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      Heart of the World’s Top Ultramarathon Runner—Not Necessarily Much Different from Normal

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          Abstract

          The impact of ultramarathon (UM) runs on the organs of competitors, especially elite individuals, is poorly understood. We tested a 36-year-old UM runner before, 1–2 days after, and 10–11 days after winning a 24-h UM as a part of the Polish Championships (258.228 km). During each testing session, we performed an electrocardiogram (ECG), transthoracic echocardiography (TTE), cardiac magnetic resonance imaging (MRI), cardiac 31P magnetic resonance spectroscopy ( 31P MRS), and blood tests. Initially, increased cholesterol and low-density lipoprotein cholesterol (LDL-C) levels were identified. The day after the UM, increased levels of white blood cells, neutrophils, fibrinogen, alanine aminotransferase, aspartate aminotransferase, creatine kinase, C-reactive protein, and N-terminal type B natriuretic propeptide were observed. Additionally, decreases in hemoglobin, hematocrit, cholesterol, LDL-C, and hyponatremia were observed. On day 10, all measurements returned to normal levels, and cholesterol and LDL-C returned to their baseline abnormal values. ECG, TTE, MRI, and 31P MRS remained within the normal ranges, demonstrating physiological adaptation to exercise. The transient changes in laboratory test results were typical for the extreme efforts of the athlete and most likely reflected transient but massive striated muscle damage, liver cell damage, activation of inflammatory processes, effects on the coagulation system, exercise-associated hyponatremia, and cytoprotective or growth-regulatory effects. These results indicated that many years of intensive endurance training and numerous UMs (including the last 24-h UM) did not have a permanent adverse effect on this world-class UM runner’s body and heart. Transient post-competition anomalies in laboratory test results were typical of those commonly observed after UM efforts.

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          The athlete's heart. A meta-analysis of cardiac structure and function.

          It has been postulated that depending on the type of exercise performed, 2 different morphological forms of athlete's heart may be distinguished: a strength-trained heart and an endurance-trained heart. Individual studies have not tested this hypothesis satisfactorily. The hypothesis of divergent cardiac adaptations in endurance-trained and strength-trained athletes was tested by applying meta-analytical techniques with the assumption of a random study effects model incorporating all published echocardiographic data on structure and function of male athletes engaged in purely dynamic (running) or static (weight lifting, power lifting, bodybuilding, throwing, wrestling) sports and combined dynamic and static sports (cycling and rowing). The analysis encompassed 59 studies and 1451 athletes. The overall mean relative left ventricular wall thickness of control subjects (0.36 mm) was significantly smaller than that of endurance-trained athletes (0.39 mm, P=0.001), combined endurance- and strength-trained athletes (0.40 mm, P=0.001), or strength-trained athletes (0.44 mm, P<0.001). There was a significant difference between the 3 groups of athletes and control subjects with respect to left ventricular internal diameter (P<0. 001), posterior wall thickness (P<0.001), and interventricular septum thickness (P<0.001). In addition, endurance-trained athletes and strength-trained athletes differed significantly with respect to mean relative wall thickness (0.39 versus 0.44, P=0.006) and interventricular septum thickness (10.5 versus 11.8 mm, P=0.005) and showed a trend toward a difference with respect to posterior wall thickness (10.3 versus 11.0 mm, P=0.078) and left ventricular internal diameter (53.7 versus 52.1 mm, P=0.055). With respect to cardiac function, there were no significant differences between athletes and control subjects in left ventricular ejection fraction, fractional shortening, and E/A ratio. Results of this meta-analysis regarding athlete's heart confirm the hypothesis of divergent cardiac adaptations in dynamic and static sports. Overall, athlete's heart demonstrated normal systolic and diastolic cardiac functions.
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            Myocardial injury and ventricular dysfunction related to training levels among nonelite participants in the Boston marathon.

            Multiple studies have individually documented cardiac dysfunction and biochemical evidence of cardiac injury after endurance sports; however, convincing associations between the two are lacking. We aimed to determine the associations between the observed transient cardiac dysfunction and biochemical evidence of cardiac injury in amateur participants in endurance sports and to elicit the risk factors for the observed injury and dysfunction. We screened 60 nonelite participants, before and after the 2004 and 2005 Boston Marathons, with echocardiography and serum biomarkers. Echocardiography included conventional measures as well as tissue Doppler-derived strain and strain rate imaging. Biomarkers included cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP). All subjects completed the race. Echocardiographic abnormalities after the race included altered diastolic filling, increased pulmonary pressures and right ventricular dimensions, and decreased right ventricular systolic function. At baseline, all had unmeasurable troponin. After the race, > 60% of participants had increased cTnT > 99th percentile of normal (> 0.01 ng/mL), whereas 40% had a cTnT level at or above the decision limit for acute myocardial necrosis (> or = 0.03 ng/mL). After the race, NT-proBNP concentrations increased from 63 (interquartile range [IQR] 21 to 81) pg/mL to 131 (IQR 82 to 193) pg/mL (P 45 miles/wk, athletes who trained < or = 35 miles/wk demonstrated increased pulmonary pressures, right ventricular dysfunction (mid strain 16+/-5% versus 25+/-4%, P<0.001), myocyte injury (cTnT 0.09 versus < 0.01 ng/mL, P<0.001), and stress (NT-proBNP 182 versus 106 pg/mL, P<0.001). Completion of a marathon is associated with correlative biochemical and echocardiographic evidence of cardiac dysfunction and injury, and this risk is increased in those participants with less training.
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              International recommendations for electrocardiographic interpretation in athletes

              Sudden cardiac death (SCD) is the leading cause of mortality in athletes during sport. A variety of mostly hereditary, structural, or electrical cardiac disorders are associated with SCD in young athletes, the majority of which can be identified or suggested by abnormalities on a resting 12-lead electrocardiogram (ECG). Whether used for diagnostic or screening purposes, physicians responsible for the cardiovascular care of athletes should be knowledgeable and competent in ECG interpretation in athletes. However, in most countries a shortage of physician expertise limits wider application of the ECG in the care of the athlete. A critical need exists for physician education in modern ECG interpretation that distinguishes normal physiological adaptations in athletes from distinctly abnormal findings suggestive of underlying pathology. Since the original 2010 European Society of Cardiology recommendations for ECG interpretation in athletes, ECG standards have evolved quickly over the last decade; pushed by a growing body of scientific data that both tests proposed criteria sets and establishes new evidence to guide refinements. On 26-27 February 2015, an international group of experts in sports cardiology, inherited cardiac disease, and sports medicine convened in Seattle, Washington, to update contemporary standards for ECG interpretation in athletes. The objective of the meeting was to define and revise ECG interpretation standards based on new and emerging research and to develop a clear guide to the proper evaluation of ECG abnormalities in athletes. This statement represents an international consensus for ECG interpretation in athletes and provides expert opinion-based recommendations linking specific ECG abnormalities and the secondary evaluation for conditions associated with SCD.
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                Author and article information

                Journal
                Diagnostics (Basel)
                Diagnostics (Basel)
                diagnostics
                Diagnostics
                MDPI
                2075-4418
                28 January 2020
                February 2020
                : 10
                : 2
                : 73
                Affiliations
                [1 ]Center for Sports Cardiology at the Gajda-Med Medical Center in Pułtusk, ul. Piotra Skargi 23/29, 06-100 Pułtusk, Poland
                [2 ]The Cardinal Stefan Wyszyński National Institute of Cardiology, ul. Alpejska 42, 04-628 Warszawa, Poland; aklisiewicz@ 123456ikard.pl (A.K.); k.biernacka@ 123456ikard.pl (E.K.B.)
                [3 ]The 2nd Department of Clinical Radiology, Medical University of Warsaw, ul. Banacha 1A, 02-097 Warsaw, Poland; vadym.matsibora@ 123456gmail.com
                [4 ]The 1st Department of Radiology, Medical University of Warsaw, ul. Żwirki i Wigury 61, 02-091 Warsaw, Poland; dodo@ 123456mrlab.pl
                Author notes
                [* ]Correspondence: gajda@ 123456gajdamed.pl ; Tel.: +48-604286030; Fax: +48-23-6920199
                Author information
                https://orcid.org/0000-0002-8305-8130
                https://orcid.org/0000-0003-3215-5085
                Article
                diagnostics-10-00073
                10.3390/diagnostics10020073
                7168911
                32012817
                91419256-4796-4006-8c23-faafc0d8854b
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 23 December 2019
                : 25 January 2020
                Categories
                Article

                professional ultramarathon runner,echocardiography,electrocardiogram,magnetic resonance imaging,cardiac 31p-mr spectroscopy,blood tests

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