https://orcid.org/0000-0001-9693-4083
There are in fact two things, science and opinion. The former begets knowledge, the latter ignorance..
Hippocrates, Paul Potter (1984). ‘Hippocrates’
‘Joy to you, we have won!’ the last words pronounced by Philippides before the occurrence of the first sudden cardiac death (SCD) in sport. Legend has it that Philippides died after running ∼40 km from Marathon to Athens to announce the victory of the Greek forces against the Persians. Further research demonstrated that Philippides had run actually almost 500 km, as he went from Marathon to Athens, from Athens to Sparta, and back to Athens. Indeed, despite this distance, he actually survived as his story was merged with that of another runner, Eucles, who 50 years later ran to Athens to announce victory and died. This first SCD of an athlete did not question the upheld benefits of sports and physical exercise in the classic world, where through the teachings of philosophers such as Plato (428–348 BC), in his Republic, but also the works of Herodicus (5th century BC) and his most famous pupil Hippocrates (460–370 BC), physical exercise became a core part of the education of the citizen in ancient Greece. This concept of benefits without significant harm was passed on through the works of Galen (129–210 AD) and handed down through the centuries relatively unexamined until the 1800s1 (Figure 1).
Historical milestones in the description of the athlete’s heart. Free cliparts by https://creazilla.com.
The athlete’s heart
In 1862, the American Civil War was in its second year when Jacob Mendez Da Costa (1833–1900) first described a syndrome caused by the excessive physical demands of long military campaigns, characterized by dyspnoea, palpitations, tachycardia, and dizziness—he called it the ‘soldiers heart’ opening the debate on the perils of overtraining2 (Figure 2).
Painting of Philippides announcement of the Greek victory by Luc-Olivier Merson (1869) framed by some of the physicians that have contributed to the athletes’ heart history. 1. Jacob Mendez Da Costa (1833–1900); 2. Frederic Carpenter Skey (1798–1872); 3. Thomas Allbutt (1836–1925); 4. William Osler (1849–1919); 5. Salomon Eberhard Henschen (1847–1930); 6. Thomas Barlow (1845–1945); 7. William Hale-White (1857–1949); 8. Benjamin Ward Richardson (1828–96); 9. Adolphe Abrahams (1883–1967); 10. Robert Tait McKenzie (1867–1938); 11. Edward Hickling Bradford (1848–1926); 12. Paul Dudley White (1886–1973); 13. Hugo Wilhelm Knipping (1895–1984); 14. Per-Olof Astrand (1922–2015); 15. Wildor Hollman (1925–2021); 16. Bengt Saltin (1935–2014); 17. Noah ‘Jerry’ Morris (1910–2009); 18. Lionel Henry Opie (1933–2020); 19. Paul Davis Thompson (1947–); 20. David Stuart Siscovick (1951–); 21. Barry Joel Maron (1941–); 22. Paolo Zeppilli (1946–); 23. Jonathan Drezner (1970–); 24. Kimberly Harmon (1966–); 25. Sanjay Sharma (1964–); 26. Antonio Pelliccia (1951–); 27. Domenico Corrado (1956–).
The shift from the ‘soldier’s heart’ to the ‘athlete’s heart’ started a few years later when the English surgeon Frederic Carpenter Skey (1798–1872) in 1867 published in the London Times a series of letters on the cardiac effects of severe training. In 1873 the debate sparked. In that year, Thomas Allbutt (1836–1925) published on The Clinical Society of London his observation of overstrain of the heart and aorta by exercise, causing, in his opinion, cardiac disease. In the same year, John Edward Morgan (1828–92), a Manchester Royal Infirmary physician, published the effects of exercise on the Oxford and Cambridge rowing teams, concluding that there were no concerns for reduced life-expectancy and that only those weak and diseased were at risk. The theory of Morgan became popular and even Allbutt concurred that only people with imperfect constitution could be harmed by exercise.3
In 1892 Sir William Osler (1849–1919) documented how the ‘getting wind’ was linked to the heart's capability to become larger in the athletes. However, it is in 1899 that the expression ‘athlete’s heart’ first officially appeared, when the Swedish physician Salomon Eberhard Henschen (1847–1930) described the two main cardiac adaptations to sports: enlargement and hypertrophy.4
The reintroduction of the modern Olympic Games in 1896 opened the doors for new discussion: in 1903 an editorial titled ‘the dangers in competitive athletes’ was published on the Journal of the American Medical Association (JAMA) suggesting that ‘violent athletic exercise produces a great mechanical strain on the heart’ and ‘repeated exercise, such as prolonged training in successive years, may lead to permanent injury of the heart or kidney is unquestionable’. The same hypothesis was published in the Lancet 20 years later by Thomas Barlow (1845–1945) and William Hale-White (1857–1949).3 The debate on the cardiac effects of exercise continued for another century.
Physicians were divided: on one side those arguing for the dangers of sports, such as the English physiologist and physician Benjamin Ward Richardson (1828–96) and the English pioneer moto-cyclist physician William Collier (1856–1935), on the other side the dissenting voices of the German physician George Kolb (1863–99), the English physicians Joseph Strickland Goodall (1874–1934) and Adolphe Abrahams (1883–1967). Kolb, in particular, recognized the effects of detraining: initially convinced of the damaging cardiac effects of sports, he ended up concluding that sport is healthy, that all the changes observed were normal features for athletes and would reduce with detraining.5
Concerns were also voiced overseas, in America, where Robert Tait McKenzie (1867–1938) and Peter Karpovich (1896–1975) were concerned that the dilatation could be an expression of acute cardiac decompensation, while Edward Hickling Bradford (1848–1926) and George Louis Meylan (1873–1960) were publishing reassuring results. The majority of the observations was based on marathon runners, those of the Olympic Marathons and those of the Boston Marathons, the first of which was run in 1897: only 17 runners participated, each followed by someone riding a bicycle.3
In the first half of the 19th century, several anatomical findings were being reported on the heart of SCD athletes in the search for causation.6
Attempts to provide quantitative evaluations of the athlete’s heart were made by imaging: the Swedish group of Sven Roland Kjellberg (1905–66) first demonstrated a correlation between the radiological size of the heart and the physical capacity of work. German physicians correlated the radiological findings with the maximal oxygen pulse allowing differentiation between athlete’s heart and pathological heart dilatation by obtaining normal values for the ratio of heart dilation to oxygen pulse.6
While in Europe in the 1930–40s exercise programmes often served the growing cult of the perfect body as a promotion of racial excellence, in America Paul Dudley White (1886–1973) promoted exercise for the prevention of heart disease.3 Only in the 1940–50s, the athlete’s heart started to be accepted as a physiological phenomenon.
The clinical introduction of spiroergometry and cycle ergometer by Hugo Wilhelm Knipping (1895–1984) and Per-Olof Astrand (1922–2015), respectively, and its application in sports medicine by Wildor Hollman (1925–2021) were the basis for the research of the Swedish school around Bengt Saltin (1935–2014), describing the physical responses to training and detraining.
Widely held beliefs on the dangers of sport changed when the Scottish epidemiologist Jeremiah Noah ‘Jerry’ Morris (1910–2009) and colleagues in 1953 studied the coronary artery disease risk of London transport, postal and civil service workers, showing that those more active had significantly less coronary artery disease with fewer early fatal events.
The emergence of ultrasound imaging and increasing reports of SCD of athletes, especially among marathon runners, closed the circle to the earliest ancient reports and resulted in renewed research interest in America, quickly spreading in Europe. Virtue of the first modern day media presence at the 1960 Olympic Games in Rome, elite athlete medical care became an important topic also for the wider public.
While the first observation of electrocardiographic changes in athletes and their correlation to cardiac hypertrophy and training status in 1966 by Helmut Roskamann (1933–2018) were largely ignored, echocardiographic findings in athletes by Richard Ernst Rost (1940–98) published in 1972 provoked new debate.6 He also published the first description of eccentric hypertrophy as physiological adaptation, a concept introduced by Joel Morganroth (1945–) with his milestone publication in 1975.6
In 1975 the first quantification of the risk of SCD through exercise appeared in the Lancet by Lionel Henry Opie (1933–2020). Similarly, Paul Davis Thompson (born 1947) published on the circumstances of death and medical history of 18 elite athletes on JAMA, only 1 week after president Jimmy Carter famously collapsed after a 10 km race on September 15th 1979. Finding the cause and risk of SCD became hence a focus for further research. In 1984 David Stuart Siscovick (born 1951), in the New England Journal of Medicine (NEJM), showed that despite a transient higher risk for cardiac events in physically active men during exercise, exercise participation in general is associated with an overall decreased cardiac risk (40% of that of sedentary men).3
Simultaneously, electrocardiographic abnormalities including T-wave inversion in elite athletes were pointed out by Antonio Venerando (1923–90) and Paolo Zeppilli (born 1946).7 This observation has been meticulously studied in recent years by Sanjay Sharma’s (born 1964) group as well as those of Jonathan Drezner (born 1970) and Kimberly Harmon (born 1966) among many others worldwide. Research continued to progress when specific diseases, such as hypertrophic cardiomyopathy, were found as SCD cause in athletes, such as described in 1980 by Barry Joel Maron (born 1941).3
Consequently, echocardiography imaging as the primary tool to differentiate athlete’s heart from structural heart disease became a central research topic. Only in 1991, when the Italian group of Antonio Pelliccia (born 1951) published in the NEJM the largest echocardiographic study on athletes supporting the eccentric hypertrophy hypothesis, the concept of physiologic left ventricular hypertrophy was accepted.8 Meanwhile, another inherited cause of SCD among athletes, arrhythmogenic cardiomyopathy, was described by Domenico Corrado (born 1956).9
The observations by Thompson, Siscovick, Maron, Corrado, and many other pioneers in this area, that athletes dying suddenly harbour an underlying undiagnosed cardiac disease and that exercise can trigger SCD in those predisposed individuals, has since led to programmes aiming to preventively pick up such underlying inherited cardiac disease—the currently practised cardiac screening. From the early almost mythological descriptions of SCD in the ancient world to the modern quest of understanding the cardiac physiology of the athlete all contributed to the recent emergence of a new specialty, sports cardiology—but that is another story.10
Acknowledgements
We recognize many sports physicians and sports cardiologists have contributed to the field and we apologize we could not acknowledge all of them in our article.
Conflict of interest: No conflicts of interest.
