Killer Workouts

Jim Fixx was not exactly the healthiest of athletes at baseline. He was 35 when he took up running (The Jim Fixx Neurosis: Running Yourself to Death - The Washington Post). He had numerous risk factors, to include smoking 2 packs per day, being overweight at 220 lbs, a strong family history of premature coronary artery disease - his father suffered his first heart attack at age 35 and died after a second heart attack at age 43 (JAMES F. FIXX DIES JOGGING; AUTHOR ON RUNNING WAS 52 - The New York Times), high stress as editor of a magazine and 2 divorces.

Jim Fixx wrote a best-selling book about running. He was among other running authors of that era who encouraged readers to “listen to their bodies, instead of doctors” (​​10.1080/02701367.2002.10608990). But in yet another twist of irony, he did neither. He ran through his chest pain. Autopsy revealed severe obstructive 3-vessel coronary artery disease with 95%, 85% and 70% blockages as well as multiple infarcts in multiple stages of healing. 

While smoking certainly confounds the death of Jim Fixx, the death of an apparently healthy athlete is a perplexing and frightening event. But it is not new. Indeed, Pheidippides died shortly after running, well a marathon, from Marathon to Athens in 490 B.C. Today, Sudden Cardiac Death (SCD) during sports occurs in 5-6% in the general public. There is a 9:1 male to female ratio in those > 35 years age, considered the “older athlete” (Sudden Cardiac Death in the Older Athlete | Journal of the American College of Cardiology). Sudden cardiac death risk for runners has been reported as 0.8 to 2 per 100,000 marathon runners (Risk for sudden cardiac death associated with marathon running | Journal of the American College of Cardiology).  54% are over age 35. 57% are male (Sudden Cardiac Death in the Older Athlete | Journal of the American College of Cardiology). 

While that may not seem like a lot, when you consider there are approximately 20 million athletes (and growing) participating in foot races in the US annually, with a running craze that is attracting a more aging population, you are bound to hear about it in your community. For instance, a popular community race in Spokane, WA called “Bloomsday” brings about 45,000 runners participating in a 7.4 mile run. In 2018 there was 1 death near the finish line and reportedly 7 or 8 collapses that day. There was an aborted Sudden Cardiac Death in 2017 thanks to the quick action of nearby healthcare workers. This shocked the community and was well covered by the local news stations.

But Does Exercise TRIGGER the Heart Attack?

There is relatively sparse information on this question. There is evidence that suggests long term exercise is protective against atherosclerosis (Long-term Exercise and Atherogenic Activity of Blood Mononuclear Cells in Persons at Risk of Developing Ischemic Heart Disease | Cardiology | JAMA.)

However other data suggests exercise CAN trigger a heart attack (Triggering of Acute Myocardial Infarction by Heavy Physical Exertion -- Protection against Triggering by Regular Exertion | NEJM). But the above study suggests that the more sedentary an individual is, the more likely it is that HEAVY physical exertion will provoke an MI. Habitual and moderate to high intensity exercise appears to reduce this risk (Triggering of Sudden Death from Cardiac Causes by Vigorous Exertion | NEJM, Leisure-time physical activity and the risk of primary cardiac arrest).

What’s the Mechanism?

Not entirely clear. Possible mechanisms are sympathetic activity, ischemia, activation of hemostatic system, hemodynamic effects on vulnerable plaque, electrolyte and metabolic factors with prolonged exercise. Indeed, the length of the activity appears to be a factor. The majority of SCD occurs in the last ¼ of a marathon. There are more SCD events during marathons than ½ marathons.

So Then What’s the Deal with the Higher Coronary Artery Calcification in Athletes?

Progressive or premature coronary artery calcification has been associated with chronic intense exercise as well. It is unclear whether such athletes have the same risk as nonathletes with similar high CAC scores.

More to come on this.

So What’s the Verdict?

Yes, HEAVY exertion can kill you, but it’s rare and more likely to do so if you are not accustomed to exercise. The more you exercise, the less likely that HEAVY exertion will kill you. 

Exercise is medicine. Movement is medicine.

When tragedy strikes, it’s usually the “older” athlete (> 45 years of age) and usually due to coronary artery disease. Appropriate screening, particularly with Coronary Artery Calcium CT scans, can detect coronary artery disease in such patients. We have the tools to treat this. It’s not hard.

Can Too Much Exercise Cause Other Cardiac Issues in an Otherwise Healthy Athlete?

There can potentially be pathologic changes related to the ongoing effects from intense exercise. 

Exercise Dose

It’s debatable whether there exists a “J-shaped” curve when it comes to exercise intensity and volume. What this means is that as one begins to exercise, a small to intermediate amount of exercise intensity and volume offers protection, or an advantage over those who don’t, when it comes to death or cardiac death and other cardiac related problems. But as exercise intensity becomes more extreme, it may begin to negatively impact the risk for death, cardiac death or other bad cardiac problems. In other words, is there an appropriate “dose” of exercise that is ideal? Like Goldilocks. Not too little, not too much.

Based upon the Copenhagen Male Study, there appears to be a “dose-dependent” increase in lifespan with higher cardio fitness. Meaning, NO J-shaped curve (Midlife Cardiorespiratory Fitness and the Long-Term Risk of Mortality: 46 Years of Follow-Up).

Ok, But What if I Already Have CAD?

For those with known CAD, we have evidence that participating in cardiac rehab results in a 27% reduction in TOTAL MORTALITY! (Exercise-based rehabilitation for patients with coronary heart disease: systematic review and meta-analysis of randomized controlled trials). 

The Heidelberg Regression Studies demonstrated some evidence of regression by angiography among other findings (improved myocardial O2, measures of ischemia, well being, work capacity). Plaque regression was seen, but only in those spending 5-6 hours/week in leisure time (Various intensities of leisure time physical activity in patients with coronary artery disease: effects on cardiorespiratory fitness and progression of coronary atherosclerotic lesions.)

Atrial Fibrillation:

Atrial fibrillation is 8 times more likely to occur in endurance athletes, likely due to both mechanical and electrical remodeling of the left atrium in the setting of increased flow.

Screening Athletes

There is considerable controversy over preparticipation sports screening with EKGs and or echocardiograms due to the likelihood of false positive studies. The problem is that many athletes have “abnormal” EKGs due to normal or benign variants produced by cardiac “remodeling” in the setting of “athletic heart.” This includes eccentric left ventricular hypertrophy, right ventricular enlargement, atrial enlargement and various heart rhythm or conduction abnormalities, generally due to high vagal tone in athletes (generally a sign of optimal conditioning) such as marked sinus bradycardia, first degree AV block, ectopic atrial rhythm, junctional rhythm, incomplete right bundle branch block, right bundle branch block and more. 

Proponents of screening wish to rule out less common but potentially catastrophic congenital abnormalities (see below) more likely seen in the “younger athlete,” defined as