Running and Your Heart, Part II: The Athlete's Heart

Last week, inspired by some recent schoolwork and research, and mildly prompted by my collapse at Rocky Raccoon,  I started a series of posts on distance running and cardiac health.  The first post used my last twenty miles at Rocky as a jumping-off point to talk a little bit about pulmonary edema, and rather obliquely about cardiac illness.  I'd like to delve a little bit more into the relationship between endurance exercise, heart health, and heart disease.  In light of some of the recent media coverage of these issues, we're going to discuss some facts and address some common misconceptions and/or misinterpretations of some of the data out there, with the goal of all of us becoming better informed regarding this topic and better able to make rational decisions about our athletic future.

Before we can get into dysfunction, though, we have to talk about normal function, and about the physiologic adaptations that the heart makes to long-term endurance exercise.  Many of these adaptations are beneficial, but they're not without problems, either.

The normal heart

Chambers (and valves) of the heart

I don't think there's any need to get into a bunch of esoteric facts about the heart (It pumps six liters of blood per minute! It weighs 300 grams!) but we should first go through a few basics.  I'm sure you can remember from ninth grade biology that the heart is a muscle that pumps blood through the body.  You might also remember that the heart is split into two sides (left and right), each of which has two chambers (an atrium and a ventricle).  The right side of the heart pumps de-oxygenated blood to the lungs, where the red blood cells bind to oxygen.  Blood from the lungs then returns to the left side of the heart, from where (whence?) it is pumped out to the rest of the body so that the various tissues and organs can use that oxygen.  Having delivered oxygen to the tissues, the blood then returns to the right side of the heart to begin the cycle again.  Blood flows throughout the circulatory system in what is essentially a series of tubes; veins carry blood to the heart, while arteries carry blood from the heart.

OK, simple enough.  From a basic standpoint, that's all we need the heart to do: pump oxygen-poor blood to the lungs, deliver oxygen-rich blood to the rest of the body.  So when we talk about cardiac disease, we're most generally talking about a failure of the heart to fulfill that function.  But there are a bunch of different ways in which this basic function can be compromised.  For our purposes, there are three systems inherent to normal heart function that we want to be familiar with in order to understand possible dysfunction: the coronary arteries, the conduction system, and the heart muscle itself.

Coronary arteries

We spoke briefly about the heart muscle last week; simply put, the muscle squeezes, increasing the pressure within the chambers of the heart, and forces blood out into the circulation.  The muscle is the heart's engine.  The coronary arteries are responsible for delivering oxygen to the heart muscle.  Wait a minute, you're saying, didn't you just say that arteries carry blood AWAY from the heart?  Yes, I did!  Thanks for paying attention!  Arteries do indeed carry blood away from the ventricles, but in this case they don't have to go very far.  The coronary arteries arise from the aorta immediately after the blood leaves the left ventricle, and they surround the heart, supplying oxygen-rich blood to the muscle.  When you hear the term "heart attack," this is usually used to mean an interruption of blood flow to the heart muscle, usually due to a narrowing of, or blockage within, the coronary arteries. We're going to do an entire post about the coronary arteries next week, so for now, just think of them as the heart's plumbing system.

The conduction system, then, is the wiring.  This system is comprised of electrical fibers that coordinate the heartbeat.  The depolarization of these electrical cells causes the atria, and then the ventricles, to contract synchronously.  The contraction of the atria forces blood into the ventricles, and the contraction of the ventricles forces blood out into the circulation.  When you see that familiar tracing that we all know represents a beating heart:

what you're looking at is a graphic representation of the heart's electrical activity.  (I'm not going to go into what each of those little squiggles means, but if you're interested, read this.)  Without the orderly input of the electrical/conduction system, these contractions may lose their synchronicity, robbing the heart muscle of its ability to pump blood effectively--or contractions can cease altogether.

The athlete's heart

Note the enlarged (dilated) cardiac chambers
in the athlete's vs. non-athlete's heart.
Photo: cyclingtips.com

Like any other muscle, the heart responds to exercise by adapting to stress.  Weight lifting, for example, places the skeletal muscles under stress, ultimately causing the muscles to adapt by increasing muscle mass and size (hypertrophy).  Similarly, aerobic exercise means that the muscles requires more oxygen, necessitating increased cardiac output (the amount of blood the heart pumps).  Over time, the heart muscle adapts by increasing the mass and thickness of the muscular wall of the left ventricle.  Other adaptations include dilation (or enlargement) of the various heart chambers, and dilation of the coronary arteries (which I'll discuss more in next week's post).   In the absence of a history of vigorous exercise, many of these structural changes--hypertrophic ventricular walls, atrial dilation--would be considered pathologic.  That is to say, when we see these sorts of things in the population at large, they are usually the result of chronic high blood pressure or underlying cardiac disease, are usually associated with a loss of the heart's pump function, and can lead to congestive heart failure, pulmonary edema, and other general badness.  But in endurance athletes, who demonstrate these changes in the setting of preserved pump function, they are usually considered normal adaptations to long-term vigorous exercise that we term the athlete's heart.

What's the big deal? Aren't adaptations good?

So, in general, we think of the chronic adaptations associated with the athlete's heart to be beneficial, or at the very least neutral.  They allow for us to increase our cardiac output to meet the demands of intense aerobic activity, and do not appear to be associated with the sort of pathology we would otherwise expect from these kinds of changes in heart morphology.  However, there is some evidence that suggests that there may be some downside to some of the adaptations of the athlete's heart.

For example, take the dilation seen in the heart's chambers, particularly the left atrium and right ventricle.  There is a hereditary disease called arrhythmogenic right ventricular cardiomyopathy, a rare condition that causes dilation of the right ventricle and fibrous deposition or "scarring" within the myocardium (the muscular layer of the heart wall).  This fibrous tissue can interrupt the electrical pathways of the heart (remember that conduction system stuff?), serving as an origination point for life-threatening ventricular arrhythmias (abnormal heart rhythms).  The dilated RV seen in long term athletes can be accompanied by similar fibrous deposition, leading to some speculation that there may be an "exercise-induced arrhythmogenic right ventricle" that may mimic the inherited condition.  (Some have posited this as the theoretical framework for the death of Ryan Shay at the US Olympic Trials marathon in 2007, though that--in fact, all of this--remains unproven.)  Dilation of the left atrium also seems to place athletes at increased risk of atrial fibrillation or atrial flutter, two abnormal heart rhythms that, while not as dangerous as ventricular arrhythmias, can still cause significant cardiovascular complications.

No bueno.

Another interesting cardiac finding associated with ultra-endurance exercise relates to cardiac enzymes.  Many of you are probably familiar with rhabdomyolysis, a fun little problem in which repeated skeletal muscle trauma (as seen in, say, a 100-mile run) causes breakdown of muscle tissue and the release of enzymes called myoglobin and creating phosphokinase into the bloodstream.  Just like skeletal muscles, heart muscle contains these enzymes; but there are also enzymes that are specific to cardiac muscle, notably troponin.  Troponin is generally only minimally detectable in the bloodstream; elevated troponin levels generally imply damage to the heart muscle, usually from ischemia (lack of blood flow)-- a "heart attack."  Now, several studies have detected significant elevations in troponin levels following prolonged exercise.  Does this mean that we're giving ourselves small heart attacks during every ultra we run?  Probably not; while troponin elevations following heart attacks tend to peak many hours after the event, and persist for several days to weeks, post-exercise troponin elevations typically appear, and resolve, very rapidly.  Furthermore, while there have been studies showing reduction in LV and RV function following ultra endurance events, in almost every case function has been demonstrated to return to normal within one week, unlike what we would see in a "heart attack."  It appears possible that the transient elevation in troponin following extreme exercise is related to increased permeability (leakiness) of the cardiac cell membranes rather than ischemia, cell death, or permanent heart damage.

What does all this mean?

I know, I hit you with a lot of information, and right now you might be freaking out a little bit.  Freaking you out is not the objective of this post.  We're going to talk big picture in a couple of weeks, and hopefully when we're done you'll feel pretty comfortable with the whole deal.  For now, here's the take-home points:

• there are several adaptations that the heart makes to accommodate long-term, vigorous aerobic exercise
• most of these adaptations are generally beneficial
• there are some morphologic changes (that is, the the size/shape of the heart) that may increase the risk of arrhythmias in athletes
• most of the evidence we have at this time shows correlation, not causation, and much of the framework surrounding this remains theoretical/speculative

Again, we'll go big picture in a couple of weeks, and I'll be able to draw things together a little bit more.  The point of all this is just to make you a little more aware and informed about some of the interesting stuff that's out there, and maybe to generate some fodder for a discussion with your doctor if you have questions or concerns.  

If you want some really detailed reading on this stuff, check our these highly scientific articles:

George K, Whyte GP, Green DJ, Oxborough D, Shave RE, Gaze D, and Somauroo J. (2012). The endurance athletes heart: acute stress and chronic adaptation. British Journal of Sports Medicine, 46(S1), i29-i36.

O'Keefe JH, Patil HR, Lavie CJ, Magalski A, Vogel RA, and McCullough PA. (2012). Potential Adverse Cardiovascular Effects From Excessive Endurance Exercise. Mayo Clinic Proceedings, 87(6), 587-595.

Running and Your Heart, Part I

So...it's been an interesting couple of months.  I think I've mentioned this before, but since late last year I've been involved with the Heart Center, the preeminent cardiology group in the Hudson Valley, in establishing a new sports cardiology practice.  I'm not a cardiologist (which will become eminently obvious over the course of the next couple of posts) but I have more than a layman's understanding of the athlete's heart and many of the cardiac issues that endurance athletes deal with.  Plus, I've always had a major interest in exercise physiology, and have been looking for an opportunity to break into that field for some time.  Starting within the next couple of months, we'll be opening the doors on our new sports cardiology practice (spiffy title pending) and I'll be working part-time as the group's exercise physiologist.  So exercise science and the athlete's heart have been on my mind quite a bit recently.

This was obviously at the forefront of my thoughts during and after Rocky Raccoon.  As a brief recap, I was running very well at Rocky through 60 miles (9:12) and, despite a nosebleed and some other minor issues, was still on pace for a top-6, sub-16 hour finish through 80 miles (12:45).  In the last twenty miles, however, I developed some rather scary breathing issues, including some rattling breath sounds starting around mile 88 that had me concerned I might be developing pulmonary edema.  Pulmonary edema is basically fluid buildup in the lungs; it can occur for a variety of reasons in sick or elderly individuals, but is much less common in young, healthy folks.  (I'm referring to fluid within the lungs; this is different from a pleural effusion, or fluid around the lungs, which is an entirely different issue I'm not going to address here.)  Mountain climbers can experience high-altitude pulmonary edema (HAPE), which is basically a failure of the pulmonary (lung) vasculature (blood vessels) in response to the physiologic demands of altitude--obviously not an issue in Huntsville, TX.

The most common reasons for a buildup of fluid in the lungs are basically an inability to remove fluid (kidney failure) or an inability to circulate fluid (heart failure).  Reports of kidney failure following extreme endurance events, due to a condition called rhabdomyolysis, are not uncommon.  Rhabdomyolysis occurs as a result of extreme muscle breakdown, when large amounts of a muscle-based proteins myoglobin and creatine phosphokinase (CPK) are released into the bloodstream.  Without proper fluid intake, these proteins can accumulate in the renal tubular system, causing kidney failure.  Kidney failure can lead to anuria (inability to urinate) and pulmonary edema, as the body cannot excrete excess fluid and hydrostatic pressure causes fluid to leak into the lungs and other tissues.  In a 100-mile race, this is certainly a possibility (though remote).  However, I wasn't terribly concerned; I had urinated several times during the race, without any blood (a telltale sign of muscle breakdown called myoglobinuria), I had been taking in adequate fluids, and it was not an overly warm day.  Also, rhabdo-induced renal failure is usually a later finding; it was hard to believe that my kidneys could have already failed to the point where I was going into pulmonary edema less that fourteen hours into the event.  My real fear was my heart.

The most common cause of pulmonary edema is heart failure.  Basically, if the heart muscle is weakened (by any of a variety of mechanisms; most commonly, a heart attack), its ability to pump blood adequately can be compromised.  This can lead to a backup of blood flow throughout the body. When the blood does not flow adequately through the venous system, that can cause an increase in the amount of pressure within the veins.  That increased pressure can cause fluid to leak out of the veins, where it doesn't belong--including into the lungs.

Fortunately, not my chest X-ray
photo: wikipedia.org

Now, I had no real reason to be concerned about my heart.  Other than some mild hypertension, I have no personal history of heart disease, and no other significant risk factors; I had even undergone a recent CT angiogram of the coronary vessels (more on this in subsequent postings), which was normal.  But as I mentioned, I've been rather immersed in sports cardiology and the athlete's heart recently, and as I'll talk about in the next few posts, there are a lot of unlikely but unpleasant possibilities that can befall those of us who take this running thing a bit too seriously.  At its essence, the heart is a rather simple pump, but the underlying components of the organ are a bit more complex, and therein lies a lot of potential problems.  The relationship between exercise, heart health, and heart pathology is actually quite fascinating, and I'll explore that a little more as promised in coming posts. But certainly in real time I was less fascinated and more, well, freaked out.

Anyway, I finished the race by walking the vast majority of the last 18 miles or so, and since then have recovered more or less normally.  I had the usual post-race leg swelling, which in this case brought on some additional anxiety but ultimately resolved as expected.  For a few days afterwards I felt as though I was getting short of breath just walking around or climbing stairs, but I think that may have all been in my head.  A week later I went for an echocardiogram, which is an ultrasound of the heart.  This test shows the activity of the heart muscle in real time; it can show if there are areas of the muscle which are not functioning normally (wall motion abnormalities), if there are problems with leaky heart valves, and how much blood the heart pumps with each beat (ejection fraction).  My cardiologist said my heart was very photogenic:



He also told me that, other than some normal findings associated with the athlete's heart, everything looked good, and that my ejection fraction was normal.  And after a two-week break, I started running slowly again.  It's been a longish recovery period, but now five weeks post-Rocky I'm running more or less normal mileage and feeling just about ready to get back to some harder training again.  (Though the estimated 24" of snow coming our way tomorrow may preclude that for a little while.)

So, apparently this has all been much ado about nothing, fortunately, though it's forced me to think a bit about the role of the sport in my life.  It's a silly pursuit, of course, for those of us who are not making a living at it; sure, it's better than plenty of other bad habits we could have, but there probably isn't anything in our lives that needs to be taken to the extremes that we ultrarunners face regularly.  I did have some fleeting thoughts about what life would look like without 110-mile training weeks.  Unfortunately I don't think I'm mature enough to make any difficult decisions about it at this point, though with a clean bill of health it doesn't seem I'll be forced to do so for awhile.  So for now I'll keep plugging away and trying to slay whatever dragons strike my fancy in the coming months.  (Plus there's always the Western States lottery to look forward to.)

However, there's an awful lot of information out there regarding distance running and long-term health, and a lot of it can be very confusing.  So in the next few weeks I thought I'd try to demystify some of that information, in case anyone else is struggling with some of these decisions regarding their future in the sport.  Next post we'll talk a little bit about the athlete's heart and some of the various changes related to distance running, and whether or not we need to worry about those things.  After that we'll go into the association between ultrarunning and coronary artery disease.  And I'd like to spend a post on the relationship between strenuous exercise and overall mortality, which has been in the news quite a bit recently.  So, check back soon for more possibly accurate, semi-scientific information.