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☆
Lang, R. M., Bierig, M., Devereux, R. B., Flachskampf, F. A., Foster, E., Pellikka, P. A., Picard, M. H., Roman, M. J., Seward, J. B., & Shanewise, J. S. (2006) · European Journal of Echocardiography · doi:10.1016/j.euje.2005.12.014 · Cited by 3,588
Marcus, F. I., McKenna, W. J., Sherrill, D., Basso, C., Bauce, B., Bluemke, D. A., Calkins, H., Corrado, D., Cox, M. G. P. J., Daubert, J. P., et al. (2010) · Circulation · doi:10.1161/circulationaha.108.840827 · Cited by 2,676
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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 501–600 of 773
Bosscher, R. D., Heidbüchel, H., Claessen, G., & Gerche, A. L. (2022) · British Journal of Sports Medicine · doi:10.1136/bjsports-2022-105440 · Cited by 4
Self-citationRight Ventricle Chamber of Young Trained Athletes: Morphology and Function
Luca, A. D., Stefani, L., & Galanti, G. (2013) · Asian Journal of Sports Medicine · doi:10.5812/asjsm.34248 · Cited by 4
(2012) · European Heart Journal · doi:10.1093/eurheartj/ehs094 · Cited by 4
The hearts of competitive athletes: An up-to-date overview of exercise-induced cardiac adaptations
Dores, H., Freitas, A., Malhotra, A., Mendes, M., & Sharma, S. (2015) · Revista Portuguesa de Cardiologia (English Edition) · doi:10.1016/j.repce.2014.07.008 · Cited by 4
“La Gerche et al.20 showed that RV volumes increase after endurance races, whereas LV volumes decrease, resulting in decreased RV but not LV ejection fraction (LVEF).”
BackgroundEndurance Exercise and Myocardial Fibrosis
Shave, R., & Oxborough, D. (2016) · Circulation Cardiovascular Imaging · doi:10.1161/circimaging.116.005730 · Cited by 4
“small number of elite or veteran athletes evidence of focal myocardial fibrosis.(10,11) These authors suggest that this is evidence of the Phidippides Cardiomyopathy,(9) with a cause”
BackgroundCardiovascular Imaging Considerations for Masters-Aged Athletes
Phelan, D. M. J., Claessen, G., Eijsvogels, T. M. H., Churchill, T. W., Dineen, E. H., Gati, S., Guseh, J. S., Hsu, J. J., Shah, A. B., Sperry, B. W., et al. (2025) · JACC. Cardiovascular imaging · doi:10.1016/j.jcmg.2025.10.024 · Cited by 5
Long-Term Changes in Ventricular Function in Recreational Marathon Runners
Schindler, M., Schoenfeld, J., Trommler, A., Haller, B., Nieman, D. C., Halle, M., & Scherr, J. (2025) · JAMA Cardiology · doi:10.1001/jamacardio.2025.4456 · Cited by 3
Suppression of tumorigenicity 2 after exercise: a systematic review
da Costa, A. M., Teixeira, R., Vilela, E., Tavares, A., Torres, S., Sampaio, F., Teixeira, M., Fontes‐Carvalho, R., & Nunes, J. P. L. (2021) · Monaldi Archives for Chest Disease · doi:10.4081/monaldi.2021.1839 · Cited by 3
Dausin, C., Tironi, R. M., Cornelissen, V., Hespel, P., Willems, R., Haykowsky, M. J., Gerche, A. L., Claessen, G., & Foulkes, S. (2024) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2024.12.009 · Cited by 5
Guo, C., Zhang, H., Yang, C., Hu, P., Ma, H., Ma, Y., & Gao, F. (2025) · BMC Cardiovascular Disorders · doi:10.1186/s12872-024-04455-0 · Cited by 4
“…that prolonged endurance exercise is associated with structural, functional, and bio-chemical markers of cardiac dysfunction in highly trained athletes [6], a mechanism called ‘cardiac fatigue’ has been proposed to explain the decline in resting heart function of athletes after intense exercise.”
InfluentialMoser, O., Schunk, S. J., Schöffl, V., Schierbauer, J., & Zimmermann, P. (2025) · Life · doi:10.3390/life15071095 · Cited by 4
Sudden cardiac death in athletes
Król, W., Mamcarz, A., & Braksator, W. (2016) · Kardiologia Polska · doi:10.5603/kp.a2016.0017 · Cited by 3
“Recently there has been intensive ongoing discussion on a possible acquired form of pathologic RV remodelling due to intensive exercise, triggered by the observations of group of athletes (predominantly cyclist) with complex ventricular arrhythmias [35, 36].”
BackgroundCardiovascular risk among ultra-endurance runners
Shah, A. B., Torguson, R., Alexander, K., Umar, K. H. A. N., Zhang, C., Fisher, C., Hoffman, M. D., Sedgley, M. D., Lincoln, A. E., & Baggish, A. L. (2021) · The Journal of Sports Medicine and Physical Fitness · doi:10.23736/s0022-4707.21.11903-6 · Cited by 4
Decreased Native T1 Values and Impaired Myocardial Contractility in Anabolic Steroid Users
de Souza, F. R., dos Santos, M. R., Rochitte, C. E., et al. (2021) · International Journal of Sports Medicine · doi:10.1055/a-1518-7953 · Cited by 3
“Moreover, prolonged endurance training may trigger cardiac injury with consequent myocardial fibrosis [32].”
BackgroundRight Heart Resilience and Atrial Fibrillation Risk in Long-Term Endurance Athletes
Petek, B. J., Hayes, D., & Wasfy, M. M. (2022) · Journal of the American Society of Echocardiography · doi:10.1016/j.echo.2022.09.019 · Cited by 4
Ping, Z., Li, J., Sun, Y., Zhang, X., Wang, Z., & Cao, X. (2022) · The Chinese Journal of Physiology · doi:10.4103/0304-4920.365457 · Cited by 4
Kerstens, T. P., Donker, S. C. M., Kleinnibbelink, G., et al. (2024) · Echo Research and Practice · doi:10.1186/s44156-024-00046-z · Cited by 3
“These latter volumetric changes have been reported previously in the literature [30].”
BackgroundMaleki, F., & Mehrabani, J. (2024) · International Journal of Cardiology · doi:10.1016/j.ijcard.2024.132316 · Cited by 3
Features of cardiac remodeling depending on the mode of training session
Малахова, С. Н., Сыволап, В. В., & Потапенко, М. С. (2020) · Zaporozhye Medical Journal · doi:10.14739/2310-1210.2020.5.214735 · Cited by 3
“It is well known, that myocardial fibrosis can be a substrate for ventricular tachycardia and sudden death in susceptible individuals [18].”
BackgroundSports cardiology: lessons from the past and perspectives for the future
Leischik, R. (2015) · F1000Research · doi:10.12688/f1000research.6318.1 · Cited by 3
Hazebroek, M. R., van Paassen, P., Weerwind, P. W., et al. (2013) · International Journal of Cardiology · doi:10.1016/j.ijcard.2013.11.028 · Cited by 3
“The incessant RV arrhythmogeneity was intriguing and, interestingly, related to a reduced expression of desmosomal plakoglobin, associated with RV arrhythmias in athletes and other arrhythmogenic RV cardiomyopathies [4,5] (Appendix 3).”
BackgroundAppelman, Y., Borgh, R. V., van Dantzig, J. M., Mosterd, A., Daniels, M. C. G., & Doevendans, P. A. (2014) · European Journal of Preventive Cardiology · doi:10.1177/2047487314553781 · Cited by 3
“in 2008 and 2012, in which they found a reduced right ventricular function and TAPSE.(3,7,8) This contrast might be explained by the fact that they presented data following Figure 1.”
BackgroundBohm, P., Kindermann, W., Meyer, T., & Scharhag, J. (2016) · Circulation · doi:10.1161/circulationaha.116.024362 · Cited by 3
Right Heart-Pulmonary Circulation Unit in Cardiomyopathies and Storage Diseases
D’Andrea, A., Formisano, T., Gerche, A. L., Cardim, N. M., Carbone, A., Scarafile, R., Martone, F., D’Alto, M., Bossone, E., & Galderisi, M. (2018) · Heart Failure Clinics · doi:10.1016/j.hfc.2018.03.001 · Cited by 5
Weihl, F. M., & Guilder, G. P. V. (2018) · The Journal of Strength and Conditioning Research · doi:10.1519/jsc.0000000000002769 · Cited by 3
“Clinical studies in young- to middle-aged athletes suggest that a single bout of ultraendurance exercise elicits acute changes in heart structure (20) and function (34).”
BackgroundThe influence of non-modifiable and modifiable factors on cardiac biomarkers after marathon running
Martin, T. G., Pata, R. W., Jou, D., Narowska, G., Myrick, K. M., Malloy, K. A., Lafalce, A., & Feinn, R. (2019) · The Journal of Sports Medicine and Physical Fitness · doi:10.23736/s0022-4707.19.09247-8 · Cited by 3
Marked Disparity in Regional and Transmural Cardiac Mechanics in the Athlete’s Heart
Stewart, G. M., Chan, J. H., Kane, G. C., Johnson, B. D., Balmain, B. N., Yamada, A., Shiino, K., Haseler, L. J., & Sabapathy, S. (2020) · Medicine & Science in Sports & Exercise · doi:10.1249/mss.0000000000002336 · Cited by 3
“Furthermore, it is speculated that the reduced LV and RV strain in the athlete’s heart could represent myocardial maladaptation (11), given evidence of acute cardiac injury and rare cases of controversial adaptive remodeling with extreme volumes of endurance exercise (16).”
BackgroundLeischik, R., Spelsberg, N., Niggemann, H., Dworrak, B., & Tiroch, K. A. (2014) · F1000Research · doi:10.12688/f1000research.4288 · Cited by 3
The Acute Impact of Endurance Exercise on Right Ventricular Structure and Function
Ramcharan, T., Edwards, J. J., O’Driscoll, J. M., & Papadakis, M. (2022) · Cardiology Clinics · doi:10.1016/j.ccl.2022.08.004 · Cited by 3
Insights from Exercise-induced Cardioprotection-from Clinical Application to Basic Research
Jiang, H., Zhang, B., Jia, D., Yang, W., Sun, A., & Ge, J. (2019) · Current Pharmaceutical Design · doi:10.2174/1381612825666191008102047 · Cited by 3
Unraveling the Unsolved Mysteries of the Athletic Heart
Cornwell, W. K., & Levine, B. D. (2024) · Circulation · doi:10.1161/circulationaha.124.064534 · Cited by 3
De Paepe, J., D’Ambrosio, P., De Bosscher, R., Bekhuis, Y., Pauwels, R., Dausin, C., Janssens, K., Mitchell, A., Elliott, A., Van De Heyning, C. M., et al. (2026) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwaf715 · Cited by 2
Self-citationCardiac Effects of Prolonged Endurance Exercise in Young and Older Athletes
Frandsen, J., Aarøe, M., Sehestedt, T. B., Sahl, R. E., Hansen, M. T., Lie‐Olesen, M. M., Nielsen, A. B., Rømer, T., Ingersen, A., Larsen, S., et al. (2025) · Scandinavian Journal of Medicine and Science in Sports · doi:10.1111/sms.70104 · Cited by 2
“La Gerche et al. further described a post-exercise duration-dependent RV deterioration with greater functional impairment in those who competed at high intensity for the longest time (> 12 h) [29].”
Physical Activity and Cardiovascular Outcomes in Phenotype-Negative Cardiomyopathy Variant Carriers
Ajufo, E. C., Kany, S., Jurgens, S. J., Churchill, T. W., Guseh, J. S., Aragam, K. G., Nauffal, V., Pirruccello, J. P., Choi, S. H., Lakdawala, N. K., et al. (2025) · JAMA Cardiology · doi:10.1001/jamacardio.2025.4466 · Cited by 2
New Insights in Exercise for Arrhythmogenic Cardiomyopathy: A Narrative Review
Aljohar, A., Laksman, Z., Boroditsky, N. D., Moulson, N., & McKinney, J. (2025) · CJC Open · doi:10.1016/j.cjco.2025.12.012 · Cited by 2
“15 For these reasons, along with the thinner wall of the RV, the hemodynamic stresses of exercise may disproportionately affect the RV. 16 Participation in intense endurance races resulted in acute dysfunction of the RV with no deleterious effect on the LV. 17 Therefore, a biologically and physiologically plausible re…”
Waxman, A. B., Babu, A. S., Badagliacca, R., et al. (2026) · Pulmonary Circulation · doi:10.1002/pul2.70240 · Cited by 2
“Since RV dysfunction severity depends on the exercise intensity and duration [135, 136], results can guide individualized exercise prescriptions for patients with PH.”
Wang, Y., Du, X., & Wang, Q. (2026) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2026.1746819 · Cited by 5
Preventive Cardiology: The Effects of Exercise
Khera, A., Mitchell, J. H., & Levine, B. D. (2007) · Springer eBooks · doi:10.1007/978-1-84628-715-2_129 · Cited by 2
Leischik, R., & Spelsberg, N. (2014) · Journal für Kardiologie · Cited by 2
Common electrocardiogram variations pre‐ and post‐marathon
Martin-Beaulleu, J., Myrick, K. M., Martin, T., Pata, R. W., & Feinn, R. (2016) · Clinical Case Reports · doi:10.1002/ccr3.650 · Cited by 2
“They found the right ventricle more profoundly affected by high-intensity exercise than the left, and although the insult was transient, led to speculation about a dose-dependent arrhythmogenic effect of exercise on the RV [12].”
BackgroundCan too much exercise be dangerous: what can we learn from the athlete’s heart?
Goh, F. Q. (2021) · British Journal of Cardiology · doi:10.5837/bjc.2021.030 · Cited by 4
Preventive Cardiology: The Effects of Exercise
Schopfer, D. W., Khera, A., Levine, B. D., & Forman, D. E. (2015) · Cardiovascular medicine · doi:10.1007/978-1-4471-2828-1_28 · Cited by 2
Role of cardiac magnetic resonance imaging in troponinemia syndromes
Nguyen, N. N., Assad, J., Femia, G., Schuster, A., Otton, J. M., & Nguyen, T. L. (2022) · World Journal of Cardiology · doi:10.4330/wjc.v14.i4.190 · Cited by 3
Difference in cardiac remodeling between female athletes and pregnant women: a case control study
Toncelli, L., Pasquini, L., Masini, G., et al. (2022) · Cardiovascular Ultrasound · doi:10.1186/s12947-022-00280-7 · Cited by 2
Cardiovascular adaptations and inflammation in marathon runners
Tsarouhas, K., Tsitsimpikou, C., Samaras, A., Saravanis, C., Kolovou, G. D., Bacopoulou, F., Spandidos, D. A., & Kouretas, D. (2022) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2022.11635 · Cited by 4
An Athlete With Bicuspid Aortic Valve Regurgitation and Left Ventricular Dilatation
Chatrath, N., Bhatia, R., Fyyaz, S., et al. (2022) · JACC Case Reports · doi:10.1016/j.jaccas.2022.05.021 · Cited by 2
“Furthermore, in athletes with a dilated LV, other cardiovascular adaptations (eg, proportional RV dilatation) are expected.(3) In our case, the right ventricle remained normal in size, thus further suggesting that the degree of LV dilatation was beyond physiologic cardiac adaptation to exercise.”
BackgroundTakeshita, M., Arai, H., Nagaoka, E., et al. (2023) · European Journal of Cardio-Thoracic Surgery · doi:10.1093/ejcts/ezad108 · Cited by 2
Mechanobiology of Exercise-Induced Cardiac Remodeling in Health and Disease
Cornwell, W. K., & Buttrick, P. M. (2023) · Cardiac and vascular biology · doi:10.1007/978-3-031-23965-6_9 · Cited by 2
The Acute Impact of Endurance Exercise on Right Ventricular Structure and Function
Ramcharan, T., Edwards, J. J., O’Driscoll, J. M., & Papadakis, M. (2024) · Cardiac Electrophysiology Clinics · doi:10.1016/j.ccep.2023.09.005 · Cited by 2
Aaserud, L. T., Rootwelt‐Norberg, C., Five, C. K., Aabel, E. W., Hasselberg, N. E., Lyseggen, E., Haugaa, K. H., & Lie, Ø. H. (2024) · Heart Rhythm O2 · doi:10.1016/j.hroo.2024.08.003 · Cited by 2
Jean, C., Laprérie, A.-L., Guyomarch, B., et al. (2025) · JACC. Clinical electrophysiology · doi:10.1016/j.jacep.2025.05.007 · Cited by 2
Modalities to Improve the Spinal Column Dysfunctions by using Some Complementary Kinetic Means
Acasandrei, L., & Macovei, S. (2014) · Procedia - Social and Behavioral Sciences · doi:10.1016/j.sbspro.2014.02.260 · Cited by 2
Implantable Cardioverter Defibrillator in Sport Participation
Mascia, G., Biase, L. D., Galanti, G., Natale, A., & Padeletti, L. (2014) · International Journal of Sports Medicine · doi:10.1055/s-0033-1361185 · Cited by 2
Stavroulakis, G. A., Methenitis, S. K., Koutroulis, G., Xanthis, D., Cherouveim, E. D., Κroupis, C., Anastasiadis, G., Ketselidi, K., Vlachopoulou, E., Tsolakis, C. K., et al. (2022) · Biomarkers · doi:10.1080/1354750x.2022.2062449 · Cited by 2
Pathologies cardiaques à risque chez le jeune sportif
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“[22] La Gerche A, Burns AT, Mooney DJ et al.”
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“This septal fibrosis was encountered among individuals with the most marked RV dilation and was associated with an increased incidence of ventricular arrhythmias [51].”
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Cardiovascular Evaluation and Treatment of the Endurance Athlete
Michaud-Finch, J., & Baggish, A. L. (2016) · Springer eBooks · doi:10.1007/978-3-319-32982-6_1 · Cited by 3
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“Other controversial data suggest that chronic exposure to ultra-endurance exercise is associated with an ARVC-like exercise-induced RV cardiomyopathy.(4) We present an unusual case of a marathon runner who had symptomatic VT and nonpathologic f indings on cardiac imaging studies.”
BackgroundEinführung in das Herz-Kreislauf-System
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Prolonged Intensive Exercise: When the Right Ventricle Goes Wrong
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Endurance exercise and myocardial injury
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Cardiac Troponin in Endurance Exercise—Fragments of the Imagination or Clinical Significance?
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“Although these changes are physiological, myocardial damage can occur when exercise is strenuous and prolonged, and although either of the two ventricles can be involved, the right ventricle (RV) is the most commonly affected.(8) The degree of right ventricular dysfunction seems to depend on the intensity and duration…”
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Medical Evaluation of Athletes: Echocardiography
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Intense Endurance Exercise: A Potential Risk Factor in the Development of Heart Disease
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“[10] were that the effects of myocardial fibrosis and cardiac remodelling were directly linked to cardiac dysfunction, which shed light on possible mechanisms that endurance exercise affects the heart.”
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“Studies in relatively amateur marathon runners [ 57 – 59 ] as well as well-trained ultraendurance runners [ 60 ] and triathletes [ 61 , 62 ] have consistently demonstrated signifi cant decrements in RV function immediately following exercise, whereas LV function is preserved.”
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“However, importantly, none of these athletes had ventricular arrhythmias (2,3).”
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Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy
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Exercise-induced right ventricular cardiomyopathy in an endurance cyclist: a case report
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“This also acts as a causative mechanism to explain chronic adverse remodelling.(3,13) While scar burden and positioning could form the basis for screening tools assessing risk of RV remodelling or SCD, ICD implantation remains a cornerstone preventative strategy of SCD.”
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Influence of a 7‐day Transalpine Trail Run on cardiac biomarkers and myocardial function
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“12,13,27 Our findings add to these data, showing no significant changes in CMR directly after the race in large sample of athletes of both genders.”
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Prediction of cardiac remodeling and myocardial fibrosis in athletes based on IVIM-DWI images
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“La Gerche et al. (2011) despite these elevated values, FAC remained within the normal reference range (Rudski et al. 2010).”
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“These ECG patterns should be interpreted for a differential diagnosis between physiological remodeling and arrhythmogenic cardiomyopathy [24].”
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Clinical Considerations for the Care of the Tactical Athlete With Cardiovascular Abnormalities
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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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