Run for Your Life… at a Comfortable Speed and Not Too Far


The following are points to remember about this is editorial, which states the authors’ view that a low level of light or moderate exercise confers greater cardiovascular risk reduction compared to exercise at higher levels and/or of longer duration:

1. The authors cite the death of the Greek runner Phidippides in 490 BCE as an example of exercise-associated sudden cardiac death.

2. The authors cite potential adverse effects of exercise including:

• Acute volume overload of the atria and the right ventricle.
• Stretching caused by volume overload results in myocardial micro-tears, evidenced by elevations in cardiac troponin and B-type natriuretic peptide (BNP); and decrease in right ventricular ejection fraction following endurance exercise.
• Prolonged endurance exercise results in patchy myocardial fibrosis, which in turn is a substrate for atrial fibrillation and for ventricular arrhythmias.
• Exercise results in ‘aging’ of the heart, manifest by increased coronary calcification, ventricular diastolic dysfunction, and large-artery wall stiffening.
• Vigorous exercise for 60 minutes increases oxidative stress and worsens vascular stiffness.

3. The authors cite a study that showed that mice forced to run to exhaustion daily for 4 months developed evidence of cardiac enlargement, scarring, and predisposition to dangerous arrhythmias; cardiac abnormalities and myocardial fibrosis improved after cessation of exercise.

4. The authors cite the March 2012 death during a moderate-distance run of Micah True, an ultra-distance runner and the man on whom the 2009 book Born to Run was based, as evidence that distance running causes potentially fatal cardiac disease. The authors cite the autopsy report as showing ‘focal areas of interstitial chronic inflammatory infiltrate’ and coronary arteries that were ‘focally thickened with mild coronary arteriosclerosis.’

5. The authors cite two abstracts that they use to support that small amounts of low-level exercise is better than either exercise of longer duration or of higher intensity:

• One observational study found that there was a 19% reduction in death among runners compared to nonrunners, but that the benefit was enjoyed only for those who ran less (5-20 miles/week), infrequently (2-5 days per week), and slowly (≤6-7 miles/hour).
• The other study similarly found that joggers had a 44% lower risk of death with an added 6 years of life compared to nonjoggers, but that the benefit was greatest for slow-to-average pace jogging for a total of 1-2.5 hours per week in a total of 2-3 sessions.

6. The authors recognize that a sedentary lifestyle leads to disability, disease, and a shortened life expectancy.

7. The authors propose a ‘U’-shaped curve for exercise and cardiovascular risk reduction, suggesting that the powerful health benefits of exercise disappear with more exercise. The authors cite Hippocrates, a contemporary of Phidippides in ancient Greece, in prescribing moderation in nourishment and exercise as the safest way to health.


There are conflicting data regarding the ‘dose-response’ between exercise and reduction of cardiovascular risk. As with so many other areas in medicine in which data are conflicting, they can be ‘spun’ to create a compelling message. With no intended disrespect, the following are a few points of fact-checking and rebuttal:

• There was no Phidippides. It is not an ancient Greek name. The histories of the Greco-Persian wars were recorded by Herodotus ~50 years after the fact. In his accounting, a runner named Philippides was sent to Sparta before the battle on the plain of Marathon to try to enlist their help. The Spartans declined, and the battle was won without them. There is no mention of a runner sent to Athens after the battle. Rather, Phidippides first was mentioned in the histories of Lucian of Samosata about 250 years later, and was popularized in an 1879 poem by Robert Browning. That poem shortly predated the 1896 first modern Olympic marathon.
• Surrogate endpoints like troponin, BNP, and right ventricular ejection fraction are not clinical endpoints, and should be interpreted with caution.
• The study which showed that mice develop cardiomyopathies, fibrosis, and ventricular tachyardia (VT)? The study used rats, not mice. The structural changes in the rat hearts were compatible with athletic conditioning. And the only VT that was seen was after specific induction attempts; no spontaneous ventricular arrhythmias were reported.
• The autopsy report on Micah True notes coronary arteries that were ‘focally thickened, but the lumens are nowhere compromised’––different than what was cited in quotations in this editorial. The quote stating: ’focal areas of interstitial chronic inflammatory infiltrate’ is taken from the autopsy findings of the lungs. Microscopic examination of the heart states: ’rare focus of chronic inflammatory infiltrate.’ If anything was going on in the heart, it also was going on (and more so) in the lungs. No one to my knowledge has described Phidippides pulmotoxicity, though.
• Beware the tyranny of the anecdote. One (or a few) endurance athlete(s) who suffer(s) sudden death do(es) not an epidemic make. Neither does it science make.
• One of the cited abstracts on population-based outcome studies is available for review in a peer-reviewed publication, and one still is not. In the one that is, the authors recognize the small number of events in their subanalyses of jogging quantity, pace, and frequency, and urge caution in interpretation of the results.
• Hippocrates (~460-370 BCE) could not have been a contemporary of the 490 BCE there-never-was-a-Phidippides.

Some of what is listed here might seem like silly perseveration over detail. Rats or mice––who cares? But if data are conflicting, at least existing data (and history) should be accurately quoted.

Exercise has dramatic physical and psychological benefits. The jury is still out on whether the endurance athlete really loses all cardiovascular benefits of exercise, and it seems reasonable to state that a controversy exists. Notably, though, most endurance athletes probably do not think that they are immortal. If an endurance athlete finds joy in his or her sport, he or she might pursue it even independent of any cardiovascular benefit. Meanwhile, the population is becoming increasingly sedentary and increasingly obese. A health policy message of ‘exercise is good’ might save more lives than trying to convince the addicted ultra-marathoner that he or she is not immortal.

Clinical Topics: Arrhythmias and Clinical EP, Congenital Heart Disease and Pediatric Cardiology, Diabetes and Cardiometabolic Disease, Dyslipidemia, Heart Failure and Cardiomyopathies, Prevention, Sports and Exercise Cardiology, Atherosclerotic Disease (CAD/PAD), SCD/Ventricular Arrhythmias, Congenital Heart Disease, CHD and Pediatrics and Arrhythmias, CHD and Pediatrics and Prevention, CHD and Pediatrics and Quality Improvement, Lipid Metabolism, Novel Agents, Acute Heart Failure, Heart Failure and Cardiac Biomarkers, Exercise, Stress, Sports and Exercise and Congenital Heart Disease and Pediatric Cardiology

Keywords: Athletes, Health Policy, Ventricular Function, Right, Coronary Artery Disease, Conflict (Psychology), Heart Atria, Greece, Exercise, Sports, Risk Factors, Autopsy, Furin, Nervous System Diseases, Microscopy, Biological Markers, Cardiomyopathies, Cardiovascular Diseases, Stroke Volume, Obesity, Death, Sudden, Cardiac, Natriuretic Peptide, Brain, Outcome Assessment (Health Care), Disabled Persons, Heart Defects, Congenital, Risk Reduction Behavior, Life Expectancy, Drug-Related Side Effects and Adverse Reactions, Oxidative Stress, Vascular Stiffness, Cardiomegaly, Heart Failure, Sedentary Lifestyle, Coronary Vessels, Diastole, Heart Ventricles, Troponin

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