Post marathon cardiac troponin T is associated with relative exercise intensity

Richardson, Alan; Leckie, Todd; Watkins, Emily; Fitzpatrick, Daniel; Galloway, Rob; Grimaldi, Rachael; Baker, Polly

doi:10.1016/j.jsams.2018.02.005

Cited by 43 publications

(60 citation statements)

References 28 publications

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“…The results concerning skeletal muscle damage, temporary decline of kidney function and inflammation markers after the Kalmar Ironman 2016 are in line with previous research in athletes engaging in either triathlon12 13 or other types of endurance sports such as marathon11 19 or ultradistance running 20. Given the amount of exercise, the results are neither surprising nor do they lead to any debate about long-term consequences.…”

Section: Discussionsupporting

confidence: 85%

Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death

Danielsson

Schreyer

Woksepp

et al. 2019

BMJ Open Sport Exerc Med

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ObjectiveIt has been suggested that the mechanism behind cardiac troponin elevation after strenuous exercise is passage through a cell membrane with changed permeability rather than myocardial cell death. We hypothesised that an increase of cardiac specific myosin heavy chain-alpha (MHC-α; 224 kDa compared with cardiac troponin T’s (cTnT) 37 kDa) could hardly be explained by passage through a cell membrane.MethodsBlood samples were collected from 56 athletes (15 female, age 42.5±9.7, range 24–70 years) before, directly after and on days 1–8 after an Ironman. Biomarkers (C reactive protein (CRP), cTnT, creatine kinase (CK), MHC-α, myoglobin (MG), creatinine (C) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) were measured.ResultsThe course of MHC-α concentration (µg/L) was 1.33±0.53 (before), 2.57±0.78 (directly after), 1.51±0.53 (day 1), 2.74±0.55 (day 4) and 1.83±0.76 (day 6). Other biomarkers showed a one-peaked increase with maximal values either directly after the race or at day 1: cTnT 76 ± 80 ng/L (12–440; reference<15), NT-proBNP 776±684 ng/L (92–4700; ref.<300), CK 68±55 µkat/L (5–280; ref.<1.9), MG 2088±2350 µg/L (130–17 000; ref.<72) and creatinine 100±20 µmol/L (74–161; ref.<100), CRP 49±23 mg/L (15–119; ref.<5).ConclusionMHC-α exhibited a two-peaked increase which could represent a first release from the cytosolic pool and later from cell necrosis. This is the first investigation of MHC-α plasma concentration after exercise.

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Section: Discussionsupporting

confidence: 85%

Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death

Danielsson

Schreyer

Woksepp

et al. 2019

BMJ Open Sport Exerc Med

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“…Our findings for the effect of intensity of intermittent exercise are consistent with other studies, reviewed in the Introduction, showing greater elevation of cardiac biomarkers with higher intensity exercise. In particular, it obtained pronounced high-sensitivity cardiac troponin-T elevation after intermittent exercise with average heart rate of 160 min −1 , which was similar to the mean heart rate of our runners (Richardson et al, 2018). Stewart et al (2016) suggested that a heart rate of 145 min −1 was a threshold for the elevation of cardiac troponin.…”

Section: Discussionsupporting

confidence: 83%

“…A transient increase in myocardial membrane permeability appears to be responsible, but the mechanism is still under debate (Nie et al, 2010(Nie et al, , 2016Li et al, 2016b). Eijsvogels et al (2016) concluded that exercise intensity was the strongest single predictor of exerciseinduced cardiac troponin elevation, and Richardson et al (2018) found that cardiac troponin was associated with both mean and peak heart rate during exercise. Gresslien and Agewall (2016) hypothesized that there might be a threshold exercise intensity where cardiac troponin release became more marked.…”

Section: Introductionmentioning

confidence: 99%

Effects of Matched Intermittent and Continuous Exercise on Changes of Cardiac Biomarkers in Endurance Runners

Nie

Zhang

et al. 2020

Front. Physiol.

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Exercise Physiology, a section of the journal Frontiers in PhysiologyPurpose: Endurance runners training with high-intensity intermittent exercise might experience damage to cardiac muscle. We have therefore compared changes of cardiac biomarkers after workload-matched intermittent and continuous exercise.Methods: Twelve endurance runners [11 males, 1 female; means ± SDVO 2max , 62.4 ± 5.4 ml kg −1 min −1 ; velocity ofVO 2max (vVO 2max ), 17.1 ± 1.4 km h −1 ] completed an intermittent and continuous exercise trial in random order. Intermittent exercise consisted of running at 90% vVO 2max for 2 min followed by 50% vVO 2max for 2 min, repeated for 92 min. Continuous exercise was performed at 70% vVO 2max for 92 min. Blood samples were drawn before and 0, 2, 4, 24, and 48 h after exercise for assay of various cardiac biomarkers. Changes in concentration of biomarkers were averaged for the comparison of intermittent with continuous exercise after adjustment for baseline concentration and exercise intensity expressed as percent of heart-rate reserve (%HRR); magnitudes were assessed by standardization.Results: There were moderate and large increases in high-sensitivity cardiac troponin-I and -T respectively following exercise. The differences between the increases adjusted to the mean intensity of 78 %HRR were trivial, but at 85 %HRR the increases for cardiac troponin-I and -T were moderately higher for intermittent compared with continuous exercise (factor difference, ×/÷90% confidence limits: 3.4, ×/÷1.9 and 2.1, ×/÷1.8 respectively). Differences in the changes in other cardiac biomarkers were trivial.Conclusion: Prolonged intermittent exercise is potentially more damaging to cardiac muscle than continuous exercise of the same average running speed at higher average heart rates in endurance runners.

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“…Exhaustive exercise could cause myocardial cell edema and increased membrane permeability, and the rupture of myocardial fibers caused the release of cTn-I in cardiomyocyte to peripheral blood [21]. e acute overload exercise increased the level of cardiac calcium protein in the peripheral blood, and the increase of the serum myocardial injury marker enzyme was related to exercise intensity [22]. After EP, the content of myocardial enzyme in serum of exhausted rats decreased, which indicated that EP had the ability to resist the myocardial injury.…”

Section: Discussionmentioning

confidence: 99%

Exercise Preconditioning Plays a Protective Role in Exhaustive Rats by Activating the PI3K‐Akt Signaling Pathway

Li¹,

Xu²,

Wang³

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Objective. To investigate whether exercise preconditioning (EP) protects the rat heart from exhaustive exercise- (EE-) induced injury by inducing the PI3K-Akt signaling pathway. Methods. 84 male Sprague-Dawley rats were randomly divided into 6 groups (n = 14 rats per group): control group (Con), exhaustive exercise group (EE), exercise preconditioning group (EP), exercise preconditioning + exhaustive exercise group (EP + EE), LY294002 (PI3K inhibitor) + exercise preconditioning + exhaustive exercise group (LY + EP + EE), and LY294002 group (LY). The Con and LY did not exercise. The remaining groups were subjected to treadmill running. The structure of myocardial tissue and serum biomarkers of myocardial injury were observed. Hemodynamic parameters were recorded with a pressure-volume catheter. TUNEL assay was used to detect the apoptosis of cardiac myocytes, and the level of mitochondrial membrane permeability transforming pore (mPTP) in myocardium was evaluated using ELISA. Pathway and apoptosis-related proteins in myocardium were assessed using western blotting. Results. Compared to the Con group, the EE group showed remarkable myocardial injury, such as cardiac dysfunction and myocardial apoptosis. Compared to the EE group, the injuries in the EP + EE group were improved. EP increased the PI3K-Akt signaling pathway and regulated Bcl-2 family to decrease the mPTP openness level. However, the cardioprotective effects of EP were attenuated when pretreated with the LY294002. Conclusions. EP protected the heart from EE-induced injury, and it may improve the cardiac function and reduce the cardiomyocyte apoptosis by activating the PI3K-Akt signaling pathway.

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Post marathon cardiac troponin T is associated with relative exercise intensity

Abstract: CTnT increases above reference limits during a marathon. Magnitude of cTnT rise is related to exercise intensity relative to ventilatory threshold and V˙Omax, but not individuals' absolute cardiopulmonary fitness, training state or running history.

Cited by 43 publications

References 28 publications

Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death

Two-peaked increase of serum myosin heavy chain-α after triathlon suggests heart muscle cell death

Effects of Matched Intermittent and Continuous Exercise on Changes of Cardiac Biomarkers in Endurance Runners

Exercise Preconditioning Plays a Protective Role in Exhaustive Rats by Activating the PI3K‐Akt Signaling Pathway

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