Changes to the cardiac biomarkers of non-elite athletes completing the 2009 London Marathon

Baker, Polly; Davies, Sarah L.; Larkin, Joanne; Moult, Daniel; Benton, Sally C; Roberts, Andrew; Harris, T. J. R.

doi:10.1136/emermed-2012-201465

Cited by 24 publications

(31 citation statements)

References 22 publications

(14 reference statements)

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“…19,32 However, conflicting data exist regarding the prognostic significance of cardiac biomarkers at exercise, because Baker et al reported higher release among marathon runners who collapsed than among control subjects. 33 To our knowledge, this is the first study in which the presence of EVLF and BNP levels were simultaneously assessed during a climbing expedition, using a handheld echography and a point-of-care capillary assay, allowing immediate results. Previous studies 12,13,15,34 used venous blood samples, which imply more complex logistics and some technical expertise that preclude their use in the hostile environment of HA expeditions.…”

Section: Discussionmentioning

confidence: 99%

Brain Natriuretic Peptide Levels and the Occurrence of Subclinical Pulmonary Edema in Healthy Lowlanders at High Altitude

Pagé

Henri

Pagé

et al. 2015

Canadian Journal of Cardiology

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Section: Discussionmentioning

confidence: 99%

Brain Natriuretic Peptide Levels and the Occurrence of Subclinical Pulmonary Edema in Healthy Lowlanders at High Altitude

Pagé

Henri

Pagé

et al. 2015

Canadian Journal of Cardiology

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“…Acute, prolonged, strenuous‐exercise induced cTn release, including cTn T and I (cTnT and cTnI) has been widely reported in healthy and asymptomatic athletes (Shave et al., ). Both continuous exercise, such as marathon running (Serrano‐Ostáriz et al., ) and cycling (Baker et al., ), and intermittent exercise, such as basketball in adolescents (Nie et al., ), have been shown to trigger the elevation of cTn. With regard to the potential mechanisms, it is assumed that mechanical stretch (George et al., ), myocardial cell ischemia (Hickman et al., ), necrosis (Shave et al., ), or the oxidative stress‐induced increase in membrane permeability (Nie et al., ; Howatson et al., ) may be involved.…”

mentioning

confidence: 99%

Effects of acute, intermittent exercise in hypoxic environments on the release of cardiac troponin

Nie

et al. 2015

Scandinavian Med Sci Sports

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The purpose of this study was to examine the effects of acute, intermittent exercise performed in hypoxic environments on the release of cardiac troponin (cTn). Ten well-trained, male marathon runners (22.1 ± 2.6 years, 64.0 ± 4.9 kg and 177.3 ± 3.9 cm) completed three intermittent exercise protocols under normoxic (trial N) and hypoxic (trial AH and RH) conditions. In trial N, the fraction of inspiration oxygen (FIO2 ) was 21.0% and exercise intensity was 90% and 50% normoxic velocity of VO2max (vVO2max). In trial AH, FIO2 was 14.4% (simulated altitude of 3000 m) and exercise intensity was 90% and 50% normoxic vVO2max. In trial RH, FIO2 was 14.4% and exercise intensity was 90% and 50% hypoxic vVO2max. High-sensitivity cardiac troponin T (hs-cTnT) and cardiac troponin I (cTnI) were measured pre- and 0, 2, 4, and 24 h post-exercise. Hs-cTnT was elevated in all three trials, peaking at 2 to 4 h and returning to the baseline 24 h post-exercise. CTnI increased in trial AH, peaking at 2 to 4 h and returning below the detection limit 24 h post-exercise. It is concluded that the stimulus of hypoxia did not in and of itself induce more cTn to be released, but exercise intensity could affect this response in hypoxic environments.

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“…Four prior studies have investigated cTnT rise in marathon runners utilizing the same high-sensitivity cTnT assay with an average post-marathon value of between 31.1 to 47.0 ng/L. 4,[8][9][10] The median cTnT rise of 45.6 ng/L observed in the CON group is at the higher end of the range seen in prior studies. Peak post-exercise cTnT value is not achieved immediately upon exercise completion with peak post-exercise cTnT and cTnI values reported 1-4 hours following exercise completion.…”

Section: Discussionmentioning

confidence: 93%

“…This finding is in agreement with the only other study assessing these populations. 10 Although only a relatively small number of HD runners were recruited, the cohort represented a diverse spectrum of HD pathology. The similarity of the cTnT rise with the CON runners demonstrates that variations in post-marathon cTnT rise cannot be used to reliably identify individuals with undiagnosed cardiac abnormalities.…”

Section: Discussionmentioning

confidence: 99%

High‐sensitivity troponin T in marathon runners, marathon runners with heart disease and collapsed marathon runners

Leckie

Richardson

Watkins

et al. 2019

Scandinavian Med Sci Sports

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Endurance exercise is an established cause of cardiac troponin (cTn) elevation, of further interest is whether this rise represents clinical significance. This study compared cTnT rise in three cohorts of marathon runners using a high-sensitivity assay; control runners, those with known heart disease and runners who collapsed at the finish line. Control runners (n = 126) and runners with heart disease (n = 12) were prospectively recruited with cTnT levels measured pre-race and at race completion.Collapsed runners (n = 15) were retrospectively recruited. A mixed model ANCOVA was used to compare the three groups. Pre-race median cTnT for the control group and heart disease groups was 3.9 ng/L (IQR 3.1 ng/L) and 4.1 ng/L (IQR 3.4 ng/L).Post-race values for the three groups were control 45.6 ng/L (IQR 42.5 ng/L), heart disease 41.2 ng/L (IQR 36.1 ng/L), and collapsed 41.9 ng/L (IQR 57.8 ng/L). Postrace cTnT and cTnT change were significantly correlated with pre-race cTnT within the control group (r = 0.38 and 0.30, P < 0.01). There was no difference in post-race cTnT (adjusted for pre-race cTnT) between the three groups. None of the runners reported symptoms suggestive of acute myocardial infarction on follow-up. These results demonstrate that marathon running is associated with an asymptomatic cTnT rise for all runners, and this rise is significantly correlated to baseline cTnT levels, in addition, marathon runners with pre-existing cardiac pathology or who collapse at the finish line do not exhibit an increased cTnT rise compared to healthy runners. K E Y W O R D Scardiac, Marathon, running, troponin

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Changes to the cardiac biomarkers of non-elite athletes completing the 2009 London Marathon

Cited by 24 publications

References 22 publications

Brain Natriuretic Peptide Levels and the Occurrence of Subclinical Pulmonary Edema in Healthy Lowlanders at High Altitude

Brain Natriuretic Peptide Levels and the Occurrence of Subclinical Pulmonary Edema in Healthy Lowlanders at High Altitude

Effects of acute, intermittent exercise in hypoxic environments on the release of cardiac troponin

High‐sensitivity troponin T in marathon runners, marathon runners with heart disease and collapsed marathon runners

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