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by Harshal R. Patil, MD, James H. O’Keefe, MD, Carl J. Lavie, MD, Anthony Magalski, MD, Robert A. Vogel, MD & Peter A. McCullough, MD

Abstract

A daily routine of physical activity is highly beneficial in the prevention and treatment of many prevalent chronic diseases, especially of the cardiovascular (CV) system. However, chronic, excessive sustained endurance exercise may cause adverse structural remodeling of the heart and large arteries. An evolving body of data indicates that chronically training for and participating in extreme endurance competitions such as marathons, ultra-marathons, Iron-man distance triathlons, very long distance bicycle racing, etc., can cause transient acute volume overload of the atria and right ventricle, with transient reductions in right ventricular ejection fraction and elevations of cardiac biomarkers, all of which generally return to normal within seven to ten days.  In veteran extreme endurance athletes, this recurrent myocardial injury and repair may eventually result in patchy myocardial fibrosis, particularly in the atria, interventricular septum and right ventricle, potentially creating a substrate for atrial and ventricular arrhythmias. Furthermore, chronic, excessive, sustained, high-intensity endurance exercise may be associated with diastolic dysfunction, large-artery wall stiffening and coronary artery calcification. Not all veteran extreme endurance athletes develop pathological remodeling, and indeed lifelong exercisers generally have low mortality rates and excellent functional capacity. The aim of this review is to discuss the emerging understanding of the cardiac pathophysiology of extreme endurance exercise, and make suggestions about healthier fitness patterns for promoting optimal CV health and longevity.

Introduction

Although exercise is not a pharmacologic agent, in many ways its effects resemble those of a powerful drug. Daily physical activity (PA) and exercise produces numerous favorable changes in gene expression, with improvements in physiological function, structure, and body composition.^1-4 A regimen of regular exercise training (ET) is extremely efficacious in the prevention and treatment of many of our most common and deadly chronic diseases including: coronary artery disease (CAD), diabetes, obesity, high blood pressure, heart failure (HF) and depression.⁵ Individuals who regularly engage in more PA have markedly lower rates of disability, and an average life expectancy that is about seven years longer than sedentary people.^6,7 For this reason, enlightened health care providers routinely recommend to patients regular PA as an indispensable element of their day-to-day routine.

Figure 1. Exercise improved overall survival in a dose-dependent fashion up to about 60 minutes of daily vigorous PA.

As can be expected with any drug, a safe upper range dose of ET may exist, above which the adverse effects of sustained intense PA and exercise may outweigh its benefits. Even a modest dose of regular PA, as little as 15 minutes daily, can confer substantial health benefits, as shown in a recent observational long-term study in involving 416,000 individuals.⁹ That study also found that exercise improved overall survival in a dose-dependent fashion up to about 60 minutes of daily vigorous PA; beyond that a point of diminishing returns was apparent (See Figure 1). Similarly, a 15-year observational study of 52,000 adults reported that long-term runners had a 19% lower risk of all-cause mortality compared with non-runners.  However, U-shaped mortality curves were apparent for running distances, speeds, and frequencies (See Figure 2). Running speeds of six to seven miles/hour, running distances of about one to twenty miles/week, and frequencies of runs of two to five days/week were associated with lower rates of all-cause mortality; while higher weekly mileage, faster running paces, and more frequent runs diminished some of the survival benefits noted with more moderate running.¹⁰ From this large study, more not only did not appear to be better, but actually more running appeared to be worse, in that there was a loss of the survival benefit that was noted at lower levels of running. A recently published trial randomized 60 male CAD patients to regular vigorous exercise training sessions of either 30 or 60 minutes. The 30-minute physical activity sessions produced less oxidant stress and augmented arterial elasticity; sixty-minute workouts increased oxidant stress and worsened vascular stiffness as assessed by pulse wave velocity.  These adverse effects were mainly apparent in older subjects.¹¹

Figure 2. A 15-year observational study of 52,000 adults reported that long-term runners had a 19% lower risk of all-cause mortality compared with non-runners.  However, U-shaped mortality curves were apparent for running distances, speeds, and frequencies.

Thus, exercise confers benefits even with relatively modest levels of regular PA. Competitive ultra-endurance athletes often engage in daily vigorous aerobic exercise for anywhere from 90 to 300 minutes per day, commonly accumulating workloads of 200 to 300 metabolic equivalent hours (METS X hours) weekly; this is about five to ten times more than the weekly cumulative exercise workload recommended by consensus guidelines for prevention of CAD.^5,12 The purpose of this review is to explore the possibility that chronic intense sustained endurance exercise may cause adverse structural and electrical remodeling of the heart and large arteries that could attenuate some of the benefits conferred by more moderate intensities and durations of exercise training.

In the environment of our evolution, our ancient ancestors performed a wide variety of PA usually done intermittently, at moderate intensities, for moderate durations; when high intensity exercise was performed, it was typically performed for short or intermediate bursts.^1-3 Humans are not genetically adapted for protracted, sustained, and extreme aerobic exercise efforts.^1,2

Even in highly trained individuals, high-intensity, sustained multi-hour endurance exercise efforts are often associated with cardiac strain, elevated levels of troponin and B-type natriuretic peptide (BNP), and subsequent patchy myocardial fibrosis.^13-17 Especially, right ventricular (RV) function may be more profoundly affected by chronic excessive endurance exercise (EEE)^17-20 and, in some cases, RV recovery may be incomplete^20-22 which may represent a substrate for proarrhythmic RV remodeling in some highly trained athletes^23,24 even in the absence of a known familial disposition²⁵ (See Figure 3). Long-term exercise training and racing involving marathons and ultra-marathons, Iron-man distance triathlons, and very long distance bicycling can exact a toll on the health and integrity of the heart and blood vessels.²⁶

Figure 3. Right ventricular (RV) function may be more profoundly affected by chronic excessive endurance exercise.

Sudden Death and Endurance Exercise

Over the past 35 years, the number of Americans participating in a marathon annually has risen twenty-fold.  In 2010, there were an estimated half million marathon finishers.²⁹ Recent analyses^30,31a estimated the rate of sudden cardiac death (SCD) among marathoners as approximately 1 per 100,000-200,000 participants; while that per participant risk has not changed over the decades, absolute mortality has increased as the number of participants has risen. The final mile of the 26.2 mile marathon run represents less than 5% of the total distance yet accounts for almost 50% of the SCDs.³¹

 The fatality rate for triathlons is approximately twice that of marathons, largely due to increased CV events and drowning during the swim portion of the races.³² The incidence of SCD among collegiate athletes during competition is about 1 per 40,000 participants per year for all athletes, but rises to 1 per 3,000 for Division I male basketball players.³³  However, the rare occurrence of sudden cardiac death during marathons, triathlons, and collegiate athletic events does not convey the full spectrum of potential adverse effects induced by chronic EEE training and racing.

The etiologies of sudden cardiac death during or after extreme exertion in individuals younger than age 40 most commonly include genetic causes such as hypertrophic cardiomyopathy, anomalous coronary arteries, dilated cardiomyopathy, and congenital long QT syndrome. In athletes over age 30, CAD and acute myocardial ischemia are the predominant causes of exercise related SCD.^34-40  All of these causes should be excluded, and in the remaining cases with sudden cardiac death and no discernable cause, an acquired structural cardiac abnormality due to chronic and repetitive sessions of extreme exertion should be considered.

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