Book Review: Haywire Heart









Check out the recently published “The Haywire Heart” by Chris Case, John Mandrola, MD, and Lennard Zinn.  The book is available at Amazon and other outlets.

You may recall that Case, Mandrola, and Zinn authored an article in VeloNews, entitled “Cycling to Extremes:  Are endurance athletes hurting their hearts by repeatedly pushing beyond what is normal?”  This was a terrific read.  I wrote a previous blog post sharing my thoughts about the article and about the issue of arrhythmias and endurance sport, more generally.  Their article generated much discussion in the cycling and broader endurance sports communities and the interest of readers served as the motivation for their new book.

This is a book about electrical problems in the heart–the various arrhythmias.  Case, Mandrola, and Zinn are in a unique position to bring this topic to life because each has dealt personally with some form of arrhythmia.  And as long time cyclists (and perhaps with some triathlon experience as well), they’re able fashion the discussion to the avid endurance athlete.  From the medical perspective, the field of arrhythmias is rather complicated, both in terms of the underlying mechanisms of disease and the evaluation and treatment of affected patients, but here the authors have found a writing style that is captivating and accessible to the non-medical reader, while retaining much medical detail that will be of interest.  I give them credit because this is hard to do!

I love the title.  With an arrhythmia, the heart is truly “haywire.”  Ignore the line on the cover, though, about “How too much exercise can kill you.”  That’s unlikely to happen and there’s little in the book about that particular issue.  Instead, focus on “what you can do to protect your heart.”  That’s where the value lies here.

The book is organized into 9 chapters.  In Chapters 1-3, the authors describe in detail how the normal heart works, outline how the heart adapts over time to endurance exercise, and introduce the medical aspects of heart attack and arrhythmias, especially for the endurance athlete.  These sections are well-illustrated and are a great primer for any athlete interested in learning more about the heart.

Chapters 4-6 focus on the evidence of a link between long-time endurance exercise and arrhythmias, what to look for in yourself, and what it’s like to receive the diagnosis of an arrhythmia.  Here, the authors speak from personal experience and their observations and advice are valuable.

Chapter 7 deals with the issue of exercise addiction.  We know that exercise is generally healthy, but most of the benefits of exercise accrue with the first few hours per week.  Why, then, do athletes exercise more?  When does one become addicted?  What are the implications?  This is an interesting and pertinent discussion and might provoke some warranted introspection.

Chapter 8 covers the various treatment options for athletes with various arrhythmia problems.  For athletes who don’t have trouble with arrhythmias, the discussion is educational in a broad sense.  For those who do have arrhthymias, though, there is ample detail here to become educated and be better engaged with your doctor(s) as you sort out the best treatment for you.

Finally, in Chapter 9, the authors wrap up with their “takeaway” on how we might prevent arrhythmia problems.

One of my favorite aspects of the book is the inclusion of Case Studies sprinkled throughout the text, where the authors illustrate their points in a side bar with the personal account of an athlete.  These stories bring us the human side of arrhythmias and show how difficult these problems can sometimes be.

This book is for….

  • the athlete with an arrhythmia problem.  There’s a lot of familiar territory here as well as the opportunity to learn more.  An educated patient is the ideal patient.
  • the athlete with simply an interest in the heart.  I can’t think of a better resource to become educated about the workings of the heart, particularly as they relate to the endurance athlete.
  • the athlete (or the athlete’s spouse or parent) who’s afraid of causing harm to the heart through exercise.  Be forewarned and be vigilant.


Related Posts:

  1. Heart to Start, by James Beckerman, MD
  2. The Exercise Cure, by Jordan Metzl, MD
  3. Cardiac Athletes, by Lars Andrews

Thoughts on the Recent VeloNews Article








I enjoyed reading a recent article in VeloNews by Chris Case, entitled “Cycling to Extremes: Are endurance athletes hurting their hearts by repeatedly pushing beyond what is normal?”  The article is good reading.

First, I give a lot of credit to Chris Case and the editors at VeloNews.  It’s great that a publication with such a broad audience would devote time and space to the issue of heart health and endurance sport.  In recent months, they’ve also brought attention to the heart problems of pro cyclists, Robert Gesink, Olivier Kaisen, and Eddy Merckx.  I wish that other writers and publications would do the same.

I also thank Lennard Zinn and Mike Endicott for sharing their personal stories with their heart problems.  It would be very easy to keep quiet.  I very much enjoy reading personal accounts such as these.  Their stories are real and also familiar.  This is how we learn.

Since the article was published, I’ve gotten a bunch of inquiries asking my opinion about the article in general or about specific information that was presented.  Let me share a few thoughts that may be helpful to readers here at the blog….

Don’t be scared (too much)!  For most people, cycling is a healthy pursuit.  In general, exercise is healthy and provides a myriad of benefits.  So don’t stop cycling!  It’s important to keep in mind that the stories of Zinn and Endicott are not the norm, even among veteran endurance athletes.  Zinn’s multifocal atrial tachycardia (MAT) is one of the least common atrial arrhythmias and Endicott’s sudden cardiac death is rare.  As you absorb their stories, focus not on the particular arrhythmias but rather on the possibility that an arrhythmia–any arrhythmia–can cause significant problems or be an indication that things are amiss with the heart.  In that sense, their stories should cause you to put on your thinking cap.

My favorite quote from the article?  “But fit for racing doesn’t necessarily equal healthy.”  Readers here at the blog will know that I’ve said this repeatedly.  It’s easy for seemingly healthy endurance athletes, particularly men, to believe that fitness is the same thing as healthiness.  This isn’t necessarily true.  To dispel the myth, I’ve shared the stories of many elite endurance athletes who’ve struggled with heart problems of various sorts.  We can add Zinn and Endicott to these lists.  Heart problems are common….and athletes aren’t exempt.  This is the most important take-home message from the article.

Arrhythmias are common–in athletes and non-athletes, alike.  All athletes experience arrhythmias.  Infrequent premature beats, originating in either the atrium (premature atrial contractions, or PAC’s) or in the ventricles (premature ventricular contractions, or PVC’s) most likely have no consequence.  Sustained arrhythmias, on the other hand, deserve attention and evaluation.  There are far too many varieties of arrhythmias to consider here, other than to mention some of their names:  SVT, or supraventricular tachycardia; WPW, or Wolff-Parkinson-White syndrome; atrioventricular (AV) nodal re-entry tachycardia; atrial or ventricular bigeminy; sick sinus syndrome; sinus bradycardia; atrial fibrillation (AF); atrial tachycardia; MAT; ventricular tachycardia (VT); and ventricular fibrillation (VF).

The last part of the VeloNews article alludes to AF.  Other than sinus bradycardia (simply a heart rate slower than 60 beats per minute, which may be very healthy in athletes) or innocuous premature beats, AF is probably the most common arrhythmia in athletes.  We know from longitudinal studies that the lifetime risk of having AF is approximately 25% in the general population.  The question of whether athletes–and endurance athletes, specifically–are more prone to AF is a current controversy, with important implications for long-term endurance athletes.  I’ll try to finish up a separate blog post that summarizes the accumulated evidence on this issue.  For men, there may be an association with long-term exercise and the prevalence of AF, but there is certainly no consensus among experts.  For women, the evidence does not suggest an association between long-term exercise and AF.

Pay attention to warning signs.  I particularly like the last section of the article, written by Dr. John Mandrola.  He’s a cardiologist who specializes in arrhythmias and who is also a (former?) triathlete and current avid cyclist.  He provides good advice in the Q&A.  I like to talk about 5 important warning signs of possible heart disease:  chest pain or discomfort, especially during exercise; unexplained shortness of breath; light-headedness or blacking out (syncope), especially during exercise; unexplained fatigue; and palpitations–the sense of a rapid or irregular heartbeat.  Any of these warning signs may be due to an arrhythmia.  All deserve investigation.  Dr. John makes the apt point that, very often, heart rhythm problems start off small and get worse with time.  Not surprisingly, it’s best to get things sorted out earlier rather than later.

Less may be more.  Lastly, I would encourage athletes with identified arrhythmias to be open to the idea that less exercise may be helpful.  In fact, this may be the most appropriate prescription.  For the long-term endurance athlete, this can be difficult to accept.  In this regard, the stories of Zinn and Endicott are particularly poignant.


Related Posts:

1.  Physical Activity Levels and Atrial Fibrillation

2.  Atrial Fibrillation in Athletes (in a Nutshell)

3.  Too Much Exercise, Revisited

4.  Don’t Stop Running Yet!


Triathlon, Open Water Swimming, and the Heart: What Can We Learn From Dolphins and Seals?








A recent study about marine mammals caught my eye.  I don’t know much about non-human biology and physiology, but this study on dolphins and seals may shed some light on the problem of fatalities during open water swimming or triathlon events.

The Study

A group of investigators headed by Terrie Williams from the University of California at Santa Cruz shared their report, “Exercise at depth alters bradycardia and incidence of cardiac anomalies in deep-diving marine mammals” in the January 16th edition of Nature Communications (1).

This group of investigators has been interested in the physiology of the so-called “dive response” in marine mammals.  This is a response that is governed by the involuntary, or autonomic, nervous system, which has two antagonistic components:  the parasympathetic nervous system and the sympathetic nervous system.  As a group, the marine mammals depend on feeding by chasing pray to depths that can range up to 3,000 m.  Even at lesser depths, these mammals must maintain a breath-hold under large hydrostatic pressures while they undergo extreme exertion to catch their pray.  During a dive, breath-holding stimulates the parasympathetic nervous system to slow the heart rate (producing bradycardia).  At the same time, the exertion required to chase pray stimulates the sympathetic nervous system, producing an increase in the heart rate.  The current study offers the first detailed study of the interplay between the components of the autonomic nervous system during routine diving and feeding activity in these animals.

The investigators created an electrocardiograph-accelerometer depth monitor that was deployed on 10 Atlantic bottle-nosed dolphins and 3 Weddell seals.  This device allowed high-fidelity recording of the heart rate, ECG, water depth, and swimming stroke frequency (a measure of exertion) during dives.  For the dolphins, measurements were made for 74 dives to depths of up to 210 m.  For the seals, measurements were made for 91 dives to depths of up to 390 m.

The Results

As expected, there was a strong relationship between diving depth and heart rate for both species, with heart rates falling during descent and reaching a minimum at the lowest depth of the dive.  Superimposed on this effect was an additional effect of exertion.  For the dolphins, the maximum heart rate was 1.7 to 3.7 times greater during periods of extreme exercise compared to gliding alone.  For the seals, the maximum heart rate was 1.5 to 1.8 times greater during periods of extreme exercise compared to gliding alone.

The surprising finding was that cardiac arrhythmias occurred in more than 73% of the dives.  The investigators defined arrhythmias to include ectopic beats or significantly increased variability in the interbeat interval (IBI).  There were apparently no sustained or fatal arrhythmias., but there were discrete examples of “wandering pacemaker” and ventricular premature beats.  In the Weddell seals, there were often patterns of alternating periods of tachycardia (fast heart rate) and bradycardia (low heart rate) during periods of constant, intense exertion.

The presence of cardiac arrhythmias was strongly correlated with increased depth of dive (parasympathetic activation) and increased exertion (sympathetic activation).  As an example, cardiac arrhythmias occurred in 81% of the dolphin dives to >210 m but in only 26% of dives to <100 m.

The authors concluded that our previous understanding of the dive reflex in marine mammals was not totally correct.  Given that these animals depend on diving for their food sources, the development of cardiac arrhythmias during feeding appears to be mal-adaptive.  In fact, feeding might actually be dangerous.

My Thoughts

At first glance, the physiology of the diving response of dolphins and seals during feeding seems far afield from open water swimming and triathlon.  And moreover, we already know about the development of cardiac arrhythmias during submersion in breath-holding humans as well as other marine species.  The important observation here, though, is what I might call “irritability” or “instability” in the heart rhythm during periods of intense parasympathetic and intense sympathetic activation….and that’s the possible link to human fatalities during open water swimming or triathlon.

We know from autopsy reports of triathletes who’ve died during the swim portion of an event that there are sometimes only subtle abnormalities of the heart, and often nothing that seems explanatory.  That leaves us in a difficult position to explain such deaths.  In a previous blog post, I wrote about one very plausible hypothesis. Two UK physiologist,s X and X, proposed the concept of “autonomic conflict,” where a surge in both the parasympathetic and sympathetic stimulation of the heart might lead to a fatal arrhythmia.  I’ve been intrigued with this hypothesis because it seems to fit many of the observations made about the swim victims.  It is easy to see where exertion, cold water, anxiety, etc. might lead to strong sympathetic activation.  And it’s equally easy to see where facial wetting, water entering the mouth/hypopharynx/nasopharynx, and breath-holding, even without diving, might lead to strong parasympathetic activation.  In that instant, in an athlete with some sort of susceptible heart, a fatal arrhythmia might occur.

The new observations about the dolphins and seals seem to play into this hypothesis.


Related Posts:

1. Fatalities in Open Water Swimming:  What’s the Mechanism?

2. Triathlon Fatalities:  2013 in Review



1.  Williams TM, Fuirman LA, Kendall T, et al.  Exercise at depth alters bradycardia and incidence of cardiac anomalies in deep-diving marine mammals.  Nature Communications 2015;6:6055.




Physical Activity Levels and Atrial Fibrillation

 Afib strip 2 - Copy




In the medical news last week came another interesting report on the relationship between physical activity and atrial fibrillation (AF).  Reported in the medical journal, Heart, a team of investigators led by Nikola Drca from the Karolinska Institute in Stockholm gave us a study entitled “Atrial fibrillation is associated with different levels of physical activity levels at different ages in men.”  This is the largest-ever study of the relationship between physical activity and AF, so the findings and conclusions deserve our attention here in the athlete community.

To set the stage for our discussion, recall that AF is a fairly common arrhythmia that is generated in the upper chambers of the heart–the left and right atrium.  I’e written about AF here at the blog previously, in general terms for athletes.  We’ve known for a long time that AF is associated with some other types of heart disease, particularly heart valve disease, and increases in prevalence as we age.  The problem of AF is not benign.  For athletes, the arrhythmia disrupts training or competition, but over the long term there is a small but real risk of stroke and also the chance of harm to the heart itself.  Moreover, the available treatments–medications or ablation procedures–carry risk as well.

We also know that AF is associated with exercise.  We know from prospective, longitudinal population studies that long-time, regular exercisers are more likely to develop AF over the years.  And we know from targeted studies that athletes in the endurance sports are particularly at risk for developing AF.

Healthy endurance athletes should be asking the questions like:

  • What are my chances of developing AF?
  • How can I exercise safely and avoid developing AF?

Questions like these motivated the current study.  Let’s take a look….

The Study

The purpose of the study was to determine if there was an association between physical activity level and the development of new AF in middle-aged men.

Back in 1997-1998, the investigators contacted all of the men aged 45-70 years who were residing in 2 counties in central Sweden and asked them to participate.  About half (48,850 men, or 49%) responded by completing a questionnaire.  From these, several thousand were excluded from further study because of:  missing data on the questionnaire, death before the study’s follow-up period began, a current diagnosis of AF (1,496 men, or about 3% of the entire group), and the current diagnosis of some forms of cancer.  This left 44,410 men to be part of the study.  The average age of the participants at the time of enrollment was 60 years.

The questionnaire asked 2 questions about the amount of physical activity that the men engaged in.  They were asked to think back and to recall their activity levels at age 15, at age 30, at age 50, and at the current (“baseline”) time.  The participants younger than 50 years only answered for age 15 and for age 30 and “baseline.”  The questions were:

“How many hours per week do you engage in leisure-time exercise (such as running, soccer, bicycling, swimming, floorball, gymnastics, cross-country skiing, etc.)?”

The respondents had to choose between:

  • <1 hour
  • 1 hour
  • 2-3 hours
  • 4-5 hours
  • >5 hours.

“How much time each day do you spend walking or bicycling for everyday transportation purposes?”

The respondents had to choose between:

  • <20 min per day
  • 20-40 min per day
  • 40-60 min per day
  • >1 hour per day

In addition to the questions about physical activity, the respondents provided information about their medical history, smoking history, family medical history, medications, alcohol consumption, and level of education.

The respondents were then followed for 12 years to see what happened to them….and, in particular, to see if they developed AF.

The Results

At the end of the 12 years, there was an accumulated experience of 476,112 person-years!  And during that time, there were 4,568 new cases of AF.  Doing the math, that works out to 9.6 cases of AF per 1,000 person-years.  Put another way, of the 44,410 participants, about 10.3% developed AF.

But the goal of the study was to determine if the individuals’ activity level was related to their chance of developing AF.

The primary finding of the study was that the self-reported leisure-time exercise at age 30 was indeed associated with the risk of developing AF.  The investigators performed a statistical analysis designed to isolate the effect of the number of hours of exercise per week (and eliminating, as best possible, the effects of other influences on the risk of AF).  They showed that the risk of developing AF was 19% greater among the individual who exercised >5 hours per week (at age 30) compared to those who exercised <1 hour per week.  Remember that overall, 10.3% developed AF….so in terms of absolute risk difference between the extremes of exercise level reported at age 30, we’re talking about a couple percentage points different in the chances of developing AF.  It’s because of such a large number of participants that differences this small can be detected.

Another important finding of the study was that the self-reported leisure-time exercise at baseline (when participants enrolled in the study, at mean age 60 years) was not related to the development of AF.  And furthermore, the investigators found no relationship between the amount of self-reported leisure-time exercise at age 15 or at age 50 and the development of AF.  The only such relationship was for the activity level at age 30.

The last important finding of the study came from a subgroup analysis.  The participants who were at greatest risk of developing AF were those who reported >5 hours per week of leisure-time exercise at age 30….and <1 hour per week of leisure-time exercise at the time of enrollment in the study.  These individuals were 49% more likely to develop AF during the 12-year follow-up period than individuals who exercised <1 hour per week at both age 30 and at the time of enrollment in the study.

There was no relationship between the amount of walking/cycling for transportation purposes at any age and the development of AF.

The Take-home Messages

  • The current study adds to our knowledge about exercise and AF.  I hope that more studies are to come.
  • The relationship between exercise and AF is not completely understood and, indeed, the relationship may not be straightforward.  Studies like this one ask participants to recall and note their activity levels at just a few moments during their lifetime.  That can be hard to do, memory being what it is.  Undoubtedly, the risk for developing AF must be related to some sort of dose of exercise over time.  In retrospect, that’s hard to quantify.  People exercise more some years than others.  Some start exercising and some stop.  They start and stop different types of exercise.  I’ll bet that the intensity is important, too, yet how do we quantify this (in some straightforward way) so that analyses can be performed?
  • Previous studies, both in large longitudinal cohorts as well smaller invetigations of particular endurance athletes, have shown an increased risk of AF over the long term among individuals who exercised a lot.  This phenomenon has been shown best for individuals in young to middle age, and for men more so than women.  This relationship has been shown in enough different populations that we should accept it as fact.  The current study points out that the increased relative risk compared to non-exercisers may reflect a rather modest increase in absolute risk.  But that’s at odds with previous studies that have shown as much as a several-fold increased risk for AF among heavy exercisers.  But whatever the magnitude, that risk must be considered together with the other, well-established benefits of exercise over the long term when athletes are making decisions about their activity level.  Don’t forget that exercisers live longer.  That’s an important endpoint to keep in mind.
  • The current study is curious in at least one respect.  At first glance, it seems a bit odd that a relationship between exercise and development of AF could only be established for the amount of exercise reported at age 30…..and not at age 15, 50, or at the time of enrollment.  Why is that?  Could it be possible that we should exercise freely, with no worry about AF, while we’re young….and then again when we’re old?  Maybe the 30-year-olds exercise with greater intensity.  Maybe they accumulate more hours of exercise over more years.  Maybe they engage in different forms of exercise that carry more risk.  Perhaps “>5 hours” for the 30-year-olds was actually much more than 5 hours.  The current study doesn’t provide answers.  This needs to get sorted out with future studies.  We need to better define the safe dose of exercise with respect to AF.
  • Finally, why is exercise associated with AF?  In truth, we don’t know in any detail.  It seems that it must have something to do with the structure of the atrium that changes over years’ time with exercise.  The investigators note several of the potential reasons:  enlargement of the atrium, inflammatory changes in the atrium, and overdevelopment of the parasympathetic portion of the autonomic nervous system.  Perhaps all of these play a role.  I like Dr. John Mandrola’s blog post this week about this issue.  I like his take.

Related Posts

 1. Cyclist’s Account of Atrial Fibrillation

2. In the News:  Atrial Fibrillation in Cross Country Skiers

3. Atrial Fibrillation in Athletes (In a Nutshell)

In the Medical News: Your Heart Rate Monitor May Help Your Doctor!


Arrhythmias–abnormal heart rhythms–are one of the most common heart-related problems for athletes.  Sometimes an athlete may notice nothing more than a “skipped heartbeat.”  At other times, there can be palpitations, lightheadedness, or even unconsciousness associated with a sustained arrhythmia.

By their very nature, many types of arrhythmias are transient or paroxysmal–that is, they are fleeting.  And often, they can be provoked by exercise.  Because these arrhythmias can be transient and exercise-related, it can often be challenging for the doctor to sort things out.  The athlete-patient arrives at the office with a normal heart rhythm and only a story of a problem that happened during a workout 2 weeks ago.  There’s no lasting “evidence” of the episode.

For diagnostic purposes, we typically use a Holter monitor–an EKG “tape recorder” of sorts–for periods of 24 to 72 hours to make recordings of the heart rhythm for extended periods of time.  The patient, or athlete, wears a set of skin electrodes that attach to a recording device.  The set-up would be something like wearing a bulky iPod.  And although longer time-frame devices are increasingly available, it’s often challenging for an athlete to capture his/her arrhythmia on such a recording.


Published last week in the medical journal, Medicine and Science in Sports and Exercise, a group of investigators from Leipzig Germany issued a report entitled “Diagnosis of arrhythmias in athletes using leadless, ambulatory heart rate monitors.” [1]  They call our attention to 3 case reports of athletes in whom a standard exercise heart rate monitor provided useful clues to the diagnosis of their arrhythmias.

In Case #1, a 32-year-old cyclist with palpitations was found during an ER visit to have a brief episode of paroxysmal atrial fibrillation.  Review of stored heart rate tracings from his heart rate monitor revealed evidence of heart rate (and cycle length variability) suggestive of atrial fibrillation that correlated temporally with his reported symptoms.

In Case #2, a 36-year-old cross country skier with palpitations during exercise presented for evaluation.  The resting EKG, echocardiogram, and stress testing could not reproduce the arrhythmia.  Subsequently, the arrhythmia recurred during exercise and the skier’s heart rate monitor captured the event, with a heart rate of 230+.  With specialized invasive electrophysiologic testing, the diagnosis of atrioventricular nodal re-entrant tachycardia (AVNRT) was made.  The athlete underwent a successful ablation procedure.

In Case #3, a 28-year-old triathlete experienced episodes of tachycardia during exercise.  Efforts at recording the arrhythmia on a typical Holter monitor were unsuccessful.  His exercise heart rate monitor recording showed clear evidence of episodes of tachycardia, with heart rates of 170-200.  He underwent invasive electrophysiologic testing and was found to have an ectopic atrial tachycardia and underwent a successful ablation procedure.

The authors report that different brands and/or models of heart rate monitors (Polar, Garmin) were used for each of these three patients.  They noted that the important features were the ability to use vendor-supplied software to retrieve tracings of the heart rate information during periods of exercise.


The report isn’t surprising and I don’t doubt that there are many athletes who’ve already thought to take their heart rate monitor tracings to their doctor or cardiologist.  In a previous column at Endurance Corner, I shared a heart rate monitor strip from an athlete who was bothered with paroxysmal atrial fibrillation.  The new report reminds us, though, to take advantage of ALL of the information that’s available to us as we sort out arrhythmia problems in athletes.


1.  Mussigbrodt A, et al. Diagnosis of arrhythmias in athletes using leadless, ambulatory heart rate monitors.  Med Sci Sports Exercise 2013; epub ahead of print.