Human Limits

Today’s post was stimulated by an e-mail exchange with Amby Burfoot of Runner’s World on reports over the past few months suggesting that lifelong intensive exercise training might be “bad” and actually increase the risk of heart problems.  The idea is that during exercise adrenaline and related hormones cause the heart to beat faster and harder.  Do this day after day for years and the thinking goes that areas of micro damage might occur.  In addition to leading to small areas of heart damage, there might also be a buildup of calcium in the blood vessels that supply the heart.  So what is the evidence to support these ideas?

First, after extremely prolonged and intense exercise like a marathon or ironman triathlon the pumping ability of the heart can be reduced by a few percent for a few days and there can be a rise in blood levels of substances released from the heart.  However, the pumping function of the heart returns to normal within a week and there is no evidence of long term heart damage.   The blood levels of substances released from the heart also return to normal.  The other tricky thing here is that the skeletal muscles of highly trained athletes undergo biochemical changes that make them more like heart muscle.  The wear and tear on skeletal muscles during a competitive event can then cause a rise in the blood levels of so-called cardiac markers that are in fact released from skeletal muscle and set off all kinds of false alarms about heart damage.

Second, no one is sure exactly what finding calcium in the coronary arteries means in asymptomatic people especially older athletes.   Also, case reports in a few people are hard to interpret and in more controlled studies it appears that the coronary arteries of lifelong ultramarathon runners are a bit bigger than those of non-runners and can also dilate more.   The figure below shows this data, and bigger coronary arteries that relax more are almost certainly a very good thing.

Third, there is some data in animal models that areas of micro damage caused by prolonged intense exercise make the heart more susceptible to dangerous irregular heartbeats.  However, in these studies aversive stimuli (tail shock) were used to get the animals to run so there is the added issue of “mental stress” in addition to exercise.   Also, the animals were doing a training regimen that was truly heroic in terms of both daily duration and intensity and how this translates to what even the most fanatical human might do over 10 or 20 years is unclear.   In other animal models, exercise training tends to protect the heart from irregular beats.

Fourth, when detailed research and data collection is done on who dies during exercise a couple of patterns emerge.  Young people who die suddenly typically have congenital problems with the electrical system in their hearts or defective coronary arteries.   Middle aged and older people typically have evidence of heart disease that in many cases probably started before they became fit or started to train.   There are also cases of heart problems in athletes likely related to acute inflammation of the heart perhaps associated with a viral illness.   However, marathon running as a whole appears to be very safe.

Fifth, all the news is not positive.  There is some evidence that lifelong training is associated with a condition known as lone atrial fibrillation.   However, the data are only suggestive and much bigger and better controlled studies are required on this topic.   This condition while bothersome is typically not life threatening and can be treated.

Perspective:  Over the last few months I have been making the case that one of the biggest public health and ultimately medical problems out there is inactivity.   Is there a cardiac risk associated with being super fit and training a whole lot?  To the extent there is comprehensive and well controlled data the answer appears to be no.  It does appear that in terms of health there are diminishing returns and that people who train “a whole lot” (say more than an hour almost every day) are not  better off than people who just do “a lot” (30-60 minutes most days).  However, people who do a whole lot of training are probably doing it for reasons other than health that include things like a need to compete, a need for time alone, or the need for some sort of big challenge in life.  Not exercising enough is extremely common and dangerous.  By contrast, a life time of exercising “too much” is extremely rare and the evidence to suggest it does long term harm to the heart is pretty speculative.

Last week in the Opinion section of the New York Times, the food writer Mark Bittman made the case in layman’s terms that Alzheimer’s disease might be considered “type 3” diabetes.   There are two main lines of evidence in support of this idea.  The first is that glucose and insulin in large amounts do bad things to the brain.   In type 2 diabetes blood levels of both glucose and insulin can be high.   The second is that diabetes is a risk factor for Alzheimer’s disease, and the increased rates of diabetes and Alzheimer’s in the population tend track each other.  However, the story is a bit more complex than simple “type 3” diabetes.

The current thinking is that Alzheimer’s is caused by the buildup of one or more proteins (one of the major ones is called beta-amyloid) in the brain that damage nerve cells and ultimately cause brain function to decline.  However, there are holes in the protein theories and drug therapies designed to lower the levels of amyloid have not improved brain function in clinical trials.   It is also interesting to note that in addition to diabetes, several behavioral risk factors seem to put people at increased risk for Alzheimer’s disease.

When I look at these risk factors I am struck by how similar they are to traditional risk factors for heart disease.   For both heart disease and Alzheimer’s, diabetes, hypertension, obesity, inactivity, and smoking all damage blood vessels and their negative effects tend to multiply in people with more than one risk factor.   Also, the only genetic risk factor with a big effect in Alzheimer’s some something called ApoE4 which affects cholesterol metabolism and can also damage blood vessels.  To me this suggests that there is an interaction between the buildup of “bad” proteins in the brain and poor blood flow to the brain.   There is also some evidence that exercise causes an increase in the levels of something called BDNF (brain derived neurotrophic factor), which promotes the growth of new brain cells even in middle aged and older people.

If you take the evidence outlined above a step further and ask what effect improvements in “life style” might have on Alzheimer’s the data is pretty startling.  Here is a quote from the summary of the key paper on behavioral risk factors mentioned above.

“At present, about 33.9 million people worldwide have Alzheimer’s disease (AD), and the prevalence is expected to triple over the next 40 years. The aim of this Review was to summarize the evidence regarding seven potentially modifiable risk factors for AD: diabetes, midlife hypertension, midlife obesity, smoking, depression, cognitive inactivity or low educational attainment, and physical inactivity…….Together, up to half of AD cases worldwide (17.2 million) and in the USA (2.9 million) are potentially attributable to these factors. “

Who knows if there will ever be a simple explanation for Alzheimer’s disease that will lead to effective drug therapy.  However, it is pretty clear that what is good for your heart is good for your brain.