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!


Interesting Research Studies from the ACC’15 Meeting





This year’s annual meeting of the American College of Cardiology (ACC) was held recently in San Diego.  I thought I’d share a round-up of some of the sports cardiology studies that caught my eye.  In the months ahead, we can look forward to seeing the published reports.  Here are my Top 8:

1. Life expectancy of elite long and short distance runners.  In a study reported by Lee-Heidenreich D et al., the longevity of male Olympic athletes who competed in either the 100m dash or the marathon was examined.  The study included the top 20 finishers in each event at the Olympic Games from 1928 to 1960.  The investigators were able to determine the date of death for the majority (67%) of these athletes.  At the time of their Olympic races, the short distance runners were younger than the long distance runners (23.8 vs 30.5 years).  The life expectancy after their races were fairly similar (45.5 vs. 43.8 years), slightly favoring the short distance runners.  But because of their older age at the time of their Olympic event, the marathoners actually enjoyed greater longevity overall.

My take:  This is an interesting observation.  No doubt, though, many variables influence longevity and it’s probably simplistic to think that the long- vs. short-distance issue explains all (or even most) of the longevity difference.  I certainly wouldn’t encourage short distance runners to go long!

2.  An assessment of the performance of pre-participation guidelines applied to novice older endurance athletes.  This continues to be an important topic because there is no consensus about the best approach to screen adult recreational athletes for underlying cardiac conditions that might place them at risk.  In this report by Matsumura ME et al., the use of either the American Heart Association (AHA)/American College of Sports Medicine (ACSM) Pre-Participation Questionnaire (AAPQ) or the 2001 Working Group on Masters Athletes guidelines were considered.  The investigators surveyed 1457 novice runners and triathletes who were 35+ years old about the items included in the 2 screening tools.  If the AAPQ criteria were applied, 42% of the athletes would be told they should have additional cardiac testing.  If the Masters criteria were applied, 75% of the athletes would be told they should have additional cardiac testing.

My take:  These screening questionnaires identify a rather large group of masters athletes who would require additional testing.  It’s difficult to know how to find the balance here.  We want to find athletes who truly have an important (hidden) heart problem, but avoid unnecessary diagnostic testing in those who don’t.  It’s worth reading my previous blog post on another, recently published report on the topic of cardiac screening in adult recreational athletes.

3.  Results from the coronary anomalies program at Texas Children’s Hospital.  Anomalous coronary arteries (ACA, an inherited condition in which a coronary artery has an abnormal anatomy) are the 2nd leading cause of sudden cardiac death in young athletes.  The investigators report on the successes of a multidisciplinary team approach to patient care, imaging studies, treatment, and long-term follow-up of pediatric patients with ACA.  Among 58 patients, operation for surgical repair was recommend in 29 patients; 4 declined and 25 underwent operation.  There were significant surgical complications in 4 patients.  After operation, all 25 patients were able to return to exercise activities without restriction and none of these patients experienced any cardiac difficulties after operation.

My take:  A multidisciplinary team that includes pediatric cardiologists, radiologists, and cardiac surgeons is almost essential to care for patients with ACA.

4.  Screening with echocardiography or stress testing in asymptomatic USAF aviators–Not efficacious.  The issue of cardiac screening for seemingly healthy adult athletes continues to be debated.  In this study, the investigators report on an interesting experience with US Air Force (USAF) pilot applicants who, prior to 2008, underwent routine screening with echocardiogram and some form of exercise stress testing.  Between 1994 and 2006, 20,208 screening echocardiograms were performed; a “permanently disqualifying diagnosis” was found in only 9 individuals (0.045%).  The most common abnormalities detected were bicuspid aortic valve (in 0.76%), mitral valve prolapse (in 0.025%), and mild aortic regurgitation (in 0.29%).  In a subgroup of 903 aviators who underwent stress testing, only 16% of those with an abnormal results were later found to have significant coronary artery disease with coronary arteriography.  And moreover, regardless of the results of the stress testing, there was a very low rate (~0.5%) of later problems with death, heart attack, or need for revascularization (bypass surgery or coronary stent).  The authors concluded that screening echocardiography and stress testing was not useful in healthy individuals without cardiac risk factors and suggested that the results could be extended to the healthy athlete population as well.

My take:  The diagnostic yield for screening tests among healthy individuals will always be low.  That’s how screening tests work, by design.  We have to ask ourselves:  What’s it worth to identify the 9 individuals who were disqualified from flying?  Perspective matters here.  If you were a member of a potential flight crew or a potential passenger, you’d want to know that your pilot was healthy!

5.  Are years of training an independent predictor of atrial fibrillation in older runners?  There’s plenty of evidence to suggest a link between long-term endurance sport and atrial arrhythmias like atrial fibrillation (AF).  In this study, the investigators wanted to determine for runners if this relationship was independent from other known risk factors for AF such as age.  They reviewed data on 2819 runners that was collected as part of the MASTERS Athletic Study, a web-based survey of endurance athletes.  The data set included information about AF as well as the athletes’ run training and race participation.  The mean age of the athletes was 48.4 years and the median range of running career duration was 11-15 years.  The rate of reported AF was 2.4%.  There was a significant correlation between the accumulated years of running and the rate of AF, with a 6.1% rate of AF among those who had run for 30 years.  Independent risk factors for AF included:  increasing athlete age, high blood pressure, and years of accumulated running.  Variables that were not risk factors included:  diabetes, average running pace, use of speed training, and participation in marathons/ultramarathons.

My take:  There is ample evidence that long-term endurance sport is associated with AF.  There’s no good reason not to believe that the exercise is somehow causal, even if the mechanism remains uncertain.

6.  Incidence of sudden cardiac death associated with physical exertion in the Unites States military.  The Armed Forces Medical Examiner Tracking System includes information about all fatalities among military service members, including autopsy reports, death certificates, and official investigations.  From 2005-2010, there were 135 sudden cardiac deaths associated with exertion (SCDE) among 8,298,606 person-years of observation, giving an incidence rate of 1.63 per 100,000 person-years (p-y).  The incidence rate was higher for those >35 years (3.84 per 100,000 p-y), males (1.87 per 100,000 p-y), and African-Americans (3.00 per 100,000 p-y).

My take:  The US military is probably a relatively healthy cohort.  Nonetheless, we shouldn’t be surprised that there would be a small rate of SCDE.  Mention is not made in the abstract about what forms of exertion were involved, but we know that there is a finite rate of SCD associated with virtually any form of sporting activity, even if it doesn’t seem very strenuous.

7. Activities performed during sudden cardiac death associated with physical exertion in the United States military.  This is a companion study with #6, above, using the same source of data.  Here, the investigators studied the type of exercise that was associated with 200 cases of sudden cardiac death (SCD).  The most common types of exercise were:  running/elliptical (in 60%), generalized exercise such as furniture moving, construction, lawn mowing, dancing (in 10%), military P.T. (in 9%), walking (in 7%), swimming (in 4%), basketball (in 4%), and weight lifting (in 4%).  Interestingly, 20% of SCD events occurred during mandatory physical fitness tests; of these, 32% of events occurred during the test and 68% occurred within 1 hour afterwards.

My take:  Again, SCD can occur with any form of exercise.  The data here also point out that SCD may occur soon after exercise.  In the case of mandatory physical fitness testing, just as for athletic competition events, it’s important to organize medical support teams for the possibility of emergencies even after the event is completed.

8. QT interval in elite athletes.  We know that prolonged QT interval on the ECG, either inherited or acquired, is associated with increased risk for sudden cardiac death during exercise.  Here, the investigators wanted to learn if participation in sport, along with cardiac adaptations to exercise training, could itself cause prolongation of the QT interval.  The investigators reviewed the medical literature and identified 10 studies on 5354 elite athletes and 448 controls for whom QT interval data were available.  The QT interval in the elite athletes was, on average, 36 msec longer than for the non-athletic controls.  But once the data were corrected for the slower heart rates in the elite athletes, the corrected QT, or QTc, was not significantly different for the elite athletes and the non-athletic controls.

My take:  Participation is sport probably doesn’t cause prolongation of the QT interval and by itself lead to an increased risk of SCD.


Related Posts:

1.  Interesting Research Studies from the ACC’14 Meeting

Update on Swimming Induced Pulmonary Edema (SIPE)







I saw this week that there was an important new paper on swimming induced pulmonary edema (SIPE).  Richard Moon, MD, and his colleagues at Duke University published a report entitled, “Immersion Pulmonary Edema and Comorbidities:  Case Series and Updated Review” in a recent edition of the sports medicine journal, Medicine & Science in Sports & Exercise (1).

SIPE is known to occur not only in recreational or competitive swimmers, but also in divers.  In fact, the condition was first recognized because of breathing difficulties encountered by military divers.  As triathlete and swimmer readers here will know, there are many reasons why an athlete might develop shortness of breath during an open water swim.  Water conditions, water and air temperature, exertion, and anxiety all play a role.  SIPE is something different, altogether, though.  This is a condition that develops because of immersion in the water, in which fluid builds up in the lungs and makes breathing difficult.  The condition is believed to be self-limiting; if a swimmer gets out of the water, the condition will resolve.  The underlying mechanisms and risk factors are not completely understood.

I’ve written about this condition in 2 previous blog posts….SIPE and More on SIPE.  These posts might be a good starting point.

The newly published report is important because it reviews the medical literature and gathers all of the pertinent information about pre-existing medical conditions, or so-called comorbidities, in victims of SIPE.  Dr. Moon is probably the world’s foremost authority on the topic of SIPE, so this new report deserves our attention.


The Study

There are 2 parts to the study:  1) a look at the Duke University experience with recreational swimmers who’ve had a SIPE episode and 2) a review of the medical literature on SIPE cases, both in military and recreational divers and swimmers.

In the first part, the investigators collated information on 41 swimmers who, over the past several years, had been studied at Duke University after reporting a SIPE episode.  The mean age was 50.1 +/- 10.8 years (range, 25-71 years).  Complete medical history data was available for 36 of the 41 swimmers.

In the second part, the investigators collected 45 previously published articles in the medical literature that reported on 292 cases of SIPE.  There were 156 recreational swimmers or divers (89 men and 67 women), with a mean age of approximately 47.8 +/- 11.3 years.  There were also 136 military swimmers or divers (135 men and 1 woman), with a mean age of approximately 23.3 years (range, 18-47 years).

For each of these groups, the investigators gathered information about pre-existing medical conditions in order to determine potential risk factors for the development of SIPE, focusing on:  hypertension (high blood pressure), lung disease, overweight/obesity, sleep apnea, hypothyroidism, and cardiac abnormalities).


The Results

Among the Duke University group, 9 (25%) of the 36 swimmers with available health history were completely healthy.  The remaining 27 (75%) had 1 or more medical/health conditions, including:

  • overweight/obesity in 12
  • hypertension in 7
  • cardiac arrhythmias in 4
  • heart valve problem (mitral valve prolapse) in 1
  • reduced heart function in 2
  • repaired congenital heart conditions in 2
  • asthma in 3
  • COPD in 1
  • reactive airways disease in 1
  • hypothyroidism in 3
  • diabetes in 2
  • polycystic ovary syndrome in 1
  • obstructive sleep apnea in 2

Twelve subjects had more than one of these conditions.

In the literature review, all of the 136 military swimmers and divers were healthy; they had none of the pre-existing medical/health conditions that were surveyed.  In contrast, 70 (45%) of the 156 recreational swimmers or divers had one or more significant pre-existing risk factors:

  • asthma in 4
  • enlarged heart in 2
  • arrhythmias in 2
  • coronary artery disease in 3
  • diabetes in 4
  • exercise-induced cough in 1
  • Elevated serum lipids in 22
  • hypertension (high blood pressure) in 25
  • thickening of the left ventricle in 9
  • peripheral vascular disease in 1
  • sleep apnea in 6

As a side note, approximately 17% of cases in the literature review reported similar previous episodes or follow-up episodes that were suggestive of SIPE, giving an important look at the potential recurrence rate.  And in total, 6 fatal cases of SIPE were identified in the literature review.


My Thoughts

How can all of this collated information be useful to us?

First, it’s important to note that all of the military swimmers and divers included in the literature review were healthy.  We shouldn’t overlook the possibility that even completely healthy swimmers may experience SIPE.

Second, the recurrence rate of ~17% in the literature review is probably an underestimate.  No doubt, some swimmers who experienced a worrisome episode of SIPE might avoid future swimming altogether.  It’s very important to remember that this condition may recur.

Third, it’s very apparent that, among recreational swimmers who experience SIPE, the prevalence of important pre-existing medical conditions is rather high, at 75% in the Duke group and 45% in the recreational swimmers in the literature review.  I suspect that the Duke investigators were more thorough in their history-taking and the 75% is probably more reflective of the reality.

The investigators’ aim was to identify risk factors for SIPE.  Sadly, there’s obviously no single, unifying thread here.  Hypertension (high blood pressure) was the most commonly identified condition among the cases, but this accounted for only ~15% of the cases.  As I mentioned at the top, the physiologic underpinnings of SIPE are not completely understood and indeed there may be more than one responsible mechanism leading to some common final pathway by which fluid accumulates in the lungs.  All of the various cardiovascular abnormalities identified in the cases might conceivably play a role.  There’s more to learn.

It’s worth noting that the long list of medical conditions that were identified deserve careful medical attention before participating in recreational swimming events.



I’ll reprint here my best advice to athletes and event organizers regarding SIPE.  I originally included this in another blog post, but this is still my best advice!

  1. Triathletes and open water swimmers should be aware of SIPE and the possibility that this condition can be lethal.
  2. Symptoms of SIPE can manifest for the first time even in experienced swimmers.  Symptoms may develop rapidly, be unexpected, and confuse the athlete about the cause.
  3. The development of SIPE does not appear to be confined to cold water swims or only to victims who are wearing a wetsuit at the time.
  4. SIPE appears to be self-limiting–that is, the symptoms will subside if the victim stops exercising and gets out of the water.
  5. Because of #2, #3, and #4, athletes who experience breathing difficulties in the open water should treat the problem like a medical emergency and STOP swimming and SEEK immediate assistance.  Because of the challenges of rescue in the open water, your life could depend on recognizing a problem early and getting out of the water.  I would encourage affected athletes to get complete medical evaluation as soon as possible after an episode.
  6. There appear to be no effects on lung function after an episode of SIPE, but repeat episodes of SIPE may occur.
  7. Affected athletes have described a variety of strategies for preventing repeat episodes of SIPE.  From athlete accounts, no single strategy appears to be universally successful.
  8. Affected athletes should use EXTREME CAUTION in subsequent open water training and races, being hypervigilant for warning signs.
  9. Event organizers and on-water rescue personnel should be familiar with SIPE.  The safety plan should allow for athletes with breathing difficulties to be removed from the water as quickly as possible.



1.  Peacher DF, Martina S, Otteni C, et al.  Immersion pulmonary edema and comorbidities:  Case series and updated review.  Med Sci Sports Exerc 2015;47(6):1128-1134.


Related Posts:

1.  Swimming Induced Pulmonary Edema (SIPE)

2.  More on Swimming Induced Pulmonary Edema (SIPE)

USAT Medical Multisport Conference








I had the chance to be a speaker at the November, 2014 USA Triathlon (USAT) Medical Multisport Conference that was held at the Olympic Training Center in Colorado Springs.  The weekend brought 2 days of talks that focused on aspects of sports medicine that were particularly relevant to triathlon and multisport.

Travis Tygart, CEO of the United States Anti-Doping Agency (USADA) was the keynote speaker.  We heard about event and safety planning from a very experienced group of USAT-affiliated physicians, including W. Douglas Hiller, MD, Andrew Hunt, MD, and John M. Martinez, MD.  I gave talks on some of my favorite topics:  “Triathlon Fatalities,” “Endurance Sport:  Is it Heart Healthy?,” and “Cardiovascular Considerations in the Aging Athlete.”  We had lunch with Kathy Matejka, the USAT Event Services Director and dinner with Rob Urbach, CEO of USAT.

I met some terrific folks and I learned a lot.

It was great to visit the Olympic Training Center.  I particularly enjoyed the museum area and a workout at the pool.  The snow and cold weather got the best of a planned group run, though.

This year’s Conference is planned for November 5-7, 2015, again at the Olympic Training Center in Colorado Springs.  This year’s keynote speaker will be Robert Laird, MD, the original and long-time medical director for the Ironman World Championship race in Kona, Hawaii.  This would be a worthwhile meeting for anybody who’s involved with medical care of multisport athletes, including nurses, physicians, and allied health professionals.  Information about the meeting schedule, speakers, and registration can be found at the USAT website.

I hope that you’re able to join us in November!

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.