ReviewPotential Adverse Cardiovascular Effects From Excessive Endurance Exercise
Section snippets
Sudden Cardiac Death and Endurance ET
Over the past 35 years, the number of Americans participating in a marathon annually has risen 20-fold; in 2010, an estimated half-million runners completed a marathon in the United States.10 Sudden cardiac death (SCD) among marathoners is very rare, with 1 event per 100,000 participants.6, 7, 11, 12 Although that per-participant risk has not changed over the decades, absolute mortality rates have increased as the number of participants has risen. The final 1 mile of the marathon course
Animal Studies
In an elegant animal model of excessive endurance ET, rats were trained (in part by prodding with electrical shocks to maintain high-intensity effort) to run strenuously and continuously for 60 minutes daily for 16 weeks, and then they were compared with control sedentary rats.8, 24 The running rats developed hypertrophy of the left ventricle (LV) and the right ventricle (RV), diastolic dysfunction, and dilation of the left atria and the right atria (RA); they also showed increased collagen
Athlete's Heart
Chronic ET imposes increased hemodynamic demands that alter the loading conditions of the heart, particularly among athletes participating in sports requiring sustained elevations in cardiac work, such as long-distance running, rowing, swimming, and cycling.26 Highly trained individuals develop cardiac adaptations including enlarged LV and RV volumes, increased LV wall thickness and cardiac mass, and increased left atrial size.21, 22, 23 In the general population, these structural changes are
Biomarker Evidence for Cardiac Damage With Extreme Endurance ET
Running is a prototypical natural PA and often plays an integral and important role in an active, healthy lifestyle.9, 34, 35, 36 However, uninterrupted very long distance running as is generally done while training for and participating in marathons and other extreme endurance events may produce adverse CV effects in susceptible individuals. Serologic markers of cardiac damage, including cardiac troponin, creatine kinase MB, and B-type natriuretic peptide, have been documented to increase in
Adverse Structural Remodeling
Accumulating evidence suggests that the adverse effects of both short-term intense PA and cumulative endurance exercise are most apparent in the right-sided cardiac chambers. Cardiac output at rest is approximately 5 L/min but typically increases 5-fold to about 25 L/min during vigorous ET.21 Long-term daily sessions of hours of continuous strenuous PA cause dilation of the RA and RV. During the postexercise period, the cardiac geometric dimensions are restored, but with this recurrent stretch
Coronary Artery Changes
Veteran endurance marathon runners in one study had coronary arteries that, at resting baseline, were similar in size to those of sedentary controls, but the marathoners had greater coronary artery dilating capacity.52 Mohlenkamp et al30 studied 108 middle-aged German long-term marathon runners and compared them with matched nonrunner controls. They observed a greater atherosclerotic burden in the marathoners as documented by higher coronary artery calcium (CAC) scores. Additionally, during
Pathophysiology of Long-Term Extreme ET
Figure 7 shows the pathophysiology and possible adverse CV consequences (fibrosis, atrial arrhythmias, VAs, and SCD) associated with endurance ET and competition, such as marathon running. Individuals who do long-term ET and race over very long distances induce sustained (often for 1 to several hours daily) elevations in heart rate, blood pressure, cardiac output, and cardiac chamber volumes.9 Heavy and sustained ET generates large quantities of free radicals55 that likely outstrip the
Proarrhythmic Effects of Excessive Endurance ET
Although it has been recognized that elite-level endurance athletes commonly have electrocardiographic abnormalities and atrial and ventricular ectopy,28, 44, 54 these functional adaptations traditionally have not been thought to predispose to serious arrhythmias or SCD. However, it appears that adverse cardiac remodeling induced by excessive ET can create an arrhythmogenic substrate, and rhythm abnormalities may be the most common CV problems encountered by veteran endurance athletes.29, 31, 54
Risk Stratification For Endurance Athletes
Currently, we have no proven screening methods for detecting potential CV pathologic changes associated with extreme endurance ET. A logical strategy for now might be to deploy postcompetition cardiac biomarkers, echocardiography, and/or advanced imaging such as cardiac MRI to identify individuals at risk for and/or with subclinical adverse structural remodeling and substrate for arrhythmias, but the cost would likely be prohibitive.65 Computed tomography for CAC scoring may be useful,
Conclusion
In some individuals, long-term excessive endurance ET may cause adverse structural and electrical cardiac remodeling, including fibrosis and stiffening of the atria, RV, and large arteries. This theoretically might provide a substrate for atrial and ventricular arrhythmias and increase CV risk. Further investigation is warranted to identify the exercise threshold for potential toxicity, screening for at-risk individuals, and ideal ET regimens for optimizing CV health. For now, on the basis of
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