The Marathon des Sables

 

The following is an excerpt from my book on the Marathon des Sables.  It is based upon a scientific review of the relevant research available at the time of publication.  I was prompted to write the chapter as one athlete died during the race in 2007, and I soon became aware of the lack of information available to runners on how the heart adapts to ultra-endurance running.  The media has also done what it can, at times, to promote the idea that exercise is unhealthy for the heart. 

   This is a concept that has not been helped by so-called 'experts', who regard any changes in heart structure or function in athletes as a sign of bad health.  Such individuals might be highly experienced at assessing heart structure and function in sedentary individuals, but are likely not aware of the growing body of research on the normal, expected structural and functional changes that can occur in athletes.  This is not to say that all changes are healthy in all individuals, but rather that a more sensible, measured consideration is required than assumptions that change is either always healthy or always unhealthy.

The Athlete's Heart


Regular aerobic exercise is important for supporting a healthy cardiovascular system and preventing many modern diseases (Wilson et al., 2010). However - and as difficult as it might be for athletes to hear -too much exercise, by definition of its being 'too much', can be detrimental for health.


Physiologic Change

The whole cardiovascular system will undergo changes in response to aerobic training, so as to promote efficiency and support future exercise. In athletes who regularly push themselves, in terms of high mileages or high exercise intensities, changes occur in the heart muscle itself. A concern is that if these physiological adaptations can influence the electrical characteristics of the heart, there might be a potential for anomalies to occur in how the heart beats, potentially increasing the risk of sudden cardiac death. 

   Whether changes in the heart are physiological (i.e. normal, healthy) or pathological (i.e. abnormal, potentially harmful) can only be determined via an individual cardiovascular assessment, typically involving ultrasound (echocardiogram) and electrical monitoring (simple ECG, stress tests, 24-hour ECG monitoring). Importantly, for the vast majority of athletes, the changes are physiological and predictable, being influenced by the type of exercise undertaken, but pathological changes do happen, and can represent a serious risk.

 

Media Hype

Even when pathological changes do occur, there are very few individuals who should actually be advised against exercise, and in the majority of cases there need be no change, or perhaps a reasonable reduction in training miles or intensities at the very most. The media seems more interested in sensationalising the rare negatives of exercise, including the very few cases of exercise-induced sudden cardiac death, in preference to being useful and promoting the benefits of physical activity for health. 

   As a brief but related aside, there has been some media attention focussing on the 'negative' health effects of running in general. Mostly, this refers to short-term, reversible effects of running above what an individual is fit for, as happens when some people participate in a marathon having never run close to that distance in training. Alternatively, racing in an unusually hot climate (for the individual) might equally have its temporary negative consequences. 

   The negative consequences of a sudden high mileage bout of exercise, or an extended running session in an extreme environment, tend to be similar. The effects include inflammation of the cardiovascular system (heart, blood vessels), a reduction in immune function, increased susceptibility to infection, and various blood and muscle indicators of increased stress.  What is often overlooked is that these changes are short-term, and in themselves a stimulus for the body to improve in fitness. 

   Athletes are unlikely to think it is healthy to train minimally and then attempt a marathon, because most of us do not do this - we increase our training mileages and intensities gradually, over time, and through common sense are better protected against any negative effects of running. Compared to sedentary individuals, we are less likely to suffer from cardiovascular disease, will have more efficient immune systems, recover better from injury, are better protected against
certain types of cancer, and have healthier muscles and bones. Regrettably, that sort of news fails to grab people's attention, and so is rarely considered newsworthy.

 


The Origins of our Understanding


Athlete's heart was first described in a short article published in 1899 (Henschen, 1899). In all this time, although the main adaptations that occur in the heart have been well-documented, there is extremely limited research on the pathological changes we would benefit from being aware of. Further, the research that does exist is widely-spread, with subject groups including all manner of athletes, rather than being focussed on endurance runners in particular. 

   Fortunately, when it comes to interpreting the research, the variety of potential adaptations that occur through aerobic exercise will be broadly similar (compared with strength athletes, for example), regardless of the actual sporting activities of those being studied. A growing body of research is being developed thanks to the cyclists, cross-country skiers, canoeists, and other aerobically-trained athletes who have volunteered for such studies. 

 

Heart Dimensions

As a warning (or even apology), there is a considerable amount of detail and terminology within this chapter, which I have tried to explain as it appears. The 'jargon' is included because the unusual terms might crop up on medical reports, and so perhaps be of direct use sometime. 

   A study published in 2005 (Karakayaet al., 2005) compared 50 athletes to 40 sedentary individuals. The athletes had been involved in competition for an average of 7.5 years, and participated in an average of 10 hours of exercise each week. In these athletes, it was found that most measurements of their hearts were similar to those of untrained, 'control' subjects. However, the thickness of the left ventricles and the interventricular septums (a thick line of fibres that separate the left and right ventricles) 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, an Italian research group (Pellicciaet al., 2005) 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 often a requirement of the ethics committees that permit the studies to take place, although as a reader we would often like to know much more about those individuals deliberately excluded. Was it possible that the abnormalities were an unusual response to training, were there genetic or congenital factors, other lifestyle factors, or was it a combination of these? 

   In that study, 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 enlarged left atria (>45 mm). 

   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 any case, it appears that all chambers of the heart are able to adapt to become more efficient for cardiovascular exercise, and not only the left ventricle.

 


The Electrical Heart

In addition to measuring structural adaptations in athletes' hearts, some researchers (Biffiet al., 2008) have looked for electrical abnormalities, via 24-hour 'ambulatory' ECG units. Ambulatory ECG units require the individual to have a few electrodes (sensors) placed in key positions over the chest, with leads from the sensors connected to a small receiver box that can be worn on a belt. The idea is that it is minimally-invasive, yet sufficiently accurate for measuring useful information about the heart, whilst a person goes about his or her normal daily routine, including training. 

   Investigators have found no relationship between more frequent irregular beats (arrhythmias) and increased size of the left ventricle. If anything, there is a trend towards those athletes with the greatest number of 'premature ventricular contractions' (more than 1000 in a 24-hour period), having the smallest left ventricles. This finding suggests 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 (Biffiet al., 2008). Perhaps it is also noteworthy that the ECG analysis assesses the atria and ventricles independently, hence references to anomalies in the ventricles, specifically, rather than the heart as a whole (atria and ventricles). 

   There is an almost inverse relationship between left ventricle size and ventricular arrhythmias in athletes, which is opposite to what occurs in 'hypertrophic cardiomyopathy' (an enlargement of the heart muscle due to pathology). In hypertrophic cardiomyopathy, greater left ventricle mass is associated with ventricular tachyarrhythmias (irregular beating of the ventricle, in which its rate of contraction is unusually increased) (Biffiet al., 2008).

 

Structural versus Electrical Change

The lack of any clear relationship between the electrical aspects of the heart and the structural adaptations seems unexpected. As the heart becomes enlarged 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 been brought about through training, then surely these would be related to the very same factors that can lead to structural changes?  This apparent case of logic has not been supported by the evidence. 

   In the Italian study previously mentioned (Pellicciaet al., 2005), in which 1,777 athletes had been recruited, less than 1% (14 subjects)experienced tachyarrhythmias' (irregular heart rhythms involving an increased number of beats) in the region above the ventricles, from where heart rate is normally set. 11 of those subjects reported prolonged palpitations during exercise, and the other 3 experienced them at rest. 

   347 of the Italian athletes were incorporated into an in-depth analysis of their 'electro-physiology' (Pellicciaet al., 2005). The ECG traces were found to be normal in 34% of the athletes (117 individuals). In the remaining 230, ECG traces were indicative of increased left ventricular muscle size (hypertrophy) (54%), whilst others were found to have anomalies in how the cells of their ventricles behaved electrically. 

   In all these studies, there appeared to be no clear relationship between structural adaptations in the heart (i.e. chamber size increasing, heart muscle size increasing) and electrical activity. If anything, there are trends towards the majority of electrical anomalies occurring in those whose hearts change the least due to training. This in itself might suggest that if the heart is unable to develop structurally to match training demands, there is an increased susceptibility to electrical anomalies, although such conjecture is far from supported. 

   On the whole, an athlete engaged in regular cardiovascular exercise is likely to stimulate his or her heart to increase in size, both in terms of the muscular walls of the chambers and the space within the chambers themselves. These changes are considered entirely physiologic in nature, rather than a potentially harmful, pathologic change.

 

 

 

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