Perspective:

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.