Figure 8 describes the pathophysiology and adverse CV consequences (fibrosis, atrial arrhythmias, VA, and SCD) associated with endurance exercise training and competition, such as marathon running. Although the accelerated atherosclerosis in chronic marathoners is somewhat surprising and counterintuitive, the metabolic and mechanical stresses involved in chronic extreme endurance efforts may be playing a critical pathophysiological role. Individuals who chronically train and race over very long-distances have sustained elevations in heart rates, blood pressures, cardiac output, and cardiac chamber volumes for as much as several hours daily. Heavy and sustained exercise training generates large quantities of free-radicals that likely outstrip the buffering capacity of the system, leaving these individuals susceptible to oxidative stress and transient myocyte dysfunction, perhaps inducing adverse changes in the quality and quantity of desmosomes and other cell anchoring structures. This process causes dilation of the RA and RV resulting from hours of strenuous physical activity and increased cardiac demands. This repetitive cycle may stimulate immune cells including lymphocytes, macrophages, and mast cells to secrete cytokines that signal the myofibroblasts to proliferate and secrete procollagen which is then cross-linked to form mature collagen. This eventually results in fibrosis deposited in patches in the myocardium and more diffusely in the large arteries.
Although it has been recognized that elite-level athletes commonly develop abnormal electrocardiograms and benign atrial and ventricular ectopy52-54 the “athlete’s heart” adaptations to long-term, high-level exercise training traditionally have not been thought to predispose to serious arrhythmias, HF, myocardial infarction, or suddent cardiac death. However, recent data indicate that adverse cardiac remodeling induced by EEE can, among other issues, create an arrhythmogenic substrate17, 26, 45, 54 Indeed, chronic sustained vigorous aerobic ET such as marathon or ultra-marathon running or professional cycling has been associated with increased risk of atrial fibrillation,17, 36, 45, 48-50, 55-60, 67 and complex ventricular ectopy including ventricular tachycardia and SCD30 even in very fit individuals.52 Despite the fact that these studies excluded athletes with findings to suggest arrhythmogenic RV dysplasia, the VA typically originate from a mildly dysfunctional RV,23,24,54,61 that may be the result of prior myocardial injury from excessive and sustained aerobic exercise training. Myocardial fibrosis (fibrillary collagen deposition) develops as a reparative process in response to damaged myocardium. This patchy myocardial scarring can favor reentry and is well established as a substrate for arrhythmia susceptibility.62, 63
Chronic excessive endurance exercise training and competition also stimulates multiple other disruptions within the system including episodic release of excessive catecholamine and resultant coronary vasoconstriction, chronic elevations of heart rate during sessions of protracted aerobic ET leading to decreased diastolic filling time of the coronary arteries, increased demand for oxygen, changes in free fatty acid metabolism, lactic acidosis, and metabolic derangements.43 During an extreme endurance event, in susceptible individuals the heart may not be able to cope with the prolonged and sustained excessive physiological demands, thus increasing right heart preload and afterload, which initiates stretch and subsequent chamber dilatation in response to these hemodynamic changes.58 Right heart dilation and hypokinesis following protracted exhaustive exercise training has been documented using both CMR and echocardiography.23,45 Diastolic dysfunction of both the RV and LV has also been observed in individuals doing chronic EEE and racing.64
During the post-endurance exercise period, the cardiac geometric dimensions are restored and many athletes continue this cycle with long distance exercise training, marathon running, transient chamber enlargement, and subsequent myocardial recovery. With this recurrent stretch of the chambers and re-establishment of the chamber geometry, some individuals may be prone to the development of chronic structural changes including dilation of the heart chambers and patchy myocardial scarring in response to the recurrent volume overload and excessive cardiac strain.59 Approximately one in three finishers of a marathon, irrespective of baseline fitness level or the time it took to complete the race, will have a post-race spike and fall in cardiac troponin and BNP.60 It is logical to hypothesize that a subset of these individuals eventually go on to develop patchy cardiac fibrosis. These abnormalities are often asymptomatic and probably accrue over many years; and may predispose to serious arrhythmias and/or sudden cardiac death.
Currently, we have no proven screening methods for detecting the CV pathology associated with EEE. A logical strategy for now would deploy post-competition cardiac biomarkers, echocardiography and/or advanced imaging such as CMR to identify individuals at risk for and with subclinical adverse structural remodeling and the substrate for arrhythmias.61 For any individual who is considering EEE efforts such as marathons or day long aerobic races for any other activity that elevates cardiac output for a sustained period of time (continuously over several hours), it may be reasonable to obtain a maximal treadmill exercise test to screen for ischemia and/or exercise induced arrhythmias24 and Heart CT for CAC scoring, particularly for those who are over age 50 and who have been chronically training for and competing in EEE events. Aortic pulse wave velocity could give an inference into the development of vascular stiffness that may not be readily appreciated by cuff blood pressure measurement.
Suggestions for an exercise routine that will optimize heath, fitness and longevity without causing adverse cardiovascular structural and electrical remodeling:
Avoid a daily routine of exhaustive strenuous exercise training for periods greater than one hour continuously. An ideal target might be not more than seven hours weekly of cumulative strenuous endurance ET.1,2,9,51
When doing exhaustive aerobic ET, take intermittent rest periods (even for a few minutes at an easier pace, such slowing down to walk in the middle of a run). This allows the cardiac output normalize temporarily, providing a ‘cardiac rest period’ when the chamber dimensions, blood pressure and pulse come down closer to baseline resting parameters before resuming strenuous exercise again.2
Accumulate a large amount of daily light-to-moderate physical activity, such as walking, gardening, housekeeping, etc. Avoid prolonged sitting. Walk intermittently throughout the day. Look for opportunities to take the stairs. 1, 2 Buy a pedometer and gradually try to build up to 10,000 steps per day.
Once or twice weekly, perform high-intensity interval exercise training to improve or maintain peak aerobic fitness. This is more effective in improving overall fitness and peak aerobic capacity than is continuous aerobic exercise training, despite a much shorter total accumulated exercise time spent doing the interval workout.65, 66
Incorporate cross training using stretching, for example, yoga, and strength training into the weekly exercise routine. This confers multi-faceted fitness and reduces the burden of cardiac work compared to a routine of daily long-distance endurance exercise training. 1, 2
Avoid chronically competing in very long distance races, such as marathons, ultra-marathons, Iron-man distance triathlons, 100-mile bicycle races, etc., especially after age 45 or 50.
Individuals over 45 or 50 years of age should reduce the intensity and durations of endurance exercise training sessions, and allow more recovery time.
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