	100	LGE+: 1.96±0.16# LGE−: 2.02±0.14 m2, P=0.294 LGE+: 25.0±2.7 LGE−: 23.3±1.7 kg/m2, P<0.05	Inclusion: Minimum training 10 h/week and regular participation in competitions in the past 3 years Type: Triathlon

*Sub-study of Wilson et al.,[29] **Male subgroup as LGE+ was detected in males (1 female only had LGE+), ^#Not reported for overall group. BMI: Body mass index, BSA: Body surface area, LGE−: Negative late gadolinium enhancement, LGE+: Positive late gadolinium enhancement, MET: Metabolic equivalent of task

Athletes baseline and training characteristics

The mean age of the enrolled athletes ranged from 35 to 58 years, and they were predominantly males; 100% males in all the studies except in one (52.7%).[11] The body surface area and body mass index ranged from 1.78 m to 2.02 m and from 21.7 to 25.0 kg/m², respectively. Triathlon was the most frequent athletic sport that endurance athletes participated in. The mean lifetime training exposure varied between the reporting studies (11–43 years)[11,12,13,14,15,16] with a minimum weekly load of 10 h [Table 1]. There was not statistical difference between athletes with or without LGE in terms of training and competition history (i.e., cumulative active years of training,[11,12,13,14,15,16] training hours per week,[13,14,16] or numbers of competitions.)[14,15]

Prevalence, pattern, location, and extent of myocardial fibrosis

The prevalence of myocardial fibrosis in endurance athletes varied considerably between studies (13% to 48%). The myocardial fibrosis was mainly focal and of nonischemic and myocarditis pattern. The right ventricle insertion point seems to be the most frequent location of the myocardial fibrosis. The overall size of the fibrosis was approximately 3% of the left ventricle [Table 2].

Table 2.

Prevalence and characteristics of myocardial fibrosis

Study	Prevalence (%)	Pattern	Location	Size	Mass
Chen et al., 2023[10]	20/101 (19.8)	Nonischemic Focal Typical for myocarditis	Anterolateral, inferolateral, and inferior segments of basal LV wall	3.6±2.4% of LV	-
Domenech-Ximenos et al., 2020[11]	35/93 (37.6)	Focal	Inferior interventricular septum, where RV attaches to the septum (insertion point or hinge point)	Small	-
Eijsvogels et al., 2017[12]	4/9 (44.4)	Nonspecific in 3 athletes Myocarditis pattern in 1 athlete	Near the insertion points of RV free wall on LV in 3 athletes In epicardial lateral wall in 1 athlete	-	1–8 g
Farooq et al., 2023[13]	24/50 (48)	Nonischemic	Mid-myocardium of basal lateral wall of LV	3.0±4.0 mL (volume)	-
Ragab et al., 2023[14]	7/55 (13)	Ischemic in 1 athlete Nonischemic in 6 athletes	Midmyocardial or subepicardial in 7 athletes Subendocardial in 1 athlete	2.5±1.8% of LV	1.9±1.8 g/m2
Tahir et al., 2018[15]	9/54 (16.7)	Focal, nonischemic pattern	Subepicardial in 5 athletes (typical myocarditis) Posterior RV insertion point in 2 athletes (typical for RV pressure overload)	3.5±2.8% (0.5%–9.2%) of LV	2.9±2.3 g/m2 (0.5–7.4)
Tahir et al., 2019[16]	15/78 (19.2)	Myocarditis pattern in 13 triathletes	Subepicardial and mid-myocardial locations, and at posterior RV insertion point	Global LGE: 2.9±2.3 (0.5%–9.2%) Segmental LGE: 13.6±13.1% (range 0.3%–53%) per segment in 38 LGE+ segments	Global mass: 2.2±2.0 g/m2 (0.3–7.4)
Tahir et al., 2020[17]	10/30 (33.3)	Nonischemic pattern in all, with typical myocarditis pattern in 8 triathletes	Posterior RV insertion point, subepicardial and mid-myocardial location	2.8±1.7% of LV	2.2±1.6 g/m2

LGE: Late gadolinium enhancement, LV: Left ventricle/ventricular, RV: Right ventricle/ventricular

Outcomes

Function and volume of ventricles

All the included studies reported ventricular CMR measurements for function and volumes. In five studies, there was no statistically significant difference between athletes with or without LGE in terms of ventricular function and volumes.[10,11,13,14,15] Eijsvogels et al. suggested that athletes with LGE had larger heart dimensions than athletes without it (LVEDV [205 ± 24 vs. 173 ± 18 ml] and posterior wall thickness [11 ± 1 vs. 9 ± 1 mm]), without reported differences in LVESV, RVEDV, and RVESV between the groups. However, their study was a case series of total of nine athletes.[12] In another two studies, left ventricular mass index was significantly higher in athletes with positive LGE ([89 ± 12 vs. 81 ± 12 g/m², P < 0.05],[16] and [88 ± 7 vs. 78 ± 10 g/m², P < 0.01][17]) [Table 3].

Table 3.

Outcome measures

LGE+ versus LGE−
Study	Biomarkers	CMR (Left heart)	CMR (Right heart)
Chen et al., 2023[10] LGE+: n=20 LGE−: n=81	Troponin T 7±5 versus 6±8 pg/mL, P=0.661 NT-proBNP 58±108 versus 33±26 pg/mL, P=0.057	Ventricle CI: 3.29±0.69 versus 3.22±0.6 L/min/m2, P=0.653 LVEF: 61±8% versus 61±5%, P=0.778 LVEDVi: 98±12 versus 100±14 mL/m2, P=0.529 LVESVi: 38±9 versus 40±9 mL/m2, P=0.480 LVSVi: 60±10 versus 61±9 mL/m2, P=0.809 LV mass index: 88±10 versus 80±12 g/m2, P<0.01 Atrium LAEF: 56±9% versus 60±9%, P=0.091 LAEDVi: 21±7 versus 18±8 mL/m2, P=0.101 LAESVi: 49±12 versus 45±11 mL/m2, P=0.171 LV diastolic filling Early peak-filling rate: 212±73 versus 216±58 mL/s/m2, P=0.798 Atrial peak-filling rate: 149±50 versus 120±46 mL/s/m2, P<0.05 Peak-filling rate ratio: 1.56±0.67 versus 2.07±1.03, P<0.05	Ventricle RVEF: 60±8% versus 57±6%, P=0.097 RVEDVi: 103±21 versus 105±16 mL/m2, P=0.564 RVESVi: 42±12 versus 46±11 mL/m2, P=0.117 RVSVi: 61±14 versus 59±10 mL/m2, P=0.465 Atrium RAEF: 43±10% versus 45±11%, P=0.546 RAEDVi: 31±10 versus 31±11 mL/m2, P=0.844 RAESVi: 54±14 versus 56±14 mL/m2, P=0.501
Domenech-Ximenos et al., 2020[11] LGE+: n=49 LGE−: n=44	-	LVEF: 57±5% versus 58±5%, P=0.372 LV mass indexed: 60±12 versus 61±10 g/m2, P=0.798 LVEDVI: 102±15 versus 105±14 mL/m2, P=0.381 LVESVI: 43±9 versus 44±8 mL/m2, P=0.792 LVSVI: 57±8 versus 60±9 mL/m2, P=0.125	RVEF: 52±4% versus 54±6%, P=0.228 RVEDVI: 101±19 versus 102±18 mL/m2, P=0.717 RVESVI: 48±10 versus 47±11 mL/m2, P=0.909 RVSVI: 52±9 versus 55±10 mL/m2, P=0.257
Eijsvogels et al., 2017[12] LGE+: n=5 LGE−: n=4	-	LVEF: 64±4% versus 65±6% LVEDV: 205±24 versus 173±18 mL LVESV: 74±13 versus 61±17 mL LVSV: 131±22 versus 112±6 mL LV length: 91±7 versus 86±6 mm LV mass: 154±14 versus 140±16 g IVSd: 12±2 versus 10±1 mm PWd: 11±1 versus 9±1 mm	RVEF: 66±6% versus 64±5% RVEDV: 198±32 versus 177±16 mL RVESV: 69±20 versus 64±14 mL RVSV: 129±18 versus 114±7 mL
Farooq et al., 2023[13]	-	Ventricle LVEF: 58±5% versus 58±6%, P=1.0 LVEDVi: 108±17 versus 105±15 mL/m2, P=1.0 LV mass index: 80±11 versus 78±8 g/m2, P=0.31	Ventricle RVEF: 55±8% versus 57±9%, P=1.0 RVEDVi: 110±19 versus 107±17 mL/m2, P=1.0
Ragab et al., 2023[14]	Troponin T 6±3 versus 6±7 pg/mL, P=0.438 NT-proBNP 42±18 versus 38±28 pg/mL, P=0.304	LVEF: 65±6% versus 63±10%, P=0.729 LVEDVi: 90±7 versus 90±19 mL/m2, P=0.640 LVESVi: 31±4 versus 33±9 mL/m2, P=0.672 LVSVi: 58±9 versus 58±12 mL/m2, P=0.947 LV mass index: 86±18 versus 73±14 g/m2, P<0.05	RVEF: 58±6% versus 57±10%, P=0.928 RVEDVi: 103±11 versus 104±21 mL/m2, P=0.0.851 RVESVi: 42±6 versus 44±13 mL/m2, P=0.717 RVSVi: 61±8 versus 60±12 mL/m2, P=0.860
Tahir et al., 2018[15] LGE+: n=9 LGE−: n=45	Troponin T 9±6 versus 7±10 pg/mL, P=0.635 NT-proBNP 89±160 versus 38±31 pg/mL, P<0.05	LVEF: 62±7 versus 63±5, P=0.623 LVEDVi: 96±13 versus 98±13 mL/m2, P=0.716 LVESVi: 37±8 versus 37±9 mL/m2, P=0.971 LVSVi: 59±13 versus 61±8 mL/m2, P=0.573 LV mass index: 93±7 versus 84±11 g/m2, P<0.05 Extracellular volume: 25±3 versus 21±3 g/m2, P<0.001 Cellular volume: 69±6 versus 64±9 g/m2, P=0.131	RVEF: 59±9% versus 57±7%, P=0.406 RVEDVi: 98±17 102±15 mL/m2, P=0.497 RVESVi: 40±9 versus 44±10 mL/m2, P=0.216 RVSVi: 59±16 versus 58±9 mL/m2, P=0.859
Tahir et al., 2019[16] LGE+: n=15 LGE−: n=63	Troponin T 7±5 versus 7±9 pg/mL, P=0.734 NT-proBNP 63±125 versus 35±29 pg/mL, P=0.107	CI: 3.3±0.6 versus 3.3±0.7 L/min/m2, P=0.860 LVEF: 62±6% versus 62±5%, P=0.958 LVEDVi: 96±13 versus 100±13 mL/m2, P=0.332 LVESVi: 36±7 versus 38±9 mL/m2, P=0.492 LVSVi: 59±11 versus 62±7 mL/m2, P=0.400 LV mass index: 89±12 versus 81±12 g/m2, P<0.05	RVEF: 59±7% versus 57±6%, P=0.247 RVEDVi: 101±19 versus 103±16 mL/m2, P=0.670 RVESVi: 41±10 versus 45±11 mL/m2, P=0.230 RVSVi: 60±14 versus 58±9 mL/m2, P=0.512
Tahir et al., 2020[17] LGE+: n=10 LGE−: n=20	Troponin T 8±6 versus 6±3 pg/mL, P=0.427 NT-proBNP 88±150 versus 34±23 pg/mL, P=0.119	Ventricle CI: 3.5±0.8 versus 3.3±0.5 L/min/m2, P=0.594 LVEF: 64±8% versus 61±5%, P=0.343 LVEDVi: 100±16 versus 102±14 mL/m2, P=0.765 LVESVi: 36±9 versus 40±8 mL/m2, P=0.253 LV mass index: 88±7 versus 78±10 g/m2, P<0.01 LV septum: 12±2 versus 11±1 mm, P<0.05 Atrium LAEDVi: 22±7 versus 16±6 mL/m2, P<0.05 LAESVi: 53±14 versus 44±10 mL/m2, P<0.05 LAEF: 58±12% versus 64±9%, P=0.148 LV diastolic filling Early peak-filling rate index: 239±87 versus 242±58 mL/s/m2, P=0.889 Atrial peak-filling rate index: 161±34 versus 121±30 mL/s/m2, P<0.05 Peak-filling rate ratio: 1.6±0.7 versus 2.1±0.8, P<0.05	Ventricle CI (RV): 3.2±0.5 versus 3.5±0.8 L/min/m2, P=0.138 RVEF: 62±10% versus 58±6%, P=0.201 RVEDVi: 104±21 versus 103±19 mL/m2, P=0.952 RVESVi: 40±14 versus 44±13 mL/m2, P=0.389 Atrium RAEDVi: 30±10 versus 28±7 mL/m2, P=0.801 RAESVi: 52±16 versus 50±14 mL/m2, P=0.835 RAEF: 42±12% versus 45±9%, P=0.526

CI: Cardiac index, CMR: Cardiac magnetic resonance, IVSd: Intraventricular septum thickness, LAEDVi: Left atrial end-diastolic volume index, LAEF: Left atrial ejection fraction, LAESVi: Left atrial end-systolic volume index, LGE: Late gadolinium enhancement, LV: Left ventricle/ventricular, LVEDV(i): Left ventricular end-diastolic volume (index), LVEF: Left ventricular ejection fraction, LVESV(i): Left ventricular end-systolic volume (index), LVSV(i): Left ventricular stroke volume (index), NT-proBNP: N-terminal pro-brain natriuretic peptide, PWd: Posterior wall thickness, RAEDVi: Right atrial end-diastolic volume index, RAEF: Right atrial ejection fraction, RAESVi: Right atrial end-systolic volume index, RV: Right ventricle/ventricular, RVEF: Right ventricular ejection fraction, RVEDV(i): Right ventricular end-diastolic volume (index), RVESV(i): Right ventricular end-systolic volume (index), RVSV(i): Right ventricular stroke volume (index)

Function and volume of atria

Two studies reported atrial parameters. Chen et al. did not show significant differences in atrial parameters between the LGE-positive and LGE-negative groups,[10] whereas Tahir et al. found significantly higher LAEDVi (22 ± 7 vs. 16 ± 6 ml/m², P < 0.05) and LAESVi (53 ± 14 vs. 44 ± 10 ml/m², P < 0.05) in the presence of LGE without a difference in LAEF [Table 3].[17]

Left ventricular diastolic filling

Two studies investigated left ventricular diastolic filling patterns and showed consistent findings.[10,17] In both studies, early peak-filling rate was similar between groups, but atrial peak-filling rate was significantly higher in the athletes with positive LGE ([149 ± 50 vs. 120 ± 46 ml/s/m², P < 0.05][10] and [161 ± 34 vs. 121 ± 30 ml/s/m², P < 0.05][17]). Thus, the peak-filling rate ratio was significantly lower in the presence of LGE ([1.56 ± 0.67 vs. 2.07 ± 1.03, P < 0.05][10] and [1.6 ± 0.4 vs. 2.1 ± 0.8, P < 0.01][17]). Both atrial peak-filling rates and peak-filling rate ratios in each study were similar to that of the control nonathlete group, who were eligible if they exercised <3 h per week [Table 3].[10,17]

Myocardial strain

Tahir et al. reported lower global radial strain in LGE-positive-athletes than LGE-negative-athletes (40 ± 7% vs. 45 ± 7%, P < 0.05), without differences in global longitudinal or circumferential strains between them. Segmental radial, longitudinal, and circumferential strains were lower in the LGE-positive group. Reduced strains suggested an unfavorable effect of myocardial fibrosis on the left ventricular function. There was an inverse relationship or correlation between the size of segmental LGE and segmental strain (P < 0.01), reflecting the direct effect of myocardial fibrosis extent on the contractility of myocardium. The correlation was not noted with the relative circumferential (P = 0.84) and longitudinal (P = 0.302) strains.[16]

DISCUSSION

The currently published systematic reviews focused on the prevalence and characterization of myocardial fibrosis in athletes.[1,3,8] This review investigated the impact of myocardial fibrosis in asymptomatic endurance athletes. Eight studies were included in this qualitative synthesis that discussed CMR measurements related to ventricular and atrial functions and volumes as well as left ventricular diastolic filling and myocardial strain in endurance athletes with or without myocardial fibrosis. In the general nonathlete population, the prevalence of myocardial fibrosis was approximately 8% to 20% using CMR imaging with LGE technique.[3,12] In this review, the prevalence in endurance athletes was higher and varied considerably between studies (i.e., ranged from 13% to 48%). The prevalence of myocardial fibrosis in athletes ranged from 3% to 50% in the published literature.[18,19,20,21,22,23,24,25,26,27,28,29] On the other hand, other studies did not find myocardial fibrosis among the recruited endurance athletes[30,31,32,33,34] or reported it in only one athlete in others.[35,36] The presence of myocardial fibrosis in athletes was associated with factors such as longer endurance training period, longer training years, and more completed competitions than in athletes without myocardial fibrosis.[3,5] However, this was not shown in the studies included in this review. Interestingly, a recent study by Liu et al. used LGE-based CMR-proton density fat fraction for the assessment of liver fat content in athletes to predict cardiac fibrosis.[37] The common pattern and location of myocardial fibrosis reported in the studies included in this review are consistent with the generally reported data of being of a focal nonischemic pattern and located in the right ventricle insertion points. Myocarditis does not usually necessitate additional cardiac investigation because it is often self-limiting with benign small scars. Although asymptomatic, large areas of LGE are detected in athletes after experiencing myocarditis with abnormal electrocardiographic and echocardiographic investigations. The exact proportion of uninvestigated asymptomatic athletes after myocarditis is unclear.[4] It is also unclear whether endurance training would increase the risk of ischemic myocardial fibrosis beyond what can be inferred due to the age or other cardiovascular risk factors.[4]

The studies included in this review did not find consistent results on the impact of myocardial fibrosis on ventricular function and volume parameters. However, the only two studies[16,17] that reported left ventricular diastolic filling found similar findings that resembled those of the nonathlete controls which may suggest that the impact of myocardial fibrosis on left ventricular diastolic function may result in a pseudo-normalization due to the reduction in passive elasticity of the enlarged left ventricle.[10] Myocardial fibrosis was associated with reduced strains, and its size can affect the myocardial function, as reported by only one included study.[16] Patient clinical outcomes, such as morbidity and mortality, were not investigated in the studies included in this review. It is known that the presence of myocardial fibrosis in cardiac patients is considered a risk factor for adverse clinical outcomes, but its clinical impact on athletes has not been well studied.[3] In marathon runners with LGE, the survival rate was significantly lower (P < 0.0001),[20] cardiac troponin levels were higher during the marathon,[38] and coronary artery calcification burden was significantly higher[39] than those without LGE. Furthermore, as endurance training may cause left ventricular geometry changes and myocardial fibrosis, the risk of atrial and ventricular arrhythmias increases.[6] Vigorous exercise training such as running (marathon or ultramarathon) or professional cycling is associated with increased atrial fibrillation prevalence by up to fivefold.[2] Ventricular arrhythmias often occur due to right ventricle and/or interventricular septum dysfunction.[2,40] Despite the atrial and ventricular electrical abnormalities, the predisposition to serious arrhythmias or sudden cardiac death is considered rare.[2]

To the best of our knowledge, this is the first review to discuss the impact of myocardial fibrosis in endurance athletes. However, there are several limitations that should be acknowledged. All the studies were of small size and of an observational design with its inherent bias due to lack of power and randomization, for example. All of them were conducted in Europe with various athletic activities which may limit overall population representation and study findings extrapolation. The enrolled athletes were of middle age and were predominantly males. Furthermore, the use of illicit drugs or the presence of underlying coronary artery disease cannot be excluded. The prognostic implications of myocardial fibrosis on patient clinical outcomes, such as arrhythmias and mortality, were not reported as there was no long-term follow-up. Finally, although LGE-CMR modality is validated to identify and quantify focal myocardial fibrosis, it cannot detect diffuse myocardial fibrosis,[3,4] which may underestimate the actual prevalence of LGE or myocardial fibrosis.[3] As an alternative, other CMR techniques can be used such as T1 mapping and extracellular volume measurement.[3,4,5,10] Few studies have been published on diffuse myocardial fibrosis in athletes, but with conflicting findings.[3,4] There are clear unmet needs to encourage larger studies on myocardial fibrosis phenotypes to shed more light on the underlying mechanism, clinical consequences, and prognosis. Well-powered studies are needed to address the gaps in evidence regarding the long-term implications of myocardial fibrosis on clinical outcomes and the inclusion of more diverse sport types, female athletes, and ethnic backgrounds.

CONCLUSION

Strenuous endurance athletes exceed the recommended exercise dose, which may lead to pathologic cardiac remodeling. Emerging evidence found a higher prevalence of myocardial fibrosis among endurance athletes compared with healthy nonathletic individuals. The impact of myocardial fibrosis on cardiac chambers’ function and structure as well as clinical outcomes is not well characterized. Further research is needed to shed more light on myocardial fibrosis phenotypes and the underlying mechanism, clinical consequences, and prognosis.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.