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Background: The impact of high exercise loads on a previously healthy heart remains controversial. We examined the consequences of decades of strenuous endurance exercise at the highest competition level on heart dimensions and volumes as well as on serum biomarkers of cardiac fibrosis/remodeling. Methods and results: We compared echocardiographic measurements and serum biomarkers of cardiac fibrosis/remodeling [troponin I, galectin-3, matrix metallopeptidase-2 and -9, N-terminal pro-brain natriuretic peptide, carboxy-terminal propeptide of type I procollagen, and soluble suppressor of tumorigenicity-2 (sST-2)/interleukin(IL)-1R4] in 53 male athletes [11 former professional ('elite') and 42 amateur-level ('sub-elite') cyclists or runners, aged 40-70 years] and 18 aged-matched controls. A subset of 15 subjects (5 controls, 3 sub-elite and 7 elite athletes) also underwent cardiac magnetic resonance imaging (cMRI). Elite and sub-elite athletes had greater echocardiography-determined left ventricular myocardial mass indexed to body surface area than controls (113 +/- 22, 115.2 +/- 23.1 and 94.8 +/- 21 g/m(2), respectively, p = 0.008 for group effect), with similar results for left (50.5 +/- 4.4, 48.2 +/- 4.3 and 46.4 +/- 5.2 mm, p = 0.008) and right (38.6 +/- 3.8, 41.1 +/- 5.5 and 34.7 +/- 4.3 mm, p < 0.001) ventricular end-diastolic diameter, and cMRI-determined left atrial volume indexed to body surface area (62.7 +/- 8.1, 56.4 +/- 16.0 and 39.0 +/- 14.1 ml/m(2), p = 0.026). Two athletes showed a non-coronary pattern of small, fibrotic left ventricular patches detected by late gadolinium enhancement. No group effect was noted for biomarkers. Conclusions: Regardless of their competition level at a younger age, veteran endurance athletes showed an overall healthy, non-pathological pattern of cardiac remodeling. Nonetheless, the physiopathology of the ventricular fibrotic patches detected warrants further investigation. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

Atrial fibrillation (AF) is the most common heart arrhythmia, the risk of which typically increases with age. This condition is commonly associated with major cardiovascular diseases and structural heart damage, while it is rarely observed in healthy young people. However, increasing evidence indicates that paroxysmal AF can also onset in young or middle-aged and otherwise healthy endurance athletes (e.g., cyclists, runners and cross-country skiers). Here we review the topic of AF associated with strenuous endurance exercise (SEE), for example cycling, running and cross-country skiing, especially at a competitive level, and we propose the definition of a new syndrome based on the accumulating data in the literature: SEE-related AF under the acronym of ‘PAFIYAMA’ (‘paroxysmal AF in young and middle-aged athletes’). Special emphasis is given to the proper differentiation of PAFIYAMA from ‘classical AF’ regarding pathophysiology, diagnosis and medical management. Sin financiación 4.034 JCR (2017) Q2, 41/128 Cardiac and Cardiovascular Systems 1.200 SJR (2017) Q1, 78/369 Cardiology and Cardiovascular Medicine No data IDR 2017 UEM

Service of Biochemistry, Miguel Servet UniversityHospital, Zaragoza, SpainCorresponding author: E. Serrano-Osta´riz, Section of Physical Education and Sports, University of Zaragoza, C/DomingoMiral, s/n-50009 Zaragoza, Spain. Tel: 1349 767 610 00, Fax: 1349 767 617 20, E-mail: enrise@unizar.esAccepted for publication 17 August 2009Numerous studies have observed cardiac biomarker releasewithprolongedexercise.Despitethis,weareunsureastotheconstituent aspects of any given exercise bout that maybe important in promoting cardiac biomarker release.This study examined the influence of exercise durationand intensity on the appearance of cardiac biomarkers.Twenty-one subjects ran for 45, 90 and 180min at 85%and 95% of their individual anaerobic threshold on sixdifferent days randomized. Cardiac troponin I (cTnI) andN-terminal pro-brain natiuretic peptide (NT-proBNP)were assayed from blood samples collected before,30min and 3h post-exercise. NT-proBNP was elevatedafter all exercise trials (range before: 21–32; rangepost: 38–67ng/L). Peak post-exercise concentrationsof NT-proBNP were associated with exercise duration(P50.049), but not exercise intensity (P50.451). cTnIwas elevated after all exercise trials (range before: 0.007–0.011; range post: 0.008–0.021lg/L). Peak post-exerciseconcentrations of cTnI were associated with exercise dura-tion (P50.003) and intensity (P50.037). Data suggestthat while both cTnI and NT-proBNP increased after allexercise trials, the mediating effect of duration influencedboth NT-proBNP and cTnI while intensity influenced onlycTnI.

OBJECTIVE To determine the influence of age, training status, race time, and exercise intensity on the appearance of cardiac biomarkers after a cycle-touring event. DESIGN Pre-post exercise measurements. SETTING University of Zaragoza, Zaragoza, Spain. PARTICIPANTS Ninety-one amateur cyclists. INTERVENTION The 2005 Quebrantahuesos cycle-touring event (distance: 206 km; altitude difference: 3800 m). MAIN OUTCOME MEASURES Cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-pro-BNP) were measured the day before and immediately after the race. Heart rate (HR) monitoring was performed on 55 cyclists during the race to evaluate exercise intensity. RESULTS cTnI and NT-pro-BNP were significantly elevated immediately post race, with 43% of participants exhibiting cTnI levels greater than 0.04 microg/L and 65% of the participants measuring NT-pro-BNP levels greater than 125 ng/L. The cTnI increase was significantly associated with mean exercise intensity HR (r = 0.36, P < 0.01) but was not associated with age, training status, or race time. The increase in NT-pro-BNP correlated with race time (r = 0.40, P < 0.001) and training status (r = -0.36, P < 0.001) but was not associated with age or exercise intensity HR measures. CONCLUSIONS These results suggest that, in part, exercise intensity (HR) is responsible for the cTnI increase and that race time is responsible for the increase in NT-pro-BNP. Future standardized endurance exercise trials are recommended to further elucidate the potentially differential effects of training status, exercise time, and intensity on post-exercise increases in cTnI and NT-pro-BNP.

A recent meta-analysis by Iskandar et al. (1) nicely showed that endurance athletes have larger left atrial (LA) diameters compared with control subjects. Yet only 9 of 54 studies included in their analysis reported LA volume values corrected for body surface area (BSA). In fact, few studies have determined LA volume in young athletes, and, to the best of our knowledge, no study has reported this variable in older athletes. This is an important question given the growing debate about the potential deleterious effects of long-term strenuous endurance exercise on the human heart, notably the higher risk of atrial fibrillation (AF), a condition for which both atrial dilation and the normal aging process are thought to be potential causative mechanisms (2). Thus, we aimed to assess the long-term consequences of endurance exercise on LA volume in athletes who were highly competitive at younger ages and are still active. To this end, we compared BSA-corrected LA volumes determined with late gadolinium enhancement magnetic resonance imaging (LGE-MRI) in former elite endurance athletes and sedentary control subjects. Sin financiación 10.189 JCR (2016) Q1, 1/127 Radiology, Nuclear Medicine and Medical Imaging, 6/126 Cardiac and Cardiovascular Systems 5.038 SJR (2016) Q1, 7/375 Cardiology and Cardiovascular Medicine No data IDR 2016 UEM

We evaluated the influence of a 14-wk endurance running program on the exercise-induced release of high-sensitivity cardiac troponin T (hscTnT) and NH2-terminal pro-brain natriuretic peptide (NT-proBNP). Fifty-eight untrained participants were randomized to supervised endurance exercise (14 wk, 3–4 days/wk, 120–240 min/wk, 65–85% of maximum heart rate) or a control group. At baseline and after the training program, hs-cTnT and NT-proBNP were assessed before and 5 min, 1 h, 3 h, 6 h, 12 h, and 24 h after a 60-min maximal running test. Before training, hs-cTnT was significantly elevated in both groups with acute exercise (P , 0.0001) with no between-group differences. There was considerable heterogeneity in peak hs-cTnT concentration with the upper reference limit exceeded in 71% of the exercise tests. After training, both baseline and postexercise hs-cTnT were significantly higher compared with pretraining and the response of the control group (P 5 0.008). Acute exercise led to a small but significant increase in NT-proBNP, but this was not mediated by training (P 5 0.121). In summary, a controlled endurance training intervention resulted in higher pre- and postexercise values of hscTnT with no changes in NT-proBNP. This study was supported by the DEP 2010-16767 grants from the National Plan for Research, Development and Innovation (R + D + i) MICINN

a Faculty of Medicine, Department of Physiology, University of Valencia, Valencia, Spain b Fundacion de Investigacion del Hospital Clinico Universitario Valencia (FIHCUV-INCLIVA), Valencia, Spain c Faculty of Health and Sport Science, University of Zaragoza, Huesca, Spain d Hospital Universitario 12 de Octubre, Research Institute (i + 12), Madrid, Spain e HospitalUniversitario Miguel Servet, Zaragoza, Spain f Cardiology Service, Hospital Universitario Miguel Servet, Zaragoza, Spain g European University of Madrid, Madrid, Spain h Faculty of Medicine, Physical Education and Sports Section, University of Zaragoza, Zaragoza, Spain

The impact of intermittent exercise on cardiac biomarker release has not been clearly established. In experienced athletes, we examined the acute effect of a heavy resistance training session (n=18 males) and an indoor soccer match (n=21, 11 males, 10 females) on the release of cTnI, cTnT, and NT-proBNP. Biomarkers were assayed from blood samples collected at rest, immediately post- and at 1, 3, 6, 12, and 24 h post-exercise. The heavy resistance training session resulted in an increase in NT-proBNP (pre: 15 ± 17, peak post: 41 ± 56 ng L (-1); p=0.001) but not in cTnI (pre: 0.024 ± 0.009, peak post: 0.025 ± 0.011 μg L (-1), p=0.809) or cTnT (undetectable in all samples). The indoor soccer match led to an increase in the release of NT-proBNP (pre: 28 ± 32, peak post: 66 ± 56 ng L (-1); p=0.000) and cTnI (pre: 0.026 ± 0.047, peak post: 0.033 ± 0.051 μg L (-1); p=0.008) in both males and females but not cTnT (detectable in only one subject). The current data suggest that intermittent bouts of exercise result in only modest perturbations of cardiac biomarkers with very limited evidence of myocyte injury/insult.

We sought to determine the influence of exercise intensity on the release of cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in amateur marathon runners. Fourteen runners completed three exercise trials of the same duration but at exercise intensities corresponding to: (a) a competitive marathon [mean ± SD: heart rate 159 ± 7 beat min(-1), finish time 202 ± 14 min]; (b) 95% of individual anaerobic threshold [heart rate 144 ± 6 beat min(-1)] and; (c) 85% of individual anaerobic threshold [heart rate 129 ± 5 beat min(-1)]. cTnI and NT-proBNP were assayed from blood samples collected before, 30 min and 3 h post-exercise for each trial. cTnI and NT-proBNP were not different at baseline before each trial. After exercise at 85% of individual anaerobic threshold cTnI was not significantly elevated. Conversely, cTnI was elevated after exercise at 95% of individual anaerobic threshold (0.016 μg L(-1)) and to an even greater extent after exercise at competition intensity (0.054 μg L(-1)). Peak post-exercise values of NT-proBNP were elevated to a similar extent after all exercise trials (P0.05). The upper reference limit for cTnI (0.04 μg L(-1)) was exceeded in six subjects at competition intensity. No data for NT-proBNP surpassed its upper reference limit. Peak post-exercise values for cTnI and NT-proBNP were correlated with their respective baseline values. These data suggest exercise intensity influences the release of cTnI, but not NT-proBNP, and that competitive marathon running intensity is required for cTnI to be elevated over its upper reference limit.