Can Intensive Exercise Harm the Heart?
Introduction
Elite athletes are paragons of physical fitness in our society, and an entire sports-industrial complex has developed from playing/watching/marketing sports.1 Although the idiosyncratic example of Pheidippides has been used by some to highlight the dangers of extreme endurance efforts,2 much more ubiquitous is the Greek model of the athlete as physical perfection, allowing vigor through to great age.3
Response by La Gerche and Heidbuchel p 991
The term “athlete’s heart” was originally coined to reflect its similarities to patients with enlarged hearts from disease,4 though it is now recognized to reflect the unique physiological adaptation of the endurance athlete5,6: a heart that is big,7 muscular,8,9 compliant,10 and can pump a lot of blood very fast, to support high rates of aerobic metabolism.11 It is quite clear that prolonged, high-intensity sports training required to compete at an Olympic level is sustainable without adverse effects in young individuals, and does not lead to impairment in cardiovascular structure or function.12,13 It is also clear that there is no epidemiological signal that high-level athletics leads to premature death; indeed quite the opposite. For example, when >15 000 Olympic medalists from 9 different country groups were examined over decades after their first medal, there was a progressive increase in conditional survival (compared with age- and sex-matched controls from the general population in those countries; Figure 1) for the Olympic medalists which was greatest in the participants in endurance sports.14 Although there are many possible explanations for such a finding (such as socioeconomic status, or healthier lifestyles), the concept of increased rather than decreased survival in elite endurance athletes has been demonstrated repeatedly,15–17 and was most recently buttressed by a study of nearly 800 French Tour de France competitors who experienced a substantial reduction in mortality (40%) compared with the French male noncyclist population.18 Therefore, although there is growing evidence that the heart may show some signs of fatigue,19,20 especially of the right ventricle21 after single bouts of extraordinary endurance effort,22 which may be accompanied by the release of biomarkers of cell permeability,23 there is little evidence that such physiological signals are pathological,24 and no rash of deaths in participants of long-distance events such as marathons.25–27
Figure 1. Data from ref 14, showing increase in survival of Olympic medalists compared with controls, which increases with the time since their first medal. CI indicates confidence interval.
In contrast, the evidence that high-performing, Masters endurance athletes have healthy, youthful cardiovascular structure and function is quite robust. For example, in studies by our group, we recruited highly trained and very competitive endurance athletes who had been training for ≥25 years, competing successfully in multiple marathons, triathlons, or other endurance events and performed high-resolution studies of cardiovascular structure and performance. Using invasive methods, we created cardiac pressure–volume curves in these athletes (Figure 2) and compared them with a group of highly screened, extremely healthy but sedentary seniors of the same age and sex distribution (mean 70±3 years, half women) and young (29±5 years) sedentary controls. Despite being very healthy, the sedentary seniors had hearts that were smaller and stiffer than the Masters athletes; most impressively, the athletes had cardiac compliance that was indistinguishable from healthy young controls.28
Figure 2. Data from ref 28; Diastolic limb of the pressure-volume curves for Masters athletes, sedentary but healthy seniors, and young controls; estimated transmural pressure derived from the difference between left ventricular end-diastolic and right atrial pressures. Note increased stiffness (leftward and upward shift of the p/v curve) in sedentary seniors that is completely prevented by life-long intensive endurance training.
The large blood vessels were similarly youthful in these athletes. For example, we developed a technique that can quantify the biological age of the aorta and applied it to this same group of Masters athletes and controls.29 As expected, both the healthy, sedentary seniors and young controls had biological aortic ages that were virtually identical with their chronological ages. However, the biological aortic age of the Masters athletes was ≈30 years younger than their chronological age (Figure 3). The functional outcome of this improved myocardial and vascular compliance was that their ventricular–arterial coupling was substantially better (>2× the increase in stroke volume for any given increase in left ventricular filling pressure) than their healthy but unfit counterparts30; enhanced ventricular–arterial coupling is also a hallmark of highly trained young endurance athletes.31
Figure 3. Data from ref 29; note that the biological aortic age of both healthy, sedentary seniors and young controls matched their chronologic age exactly. However, the fit Masters athletes had biological aortic age that was 30 years younger.
This discussion is particularly important because some investigators have suggested that intense marathon training leads to cardiac fibrosis.32 However, in this high-profile study of 102 middle-aged marathon runners, there was no statistically significant difference between the prevalence of positive delayed enhancement by cMRI in the athletes compared with a group of controls from the Heinz Nixdorf recall study. Multiple other studies have failed to confirm the development of delayed enhancement in marathon runners,33–35 though it is clear that intense training in the setting of preexisting coronary artery disease can lead to the development of ischemic-type subendocardial scar.36 Indeed, training in the face of ischemia has been shown to result in prolonged and cumulative myocardial stunning and left ventricular dysfunction,37 and could be a mechanism of myocardial injury in athletes who train hard with undetected coronary artery disease. In our own studies of >100 individuals performing varying doses of life-long exercise, including 21 elite Masters athletes, none showed delayed enhancement, except for 1 casual exerciser who had a noncoronary pattern of delayed enhancement.38
Some animal studies examining structural changes with exercise training have been done, but are hard to interpret. Some do show fibrosis,39 though the training involved intense tail shock (perhaps a stress response, rather than an exercise response) to get the animals to train. Most importantly, there was no hint of fibrosis in the left ventricle—the fibrosis was only in the right ventricular free wall; and there was no evidence of progressive increases in fibrosis—the magnitude of the fibrosis was the same in rats euthanized at 4, 8, and 16 weeks of training. This time independence suggests that the fibrosis likely was not a response to prolonged training (otherwise the fibrosis would have gotten progressively worse), but supports the idea that it might have been a response to the tail shock.
The right ventricle has been shown to be susceptible to excessive strain during exercise,40 and in extraordinary, ultra-endurance athletes, a small fraction has been shown to have late gadolinium enhancement (LGE) at the right ventricle/left ventricle junction.22 However this LGE may not necessarily represent fibrosis; for example there was no LGE present in 1 of the world’s greatest ultra-endurance athletes despite many extreme events. However, a small amount of LGE was identified at the ventricular insertion point immediately after a race across America41 (Figure 4). Therefore, this type of LGE may represent edema from acute, prolonged strain, rather than actual scar42 because it has been demonstrated to be reversible in other circumstances, such as repair of an ASD.43 However, caution should be taken for those individuals who carry a desmosomal mutation for right ventricular cardiomyopathy; training in such individuals can cause deterioration of right ventricular function and accelerate the phenotype of right ventricular cardiomyopathy.44
Figure 4. Images from ref 41. Note no evidence of gadolinium uptake in 1 of the world’s most extreme endurance athletes before his race across America (Pre). However, after running 1500 km and cycling 1500 km in 30 days, including substantial time at high altitude, there was delayed enhancement present at the ventricular insertion point (yellow arrow).
There has also been some concern articulated that older marathon runners have an excessive amount of coronary atherosclerosis.45 However, in this study involving the same athletes reporting delayed enhancement in marathoners,32 there actually was no difference in coronary artery calcium (CAC) between marathoners and age-matched controls, and more of the marathoners had a CAC of 0. Most importantly, all of the marathoners in this study started training later in life, and 50% of them were smokers, raising the possibility that these individuals started training in an attempt to reverse the effects of adverse cardiovascular risk factors. Other evidence suggests that physiologically, the coronaries of elite ultra-endurance athletes are actually quite healthy.46,47 For example, invasive measurement of coronary vasodilatory capacity (Figure 5) showed a markedly increased coronary diameter in response to nitroglycerin in ultra-endurance runners compared with sedentary controls.47 In addition, for individuals with subclinical CAD, as determined by a CAC>100, a high degree of fitness reduced the risk for CV events by a remarkable 75%48 (Figure 6). Therefore, although it is plausible that some marathoners might have higher levels of CAC based on an increase in PTH levels during running,49 any increase in marathoners as a group is modest, and functionally, their coronaries have superior vasomotor reserve and reduced risk of plaque rupture.
Figure 5. Data from ref 47. Note that the total cross-sectional area of the coronary circulation increased substantially more after intracoronary nitroglycerin in ultradistance runners, than inactive men. NTG indicates nitroglycerin.
Figure 6. Data from ref 48. In a large number of patients from the Cooper Clinic Longitudinal Study with subclinical CAD as determined by a CAC score >100, high fit individuals had a dramatically reduced risk (75%) of suffering a cardiovascular event. CAC indicates coronary artery calcium; CAD, coronary artery disease; and CV, cardiovascular.
In summary, the Table highlights the take-home messages from this essay. Although it would be foolish to argue that extraordinary endurance training can never be harmful, it is equally inappropriate to frighten individuals who wish to undertake competitive endurance training, including marathons, triathlons, or even ultra-endurance events, based on fears of accelerating coronary artery disease or initiating a cardiomyopathic process.
| 1. | Athletes have large compliant hearts that generate a large stroke volume during exercise, as well as compliant arteries with large vasodilatory capacity; |
| 2. | The heart of the senior athlete, with a life-long pattern of intensive training, is youthfully compliant, equivalent to healthy 30-year-olds, and their large blood vessels have a biological age ≈30 years younger than their chronological age; |
| 3. | Acutely, extraordinary endurance exercise may cause fatigue of cardiac muscle, which seems to be more prominent in the right than the left ventricle. But this recovers quickly after even very long events and does not appear to stimulate pathological biological programs; |
| 4. | The older athlete is probably at increased risk for atrial fibrillation (not discussed), though lower doses of physical activity do not appear to increase this risk; |
| 5. | The evidence that years of intense training accelerates atherosclerosis or causes cardiac fibrosis is weak, and given the known and clear benefits of competitive training on both cardiac and vascular structure and function, not likely to be clinically important; |
| 6. | High intensity training in the presence of advanced atherosclerosis, however, likely does increase the risk, especially if ischemia is present, and exercise training does not prevent the atherosclerotic process. The role of medical therapy in this context (ie, statins) is uncertain, though likely is of benefit. |
Disclosures
None.
Footnotes
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Response to Levine
André La Gerche, MBBS, PhD, FRACP, FCSANZ, FESC; Hein Heidbuchel, MD, PhD, FESC
When comparing the 2 opposing views in this debate, there is more in agreement than in contrast. We agree with Dr Levine that athletic training promotes enlarged compliant cardiac chambers capable of generating supra-normal stroke volumes and attenuates many of the catabolic processes of aging.
The point on which we differ is when we step away from the average athlete and deal with the stochastic nature of arrhythmias. To return to a simple analogy, runners can be assured that training will increase bone and muscle strength and yet should be aware of the simultaneous increase in risk of muscle injuries and stress fractures. With reference to the heart, training increases cardiac size and improves myocardial function in a dose-related manner, but it also increases the risk of myocardial injury and arrhythmias. Professor Levine does not negate the fact that arrhythmias are more common amongst endurance athletes. He implies that we should be reassured by the excellent functional capacity of the athlete’s heart. However, as our 2 cases and previous data illustrate, a large compliant athletic heart is not necessarily immune from arrhythmias.
Thus, our job is to promote the expansive benefits of exercise in population health whilst also maintaining an open-minded appraisal of the potential harm of intense endurance exercise in individual athletes. Greater awareness will enable more prompt diagnoses, and better pathophysiological understanding of exercise-induced cardiac injury will enable more directed treatment strategies. Ultimately, it is our job to make exercise safe and enjoyable for all.
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