Study Review

Summary of review

Reviewing the 12 studies listed in
Prevalence of Myocardial Fibrosis in Intensive Endurance Training Athletes: A Systematic Review and Meta-Analysis
for dietary information. This is in reference to a curiosity I raised in a tweet here

Per the article:

12 studies involving 1,359 participants were included for analysis. Among them, 163/772 participants in the endurance athletes group showed LGE positive, compared with 19/587 participants in the comparison group.

and they all appear listed in table 1.

"Table 1. Prevalence and patterns of myocardial fibrosis in athletic populations using CMR." ref

they are cited as 8-19 (which totals 12 as a sanity check)

The article also states they extract a bunch of data, but does not mention diet.

"Extracted items of the study included: author, year, country, design, sample size, number of athletes detected with MF, characteristic of endurance athletes and inactive controls, age, and gender."

I have broken them out with notes on details about diet below, as well as highlighting interesting findings.

Attempt to get official full text links were made. Sci-hub was used when applicable.

Tentative observations

My non-doctor and non-expert analysis: This seems so freaking rare and variable that grouping everyone together under a meta-analysis is freaking dumb as fuck. Are high-endurance athletes even dying of the complications of myocardial fibrosis anyway? And none of these studies look at diet factors and for the few that did find results, they all assume it's exercise damage without question, or consider it plausibly just normal feature of heart remodeling.

We do see a build up in what appears to be scar tissues (in a very small number) of endurance athletes tho. Why are a small number of athletes accruing such damage to their hearts at all, but not the majority of them. They all get big hearts... so something is failing to heal? That is odd.

Exploration of dietary data

cited as (8):

Myocardial late gadolinium enhancement: prevalence, pattern, and prognostic relevance in marathon runners


No data on diet.

Assumption is it's exersize associated.

Although the absolute number of marathon runners with LGE was low, the higher prevalence of LGE in runners than in control subjects suggests that the amount of exercise engaged in by the marathon runners may have had a role in the development of LGE.

cited as (9):

Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes


No data on diet.

Didn't run echocardiography on the control group.

Assumption is it's exersize associated.

Accurate diary recordings of the athlete's full training and competitive histories were collected. The data are unique in as much as all athletes were documented lifelong endurance athletes still competing in intensive endurance events.

The prevalence of LGE in veteran athletes was not associated with age, height, weight, or body surface area (P > 0.05), but was significantly associated with the number of years spent training (P < 0.001), number of competitive marathons (P < 0.001), and ultraendurance (>50 miles) marathons (P < 0.007) completed. An unexpectedly high prevalence of myocardial fibrosis (50%) was observed in healthy, asymptomatic, lifelong veteran male athletes, compared with zero cases in age-matched veteran controls and young athletes. These data suggest a link between lifelong endurance exercise and myocardial fibrosis that requires further investigation.

cited as (10):



No data on diet.

In contrast to previous reports, in this prospective study of a wide range of athletes with no known cardiovascular disease, clinically significant LGE was not observed in any sub-elite endurance athletes

cited as (11):

Right and Left Ventricular Function and Mass in Male Elite Master Athletes: A Controlled Contrast-Enhanced Cardiovascular Magnetic Resonance Study


No data on diet.

Based on our results, chronic right ventricular damage in elite endurance master athletes with lifelong high training volumes seems to be unlikely. Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to be questioned.

cited as (12):

No evidence of adverse cardiac remodeling in former elite endurance athletes


No data on diet.

Veteran endurance athletes who have performed regular strenuous endurance exercise over N30 years show a cardiac remodeling pattern characterized by larger LV, RV and LA cavities when compared with non-athletic healthy controls, with the greater LV size matched by an increased LV myocardial mass and with no evidence of permanent major cardiac damage or fibrosis assessed by imaging or blood biomarkers

cited as (13):

Lifelong Physical Activity Regardless of Dose Is Not Associated With Myocardial Fibrosis


No data on diet.

A lifelong history of consistent physical activity, regardless of “dose” ranging from sedentary to competitive marathon running, was not associated with the development of focal myocardial fibrosis.

cited as (14):

Prevalence of Subclinical Coronary Artery Disease in Masters Endurance Athletes With a Low Atherosclerotic Risk Profile


No data on diet.

This study seems to emphasize the difficulty of the processes of getting good LGE readings (refer "CMR Scan" heading). Mentioned that it was assumed LGE to be myocardio fibrosis.

LGE was considered to represent focal myocardial fibrosis.

No relationship was found between myocardial fibrosis and exercise intensity, years of training, or number of competitions.

cited as (15):

Exercise-induced arrhythmogenic right ventricular remodeling in master endurance athletes


No data on diet.

Whilst longitudinal surveillance is required to fully elucidate the clinical significance, the data suggest that chronic exercise may in some cases contribute to the development of an acquired arrhythmogenic cardiomyopathy

cited as (16):

Myocardial late gadolinium enhancement and T1 mapping in highly trained endurance athletes


No data on diet.

Highly trained endurance athletes showed higher prevalence of LGE than control subjects; always confined to the hinge point. Although this pattern of LGE may be another feature of the athlete’s heart, the results suggest that those with focal fibrosis might have globally higher myocardial ECV values

cited as (17):

Myocardial remodelling and tissue characterisation by cardiovascular magnetic resonance (CMR) in endurance athletes


No data on diet.

This one goes into some detail under "Focal myocardial fibrosis" on the controversy and plasuability of the findings. It suggests perhaps this is a normal phenomena and not related to a disease state?

It is speculated that the RV distention during exercise may result in chronic structural changes of the myocardial architecture, mainly in the septal points of insertion of the right ventricular wall. In our study, we found mild LGE in the inferior septal RV insertion in 23% of athletes. However, we did not consider this finding as true reactive MF. In fact, this finding was also observed in 36% of controls (figure 2). We believe that, as previously reported,17 19 plexiform fibrosis is a normal feature of the insertion-region anatomy that may result in contrast pooling within this area.

The conclusion states

In the only three athletes with focal MF, the LGE pattern observed suggests an intercurrent event not related with the remodelling phenomenon

cited as (18):

Myocardial Fibrosis in Competitive Triathletes Detected by Contrast-Enhanced CMR Correlates With Exercise-Induced Hypertension and Competition History


No data on diet.

This one seems to have more data about tri-athletes which includes distance factors. I wonder of longer distance training means a different diet.

LGE+ triathletes completed longer distances in swimming and cycling than LGE- triathletes, suggesting that race distances have an impact on the risk for myocardial fibrosis;

It has been suggested that increased wall stress and impaired resistance to physical stress in this region are potential explanations for involvement of the inferolateral wall in these diseases (28). This explanation may also apply to triathletes, who are characterized by repetitively increased wall stress under exercise.

The presence of scar tissue was associated with exercise-induced hypertension and increased left ventricular mass but also longer lifetime race distances. Therefore, the lifetime amount of exercise seems to affect the risk for myocardial scarring, at least in male triathletes.

The clinical relevance of myocardial fibrosis in competitive triathletes is currently unclear; however, myocardial fibrosis could be the substrate for cardiac arrhythmia with subsequent sudden cardiac death and a precursor for future heart failure. Therefore, future longitudinal studies are needed

cited as (19):

Cardiovascular magnetic resonance with parametric mapping in long-term ultra-marathon runners


No data on diet.

This one points out an interesting observation: high endurance athletes hearts would look like diseased hearts if you based it on reviews of diseased hearts in existing medical literature. The implication here is that if you only sample diseased hearts you will accrue bias.

The previously underestimated degree of adaptive volumetric structural changes of the heart in this group should raise caution when suspecting the presence of cardiomyopathy. Most of those athletes would fulfil the volumetric criteria for dilated cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy. Therefore those criteria, at least to the degree studied, should not lead to suspicion of cardiomyopathy in the absence of other changes not observed in healthy athletes such as globally decreased left or right ventricular function or the presence of regional wall motion abnormalities and/or symptoms and changes observed in other tests, as elegantly depicted in summative papers

They also have the assumption it is from exercise, the in this case they do at least have a correlation with one of the features they measure.

High intensity training may compromise the immunological system and predispose these individuals to myocarditis in cases of seasonal viral respiratory tract infections [31,32]. However, small, silent, mid-wall areas of fibrosis have also been found in almost 4% of general population [33]. If these presumably post-myocarditis residual changes are limited in size, such as in our study, they do not seem to carry increased risk of arrhythmias.

Review of endurance Athlete myocarditis meta-analysis.

Are high-endurance athletes even dying of the complications of myocardial fibrosis anyway?

ultimape 🐜💩