The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index; 13 of the 33 sources its claims cite were checked for support.
Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes
Open accessAbstract
AIMS: Endurance training may be associated with arrhythmogenic cardiac remodelling of the right ventricle (RV). We examined whether myocardial dysfunction following intense endurance exercise affects the RV more than the left ventricle (LV) and whether cumulative exposure to endurance competition influences cardiac remodelling (including fibrosis) in well-trained athletes. METHODS AND RESULTS: Forty athletes were studied at baseline, immediately following an endurance race (3-11 h duration) and 1-week post-race. Evaluation included cardiac troponin (cTnI), B-type natriuretic peptide, and echocardiography [including three-dimensional volumes, ejection fraction (EF), and systolic strain rate]. Delayed gadolinium enhancement (DGE) on cardiac magnetic resonance imaging (CMR) was assessed as a marker of myocardial fibrosis. Relative to baseline, RV volumes increased and all functional measures decreased post-race, whereas LV volumes reduced and function was preserved. B-type natriuretic peptide (13.1 ± 14.0 vs. 25.4 ± 21.4 ng/L, P = 0.003) and cTnI (0.01 ± .03 vs. 0.14 ± .17 μg/L, P < 0.0001) increased post-race and correlated with reductions in RVEF (r = 0.52, P = 0.001 and r = 0.49, P = 0.002, respectively), but not LVEF. Right ventricular ejection fraction decreased with increasing race duration (r = -0.501, P < 0.0001) and VO(2)max (r = -0.359, P = 0.011). Right ventricular function mostly recovered by 1 week. On CMR, DGE localized to the interventricular septum was identified in 5 of 39 athletes who had greater cumulative exercise exposure and lower RVEF (47.1 ± 5.9 vs. 51.1 ± 3.7%, P = 0.042) than those with normal CMR. CONCLUSION: Intense endurance exercise causes acute dysfunction of the RV, but not the LV. Although short-term recovery appears complete, chronic structural changes and reduced RV function are evident in some of the most practiced athletes, the long-term clinical significance of which warrants further study.
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Written from the paper’s full text.
TL;DR
In 40 well-trained endurance athletes, intense endurance exercise caused acute right ventricular (RV) dysfunction and dilation while left ventricular (LV) function was preserved, with most RV recovery by 1 week. A minority showed septal delayed gadolinium enhancement (DGE) and greater cumulative exercise exposure, suggesting possible chronic RV-predominant remodelling.
Key findings
- Post-race RV volumes increased and all RV functional measures decreased, whereas LV volumes decreased and LV function was preserved; RVEF fell by 9% relative to baseline (P < 0.0001) and mostly recovered by 1 week, except RVSRs remained depressed.
- Post-race BNP (13.1 ± 14.0 vs. 25.4 ± 21.4 ng/L, P = 0.003) and cTnI (0.01 ± 0.03 vs. 0.14 ± 0.17 mg/L, P < 0.0001) increased and correlated with reductions in RVEF (r = 0.52, P = 0.001 and r = 0.49, P = 0.002, respectively), but not LVEF.
- RVEF decreased with increasing race duration (r = −0.501, P < 0.0001) and VO2max (r = −0.359, P = 0.011); race completion time and VO2max independently explained 34% of the variance in ΔRVEF (P = 0.001).
- DGE localized to the interventricular septum in 5 of 39 athletes (12.8%); those athletes had greater cumulative exercise exposure and lower RVEF (47.1 ± 5.9 vs. 51.1 ± 3.7%, P = 0.042) than those with normal CMR.
Methods
- Prospective study of 40 well-trained athletes competing in a marathon, endurance triathlon, alpine cycling race, or ultratriathlon; assessments were at baseline, immediately post-race, and 6–11 days after the race.
- Evaluation included cardiac troponin I, B-type natriuretic peptide, echocardiography (three-dimensional volumes, ejection fraction, systolic strain rate), and cardiac magnetic resonance imaging with delayed gadolinium enhancement for myocardial fibrosis.
- Statistical analysis used paired t-tests, ANOVA, factorial repeated-measures ANOVA, and forward stepwise multivariable analysis; the sample size of 40 was prospectively determined to have 90% power to detect a 10% relative reduction in RVEF.
Limitations
- Stated: DGE within the RV free wall was not assessed because adequate nulling of normal RV free wall myocardium was visualized in only a minority of athletes; athletic remodelling may cause fibrosis to be under-appreciated with relative-enhancement techniques.
- Stated: the cohort was relatively small and underpowered for clinical sequelae; biomarker assessment at a single time point may limit interpretation; conclusions about exercise duration are tempered by confounders such as training levels, exercise modality, race conditions, and motivation.
- Evident from text: the study reports no long-term clinical outcomes, and prognostic implications from other clinical conditions should not be extrapolated to this healthy athletic cohort.
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Claims the paper makes
32 Own result · 15 Own interpretation · 8 Own method · 7 No full text of the sources · 4 Partly supported · 3 Supported so far · 2 Supported · 1 Not checked yet · 1 No basis given · accuracy not yet measured
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“However, right ventricular (RV) function may be more profoundly affected by intense endurance exercise 6 -10”
What the sources say
- Not checked — no full text of the sourcecites [6] 2008, Biochemical and functional abnormalities of left and right ventricular function after ultra-endurance exercise, Heart source
- Not checked — no full text of the sourcecites [7] 2010, Acute cardiac effects of marathon running, J Appl Physiol source
- Not checked — no full text of the sourcecites [8] 2009, Relation of biomarkers and cardiac magnetic resonance imaging after marathon running, Am J Cardiol source
- Supportedcites [9] 2006, Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon, Circulation source
The Echocardiography section reports that RV percentage area change decreased after the marathon while LV ejection fraction remained unchanged. It also reports changes in LV diastolic function, so the comparison is clearest for systolic function; the claim’s hedged wording is consistent with these findings. Page numbers are not provided in our copy. (LLM, conf=0.90)
- Supportedcites [10] 1990, Different effects of prolonged exercise on the right and left ventricles, J Am Coll Cardiol source
The paper reports that after the Ironman Triathlon, the filling pattern of the right ventricle, but not the left, was altered (Right and left ventricular diastolic function; page unavailable). Its Conclusions also state that the ventricles responded differently to exercise. These findings support the cautious claim that right ventricular function may be more profoundly affected. (LLM, conf=0.87)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“While this could be interpreted as abnormal enhancement, it is more likely to reflect the limitations in spatial resolution of the technique, a sentiment echoed by a panel of experts who deemed that DGE assessment in the RV free wall was too unreliable to be included in the recent revision of diagnostic criteria for arrhythmogenic RV cardiomyopathy.35”
What the sources say
- Supportedcites [35] 2010, Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria, Circulation source
The citation supports the expert panel’s caution about assessing delayed enhancement in the RV free wall, not the citing authors’ observation about athletes. The Discussion (page unavailable) says RV late enhancement can be difficult to identify because the wall is thin and may be confused with fat; the Results describe revised MRI criteria based on RV size, function, and wall motion rather than late enhancement. (LLM, conf=0.88)
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The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“However, there is also emerging evidence that intense endurance exercise may be associated with an excess in arrhythmic disorders, the mechanisms for which remain unexplained.38 -41”
What the sources say
- Not matchedcites [38] 2008, Sinus node disease and arrhythmias in the long-term follow-up of former professional cyclists, Eur Heart J
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites [39] 2011, Strenuous endurance exercise: is more better for everyone? Our genes won't tell us, Br J Sports Med source
- Supportedcites [40] 2011, Marathon rat: myocardial remodeling in an animal model of vigorous endurance exercise and implications for humans, Circulation source
The Article (see p. 13) reports a higher prevalence of atrial fibrillation in sportsmen than in the general population and describes potential arrhythmia-producing changes from extreme exercise. It also says there is very little information about the myocardial tissue alterations underlying arrhythmias, consistent with the sentence’s uncertainty about mechanisms. (LLM, conf=0.91)
- Supportedcites [41] 2010, Arrhythmias and sport practice, Heart source
The ‘Atrial arrhythmias and endurance exercise’ section reports an association between endurance sport and atrial fibrillation or flutter, and the Conclusions say athlete’s heart may create a substrate for atrial and ventricular arrhythmias. The ‘Mechanisms of AF and flutter’ section describes proposed mechanisms rather than an established explanation; page numbers are unavailable in our copy. (LLM, conf=0.90)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Studies focussing on the LV of athletes have failed to provide these mechanistic insights, 4 but recent data have suggested that exercise-induced proarrhythmic substrates may develop in the RV while sparing the LV.12,13,15”
What the sources say
- Supportedcites [12] 2007, Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment, Eur Heart J source
The Patient characteristics section (page unavailable) reports an RV origin or arrhythmogenic substrate in most athletes with ventricular arrhythmias, while LV ejection fraction did not differ between athlete groups. The Discussion and Conclusions (pages unavailable) suggest that endurance exercise could promote RV changes, but explicitly leave that causal role unproven—consistent with the claim’s hedged wording. (LLM, conf=0.88)
- Supportedcites [13] 2003, High prevalence of right ventricular involvement in endurance athletes with ventricular arrhythmias. Role of an electrophysiologic study in risk stratification, Eur Heart J source
In “Presentation, electrophysiological and morphological findings” (page unavailable), the paper reports frequent RV arrhythmogenic involvement but very little evidence of underlying LV disease in its endurance athletes with ventricular arrhythmias. In “Endurance sports and arrhythmogenic structural RV damage” (page unavailable), it speculates that endurance sports may itself lead to RV structural damage. This supports the citing sentence’s hedged claim, within that studied population. (LLM, conf=0.91)
- Supportedcites [15] 2011, Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training, Circulation source
In “Chamber-Specific Myocardial Fibrosis After Intensive Exercise Training” (page not available), the paper reports RV fibrosis after long-term intensive exercise and says the LV did not appear to be affected. In “Intense Exercise Training and Arrhythmogenic Remodeling” (page not available), it suggests that the fibrosis could contribute to the increased ventricular arrhythmia susceptibility observed in exercise-trained rats. This supports the citing sentence’s hedged claim about a possible RV substrate while sparing the LV. (LLM, conf=0.92)
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- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The considerable increases in pulmonary pressures demonstrated in trained athletes during intense exercise 29,30,34 suggest a similar physiological stress, albeit only transient.”
What the sources say
- Not checked — no full text of the sourcecites [29] 2011, Disproportionate exercise load and remodeling of the athlete's right ventricle, Med Sci Sports Exerc source
- Not checked — no full text of the sourcecites [30] 2010, Pulmonary transit of agitated contrast is associated with enhanced pulmonary vascular reserve and right ventricular function during exercise, J Appl Physiol source
- Supportedcites [34] 1999, Range of tricuspid regurgitation velocity at rest and during exercise in normal adult men: implications for the diagnosis of pulmonary hypertension, J Am Coll Cardiol source
The CO section reports that pulmonary artery systolic pressure rose with workload and continued to rise in athletes after 160 watts. The Mechanisms of pressure elevation section also states that the study confirmed higher exercise pressures in athletes than in nonathletes. (LLM, conf=0.92)
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In the paper
“Extending these hypotheses to human populations, Ector et al. 12 demonstrated that RVEF (and not LVEF) was reduced in athletes with complex ventricular arrhythmias when compared with healthy athletes and non-athletes without arrhythmias.”
What the sources say
- Partly supportedcites [12] 2007, Reduced right ventricular ejection fraction in endurance athletes presenting with ventricular arrhythmias: a quantitative angiographic assessment, Eur Heart J sourceExperimental — accuracy not yet measured
The RV volumes and EF results report significantly lower RVEF in endurance athletes with ventricular arrhythmias than in athletes without them; the Discussion also describes lower RVEF than in non-athlete controls. Neither section reports an LVEF comparison, so the parenthetical claim that LVEF was not reduced is unsupported by our copy. Page numbers are not supplied. (LLM, conf=0.86)
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and VO 2 max (r ¼ 20.359, P ¼ 0.011).”
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In the paper
“Relative to baseline, RV volumes increased”
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In the paper
“and lower RVEF (47.1 + 5.9 vs. 51.1 + 3.7%, P ¼ 0.042) than those with normal CMR.”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In contrast, all measures of LV function were unchanged.”
plain- Asserted: passes — The authors put it forward as true.
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- Probably not a substantial claim. 10
- It may state two separate claims as one. 25
- The quote only partly states this claim. 2
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Benito et al. 15 recently documented that intense endurance exercise promoted RV-specific fibrosis in rats which increased vulnerability to ventricular tachycardia following programmed stimulation.”
What the sources say
- Partly supportedcites [15] 2011, Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training, Circulation sourceExperimental — accuracy not yet measured
The chamber-specific remodeling section reports right-ventricular fibrosis after intensive training, with no observed left-ventricular difference. The ventricular-arrhythmia section reports greater inducibility during programmed stimulation in exercise rats (42% versus 6%). But the discussion says fibrosis *could play a role* in that susceptibility; it does not establish that the fibrosis caused the increase. (LLM, conf=0.87)
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In the paper
“Exercise is a powerful intervention in the prevention and treatment of cardiovascular disease for which compelling evidence exists across a wide range of exercise volumes and intensities, including among competitive athletes.4,26,37”
What the sources say
- Partly supportedcites [4] 2010, Long-term clinical consequences of intense, uninterrupted endurance training in olympic athletes, J Am Coll Cardiol sourceExperimental — accuracy not yet measured
The Conclusions (page not provided) report that prolonged, intense endurance training in young Olympic athletes was not associated with cardiovascular events or deterioration in left ventricular function. That supports a limited point about competitive athletes, but the study enrolled athletes free of cardiovascular disease and does not establish exercise as a prevention or treatment intervention across a wide range of volumes and intensities. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [26] 2010, Physical activity and cardiovascular health: lessons learned from epidemiological studies across age, gender, and race/ethnicity, Circulation source
- Not matchedcites [37] 1993, Increased life expectancy of world class male athletes, Med Sci Sports Exerc
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“More recently, Wilson et al. 18 observed DGE in 6 of 12 elite veteran athletes but not in 17 young novice athletes or 20 older non-athletes.”
What the sources say
- Partly supportedcites [18] 2011, Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes, J Appl Physiol sourceExperimental — accuracy not yet measured
The Results report LGE in 6 of 12 veteran athletes and none in the 17 young athletes or 20 age-matched controls. But the Methods describe the young athletes as experienced endurance competitors with 11–31 years of training, not novices. The paper calls the imaging finding LGE rather than DGE. (LLM, conf=0.90)
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“all measures of systolic RV function were reduced post-race.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Also, focal gadolinium enhancement and increased RV remodelling were more prevalent in those athletes with a longer history of competitive sport”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“the occurrence of an early diastolic 'septal bounce' on M-mode echocardiography in 26 of 40 athletes which was not present at baseline”
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In the paper
“Significant correlations were evident between the change in RVEF and post-race troponin (r ¼ 0.494, P ¼ 0.002) and BNP levels (r ¼ 0.518, P ¼ 0.001).”
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“those with DGE had 16% greater RVEDV and 25% greater RVESV than those athletes in whom there was no DGE (P ¼ 0.029 and 0.003, respectively).”
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In the paper
“There was no correlation between changes in LVEF and post-race cTnI (r ¼ 20.065, P ¼ 0.702) or BNP (r ¼ 0.250, P ¼ 0.125).”
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Race completion time and VO 2 max remained as independent predictors in the multivariable analysis (b ¼ 0.459, P ¼ 0.002 and b ¼ 0.294, P ¼ 0.036, respectively), together explaining 34% of the variance in △RVEF (P ¼ 0.001).”
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In the paper
“athletes who had greater cumulative exercise exposure”
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In the paper
“There was a significant interaction between event type and time point (P-value) with a greater reduction in function in those completing the longest event (ultra-triathlon).”
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In the paper
“Right ventricular volumes increased in the post-race setting while left ventricular volumes decreased resulting in a decrease in right ventricular ejection fraction but not left ventricular ejection fraction.”
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In the paper
“These athletes had been competing in endurance sport for longer and had greater structural remodelling of the RV.”
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In the paper
“In addition, we demonstrate that the acute injury and chronic remodelling of the myocardium both disproportionately affect the RV”
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In the paper
“In all cases, focal DGE was confined to the interventricular septum and commonly at the site of RV attachment.”
- Also stated in: § Conclusion and clinical implications · plain
“Images of five athletes in whom focal delayed gadolinium enhancement (DGE) was identified in the interventricular septum (indicated with arrows) when compared with an athlete with a normal study (top left).”
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- Also stated in: § Conclusion and clinical implications · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Ejection fraction (A), fractional area change (B), and systolic strain rate (C ) decreased in the post-race setting.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Functional abnormalities were confined to the RV and were largely reversible 1 week following the event.”
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In the paper
“A tolerance of .0.5 was set to avoid collinearity between the five entered variables (race duration, VO 2 max, age, weekly, and career training).”
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In the paper
“Written informed consent was obtained from all subjects and the protocol was approved by the St Vincent's Hospital Human Research Ethics Committee in accordance with the Declaration of Helsinki.”
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In the paper
“Intense endurance exercise causes an acute reduction in RV function that increases with race duration and correlates with increases in biomarkers of myocardial injury.”
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“suggesting that repetitive ultra-endurance exercise may lead to more extensive RV change and possible myocardial fibrosis.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All reported values are the average of three repeated measures from separate cardiac cycles.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The sample size of 40 was prospectively determined to have a 90% power of detecting a 10% relative reduction in RVEF averaged across all four endurance events”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Delayed gadolinium enhancement within the RV free wall was not assessed because adequate nulling of normal RV free wall myocardium (the reference against which abnormal enhancement is compared) was visualized in only a minority of athletes.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Intense endurance exercise causes acute dysfunction of the RV, but not the LV.”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Post-race changes in load, myocardial substrates, and metabolites should confound right ventricular and left ventricular measures similarly.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Intense endurance exercise causes an acute reduction in RV function that increases with race duration”
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The four endurance events represent a progressive increase in exercise duration.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“To be deemed significant, DGE had to be independently identified by both clinicians and, in addition, mean signal intensities in the region of hyperenhancement were required to be more than two standard deviations (SDs) higher than the mean signal intensity of a region of adjacent myocardium”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Delayed gadolinium enhancement (DGE) was qualitatively assessed by two experienced clinicians after comparing pre-and post-contrast short-axis slices to exclude artefacts.”
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Greater reductions in RV function occurred in those athletes competing for a longer duration, suggesting that the heart has a finite capacity to maintain the increased work demands of exercise.”
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The four endurance events represent a progressive increase in exercise duration.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, BNP may provide a measure of both acute RV load and the resultant fatigue which occurs when this load is sustained.”
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“We have previously demonstrated that BNP release during intense exercise is associated with greater relative increases in RV systolic pressures, but not LV pressures.30”
What the sources say
- Not checked — no full text of the sourcecites [30] 2010, Pulmonary transit of agitated contrast is associated with enhanced pulmonary vascular reserve and right ventricular function during exercise, J Appl Physiol source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“It has been demonstrated that ventricular load increases with exercise intensity and is greater for the RV than the LV, 29”
What the sources say
- Not checked — no full text of the sourcecites [29] 2011, Disproportionate exercise load and remodeling of the athlete's right ventricle, Med Sci Sports Exerc source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
The four endurance events represent a progressive increase in exercise duration.
“The four events were selected to represent a progressive increase in exercise duration”
The paper relies on this without support.
Post-race changes in load, myocardial substrates, and metabolites should confound right ventricular and left ventricular measures similarly.
“Comparisons with the LV are most instructive, given that post-race changes in load, myocardial substrates, and metabolites should confound RV and LV measures similarly.”
The paper relies on this without support.
Athletic training results in relatively uniform cardiac remodelling.
“Secondly, athletic training results in relatively uniform cardiac remodelling and it is possible that cardiac fibrosis may be under-appreciated with current techniques that assess relative enhancement.”
The paper relies on this without support.
Focal delayed gadolinium enhancement on cardiac magnetic resonance indicates myocardial fibrosis.
“However, there remained a significant minority of athletes in whom there was evidence of myocardial fibrosis in the interventricular septum.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated major: it would touch a result — a value a result rests on, reported and recomputed p-values on opposite sides of the significance level, two passages that conflict with no sign which is right, or a cited work retracted before this paper was published.
In the paper
§ Conclusion and clinical implications
“Functional abnormalities were confined to the RV”
§ Interventricular dependence
“Post-race LV diastolic filling was impaired, as evidenced by a decrease in the ratio of early (E) to late (A) transmitral flow (EA ratio 1.84 + 0.35 at baseline vs. 1.34 + 0.35 post-race, P , 0.0001) and an increase in E deceleration time (187 + 29 vs. 212 + 40 ms, P ¼ 0.002)”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Correlation between functional and biochemical evidence of myocardial injury
“median 0.018 mg/L”
§ Correlation between functional and biochemical evidence of myocardial injury
“range 0.020-0.99mg/L”
Citations
Cites
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Recommendations for chamber quantification☆
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Neilan, T. G., Januzzi, J. L., Lee-Lewandrowski, E., Ton-Nu, T.-T., Yoerger, D. M., Jassal, D. S., Lewandrowski, K. B., Siegel, A. J., Marshall, J. E., Douglas, P. S., et al. (2006) · Circulation · doi:10.1161/circulationaha.106.647461 · Cited by 519
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Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training
Benito, B., Gay-Jordi, G., Serrano-Mollar, A., Guasch, E., Shi, Y., Tardif, J.-C., Brugada, J., Nattel, S., & Mont, L. (2011) · Circulation · doi:10.1161/circulationaha.110.938282 · Cited by 478
Cited by
Sorted by citations
Items 201–300 of 773
Scharf, M., Schmid, A., KEMMLER, W. K., von Stengel, S., May, M. S., Wuest, W., Achenbach, S. S., Uder, M., & Lell, M. (2015) · Circulation Cardiovascular Imaging · doi:10.1161/circimaging.114.002566 · Cited by 29
Schattke, S., Xing, Y., Lock, J., Brechtel, L. M., Schroeckh, S., Spethmann, S., Baumann, G., Borges, A. C., & Knebel, F. (2014) · Cardiovascular Ultrasound · doi:10.1186/1476-7120-12-11 · Cited by 32
Physiology and Pathophysiology of Marathon Running: A narrative Review
Braschler, L., Nikolaidis, P. Τ., Thuany, M., Chlíbková, D., Rosemann, T. J., Weiss, K., Wilhelm, M., & Knechtle, B. (2025) · Sports Medicine - Open · doi:10.1186/s40798-025-00810-3 · Cited by 45
Fabritz, L., Fortmueller, L., Yu, T. Y., Paul, M., & Kirchhof, P. F. (2012) · Progress in Biophysics and Molecular Biology · doi:10.1016/j.pbiomolbio.2012.08.010 · Cited by 27
Baumgartner, L., Schulz, T., Oberhoffer, R., & Weberruß, H. (2019) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2019.00148 · Cited by 28
Mahjoub, H., Blanc, O. L., Paquette, M., Imhoff, S., Labrecque, L., Drapeau, A., Poirier, P., Bédard, É., Pîbarot, P., & Brassard, P. (2019) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00196.2019 · Cited by 29
Fibrosis in Arrhythmogenic Cardiomyopathy: The Phantom Thread in the Fibro-Adipose Tissue
Maione, A. S., Pilato, C. A., Casella, M., Gasperetti, A., Stadiotti, I., Pompilio, G., & Sommariva, E. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00279 · Cited by 29
Roof, S. R., Ho, H., Little, S. C., Ostler, J. E., Brundage, E. A., Periasamy, M., Villamena, F. A., Györke, S., Biesiadecki, B. J., Heymes, C., et al. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.01.003 · Cited by 26
“While chronic, ultra-high endurance athletes (human and animals) exhibit signs of increased fibrosis [47, 48], our training protocol is not considered ultra-high endurance.”
BackgroundPrinciples of transthoracic echocardiographic evaluation
Boyd, A. C., Schiller, N. B., & Thomas, L. (2015) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2015.57 · Cited by 26
Şimşek, Z., Tas, M. H., Günay, E., & Değirmenci, H. (2013) · International journal of cardiac imaging · doi:10.1007/s10554-013-0204-z · Cited by 26
The Potential Cardiotoxic Effects of Exercise
Gerche, A. L. (2016) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2015.11.010 · Cited by 26
Differentiating Athlete’s Heart from Cardiomyopathies – The Right Side
Prior, D. (2018) · Heart Lung and Circulation · doi:10.1016/j.hlc.2018.04.300 · Cited by 26
Self-citationChristou, G. A., Pagourelias, E. D., Anifanti, M., Sotiriou, P., Κουτλιάνος, Ν., Tsironi, M., Andriopoulos, P., Christou, K., Kouidi, E. J., & Deligiannis, A. P. (2020) · European Journal of Preventive Cardiology · doi:10.1177/2047487319898782 · Cited by 27
“found that the increase in NT-proBNP correlated with the decrease in RV ejection fraction after ultra-endurance exercise.(20) However, there was no association between post-exercise NT-proBNP levels and RV end-diastolic diameters, suggesting that RV preload may not have an important role in determining post-exercise N…”
MethodKaleta-Duss, A. M., Lewicka-Potocka, Z., Dąbrowska-Kugacka, A., Raczak, G., & Lewicka, E. (2020) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph17176191 · Cited by 26
“However, other authors reported transient impairment of left [7] and right ventricular function [8] as well as the function of left atrium [9].”
BackgroundExercise induced Right Ventricular Fibrosis is Associated with Myocardial Damage and Inflammation
Rao, Z., Wang, S., Bunner, W., Chang, Y., & Shi, R. (2018) · Korean Circulation Journal · doi:10.4070/kcj.2018.0084 · Cited by 26
Li, J.-Y., Pan, S.-S., Wang, J., & Lu, J. (2019) · International Heart Journal · doi:10.1536/ihj.18-310 · Cited by 26
Kleinnibbelink, G., van Dijk, A. P. J., Fornasiero, A., Speretta, G. F. F., Johnson, C., Hopman, M. T. E., Sculthorpe, N. F., George, K., Somauroo, J. D., Thijssen, D. H. J., et al. (2020) · Journal of the American Society of Echocardiography · doi:10.1016/j.echo.2020.12.003 · Cited by 26
Christensen, D. L., Espino, D., Infante‐Ramírez, R., Brage, S., Terzic, D., Goetze, J. P., & Kjærgaard, J. (2014) · American Journal of Human Biology · doi:10.1002/ajhb.22607 · Cited by 25
Running multiple marathons is not a risk factor for premature subclinical vascular impairment
Preßler, A., Suchy, C., Friedrichs, T., Dallinger, S., Grabs, V., Haller, B., Halle, M., & Scherr, J. (2017) · European Journal of Preventive Cardiology · doi:10.1177/2047487317713326 · Cited by 26
de Carvalho, M. R., de Mendonça, M. L. M., Oliveira, J. M. L., Romanenghi, R. B., de Morais, C. S., Ota, G. E., Lima, A. R. R., Oliveira, R. J., Filiú, W. F. D. O., Okoshi, K., et al. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.118697 · Cited by 26
Myocarditis and ARVC/D: Variants or mimics?
Tanawuttiwat, T., Sager, S. J., Hare, J. M., & Myerburg, R. J. (2013) · Heart Rhythm · doi:10.1016/j.hrthm.2013.06.008 · Cited by 25
No evidence of adverse cardiac remodeling in former elite endurance athletes
Sanchis‐Gomar, F., López-Ramón, M., Alis, R., Garatachea, N., Pareja-Galeano, H., Santos‐Lozano, A., Catalán, P., Sansoni, V., Perego, S., Lombardi, G., et al. (2016) · International Journal of Cardiology · doi:10.1016/j.ijcard.2016.07.197 · Cited by 25
Hindieh, W., Adler, A., Weissler‐Snir, A., Fourey, D., Harris, S. E., & Rakowski, H. (2016) · Journal of science and medicine in sport · doi:10.1016/j.jsams.2016.09.007 · Cited by 25
Dor‐Haim, H., Barak, S., Horowitz, M., Yaakobi, E., Katzburg, S., Swissa, M., & Lotan, C. (2018) · PLoS ONE · doi:10.1371/journal.pone.0188551 · Cited by 27
Challenges of Exercise Recommendations and Sports Participation in Genetic Heart Disease Patients
Sweeting, J., Ingles, J., Ball, K., & Semsarian, C. (2015) · Circulation Cardiovascular Genetics · doi:10.1161/circgenetics.114.000784 · Cited by 24
How to interpret right ventricular remodeling in athletes
la Garza, M. S., Carro, A., & Caselli, S. (2020) · Clinical Cardiology · doi:10.1002/clc.23350 · Cited by 25
Mair, J. M. (2025) · Journal of Clinical Medicine · doi:10.3390/jcm14124241 · Cited by 25
Pérez-Sánchez, I., Romero-Puche, A. J., García-Molina, E., Molina, M. S., López-Ayala, J. M., Muñoz‐Esparza, C., López-Cuenca, D., de la Morena, G., Castro-García, F. J., & Gimeno, J. R. (2017) · Revista Española de Cardiología · doi:10.1016/j.recesp.2017.05.026 · Cited by 23
Cardiac structure and function in response to a multi-stage marathon over 4486 km
Klenk, C., Brunner, H., Nickel, T., Sagmeister, F., Yilmaz, A., Infanger, D., Billich, C., Scharhag, J., Vogeser, M., Beer, M., et al. (2019) · European Journal of Preventive Cardiology · doi:10.1177/2047487319885035 · Cited by 24
The arrhythmogenic right ventricular cardiomyopathy in comparison to the athletic heart
Mascia, G., Arbelo, E., Porto, I., Brugada, R., & Brugada, J. (2020) · Journal of Cardiovascular Electrophysiology · doi:10.1111/jce.14526 · Cited by 24
“fect the RV, increasing with duration of the race and correlating with increases in biomarkers of cardiac injury.(28) In 2016, in contrast, Bohm et al(29) examined the cardiac structure and function in 33 white competitive elite male endurance athletes and thirty‐three white male control subjects, based on CMR imaging.”
MethodMitochondrial mutations alter endurance exercise response and determinants in mice
Schaefer, P. M., Rathi, K. S., Butic, A., Tan, W., Mitchell, K. M., & Wallace, D. C. (2022) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2200549119 · Cited by 23
Risk Factors for Exercise-Associated Sudden Cardiac Death in Thoroughbred Racehorses
Nath, L. C., Stent, A. W., Elliott, A. D., et al. (2022) · Animals · doi:10.3390/ani12101297 · Cited by 23
“In human athletes, myocardial fibrosis is more prevalent in older athletes than young athletes and is likely influenced by cumulative training volume [43,44].”
BackgroundHeart Rate and Its Variability in Response to Running—Associations with Troponin
AAGAARD, P., Sahlén, A., Bergfeldt, L., & Braunschweig, F. (2014) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000000270 · Cited by 25
Exercise, the Athlete's Heart, and Sudden Cardiac Death
D’Silva, A., & Sharma, S. (2014) · The Physician and Sportsmedicine · doi:10.3810/psm.2014.05.2062 · Cited by 24
Bruaene, A. V. D., Meester, P. D., Buys, R., Vanhees, L., Delcroix, M., Voigt, J., & Budts, W. (2012) · European Journal of Preventive Cardiology · doi:10.1177/2047487312444372 · Cited by 23
“It has been shown that the impact of exercise is greatest on the RV, with structural changes being related to haemodynamic stressors during exercise.(9,29,30) We previously showed that 602 European Journal of Preventive Cardiology 20(4)”
BackgroundHeiskanen, M. A., Leskinen, T., HEINONEN, I. H. A., Löyttyniemi, E., Eskelinen, J., Virtanen, K. A., Hannukainen, J. C., & Kalliokoski, K. K. (2016) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00399.2016 · Cited by 23
“While previous studies concerning the effects of training on the RV have reported balanced hypertrophy with the LV (21, 35–37), other studies have reported RV dysfunction following intense endurance exercise (3, 9, 10, 25, 26, 40).”
Ljones, K., Ness, H. O., Solvang‐Garten, K., Gaustad, S. E., & Høydal, M. A. (2017) · PLoS ONE · doi:10.1371/journal.pone.0173449 · Cited by 23
Endurance sport and cardiac injury
Leischik, R. (2014) · Kardiologia Polska · doi:10.5603/kp.a2014.0089 · Cited by 22
“Interobserver variability to determine the volume of the RV can be as much as up to 16% using MRI [74].”
BackgroundResultInfluentialMaster Endurance Athletes and Cardiovascular Controversies
Tso, J., & Kim, J. H. (2020) · Current Sports Medicine Reports · doi:10.1249/jsr.0000000000000695 · Cited by 24
“(9) observed this physiology in a cohort of endurance athletes and elegantly demonstrated the critical role played by the RV.”
BackgroundDefining the Interaction Between Exercise and Arrhythmogenic Right Ventricular Cardiomyopathy
Gerche, A. L. (2014) · European Journal of Heart Failure · doi:10.1002/ejhf.224 · Cited by 22
Differential diagnosis of arrhythmogenic cardiomyopathy: phenocopies versus disease variants
Cipriani, A., Marra, M. P., Bariani, R., Mattesi, G., Vio, R., Bettella, N., Lazzari, M. D., Motta, R., Bauce, B., Zorzi, A., et al. (2021) · Minerva Medica · doi:10.23736/s0026-4806.20.06782-8 · Cited by 23
Arrhythmogenic right ventricular cardiomyopathy
Paul, M., Wichter, T., Fabritz, L., Waltenberger, J. L., Schulze‐Bahr, E., & Kirchhof, P. F. (2012) · Herzschrittmachertherapie + Elektrophysiologie · doi:10.1007/s00399-012-0233-7 · Cited by 21
CrossTalk proposal: Prolonged intense exercise training does lead to myocardial damage
Guasch, E., & Nattel, S. (2013) · The Journal of Physiology · doi:10.1113/jphysiol.2013.257238 · Cited by 22
Physiologic and pathophysiologic changes in the right heart in highly trained athletes
D’Andrea, A., Gerche, A. L., Golia, E., Padalino, R., Calabrò, R., Russo, M. G., & Bossone, E. (2015) · Herz · doi:10.1007/s00059-015-4220-8 · Cited by 22
Atrial fibrillation and physical activity: Should we exercise caution?
Bosomworth, N. J. (2015) · PubMed Central · Cited by 19
The Limits of Cardiac Performance: Can Too Much Exercise Damage the Heart?
Rao, P., Hutter, A. M., & Baggish, A. L. (2018) · The American Journal of Medicine · doi:10.1016/j.amjmed.2018.05.037 · Cited by 20
Gajda, R., Kowalik, E., Rybka, S., Rębowska, E., Śmigielski, W., Nowak, M. S., Kwaśniewska, M., Hoffmań, P., & Drygas, W. (2019) · Frontiers in Physiology · doi:10.3389/fphys.2019.00296 · Cited by 21
Exercise Is Medicine? The Cardiorespiratory Implications of Ultra-marathon
Tiller, N. B., Stewart, G. M., Illidi, C. R., & Levine, B. D. (2020) · Current Sports Medicine Reports · doi:10.1249/jsr.0000000000000738 · Cited by 22
Alterations in Cardiac Function Following Endurance Exercise Are Not Duration Dependent
Coates, A. M., King, T. J., Currie, K. D., Tremblay, J. C., Petrick, H. L., Slysz, J. T., Pignanelli, C., Berard, J. A., Millar, P. J., & Burr, J. F. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.581797 · Cited by 20
“…alterations are a natural and reversable response to prolonged exercise (Scott and Warburton, 2008), are indicative of structural myocardial damage (La Gerche et al., 2012), or are simply a consequence of altered loading conditions post-exercise (Middleton et al., 2006; Lord et al., 2018), is…”
BackgroundInfluentialExercise as therapy in congenital heart disease — A gamification approach
Stuart, G. (2014) · Progress in Pediatric Cardiology · doi:10.1016/j.ppedcard.2014.12.008 · Cited by 21
“The right ventricle is at particular risk from excessive endurance sport with the potential for fibrosis, dilatation and increased arrhythmias [102].”
BackgroundDynamic right ventricular function response to incremental exercise in pulmonary hypertension
Singh, I., Oliveira, R. K. F., Heerdt, P. M., et al. (2020) · Pulmonary Circulation · doi:10.1177/2045894020950187 · Cited by 20
Eijsvogels, T. M. H., Oxborough, D., O’Hanlon, R., Sharma, S., Prasad, S. K., Whyte, G. P., George, K., & Wilson, M. G. (2017) · European Journal of Sport Science · doi:10.1080/17461391.2017.1373864 · Cited by 23
“Somewhat counterintuitively, a high prevalence of MF has also been observed in veteran endurance athletes, with evidence of LGE in 12–50% of some athletic populations (Breuckmann et al., 2009; La Gerche et al., 2012; Wilson et al., 2011).”
BackgroundLu, J., Pan, S.-S., Wang, Q., & Yuan, Y. (2018) · International Heart Journal · doi:10.1536/ihj.17-003 · Cited by 20
Vio, R., Zorzi, A., & Corrado, D. (2020) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-020-09996-1 · Cited by 21
Cavigli, L., Zorzi, A., Spadotto, V., Gismondi, A., Sisti, N., Valentini, F., Anselmi, F., Mandoli, G. E., Spera, L., Florio, A. D., et al. (2021) · European Heart Journal - Cardiovascular Imaging · doi:10.1093/ehjci/jeab017 · Cited by 22
Sedentary and Active: Self-Reported Sitting Time Among Marathon and Half-Marathon Participants
Whitfield, G. P., Gabriel, K. P., & Kohl, H. W. (2013) · Journal of Physical Activity and Health · doi:10.1123/jpah.2011-0420 · Cited by 21
Exercise hypertension: Link to myocardial fibrosis in athletes?
Halle, M., Esefeld, K., Schindler, M., & Schunkert, H. (2019) · European Journal of Preventive Cardiology · doi:10.1177/2047487319868795 · Cited by 20
“In a way, these data exonerate such extreme exercise since others had generally observed discrete morphological alterations of the myocardium after endurance competitions,(6,7) including an increase of physiological strain of the myocardium during volume overload, particularly of the right ventricle.(8,9) The bad news…”
ResultStadiotti, I., Lippi, M., Maione, A. S., Compagnucci, P., Andreini, D., Casella, M., Pompilio, G., & Sommariva, E. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126500 · Cited by 22
Cardiac Risk of Extreme Exercise
Sharalaya, Z., & Phelan, D. M. J. (2018) · Sports Medicine and Arthroscopy Review · doi:10.1097/jsa.0000000000000215 · Cited by 20
Physical activity and exercise recommendations for patients with valvular heart disease
Chatrath, N., & Papadakis, M. (2022) · Heart · doi:10.1136/heartjnl-2021-319824 · Cited by 19
Cardiovascular Adaptation and Remodeling to Rigorous Athletic Training
Weiner, R. B., & Baggish, A. L. (2015) · Clinics in Sports Medicine · doi:10.1016/j.csm.2015.03.007 · Cited by 19
Luijkx, T., Cramer, M. J., Buckens, C. F. M., et al. (2013) · British Journal of Sports Medicine · doi:10.1136/bjsports-2013-092360 · Cited by 19
Complete Reversion of Cardiac Functional Adaptation Induced by Exercise Training
Oláh, A., Kellermayer, D., Mátyás, C., Németh, B. T., Lux, Á., Szabó, L., Török, M., Ruppert, M., Meltzer, A., Sayour, A. A., et al. (2016) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000001127 · Cited by 19
“According to previous human and experimental investigations, long-term intense training might be associated with myocardial fibrotic infiltrates and, thus, cardiac arrhythmogenic remodeling, principally as a result of right ventricular dilatation and diffuse interstitial collagen deposition (18).”
BackgroundShafer, K. M., Janssen, L., Carrick‐Ranson, G., Rahmani, S., Palmer, D., Fujimoto, N., Livingston, S. A., Matulevicius, S. A., Forbess, L. W., Brickner, B., et al. (2015) · The Journal of Physiology · doi:10.1113/jp270280 · Cited by 19
Focal Fibrosis in the Endurance Athlete’s Heart
Baggish, A. L. (2017) · JACC. Cardiovascular imaging · doi:10.1016/j.jcmg.2017.09.015 · Cited by 19
“Most notably, CMR demonstrated small amounts of focal “nonischemic” LGE (3.5 2.8% of total left ventricular [LV] myocardium) in 9 of 83 triathletes (11%), all of whom were men.”
BackgroundInfluentialVecchia, L. A. D., Barbic, F., MARIA, B. D., Cozzolino, D., Gatti, R., Dipaola, F., Brunetta, E., Zamunér, A. R., Porta, A., & Furlan, R. (2019) · PLoS ONE · doi:10.1371/journal.pone.0216567 · Cited by 21
Arrhythmogenic right ventricular cardiomyopathy
Basso, C., Calkins, H. G., & Corrado, D. (2023) · Oxford University Press eBooks · doi:10.1093/med/9780198891628.003.0010 · Cited by 19
Cardiac Troponin Release After Endurance Exercise: Still Much to Learn
Airaksinen, J. K. E. (2020) · Journal of the American Heart Association · doi:10.1161/jaha.120.015912 · Cited by 19
“11 Second, more marked troponin release has been observed among marathon runners with evidence of myocardial scarring, 12 and a pronounced and prolonged troponin increase may be related to obstructive atherosclerotic coronary artery disease.”
BackgroundMissenard, O., Gabaudan, C., Astier, H., Desmots, F., Garnotel, É., & Massoure, P. (2021) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2021.100196 · Cited by 18
Eyileten, C., Fitas, A., Jakubik, D., Czajka, P., Mróz, A., Czajkowska, A., Witek, K., Bakalarski, W., Rosa, S. D., Postula, M. A., et al. (2021) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph18147234 · Cited by 21
Ventricular arrhythmias in association with athletic cardiac remodelling
D’Ambrosio, P., Claessen, G., Kistler, P. M., Heidbüchel, H., Kalman, J. M., & Gerche, A. L. (2024) · EP Europace · doi:10.1093/europace/euae279 · Cited by 25
“Since the original description of EIACM, 38 there has been interest in other phenotypes of athletic remodelling predisposing to VAs and SCD, particularly demonstrated by the increasing availability and quality of CMR imaging.”
InfluentialSelf-citationRojas, A., & Calkins, H. G. (2014) · Trends in Cardiovascular Medicine · doi:10.1016/j.tcm.2014.10.007 · Cited by 18
“The disproportional increase in wall stress of the right ventricle during exercise as compared to the left can cause acute dysfunction of the right ventricle as a result of microtrauma [13,14].”
BackgroundResultRight ventricular adaptations and arrhythmias in amateur ultra-endurance athletes
Rimensberger, C., Carlen, F., Brugger, N., Seiler, C. A., & Wilhelm, M. (2013) · British Journal of Sports Medicine · doi:10.1136/bjsports-2013-092859 · Cited by 20
Bonikowske, A. R., Barout, A., Fortin-Gamero, S., Barillas-Lara, M. I., Kapa, S., & Allison, T. G. (2019) · Journal of Electrocardiology · doi:10.1016/j.jelectrocard.2019.03.009 · Cited by 18
Exercise-induced cardio-pulmonary remodelling in endurance athletes: Not only the heart adapts
Domènech-Ximenos, B., la Garza, M. S., Prat‐González, S., Sepúlveda-Martínez, Á., Crispi, F., Perea, R. J., García‐Álvarez, A., & Sitges, M. (2019) · European Journal of Preventive Cardiology · doi:10.1177/2047487319868545 · Cited by 18
Cardiovascular Remodeling Experienced by Real-World, Unsupervised, Young Novice Marathon Runners
D’Silva, A., Bhuva, A., van Zalen, J., Bastiaenen, R., Abdel‐Gadir, A., Jones, S. H., Nadarajan, N., Menacho, K., Ye, Y., Augusto, J. B., et al. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.00232 · Cited by 18
Left Ventricular Fibrosis in Middle-Age Athletes and Physically Active Adults
Banks, L., Altaha, M. A., Yan, A. T.-K., Dorian, P., Konieczny, K. M., Deva, D. P., Gerche, A. L., Akhavein, F., Bentley, R. F., Connelly, K. A., et al. (2020) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000002411 · Cited by 19
“The observed LGE findings were primarily confined to the RV inferior hinge point, consistent with previous reports (8,38), with a similar degree of focal RV hinge-point LGE”
ResultLasocka, Z., Lewicka-Potocka, Z., Kaleta-Duss, A. M., Siekierzycka, A., Kalinowski, L., Lewicka, E., & Dąbrowska-Kugacka, A. (2024) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00756.2023 · Cited by 18
Exercise Training in Group 2 Pulmonary Hypertension: Which Intensity and What Modality
Arena, R. A., Lavie, C. J., Borghi‐Silva, A., Daugherty, J., Bond, S., Phillips, S. A., & Guazzi, M. (2015) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2015.11.005 · Cited by 17
Cardiac Adaption to Exercise Training: the Female Athlete
Petek, B. J., & Wasfy, M. M. (2018) · Current Treatment Options in Cardiovascular Medicine · doi:10.1007/s11936-018-0659-2 · Cited by 17
Molitor, N., & Duru, F. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11051230 · Cited by 18
“Cardiac magnetic resonance (CMR) tissue characterization analyses in highly trained athletes have failed to show the presence of Late Gadolinium Enhancement (LGE) macroscopic fibrosis of the RV wall, with the exception of “junctional” LGE confined to the interventricular septum in the vicinity of the RV attachment, wh…”
BackgroundMy patient wants to perform strenuous endurance exercise. What's the right advice?
Sanchis‐Gomar, F., Santos‐Lozano, A., Garatachea, N., Pareja-Galeano, H., Fiuza‐Luces, C., Joyner, M. J., & Lucía, A. (2015) · International Journal of Cardiology · doi:10.1016/j.ijcard.2015.06.014 · Cited by 18
“as RA and right ventricle (RV) dilation, accompanied by decreased RV ejection fraction and elevation of biomarkers ofmyocardial stress/injury (troponin, B-type natriuretic peptide) [7,34,35], with an apparent dose– effect of event duration [34,35].”
BackgroundZaidi, A., & Sharma, S. (2012) · Future Cardiology · doi:10.2217/fca.12.81 · Cited by 18
Changes of intima-media thickness in marathon runners: A mid-term follow-up
Müller, J., Dahm, V., Lorenz, E., Preßler, A., Haller, B., Grabs, V., Halle, M., & Scherr, J. (2017) · European Journal of Preventive Cardiology · doi:10.1177/2047487317713327 · Cited by 17
Cornwell, W. K., Levine, B. D., Baptiste, D., Bhave, N. M., Desai, S., Dineen, E. H., Durstenfeld, M. S., Edward, J. A., Huang, M., Jacobsen, R. M., et al. (2025) · Circulation · doi:10.1161/cir.0000000000001348 · Cited by 17
Orgeron, G. M., & Calkins, H. G. (2016) · Current Cardiology Reports · doi:10.1007/s11886-016-0732-y · Cited by 16
Ollitrault, P., Pellissier, A., Champ‐Rigot, L., Junqua, N., Chequel, M., Reboursière, E., Saloux, É., Milliez, P., & Hodžić, A. (2020) · EP Europace · doi:10.1093/europace/euaa037 · Cited by 16
Characterizing the spectrum of right ventricular remodelling in response to chronic training
Sitges, M., Merino, B., Butakoff, C., la Garza, M. S., Paré, C., Montserrat, S., Vidal, B., Azqueta, M., Sarquella‐Brugada, G., Gutiérrez, J. A., et al. (2016) · International journal of cardiac imaging · doi:10.1007/s10554-016-1014-x · Cited by 16
“These different working conditions of the RV, despite not necessarily indicating RV dysfunction, might lead to higher wall stress when the ventricle is larger, and therefore, is more likely to develop myocardial fibrosis and scarring [7, 25, 26].”
BackgroundMarathon running for amateurs: Benefits and risks
Burkule, N. J. (2016) · Journal of Clinical and Preventive Cardiology · doi:10.4103/2250-3528.192681 · Cited by 18
Intensive Exercise Training Improves Cardiac Electrical Stability in Myocardial‐Infarcted Rats
Dor‐Haim, H., Lotan, C., Horowitz, M., & Swissa, M. (2017) · Journal of the American Heart Association · doi:10.1161/jaha.117.005989 · Cited by 16
“Furthermore, it was shown that intensive exercise enhanced left ventricular wall fibrosis and dyssynchrony and created a predisposition to arrhythmia because of electrical instability.(12,13) Recently it was shown that long-term (16 weeks), intensive exercise training in normal rats was associated with changes in card…”
BackgroundCardiac performance after an endurance open water swimming race
Martínez, V., la Garza, M. S., Grazioli, G. C., Bijnens, B. H., Trapé, J., Garcia, G., Corzan, P., Clemente, A., González, B., & Sitges, M. (2019) · European Journal of Applied Physiology · doi:10.1007/s00421-019-04085-x · Cited by 17
Physiological and Pathophysiological Consequences of a 25-Day Ultra-Endurance Exercise Challenge
Tiller, N. B., Chiesa, S. T., Roberts, J., Turner, L. A., Jones, S. H., & Romer, L. M. (2019) · Frontiers in Physiology · doi:10.3389/fphys.2019.00589 · Cited by 16
Bernardino, G., la Garza, M. S., Domènech-Ximenos, B., et al. (2020) · European Journal of Applied Physiology · doi:10.1007/s00421-020-04335-3 · Cited by 16
Nonsustained Ventricular Tachycardia in the Normal Heart
Marine, J. E. (2016) · Cardiac Electrophysiology Clinics · doi:10.1016/j.ccep.2016.04.003 · Cited by 16
“A few investigators have raised concern that endurance training may produce acute and chronic right ventricular (RV) dysfunction that may promote ventricular arrhythmias in otherwise normal athletic hearts.(64) Heidbuchel(65) reported on 46 high-level endurance athletes (80% cyclists) with ventricular arrhythmias (24…”
BackgroundRespiratory Determinants of Exercise Limitation
Dempsey, J. A. (2019) · Clinics in Chest Medicine · doi:10.1016/j.ccm.2019.02.002 · Cited by 16
Cardiac magnetic resonance in arrhythmogenic cardiomyopathies
Palumbo, P., Cannizzaro, E., Cesare, A. D., Bruno, F., Schicchi, N., Giovagnoni, A., Splendiani, A., Barile, A., Masciocchi, C., & Cesare, E. D. (2020) · La radiologia medica · doi:10.1007/s11547-020-01289-6 · Cited by 15
Franssen, W. M. A., Vanbrabant, E., Cuveele, E., Ivanova, A., Franssen, G. H. L. M., & Eijnde, B. O. (2021) · European Journal of Sport Science · doi:10.1080/17461391.2021.1955013 · Cited by 19
Differentiating Physiology from Pathology
Danielian, A., & Shah, A. B. (2022) · Clinics in Sports Medicine · doi:10.1016/j.csm.2022.02.005 · Cited by 17
Can the Heart Get an Overuse Sports Injury?
Thompson, P. D., Eijsvogels, T. M. H., & Kim, J. H. (2022) · NEJM Evidence · doi:10.1056/evidra2200175 · Cited by 15
Athlete's heart or heart disease in the athlete? Evaluation by cardiopulmonary exercise testing
Segreti, A., Picarelli, F., Gioia, G. D., Coletti, F., Crispino, S. P., Fanale, V., FOSSATI, C., Incalzi, R. A., Pigozzi, F., & Grigioni, F. (2023) · The Journal of Sports Medicine and Physical Fitness · doi:10.23736/s0022-4707.23.14536-1 · Cited by 15
Metadata
- Authors
- La Gerche, A., Burns, A. T., Mooney, D. J., Inder, W. J., Taylor, A. J., Bogaert, J., MacIsaac, A. I., Heidbüchel, H., & Prior, D. L.
- Affiliations
- St Vincent's Hospital Melbourne (AU)
- The University of Melbourne (AU)
- Baker Heart and Diabetes Institute (AU)
- Universitair Ziekenhuis Leuven (BE)
- ORCID
- Venue
- European Heart Journal
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-12-06
- Volume
- 33
- Issue
- 8
- Pages
- 998-1006
- ISSN
- 0195-668X (ISSN-L)
- 1522-9645
- OpenAlex
- W2148325692
- Semantic Scholar
- 7d299222e3e0cabc4deedc38d9035410d00d5777
- Cited by
- 776
- References
- 48
- Citations by year
- 2026: 34 · 2025: 41 · 2024: 36 · 2023: 38 · 2022: 62 · 2021: 42 · 2020: 82 · 2019: 48 · 2018: 62 · 2017: 61 · 2016: 64 · 2015: 62 · 2014: 71 · 2013: 38 · 2012: 30
- FWCI
- 28.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- European Heart Journal (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Keywords
- endurance athletes, right ventricular dysfunction, cardiac remodeling, myocardial fibrosis, arrhythmogenic cardiomyopathy, endurance exercise, right ventricular ejection fraction, late gadolinium enhancement, cardiac troponin I, brain natriuretic peptide, exercise-induced myocardial injury
- MeSH terms
- Adult, Female, Fibrosis, Humans, Male, Middle Aged, Myocardium, Physical Endurance, Stroke Volume, Biomarkers, Exercise, Ventricular Dysfunction, Right, Magnetic Resonance Angiography, Troponin I, Ventricular Remodeling, Athletes
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