Reproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes

Scharhag, Jürgen; Urhausen, Axel; Schneider, Günther; Herrmann, Markus; Schumacher, Katrin; Haschke, Michaela; Krieg, Anne; Meyer, Tim; Herrmann, Wolfgang; Kindermann, Wilfried

doi:10.1097/01.hjr.0000219117.33038.90

Cited by 71 publications

(50 citation statements)

References 36 publications

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“…While the role of ANP in the regulation of fluid balance during exercise has been widely evaluated (1), the role of BNP in fluid homeostasis has not (8). BNP is considered a marker of fluid overload (32), and has been measured after exercise primarily as an indicator of cardiac dysfunction (33). The significant increase in [NT-proBNP] P that is seen in our subjects following prolonged endurance exercise, but not highintensity or steady-state exercise, has been noted previously (33).…”

Section: Discussionmentioning

confidence: 99%

“…BNP is considered a marker of fluid overload (32), and has been measured after exercise primarily as an indicator of cardiac dysfunction (33). The significant increase in [NT-proBNP] P that is seen in our subjects following prolonged endurance exercise, but not highintensity or steady-state exercise, has been noted previously (33). Because [NT-proBNP] P was not significantly elevated after the VO 2 max test (where blood pressure, heart rate, and cardiac output would be the highest (34)) but is increased fourfold after the ultramarathon (where mean arterial pressure and left ventricular diameter are significantly reduced (35)), it appears that stimuli apart from the cardiovascular system may be responsible for the increase in BNP seen after prolonged endurance exercise.…”

Section: Discussionmentioning

confidence: 99%

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Acute changes in endocrine and fluid balance markers during high-intensity, steady-state, and prolonged endurance running: unexpected increases in oxytocin and brain natriuretic peptide during exercise

Hew‐Butler

Noakes²,

Soldin³

et al. 2008

European Journal of Endocrinology

100

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Maintenance of fluid homeostasis during periods of heightened physical stress can be best evaluated in humans using exercise as a model. Although it is well established that arginine vasopressin (AVP), aldosterone and atrial natriuretic peptide (ANP) are the principle hormones regulating fluid balance at rest, the potential contributions of other related endocrine factors, such as oxytocin (OT) and brain natriuretic peptide (BNP), have not been well described during exercise. Seven endurance-trained runners completed three separate running trials: a maximal test to exhaustion (high intensity), a 60-min treadmill run (steady state), and a 56 km ultramarathon (prolonged endurance exercise). Statistically significant pre-to post-run increases were found only following the ultramarathon in [AVP] p (1.9 vs 6.7 pg/ml; P!0.05), [OT] p (1.5 vs 3.5 pg/ml; P!0.05), [NT-proBNP] p (23.6 vs 117.9 pg/ml; P!0.01), [interleukin 6] p (4.0 vs 59.6 pg/ml; P!0.05), [cortisol] p (14.6 vs 32.6 mg/ml; P!0.01), [corticosterone] p (652.8 vs 3491.4 ng/ml; P!0.05) and [11-deoxycortisol] p (0.1 vs 0.5 mg/ml; P!0.05) while a significant post-run increase in [aldosterone] p was documented after high-intensity (4.9 vs 12.5 ng/ml; P!0.05), steady-state (6.1 vs 16.9 ng/ml; P!0.05) and prolonged endurance running (2.6 vs 19.7 ng/ml; P!0.05). Similarly, changes in fluid balance parameters were significantly different between the ultramarathon versus high-intensity and steady-state running with regard to plasma volume contraction (less % contraction), body weight loss (increased % weight loss), plasma

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Acute changes in endocrine and fluid balance markers during high-intensity, steady-state, and prolonged endurance running: unexpected increases in oxytocin and brain natriuretic peptide during exercise

Hew‐Butler

Noakes²,

Soldin³

et al. 2008

European Journal of Endocrinology

100

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“…The kinetic profile of cTnI and cTnT circulating levels after strenuous exercise in apparently healthy subjects [25,40,[52][53][54][55][56][77][78][79][80][81][82][83][84][85][86][87][88][89][90] is different from that usually observed in patients with AMI. It is well known that circulating levels of cTnI and cTnT in patients with uncomplicated type 1 AMI usually peak between 12 and 36 h from beginning of thoracic pain, gradually returning to below the 99th URL value within 5-7 days [1,3,40,76].…”

Section: Mechanisms Of Troponin Release In Cardiac Patients and Healtmentioning

confidence: 99%

The 99th percentile of reference population for cTnI and cTnT assay: methodology, pathophysiology and clinical implications

Clerico

Zaninotto

Ripoli

et al. 2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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According to recent international guidelines, including the 2012 Third Universal Definiton of Myocardial Infarction by the Joint ESC/ACCF/AHA/WHF Task Force, an increase in cardiac troponin (cTn) levels over the 99th percentile upper reference limit (99th URL) should be considered clinically relevant, this cut-off being measured with an imprecision ≤10 CV%. In theory 99th URL values strongly depend not only on demographic and physiological variables (i.e. criteria for considering the reference population "healthy"), but also on the analytical performance of cTn methods and mathematical algorithms used for the calculation. The aim of the present article was therefore to review the methodological and pathophysiological factors affecting the evaluation and calculation of the 99th URL for cTn assay. The critical analysis made showed that no uniform procedure is followed, and nor have experts or regulatory bodies provided uniform guidelines for researchers or cTn assays manufacturers as an aid in "their quest to define normality". In particular, little attention has been paid to the way in which a healthy reference population is to be selected, or the criteria for calculating the 99th URL value for cTn assays, thus highlighting the need for international recommendations not only for demographic and physiological variables criteria for defining a healthy reference population, but also for calculating mathematical algorithms for establishing/ calculating clinical decision values. An expert consensus group, comprising laboratory and clinical scientists, biomedical statisticians, industrial and regulatory representatives, should be responsible for drawing up these guidelines.

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“…16 Therefore, to date, long-term clinical consequences caused by repeated intensive endurance exercise remain speculative. Studies evaluating the clinical impact of long-term intensive endurance training and competition in high-level elite master athletes are rare.…”

Section: May 17 2016mentioning

confidence: 99%

Right and Left Ventricular Function and Mass in Male Elite Master Athletes

et al. 2016

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Background— It is under debate whether the cumulative effects of intensive endurance exercise induce chronic cardiac damage, mainly involving the right heart. The aim of this study was to examine the cardiac structure and function in long-term elite master endurance athletes with special focus on the right ventricle by contrast-enhanced cardiovascular magnetic resonance. Methods and Results— Thirty-three healthy white competitive elite male master endurance athletes (age range, 30–60 years) with a training history of 29±8 years, and 33 white control subjects pair-matched for age, height, and weight underwent cardiopulmonary exercise testing, echocardiography including tissue-Doppler imaging and speckle tracking, and cardiovascular magnetic resonance. Indexed left ventricular mass and right ventricular mass (left ventricular mass/body surface area, 96±13 and 62±10 g/m 2 ; P <0.001; right ventricular mass/body surface area, 36±7 and 24±5 g/m 2 ; P <0.001) and indexed left ventricular end-diastolic volume and right ventricular end-diastolic volume (left ventricular end-diastolic volume/body surface area, 104±13 and 69±18 mL/m 2 ; P <0.001; right ventricular end-diastolic volume/body surface area, 110±22 and 66±16 mL/m 2 ; P <0.001) were significantly increased in athletes in comparison with control subjects. Right ventricular ejection fraction did not differ between athletes and control subjects (52±8 and 54±6%; P =0.26). Pathological late enhancement was detected in 1 athlete. No correlations were found for left ventricular and right ventricular volumes and ejection fraction with N-terminal pro-brain natriuretic peptide, and high-sensitive troponin was negative in all subjects. Conclusions— Based on our results, chronic right ventricular damage in elite endurance master athletes with lifelong high training volumes seems to be unlikely. Thus, the hypothesis of an exercise-induced arrhythmogenic right ventricular cardiomyopathy has to be questioned.

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Reproducibility and clinical significance of exercise-induced increases in cardiac troponins and N-terminal pro brain natriuretic peptide in endurance athletes

Abstract: Due to the missing reproducibilty and evidence of myocardial damage, exercise-induced increases in cardiac troponins may represent a physiologic reaction under special conditions and seem to be without pathological significance in healthy athletes.

Cited by 71 publications

References 36 publications

Acute changes in endocrine and fluid balance markers during high-intensity, steady-state, and prolonged endurance running: unexpected increases in oxytocin and brain natriuretic peptide during exercise

Acute changes in endocrine and fluid balance markers during high-intensity, steady-state, and prolonged endurance running: unexpected increases in oxytocin and brain natriuretic peptide during exercise

The 99th percentile of reference population for cTnI and cTnT assay: methodology, pathophysiology and clinical implications

Right and Left Ventricular Function and Mass in Male Elite Master Athletes

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