Endurance Exercise and Myocardial Fibrosis
2016; Lippincott Williams & Wilkins; Volume: 9; Issue: 11 Linguagem: Espanhol
10.1161/circimaging.116.005730
ISSN1942-0080
Autores Tópico(s)Sports injuries and prevention
ResumoHomeCirculation: Cardiovascular ImagingVol. 9, No. 11Endurance Exercise and Myocardial Fibrosis Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBEndurance Exercise and Myocardial FibrosisLet Us Keep the Risk in Perspective Rob Shave, PhD and David Oxborough, PhD Rob ShaveRob Shave From the Cardiff Centre for Exercise and Health, Cardiff Metropolitan University, Cardiff, United Kingdom (R.S.); and Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, United Kingdom (D.O.). and David OxboroughDavid Oxborough From the Cardiff Centre for Exercise and Health, Cardiff Metropolitan University, Cardiff, United Kingdom (R.S.); and Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, United Kingdom (D.O.). Originally published10 Nov 2016https://doi.org/10.1161/CIRCIMAGING.116.005730Circulation: Cardiovascular Imaging. 2016;9:e005730If exercise could be packed in a pill, it would be the single most widely prescribed and beneficial medicine in the nation.—Robert Butler, MD, Chair of the National Institute of AgingAs captured by Robert Butler's quote, there is no disputing the wide-reaching health benefits of exercise training. Despite this, the health burden associated with the diseases of inactivity continues to rise. Each year millions of dollars are invested to promote physical activity, yet uptake remains relatively low as highlighted by data showing that only 20.2% of the US population meet the physical activity guidelines for aerobic and muscle strengthening exercise.1 Given these facts, it is imperative that any research that questions the benefits of exercise, or indeed suggests that exercise is deleterious to health, needs to be handled responsibly and placed within appropriate context.See Article by Abdullah et alA logical question following on from Butler's analogy is that if exercise acts as a medication, is it possible to overdose? This idea has received significant scientific attention, especially in relation to the impact of prolonged exercise on the heart.2–4 A body of work has emerged showing that prolonged exercise, such as that completed by elite or competitive amateur endurance athletes, results in acute reductions in right and left ventricular functions,5–7 a transient release of cardiac biomarkers8 and potentially the development of an exercise-induced cardiomyopathy.9 Several studies have shown in a small number of elite or veteran athletes evidence of focal myocardial fibrosis.10,11 These authors suggest that this is evidence of the Phidippides Cardiomyopathy,9 with a cause related to the exceptionally high volume and intensity of exercise completed by these athletes. These studies have prompted scientific concern12,13 and attracted much media attention.In this issue of Circulation: Cardiovascular Imaging, Abdullah et al14 report findings from a relatively large study examining the incidence of focal myocardial fibrosis using late gadolinium enhancement in 4 distinct groups of veterans with divergent levels of fitness and training histories. Importantly, the groups were well characterized in relation to their fitness and training history and were also highly screened so as to exclude the potential confounding influence of cardiovascular comorbidities (eg, hypertension and atherosclerosis). Across all 4 veteran groups, there was virtually no evidence of focal myocardial fibrosis, even in the high fit cohort who were extremely well trained (mean VO2peak of 39.8 mL/kg per minute) and had at least 20 years of competitive experience. The authors, therefore, conclude that increasing levels of lifelong fitness are not associated with focal myocardial fibrosis. These findings build on those recently published by Bohm et al15 similarly showing a lack of fibrosis in a younger cohort of elite athletes. Taken together, these findings should provide reassurance that high levels of competitive physical activity do not typically result in myocardial fibrosis. The current data are further supported by the relative low cardiac risk associated with competing in endurance exercise. Based on a sample population of 10.9 million runners in marathons and half-marathons, Kim et al16 have calculated a relative risk of 0.54 per 100 000 participants. If exercise-induced cardiac fibrosis, or the so-called Phidippides Cardiomyopathy, were a common consequence of completing repeated bouts of endurance exercise, one would anticipate that the cardiac event rate would be markedly higher.Although the data from Abdullah et al14 are reassuring to endurance athletes and their physicians, there are many important caveats. The high degree of clinical screening adopted by the authors, to specifically partition the effects of exercise from cardiovascular comorbidities, may have excluded veteran athletes who would have been identified by late gadolinium enhancement. It is also important to note that both the study by Abdullah et al14 and the previous publication by Bohm et al15 are cross-sectional in design and in real terms only assessed a small number of older individuals. Bohm et al15 examining elite masters athletes (mean age 29±8 years) and Abdullah et al14 examining veteran athletes, who may have come to exercise later in life and thus not have trained to a high level during their early developmental years. Accordingly, to definitively answer whether the late gadolinium enhancement observed in a small number of athletes is because of an exercise overdose, there is need for a large, well-designed prospective study conducted over the course of an elite athlete's entire career and beyond. Importantly, any such study would need to consider and control for many confounding issues (eg, genetic substrate, systemic infections, and the use of regulated and unregulated drugs).Until a carefully conducted longitudinal study is completed, it is impossible to establish whether extreme doses of intense exercise, in isolation, can cause myocardial fibrosis, or whether the phenomenon is explained by epigenetic interactions in the small number of athletes it seems to effect. Irrespective, the public health message related to physical activity should not be undermined by a phenomenon that while clinically relevant to a few, and scientifically interesting, seems not to be widespread among the majority of highly active individuals.DisclosuresNone.FootnotesThe opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.Correspondence to Rob Shave, PhD, Cardiff Centre for Exercise and Health, Cardiff Metropolitan University, Cyncoed Campus, Cyncoed Rd, Cardiff CF23 6XD, United Kingdom. E-mail [email protected]References1. Centers for Disease Control and Prevention. Nutrition, physical activity and obesity: data, trends and maps.http://nccd.cdc.gov/NPAO_DTM. Accessed October 14, 2016.Google Scholar2. Schnohr P, O'Keefe JH, Marott JL, Lange P, Jensen GB. Dose of jogging and long-term mortality: the Copenhagen City Heart Study.J Am Coll Cardiol. 2015; 65:411–419. doi: 10.1016/j.jacc.2014.11.023.CrossrefMedlineGoogle Scholar3. Armstrong ME, Green J, Reeves GK, Beral V, Cairns BJ; Million Women Study Collaborators. Frequent physical activity may not reduce vascular disease risk as much as moderate activity: large prospective study of women in the United Kingdom.Circulation. 2015; 131:721–729. doi: 10.1161/CIRCULATIONAHA.114.010296.LinkGoogle Scholar4. Mons U, Hahmann H, Brenner H. A reverse J-shaped association of leisure time physical activity with prognosis in patients with stable coronary heart disease: evidence from a large cohort with repeated measurements.Heart. 2014; 100:1043–1049. doi: 10.1136/heartjnl-2013-305242.CrossrefMedlineGoogle Scholar5. Middleton N, Shave R, George K, Whyte G, Hart E, Atkinson G. 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Shave R, Baggish A, George K, Wood M, Scharhag J, Whyte G, Gaze D, Thompson PD. Exercise-induced cardiac troponin elevation: evidence, mechanisms, and implications.J Am Coll Cardiol. 2010; 56:169–176. doi: 10.1016/j.jacc.2010.03.037.CrossrefMedlineGoogle Scholar9. Trivax JE, McCullough PA. Phidippides cardiomyopathy: a review and case illustration.Clin Cardiol. 2012; 35:69–73. doi: 10.1002/clc.20994.CrossrefMedlineGoogle Scholar10. La Gerche A, Burns AT, Mooney DJ, Inder WJ, Taylor AJ, Bogaert J, Macisaac AI, Heidbüchel H, Prior DL. Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes.Eur Heart J. 2012; 33:998–1006. doi: 10.1093/eurheartj/ehr397.CrossrefMedlineGoogle Scholar11. Wilson M, O'Hanlon R, Prasad S, Deighan A, Macmillan P, Oxborough D, Godfrey R, Smith G, Maceira A, Sharma S, George K, Whyte G. Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes.J Appl Physiol (1985). 2011; 110:1622–1626. doi: 10.1152/japplphysiol.01280.2010.CrossrefMedlineGoogle Scholar12. O'Keefe JH, Schnohr P, Lavie CJ. The dose of running that best confers longevity.Heart. 2013; 99:588–590. doi: 10.1136/heartjnl-2013-303683.CrossrefMedlineGoogle Scholar13. O'Keefe JH, Lavie CJ. Run for your life. at a comfortable speed and not too far.Heart. 2013; 99:516–519. doi: 10.1136/heartjnl-2012-302886.CrossrefMedlineGoogle Scholar14. Abdullah SM, Barkley KW, Bhella PS, Hastings JL, Matulevicius S, Fujimoto N, Shibata S, Carrick-Ranson G, Palmer MD, Nainesh G, DeFina LF, Levine BD. Lifelong physical activity regardless of dose is not associated with myocardial fibrosis.Circ Cardiovasc Imaging. 2016; 9:e00511. doi: 10.1161/CIRCIMAGING.116.005511.LinkGoogle Scholar15. Bohm P, Schneider G, Linneweber L, Rentzsch A, Krämer N, Abdul-Khaliq H, Kindermann W, Meyer T, Scharhag J. Right and left ventricular function and mass in male elite master athletes: a controlled contrast-enhanced cardiovascular magnetic resonance study.Circulation. 2016; 133:1927–1935. doi: 10.1161/CIRCULATIONAHA.115.020975.LinkGoogle Scholar16. Kim JH, Malhotra R, Chiampas G, d'Hemecourt P, Troyanos C, Cianca J, Smith RN, Wang TJ, Roberts WO, Thompson PD, Baggish AL; Race Associated Cardiac Arrest Event Registry (RACER) Study Group. Cardiac arrest during long-distance running races.N Engl J Med. 2012; 366:130–140. doi: 10.1056/NEJMoa1106468.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Soori R, Amini A, Choobineh S, Eskandari A, Behjat A, Ghram A and Voltarelli F (2019) Exercise attenuates myocardial fibrosis and increases angiogenesis-related molecules in the myocardium of aged rats, Archives of Physiology and Biochemistry, 10.1080/13813455.2019.1660370, 128:1, (1-6), Online publication date: 2-Jan-2022. Parisi E and Baggish A (2019) Exercise and Cardiovascular Risk among Masters Athletes with Type 2 Diabetes, Current Diabetes Reports, 10.1007/s11892-019-1229-z, 19:11, Online publication date: 1-Nov-2019. Contreras-Briceño F, Herrera S, Vega-Adauy J, Salinas M, Ocaranza M, Jalil J, Mandiola J, García L, Chiong M, Castro P, Lavandero S and Gabrielli L (2021) Circulating Vascular Cell Adhesion Molecule-1 (sVCAM-1) Is Associated With Left Atrial Remodeling in Long-Distance Runners, Frontiers in Cardiovascular Medicine, 10.3389/fcvm.2021.737285, 8 November 2016Vol 9, Issue 11 Advertisement Article InformationMetrics © 2016 American Heart Association, Inc.https://doi.org/10.1161/CIRCIMAGING.116.005730PMID: 27903548 Originally publishedNovember 10, 2016 Keywordsendomyocardial fibrosisEditorialsgadoliniumexerciseathletesPDF download Advertisement SubjectsCardiovascular DiseaseMagnetic Resonance Imaging (MRI)
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