The full version of this article can be found in the appendix of The Marathon des Sables, available to buy online at Amazon and Waterstone's.

The Athlete's Heart


A Review of the Literature

Cardiovascular disease (CVD) is generally associated with a lack of physical activity, amongst other lifestyle factors, for which regular exercise has been found to be beneficial in its prevention and treatment (Wilson et al., 2010). However, whilst moderate aerobic exercise might be beneficial to everyone, extremes of exercise, including ultra-endurance exercise, has the potential to profoundly influence the size and electrophysiology of the heart. It is not clear whether or not these adaptations are always physiological in nature, or if they might be, contribute to, or exacerbate pathological development.
   Athlete's heart was first described in a short article published in 1899 (Henschen, 1899). Despite the intervening time period in which to study athletes, ultra-runners in particular have not been investigated in large numbers, so data has had to be pooled from studies involving various other types of endurance athletes (such as cyclists, cross-country skiers, canoeists, and other aerobically-trained athletes). However, the cardiovascular responses are dependent upon the duration and intensity of physical activity, so mode of exercise is not so important when it comes to understanding heart-specific responses to training.
   In 2005, a study by Karakaya et al., compared 50 athletes to 40 sedentary individuals. The athletes had been involved in competition for an average of 7.7+/- 3.3 years, and participated in an average of 10.1+/- 1.6 hours of exercise each week. In these athletes, it was found that most measurements of their hearts were similar to those of the control subjects. However, the thickness of the left ventricles and the interventricular septums were significantly greater in the athletes than the controls. Because the left ventricle is the chamber responsible for ejecting blood to the whole body, the increased muscular thickness of its walls can be directly associated with its function.
   Also in 2005, Pelliccia et al., reported on athletes examined at the Italian National Institute of Sports Medicine between 1992 and 1995. Of the 1,823 athletes, 46 were excluded from further investigation, due to evidence of structural heart abnormalities, leaving 1,777 highly trained athletes for inclusion into the study. As with many investigations into the athlete's heart, subjects are often excluded if they show signs of serious cardiac damage or abnormalities that might lead to harm. This is a requirement of the ethics committees that permit the studies to take place, although as a reader or reviewer, we would often like to know much more about those individuals deliberately not included. Was it possible that the abnormalities were an unusual response to training, were there genetic factors, other lifestyle factors, or was it a combination of the three?
   Of the subjects who remained to be tested, 80% had left atria of normal dimensions (<40 mm). The remaining 20% had left atria greater than what is accepted as normal (>40 mm). 2% of those (38 individuals) had markedly dilated left atria (>45 mm). This demonstrates a difference between the report by Pelliccia et al., (2005) and that of the previously mentioned Karakaya et al., (2005), where they reported no such findings. The differences could have been due to measuring techniques, although most likely it was due to the small sample size of the first study (only 50 athletes, compared to 1,777 in the second study), and the highly trained nature of the athletes in the latter investigation.
   Importantly, the left ventricle has often been the only chamber of the heart's four to be seen to become enlarged, simply because it has always been the easiest to measure. When viewed through the chest wall, the left ventricle is the first and largest chamber that can be seen. It has only been due to the advances in echocardiography and magnetic resonance imaging (MRI) in the last decade or so, which has permitted us to more fully explore the heart in living individuals (in vivo).
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In addition to measuring structural adaptations in the athletes' hearts, Biffi et al., (2008) also assessed for electrical abnormalities, via 24-hour ambulatory ECG units. The investigators found no relationship between more frequent ventricular arrhythmias and increased LV mass. If anything, there was a trend towards those athletes with the greatest number of premature ventricular contractions (more than 1000 in a 24-hour period) and the lowest calculated LV masses and mass indexes. However, this later finding did not reach statistical significance, although it nevertheless demonstrates that electrical anomalies appear to be independent of physiological, structural adaptations. There was also no relationship between low resting heart rates (bradycardia - a resting heart rate below 60 beats per minute), and frequency of arrhythmias (Biffi et al., 2008).
   The authors of the study noted that the almost inverse relationship between LV mass and ventricular arrhythmias is opposite what occurs in hypertrophic cardiomyopathy (an enlargement of the heart muscle due to pathology). In hypertrophic cardiomyopathy, greater LV mass is associated with ventricular tachyarrhythmias (an arrhythmia of the ventricle in which its rate of contraction is unusually increased) (Biffi et al., 2008).
   The lack of any clear relationship between the electrical aspects of the heart and the structural adaptations appears unexpected. As the heart muscle hypertrophies through training, it might be expected that this should have an effect on how that muscle is stimulated to contract. Alternatively, if there are anomalies in the way the heart contracts that have become apparent through training, then surely these would be related to the very same factors that can lead to structural changes, such as increased fitness, increased loading on the heart and so on? This apparent case of logic has not been supported by the evidence.
   We previously mentioned a study by Pelliccia et al., (2005), in which 1,777 athletes had been recruited. In addition to the structural measurements, ECG assessments were also carried out. Less than 1% (14 subjects) experienced supraventricular tachyarrhythmias, including atrial fibrillation and supraventricular tachycardia. Supraventricular refers to 'above' the ventricles (i.e., somewhere in atria or AV node), and fibrillation refers to a rapid, erratic heartbeats (hence a 'defibrillator' works by eliciting a single charge to restore a normal heartbeat, but will not start a heart that has stopped beating). 11 of those subjects reported prolonged palpitations during exercise, and the other 3 experienced them at rest. It had been previously hypothesised that ventricular tachycardias could be viewed as potentially life-threatening electrical disorders, should they occur during intense physical activity (Biffi et al., 2002).
   347 athletes were incorporated into an in-depth analysis of their electrophysiology (Pelliccia et al., 2005). The ECG traces were found to be normal in 34% of the athletes (117 individuals). In the remaining 230 athletes, ECG traces were indicative of left ventricular hypertrophy (54%), whilst others were found to have anomalies in how their ventricles depolarised and repolarised. The latter refer to the process of changing the electrical gradient of a muscle cell to make it contract. Initially the cell depolarises, which leads to a contraction, and then repolarises, as it returns to its resting, relaxed state. An ECG trace typically shows a p-wave (atria depolarising, seen as an upward wave or 'deflection'), a QRS complex (ventricles depolarising, shown by a short downward deflection, a tall narrow upward spike, then another short downward deflection), followed by one or two shorter upward waves. The last two are the ventricles and then Purkinje fibres repolarising, representing the t-wave and u-wave, respectively, although the u-wave can be absent. There is no typical ECG representation of the atria repolarising, as this happens at the same time as the ventricles depolarise, which masks the electrical activity of the much smaller atria.
   As with the study by Biffi et al., (2008), the study by Pelliccia et al., (2005), reported no association between structural adaptations and electrical anomalies. Pelliccia et al., found that atrial fibrillation and supraventricular tachycardia occurred with no greater or lesser frequency in athletes with or without enlarged left atria. Again, if anything, there was almost an inverse relationship, as the 38 athletes with the largest left atria (> 45 mm) showed supraventricular tachyarrhythmias to be incredibly rare (occurring in 1 athlete out of the 38).
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Sudden Cardiac Death

Sudden cardiac death (SCD) is incredibly rare in athletes, but due to the high profile of athletes, and the wealth of evidence to show that exercise is healthy, when an athlete does die from SCD it is reported far more widely than SCD in a sedentary individual. In athletes younger than 30 years, incidence of sudden cardiac death is very low, and in most cases associated with an inherited heart disease, the effects of which may have been exacerbated by training. In older athletes, SCD is more common, and often due to arrhythmias associated with coronary artery disease (CAD) (Link et al., 2008).
   The most common causes of sudden cardiac death among young athletes include structural heart disease, electrical defects, Brugada syndrome, and external causes (presumably including impacts to the ribcage) (Link et al., 2008; Biffi et al., 2002). Genetic causes include Brugada syndrome, which has been reported to be responsible for 20% of SCD in athletes with structurally normal hearts (Link et al., 2008). The syndrome is typically inherited and due to a mutation in a gene involved in cardiac sodium channels (an essential part of how the electrical gradient is altered to facilitate contraction). The paper by Link et al., (2008), concluded that athletes with a history of malignant ventricular arrhythmias (or conditions predisposing them to ventricular arrhythmias) should be restricted from participation in moderate and high-intensity sports.
   In the study by Biffi et al., (2002), referred to previously in this chapter, one athlete had been excluded from their investigation due to cardiac abnormalities, who later died of SCD during competition. He was a 24-year-old field hockey player with arrhythmogenic right ventricular cardiomyopathy, which had been associated with 2100 premature ventricular depolarisations, two brief bouts of non-sustained ventricular tachycardia, and who had continued to participate in training and competition against medical advice (Biffi et al., 2002).
   In the 2004 study by Biffi et al., the authors reported that the risk of sudden cardiac death in young competitive athletes with cardiovascular disease (CVD) was 2.5 times greater than the risk of SCD in non-athletes with CVD. This finding supports the idea that physical activity can act as a trigger in individuals with existing cardiac abnormalities. They concluded that disqualification from intense competitive sports should permit deconditioning to reducing arrhythmias, which may be a central component in a strategy to reduce sudden cardiac deaths in susceptible athletes (Biffi et al., 2004).
   A review by Rowland (2009), reported that in young athletes there is a relationship between ventricular hypertrophy, circulating testosterone and catecholamines (i.e., noradrenaline), stimulation of the sympathetic nervous system (fight-or-flight response), and sudden cardiac death. It was suggested that repeated bouts of exercise, which were increasing the hormonal responses to training, were also promoting ventricular hypertrophy. The mechanism for sudden cardiac death appeared to be related to pathologic hypertrophy leading to fatal dysrhythmias, with exercise acting as the trigger. In the young, it seems that the normal hypertrophy associated with endurance training can be the root cause of sudden cardiac death, and that the hypertrophy may not appear as pathologic based upon echocardiogram assessments alone (Rowland, 2009).
   Currently, there is no truly effective means of guarding against sudden cardiac death, with the probable exception of detraining. In non-athletes at risk of SCD, it is possible to use implantable defibrillators, designed to detect arrhythmias and shock the heart back into normal rhythm. However, in an athletic population these are less reliable, and in a review by Maron (2010), it appears that the risk of experiencing an inappropriate shock is unsettlingly high. More, it would appear, needs to be done.
   Risk factors for sudden cardiac death include skin colour (black), gender (male), and developmental factors and/or length of training (Rowland, 2009). This reinforces the message that anyone at risk should be thoroughly checked, via 24-hour ECG (to include training and sleep), and an echocardiogram at least. Over time, it is hoped that the amount of attention paid to comprehensive assessments of athletes, will help to develop the evidence-base and understanding required to establish efficient systems for detecting those very few athletes with a real risk of SCD, at any age.
There has been such a barrage of information in this review that it is difficult to draw any specific conclusions from it. Further, due to the fact that this is merely an introductory review, and not a more broader-ranging book, it was not possible to include more information, topics or detail. But I think that this is a start. If a reader has an ECG and/or an echocardiogram, then I would like to think they at least have a head-start when it comes to understanding it all. Books would be required to gain the skills for a full understanding of the subject, which would be far beyond the scope of this humble addition to an otherwise focussed training and competition report. But I hope it stands as at least something.
   In many cases, more information could not be included simply because more information was not available. There are certain molecules that can be tested for, which may indicate remodelling of the heart, such as NT-proBNP (Florescu et al, 2010; Vianello et al., 2009), but the findings, particularly in relation to athletes, are far from clear. There are numerous websites for cardiologists, physiologists and doctors available online, and such webpages can easily provide more information on the topics I have had to gloss over for the sake of time, space and relevance.
   As for rounding off the whole subject of the athlete's heart, I think the most valuable take-home message is that there is no single condition known as 'athlete's heart', and that should any medical professional attempt to dismiss apparently physiologic adaptation as such, then it might be best to delve a little deeper. We can expect that the cavity volumes and heart muscle might increase in size, and that these enlargements affect all chambers of the heart. We know that electrical anomalies can be entirely distinct of structural adaptations, and that they are actually fairly commonplace in endurance athletes. Individuals participating in the same sport can expect to exhibit a wide variability in how they respond, both structurally and electrophysiologically, to increased levels of endurance training (Sharma, 2003). The most important point is that we have to be responsible for our own health, and as such we have a responsibility to ourselves to have any unusual cardiac occurrences investigated. It will almost certainly be nothing, or at least nothing but a predictable, physiologic adaptation to the extreme nature of our physical training, but we ought to have it checked anyway.
   We should be proud if informed our heart's dimensions are in the upper clinical limits, or even beyond, because the chances are it is due to the way our heart has adapted to the rigours of our incredible training programmes. Our very slow resting heart rates, and the occasional palpitations, come with the territory for most of us, and these are not the sort of responses to training that we should be unnecessarily worried about. But we ought to get any concerns or anomalies checked-out, because we are a highly unusual bunch, and we do not work like normal people, or even many other types of athletes. Because of that, we owe it to ourselves to monitor these adaptations to our training.
   Finally, our bodies are impressive organisms even amongst the only relatively fit and healthy. When pushed to the extreme, for almost all of us, the body will rise to the challenge in every way, with the heart, lungs, blood vessels, muscles, mind and bones all developing to suit our physiological requirements. We ought to take care and be mindful of any noticeable consequences of increased training frequency and/or mileages, but we should also be proud and impressed by how effectively we adapt to the rigours of extreme endurance exercise.
The full version of this article is contained within the appendix of the book, The Marathon des Sables: Ultra-Endurance Running in the Heat of the Sahara, and in the main text of the book is a more general chapter on cardiovascular adaptations to exercise.  The book is available to buy online at Amazon and Waterstone's.



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