Barrington resident Don Macdonald does not call himself an adrenaline junkie, but rather more of an adventurer – who has learned the art of restraint.

Macdonald, 52, previously swam the length of Tampa Bay, the Boston Harbor, Lake Zurich, Lake Michigan, off the coast of California’s Seal Beach and Manhattan Beach, and in the La Hoya Cove off the coast of San Diego.

Reprinted: Barrington Courier Bridget O'Shea

“I think water gives me a sense of freedom, but it’s a very quiet, lonely freedom,” said McDonald, noting that he has sometimes shared this freedom with jellyfish, dolphins and sea lions.

However, a different type of challenge presented itself to MacDonald in 2011, when he began to experience cardiac issues after returning from a trip overseas, where he planned to swim the English Channel but was unable to due to weather conditions.

While taking a break from swimming, MacDonald began experiencing shoulder, arm and chest pain, which he said he was not too worried about.

“When you’re training 10K a day for swimming, your body is going to ache,” he said.

However, it turned out that MacDonald did have mild heart issues. After seeing his doctor, who then referred him to a cardiologist, MacDonald was treated with stents for narrowed arteries, given a typical medication regimen and stress tests. He was later approved to begin training again for the English Channel.

“During that time, I was actually out jogging and I had a major cardiac arrhythmia event that put me in the hospital for 10 days,” he said. “I was standing at a block party after I ran and I collapsed. This kind of came out of the blue, which is why it was so challenging to wrap my head around.”

Luckily, a retired nurse was at the party and began resuscitating him.

“She saved my life,” he said.

MacDonald was taken to Advocate Good Shepherd Hospital, where cardiologists implanted a small defibrillator device just beneath his skin to detect any abnormalities and reset electrical impulses.

“It’s been challenging physically and emotionally,” said MacDonald, who was used to training by swimming up to 26 miles at a time in 50-degree water.

But instead of focusing on any setbacks, MacDonald is now using his experience as an example of the importance of proper health screenings and evaluations for open water swimmers, triathletes and others that engage in vigorous sports.

“People have to pay attention to what they are doing to their bodies,” he said. “Everybody needs to consider their health situation carefully. Here’s a guy who could swim the English Channel and look what happened to me.”

Particularly with high endurance sports, MacDonald said, a feeling of being indestructible can sometimes develop, leading to a false sense of security. He uses himself as an example.

“Before this, it had gotten to the point where I was no longer afraid to swim in any body of water regardless of seals, sharks or the temperature of the water,” he said. “The biggest thing is that you go from being able to do anything and everything to, ‘OK, what do I do now?’”

Since his 2011 stay at Good Shepherd, MacDonald has reached out to the community, working with high schools, middle schools and the District 220 Educational Foundation by speaking to young people as a living example of the importance of cardiac and other medical tests and screenings for athletes.

While less vigorous exercise is now part of his recovery, MacDonald, who has swum since he was a young child, has not lost his love for the water.

On June 28, he will kayak the perimeter of Manhattan Island in New York as his friend Doug McConnell swims in the Manhattan Island

Marathon Swim.

“Instead of curling up and being the wilting flower, I decided that instead of swimming every day, I would do kayaking,” he said.

MacDonald will kayak next to a 9-foot boat with food, water and medical supplies for the swimmers. His main objective, he said, is the safety of his friend.

MacDonald has kayaking experience, most notably the 28 miles from Catalina Island to Los Angeles, a ride that began in the middle of the night.

“It was pitch black,” he said. “You could hear dolphins and whales.”

Originally from Goshen, Ind., MacDonald said he moved to Barrington from Chicago about 15 years ago and he and his wife enjoy raising their daughter here.

“It’s a great community,” he said, describing Barrington as a place where you can go to the city, go horseback riding or go into town for ice cream.

“It truly has everything you want from a small town,” he said. “It’s kind of the quintessential experience.”

Recovery from an Almost fatal Cardia Arrhythmia - Manhattan Island Marathon Race from the Kayakers Perspective

The 28.5 kayaking trip around the Island of Manhattan will be both grueling and scenic and more importantly bringing awareness to Two important Causes (literally near and dear to my heart) - Cardiac Arrhythmia Prevention and Doug McConnell's ALS charity efforts.

Doug’s swim will be accompanied by an escort boat with two crew members (Susan and Cliff Wilson I believe) as well as the support of a kayak manned by his long-time training partner, Don Macdonald. 

Bob Lee and others will be biking around the Island as well all supporting the cause and friend in the quest for raising money and awareness.

Here is a short video clip of the perspective from the kayaker and support crew for Manhattan Island.

Don's Journey since the English Channel has taken a twisted path.

While starting my training for a second attempt the English Channel that was planned for this fall (2014) I had a sudden cardiac arrhythmia event, collapsed, received life saving help. I was found to have arrhythmia problems perhaps brought on by high intensity exercise, that had gone undetected perhaps for years despite years of grueling training and hours submerged in ice cold water and distances.

Well I survived and now find myself with an implanted ICD to prevent such future events. I was running, which I jokingly say was the problem, instead of swimming. "I think ICD stands for I Can't Die".

However my experience now takes me down a path relatively untraveled since only about 1% of such incidents leave survivor's. So onto the next chapter of my swimming journey just One Stroke At A Time and Advocate Health System, Cardiac Care Services.


I am hopeful to return to the pool in the near future. But until then kayaking for Doug and his cause is great. We been at his for five years and like open water swimming, you have to adapt. As Dori says...just keep swimming, swimming, swimming, or in my case kayaking, kayaking, and kayaking.




Doug's ALS Challenge:

After another long year of training, the A Long Swim Team is planning for the Manhattan Island Marathon Swim, a 28.5-mile circumnavigation of the most prominent island that makes up New York City, in June 2014.  In the unique world of marathon swimming, successfully completing swims across the English Channel, The Catalina Channel and around Manhattan Island is considered the “Triple Crown.”  If he completes the third leg of that challenge, Doug will be in a select club of fewer than 100 swimmers with that honor.

Barrington man takes on ‘Triple Crown’ challenge with swim around Manhattan

Don Macdonald Kayak's alongside Doug McConnell here pictured in the middle of the pacific ocean between Catalina Island and mainland California in 2013.

With Doug's swim, the third leg of the Triple Crown bearing down in several weeks, we have been focused on extending training time in open water. While Doug has the Yeoman's work in the water this time, Im in the kayak again, and support crew in the boat. Both exposed to the weather (what ever condition it is) for 9-10 hours. 

The biggest concern we have for Doug is safety. The rivers around New York Harbor are very congested and dangerous with large ocean going ships, ferries - docking, embarking at all hours. These ships also generate sizable waves that multiply both in height and length bouncing off sea walls causing both kayaker and swimmer tremendous stress to stay on course. 

The other challenge are the piers. These are not your standard piers but large loading docks, commercial businesses extending into the river sometimes 100 plus yards disrupting the flow of water, swirling ebbs, causing the kayaker and swimmer direction problems and immediate danger from a collision. 

"There's no room for error, the current never stops and at 2-4 MPH, you will get dragged into a pier pole, debris, or ship very easily", said Don Macdonald who recently went on a test run while in New York. 

As a marathon swimmer myself, I know its essential for me to remain focused on all aspects of Doug's safety but not outwardly show the slightest change in my tempo, direction and even mood as things happen. And they always do. 

As these swims progress, its not uncommon for swimmers to become depressed from the solitude of the effort coupled with the physical exhaustion. As the reach 6-8 hours mark, the swimmer hits "the wall" both physically and mentally. The slightest perception of stress can be detected from the swimmer, stress from changes to direction, hitting some debris floating in the water, swallowing some polluted water ... can weigh heavily on the swimmers mental outlook. 

For both of us, this will be another test of resilience, forged in the desire of pushing oneself to help others. 

Sometimes your simply alone

Article Reprinted from Sun Times

As harsh, cold and seemingly unending as the winter was, few were clamoring to take long dips in area lakes as of mid-May.

Doug McConnell, however, already was swimming about 20 miles a week, often in lakes registering thermometer readings in the 50s and 60s, including Lake Michigan.

No, he wasn’t wearing a wetsuit. And no, he’s not crazy. He’s on a mission.

On June 28, the 56-year-old will attempt what is known in marathon swimming circles as the MIMS, the Manhattan Island Marathon Swim. Swimming long distances in breathtakingly, bone-achingly cold lakes is all part of the training.

McConnell, of Barrington, already swam across the English and Catalina channels. Only the MIMS — a 28.5-mile swim around Manhattan through the Hudson and Harlem rivers — stands between McConnell and the Triple Crown of open water swimming. If he makes it, he’ll join just more than a dozen others who have completed all three while over the age of 50.

Perhaps equally as remarkable, through a fundraising organization he started with his swimming friend and fellow Barrington resident Don Macdonald, McConnell has turned pulling and kicking his way through waves into more than $225,000 for the Les Turner ALS Foundation.

Amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease, claimed the life of McConnell’s father, David, in 2006. Another of his relatives now battles ALS.

“It’s just dreadful,” McConnell said of the disease, which affects nerve cells in the brain and spinal cord. “It’s a slow motion shipwreck. To watch anybody you love go through that, to see them just go to pieces like that, it’s hard to watch.”

Proceeds from McConnell’s organization, A Long Swim, go to the Les Turner ALS Laboratory to advance treatments and find a cure. Researchers are making great strides, McConnell said.

“It’s a pretty gratifying and exciting time to be supporting research into a disease that has frustrated so many for such a long time,” he said. “There are drug trials going on. There are new discoveries about upper motor neurons.”

Dr. P. Hande Ozdinler is director of the Les Turner ALS Laboratory and an assistant professor in the Department of Neurology at the Feinberg School of Medicine at Northwestern University.

Support received through McConnell and A Long Swim has been vital, Ozdinler said. With it, Ozdinler developed a method of making corticospinal motor neurons fluorescent. The labeling makes it easier for doctors to discover what goes wrong in patients with ALS and other motor neuron-affecting diseases.

Because of the headway that’s been made, the National Institutes of Health has granted $3 million to further studies at the lab, Ozdinler said.

“Before we got the NIH money, the only support was from the Les Turner Foundation, which depends heavily on people like Doug,” Ozdinler said. “His efforts make a difference.”

McConnell, meanwhile, is focused on ensuring that his body is well-prepared for the MIMS. Though he swims throughout the year at Foglia YMCA, recent conditioning has meant 6 a.m. loops around Lake Zurich and adventures in Lake Michigan, as well.

“It’s just such a lift to be outside in the sunshine,” he said. “The water’s been cold, but boy oh boy, to be out there and watch the sun come up, it’s just fabulous.”

McConnell expects to encounter chilly waters in New York, which “had the same crazy winter we did,” he said.

“The only way to get acclimated to cold water is to spend a lot of time in cold water,” McConnell continued. “It can be unpleasant and so forth, but the acclimation really works.”

McConnell noted that hypothermia is not a condition to be taken lightly. His swims are monitored. The crew often includes his wife, Susan, and their four children, ranging in age from 16 to 26. Macdonald also typically is there, riding alongside in a kayak.

The Manhattan Island Marathon Swim will start at Battery Park, with a view of the Statue of Liberty in the harbor. Twenty-three swimmers are signed up to participate on June 28, McConnell said. Others are swimming June 14 and July 12.

Start time is 7:20 a.m. Central time.

“They time it carefully around an incoming tide,” McConnell said. “It’s what pushes you north up the East River. You swim on the East River to about 120th or 130th Street, and then you cut left. You take the Harlem River northwest and swim that to 210th Street.

“That’s where the Harlem dumps into the Hudson, and you take that back to Battery Park,” he said. “This is 28.5 miles. However, because of the tidal push on the East River and the downstream ride on the Hudson, most people do it in eight or nine hours. It swims more like 17 or 18 miles rather than 28.

“That, of course, is all dependent upon the day and how well you’re able to hook into the currents.”

McConnell said he looks forward to the event, which also is a race. He crossed the English Channel — a feat that included 25-knot winds and 5-foot waves as well as pitch-black darkness — in 14 hours and 18 minutes. The Catalina Channel took 12 hours, 41 minutes.

McConnell said that turning a personal goal into a charitable endeavor adds to his motivation.

The response from both corporations and individuals has been tremendous. Minneapolis-based Medtronic is among his sponsors. The company makes medical devices, including the PRESTIGE disc, one of which was implanted in McConnell’s spine in 2009.

“From individuals, we had some $5 donations and one that was $5,000. The message and the disease really resonate with people,” McConnell said. “Many of the donations were from good friends of my father’s. I have another family member battling with ALS now, and a lot of old friends of hers are donating.”

Anyone interested in learning more or donating is encouraged to visit alongswim.com.

“The funding that [McConnell] received has turned into something really big and really good,” Northwestern’s Ozdinler said. “Without him and the support of the foundation, I don’t think we would have been able to generate the tools we have today.”

The Greatest Gift of All - saving Someone's Life

In the New Year  Learn How to save someones life  Learn How to Perform CPR 2012, Triathlete dies in NY swim. As athletes we rarely consider this will happen to ourselves much less someone we know know or a fellow competitor. I can assure you it does, and when you least expect it and sometimes from the fittest people. Do you know how to perform CPR, use a defibrillator? I did not.  Try this video and see what you think. You may just save a life....  We have all walked by the Red Cross sign in malls, schools and airports indicating where a heart machine is located, learn to use one and maybe pay it forward.  Link: http://www.heartrescuenow.com/

Cardiac Arrhythmia's in Swimmers - Ignorance is Not Bliss

Reprinted from Sports Medicine Bulletin

For at least one Olympic champion this summer, competing was a matter of life and death. Srijita Sen- Chowdhry and William J McKenna explain how heart arrhythmias can affect young athletes.
Of all the success stories emerging from the memorable return of the Olympics to its birthplace this summer, one of the most remarkable is that of 16- year-old American swimmer Dana Vollmer. At the age of 12 Dana was the youngest participant at the 2000 US Olympic trials. Four years later she won a gold medal in Athens as part of the women’s 4 x 200m relay team, which set a new world record. Dana’s accomplishments, noteworthy in themselves, are made more poignant by reports of her complex cardiac history.

From newspaper articles available at www.danavollmer.com, it appears that Dana’s cardiac problems began two years ago, when she noticed abrupt surges in her heart rate to 250 beats per minute during training. The tachycardia would last up to five minutes before resolving spontaneously. Since the episodes were erratic and relatively infrequent, a wait-and-watch approach was initially adopted. This continued, even when Dana developed symptoms of impaired consciousness while exercising. During one training session, her vision ‘went black’ several times (‘pre-syncope’), although she did not actually pass out (‘syncope’). The pre-syncopal symptoms did not return, but the tachycardias continued, and a cardiac opinion was eventually sought.

The diagnostic work-up at this stage would typically have included a 12-lead electrocardiogram (ECG), two-dimensional echocardiogram (2D echo), exercise testing and ambulatory ECG monitoring. The latter apparently demonstrated QT intervals exceeding 500 milliseconds. The QT interval is a measure of the time it takes for the ventricles of the heart to both depolarise (contract) and repolarise (relax). In normal subjects, the QT interval after correcting for heart rate is usually less than 440 milliseconds. The possibility of ‘long QT syndrome’ was therefore raised.

Her tachycardias, however, appeared to be due to an additional problem: an ‘extra electrical pathway’, to use Dana’s own words, for which she underwent radio-frequency ablation, the same procedure recently performed on Tony Blair, the British prime minister.

Although Dana’s tachycardias have not recurred, the QT prolongation is likely to persist. Long QT syndrome is a recognised cause of sudden cardiac death in young people and Dana was offered an implantable cardioverter-defibrillator (ICD). Her family declined, opting instead to carry a portable defibrillator, which is on hand during all competitive events.

Arrhythmia symptoms

Dana’s story raises a number of issues relevant to sports physicians. The first is the need to investigate symptoms suggestive of arrhythmia. Atypical chest pain and mild breathlessness are common complaints, the significance of which is often difficult to determine in a population engaging in extreme physical exertion.

However, most athletes will be accustomed to the sensation of their heart rates increasing normally during exercise. The perception of palpitation in an athlete therefore merits further investigation, particularly when sudden increases in the heart rate have been noticed, as in Dana’s case.
Exercise-related syncope is the most ominous presentation. It has been suggested that syncope is the same thing as sudden death, except that you wake up⁽¹⁾; an investigative approach based on this premise is recommended in athletes. Further participation in competitive sports should be discouraged until a thorough cardiac evaluation has been performed and the athlete cleared of any possibility of arrhythmia.

Light-headedness, as opposed to blackout, is a less specific symptom. Stimulation of the sympathetic nervous system, muscle activity and decreased intrathoracic pressure all contribute to increased venous return during exercise. An abrupt stop after vigorous exercise may well cause venous pooling, hypotension and a light-headed sensation. Thus, while dizziness and a fall in blood pressure during recovery may be physiological (and ‘normal’), pre-syncopal symptoms during exercise justify concern, particularly in experienced athletes.

Types of arrhythmia

Important causes of palpitation and syncope in athletes include heart muscle diseases, mitral valve prolapse, inherited arrhythmogenic disorders and pre-excitation. Most of these diseases have a genetic basis, reinforcing the importance of obtaining a complete family history. Anomalies in the origin or anatomical course of the coronary arteries should also be considered in an athlete with exertional chest pain and/or collapse.

Notable among the heart muscle diseases are hypertrophic cardiomyopathy (HCM) and arrhythmogenic right ventricular cardiomyopathy (ARVC), which frequently present with symptoms of arrhythmia. Sudden death may be the first clinical manifestation of both diseases, leading some authorities to advocate preparticipation screening of all athletes. Dilated cardiomyopathy (DCM) is more characteristically associated with symptoms of heart failure such as breathlessness and reduced exercise capacity; arrhythmia and sudden death are recognised complications, but seldom the mode of presentation.

Long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic ventricular tachycardia fall under the collective term of inherited arrhythmogenic disorders. All have the capacity to produce malignant ventricular tachyarrhythmia (rapid, dangerous disturbances of the heart rhythm) in a structurally normal heart. Disease-causing mutations have been identified in the cellular channels, receptors, and binding proteins that regulate ion flow⁽²⁾.

Finally, pre-excitation arises when there is an extra (‘accessory’) electrical pathway within the heart that bypasses the normal conduction system. The atrial impulse is transmitted along this accessory pathway, and prematurely activates the pumping of the ventricle. The pathway may occur at several possible locations, each producing its own distinctive syndrome. Pre-excitation is associated with supraventricular tachycardia (SVT) and atrial fibrillation with a rapid ventricular response rate.
In Dana’s case the history is suggestive of recurrent SVT secondary to pre-excitation, which is frequently cured by burning off the accessory pathway with radiofrequency ablation. At present there is no established link between preexcitation and the other possible diagnosis of long QT syndrome.
Long QT syndrome is characterised by prolonged repolarisation and a predisposition to ‘torsades de pointes’, a form of polymorphic ventricular tachycardia. There are several subtypes of long QT syndrome, related to the specific gene affected; exercise-induced arrhythmia occurs in LQT1 and to a lesser extent in LQT2⁽³⁾. Swimming and diving are prominent triggers for arrhythmic events in LQT1.
Patients with long QT syndrome are discouraged from participating in competitive sports. However, establishing the diagnosis is far from straightforward, even with molecular genetic analysis. While isolation of a known long QT mutation is confirmatory, at least half of all patients will have defects in genes that have yet to be identified; hence a negative result does not rule out the disease. Clinical diagnosis is challenging because ECG findings may be non-specific and paroxysmal; risk stratification has yet to be fully defined⁽⁴⁾.

The diagnostic difficulties are not confined to long QT syndrome, underscoring the importance of referring athletes with suspected cardiac disease to a cardiologist. Abnormalities are frequently subtle or absent in early ARVC, but patients may nevertheless be at risk of sudden death, particularly during highly strenuous activity⁽⁵⁾. Furthermore, cardiac investigations may be difficult to interpret in elite athletes because of physiological adaptations to training, such as mild left ventricular hypertrophy and ventricular dilation⁽⁶⁾.

However, sustained arrhythmia, frequent ventricular premature beats, and repolarisation abnormalities on the ECG warrant concern^(7,8), in spite of previous controversies regarding their significance^(9,10).

Treatment and management

Management of the athlete with cardiac disease is equally problematic. The clinician is always tempted to play it safe in such instances, discouraging participation in competitive sports and endurance training, and instituting prophylactic treatment whenever there is a perception of increased risk. Athletes are understandably reluctant to relinquish the aspirations and investment of a lifetime. The stakes are even higher for professional sportspeople, in whom a cardiac diagnosis will threaten career and livelihood.
Unfortunately the therapeutic options may be as unpalatable to the athlete as the advice to withdraw from organised sports. Adrenaline appears to precipitate arrhythmia in many of these disorders, notably LQT1, ARVC, and catecholaminergic polymorphic VT. Consequently, the mainstay of medical therapy in these diseases is a class of drug known as betablockers, which counteract the action of adrenaline on the heart. Beta-blockers, however, have the side effect of limiting exercise capacity and performance.

The ICD is the most effective means of preventing sudden death. It has two main components: the pulse generator, containing the battery and complex electrical circuitry; and the wires (‘leads’) that connect it to the heart. The generator is implanted beneath the collarbone, and the leads are inserted through a nearby vein. The device constantly monitors the heart rhythm. On sensing a dangerous arrhythmia, it attempts to pace or shock the heart back into a normal rhythm.

Although ICDs have the potential to be life-saving, their psychosocial impact may be considerable in young patients, and the likelihood of lead-related complications increases over extended treatment periods.

Furthermore, the ICD is incompatible with contact sports because of the potential for blunt trauma and damage to the device. In spite of enhanced sensing algorithms in the new generation of ICDs, the high heart rates attained by athletes increase the likelihood of inappropriate discharge, the delivery of an unnecessary and occasionally dangerous shock to the heart.

Management of athletes with arrhythmia is therefore tailored according to the overall risk profile, tolerance for therapy and individual preference. While the clinician can advise and educate, it is the athlete who must decide whether to undergo evaluation, discontinue high-level activity and accept treatment.

The importance of patient autonomy is perhaps best illustrated by Dana Vollmer’s comment: ‘I basically said that I would rather die swimming than not do it at all.’

This attitude is probably not surprising to marathon and higher level masters swimmers.

Fatal Arrhythmias in Open Water Swimming

Fatal Arrhythmia's in Open Water Swimming: What's the Mechanism?

Reprinted from Lawrence L. Creswell, M.D.

Introduction by Don Macdonald: I recently had a sudden cardiac event, collapsed, received life saving help immediately and found to have arrhythmia problems perhaps brought on by exercise, Well I survived and now find myself with an implanted ICD to prevent such future events. I was running, which I jokingly say was the problem, instead of swimming. I think ICD stands for "I Can't Die".

However my experience now takes me down a path relatively untraveled since only about 1% of such incidents leave survivor's. So onto the next chapter of my swimming journey just One Stroke At A Time.

Cardiac rehab has me exercising already and I am hopeful to return to the pool in the near future.

We've talked previously here at the blog about the general issue of sports-related sudden cardiac death (SCD).  And we've also talked about the specific issue of swimming fatalities during triathlons and open water swims.

But what triggers a sudden, fatal arrhythmia during open water swimming?

The answer isn't known and perhaps it will never be known with certainty.  But a recent report from a group of scientists in the U.K., though, suggests a very plausible mechanism.  Their idea is worth considering.


What's been learned from studies on runners?

As I've mentioned previously here at the blog, sports-related SCD has been best studied in the setting of long-distance running events.  Last year, Dr. Kim and colleagues in Boston reported on a decade-long study of runners with race-related SCD [1].  These investigators found that fatalities during marathons are not distributed uniformly along the race distance.  Instead, they predominate during the final 3 miles or so.  And interestingly, fatalities during half marathon events also predominate during the closing miles.  But why?

In the running population, we know from autopsy studies that the majority of victims have some sort of (often previously unknown) heart disease.  And something happens during the closing miles of the race.  In the words of the investigators, their "findings suggest that demand ischemia (i.e., ischemia due to an imbalance between oxygen supply and demand) may be operative in exercise-related acute coronary events during long-distance running races."  The leading hypothesis is that this mismatch in blood (or oxygen) supply and demand in the heart occurs when the runner picks up the pace, producing an adrenaline surge and increased physiologic demands on the heart, once the finish line is mentally within sight.

Based on this hypothesis, the International Marathon Medical Directors Association issued an advisory in March, 2010 that recommended, among other things, that athletes "not sprint the last part of the race unless you have practiced this in your training."

The concept here is that a susceptible heart (in a susceptible athlete) is triggered at a particular moment in the race to have a fatal arrhythmia because of a specific trigger.  The surge hypothesis might not explain all running race-related deaths, but is a plausible explanation for the physiology behind the majority of the deaths that occur late in a race.

It's very likely that the same concept is in play in triathlon-related sudden cardiac death.


What's going on in triathlon?

In triathlon, athletes have died at any point during the race--from the first few strokes of the swim through the final strides of the run.  And a couple athletes have collapsed with SCD even a few hours after the finish.  But the majority of deaths have occurred during the swim.  USA Triathlon issued a report last year that summarizes these facts.

What might be the trigger for sudden cardiac arrest during the swim portion of a triathlon?

Recently, two researchers in the U.K.--Michael Shattock and Michael Tipton--have offered a new hypothesis that they have labeled autonomic conflict [2,3]

To understand their hypothesis, we first need to talk for a moment about some features of the heart's physiology.


Sympathetic and Parasympathetic Influences

One component of our nervous system is called the autonomic system.  This portion of the nervous system is involuntary, responding to internal and external stimuli below the level of our consciousness.  The autonomic nervous system has 2 different divisions--the sympathetic and parasympathetic systems.  Each of these divisions can operate independently, often with opposite effects on the body's organs, including the heart.

We often think of the sympathetic nervous system as being excitatory--providing the so-called "fight or flight" response.  When activated, the sympathetic nervous system has several effects on the heart:  an increase in heart rate, vasodilation of the coronary arteries (leading to more blood flow), and increased contractility (contraction strength) of the heart muscle.  And importantly for athletes, activation of the sympathetic nervous system also increases the blood flow to the skeletal muscles, decreases blood flow to the abdominal organs, and opens up the airways of the lungs.

In contrast, the parasympathetic nervous system has an inhibitory effect on the heart, acting to restore a baseline heart rate after sympathetic activation and by slowing electrical conduction in the specialized areas of the heart's electrical system known as the sino-atrial (SA) node and the atrio-ventricular (AV) node.  In well-trained endurance athletes, the parasympathetic nervous system is often highly developed, and is one cause of a very low resting heart rate.


A Hypothesis

Drs. Shattock and Tipton have proposed a mechanism where sudden activation or sudden increase in activation of both the sympathetic and parasympathetic nervous systems can produce a fatal arrhythmia.  This idea is supported by studies in isolated hearts as well as in healthy volunteers.

Let's say that an athlete's heart might be predisposed to an arrhythmia because of one or more anatomic or physiologic conditions such as:  congenital or inherited long QT syndrome, coronary artery disease, myocardial hypertrophy, ischemic heart disease, or pathologic hypertrophy (eg, hypertrophic cardiomyopathy).

During an open water swim, an athlete's sympathetic nervous system is activated because of physical exertion, (relatively) cold water temperature, anxiety, or even anxiety or overcompetitiveness.  The parasympathetic nervous system is activated because of facial wetting, water entering the mouth, nose, and pharynx, and extended breath holding--and particularly so, just at the moment of breaking a breath hold.  At that very moment, there can be maximal parasympathetic activation.

These scientists suggest that this autonomic conflict--between the sympathetic and parasympathetic nervous systems--is what triggers a sudden, potentially fatal arrhythmia.


It's Plausible

This is a plausible hypothesis.  It fits with the observations that have been made on victims of sudden cardiac death during open water swimming.  And it fits with the general concept of a susceptible heart and an arrhythmia trigger that seems to be in play in victims of SCD in other sports.



References

1.  Kim JH et al.  Cardiac arrest during long-distance running races.  N Engl J Med 2012;366:130-140.

2. Shattock MJ, Tipton MJ.  'Autonomic conflict':  a different way todiedu  ring cold water immersion?  J Physiol 2012;590:3219-3230.

3.  Tipton MJ.  Sudden cardiac death during openwater  swimming.  Br J Sports Med 2013. Online in advance.


Related Posts

1. Sports-relatd sudden cardiac death in the general population

2. Athletes, sudden death, and CPR

Stop Seeking and Start Finding: Create a Near-Perfect Life

“What could I say to you that would change your beliefs, except that perhaps you seek too much, that as a result of your seeking you cannot find. Simply put your asking the wrong questions."

'Don Macdonald - motivational speaker, open water marathon swimmer, and cardiac and resilience health advocate'.

I have a confession: I hate slowing down. When I finally let myself stop—being alone with my thoughts, vulnerable and open to the world—I become afraid.

I have another confession: There was a specific time in my life when went through a painful and scary situation. It almost broke me. And the only way I knew how to cope was to get back up. I didn't learn how to do this without years of practice, many failures and successes and good family and friends. 

Although not quite my circumstances, the story below hits the mark dead on.

Simply put: If times were hard, I ran.

I changed schools, moved to different cities, traveled to different countries, and found solace in running, a sport that calls for constant movement. I began seeking specifically for happiness: for the people, the place, and the situation that would help me find the “perfect life.”

I was a seeker who kept looking for happiness and different ways to “become a better person.” I was searching for a new life that would be “perfect” like the lives I saw on college campuses, TV shows, and Facebook feeds.

I believed my old life and my old self weren’t good enough, so I had to create a new life that would allow me to start over.

I pondered getting a Masters in global health, joining a rock band, writing a bestseller, running marathons, making music in West Africa, climbing mountains, and learning how to build lean-to’s.

I was convinced accomplishing any of these things would make me happy, make me feel deserving, and make me whole again.

A couple years passed by, and I slowly began to realize that no matter where I went, what I sought out, and the situations I was in, I was still the same exact person inside.

That’s when I realized if I wanted to find happiness, I had to first understand that the perfect life did not exist, and the acceptance of my past and my imperfections is what creates the near-perfect life. 

Most importantly, I had to find myself again, which meant I had to stop feverishly seeking.

We should all go after the things we want; we should be driven to chase after our dreams, embrace new challenges, and go on new adventures. But seeking often means deliberately searching for something that isn’t always meant to be there, or to simply run away from something that can truthfully never escape you.

By being too tunnel-visioned and too set on a goal—landing the “perfect” job, finding the “perfect partner,” or making the “perfect” group of friends—you may miss out on the less-obvious scenarios that are intended to fill your near-perfect life.

When on your journey to stop seeking, start finding, and create a life where you are whole-hearted, fulfilled, and accepting, take note of these tips:

Accept who you are. 

Know that your core self, and your emotions, outlook, and attitude, will follow you everywhere, no matter what situation you are in. Recognizing the beautiful and imperfect person you are is the first step towards accepting new challenges and allowing new experiences into your life.

Give yourself options. 

You may really want one thing—a specific job, a house in a certain part of the country, or certain fame or fortune. But if one of your dreams doesn’t come into fruition, maybe this means that another bigger and better dream is waiting for you. Don’t get discouraged, and allow yourself to be open.

Be vulnerable. 

Invite fear, uncertainty, and imperfection into your life. Once you fully open yourself up to the universe, it will allow you to see the incredible number of options for you, and let you try new things to help create the near-perfect life.

Meditate.  

Use meditation as a way to be with nothing but your present self. This helps you to slow down and stop seeking, to really get to know your true self and what you feel, want, and need.

Try again.  

Things don’t fall into place right away. There will be ten hardships before one celebration. Don’t give up. Be patient.

Don’t be stagnant.  

None of these tips mean you should stop moving completely and wait for life to work itself out on its own. Rather, it’s about finding a balance between learning what you want and inviting new opportunities, while recognizing that how you react to life’s situations is in your hands.

After nearly ten years of seeking, I found my near-perfect life in New York City, the one place I had once swore I’d never move to. I found an apartment with an old friend, and we rekindled a friendship from nearly five years prior. I discovered a support system of friends and family who were always there for me, and one company of hundreds I applied to hired me.

My time in New York has helped me uncover the happy spirit that was always within me—the spirit that once was simply too tired from my constant seeking to spread its light.

I’m still not very good at slowing down. I’m happiest when moving, when constantly trying to reach that next tier. But I’m also trying to slow down and breathe—to stop seeking for “better” and start finding myself, allowing my near-perfect life to meet me halfway.

Reprinted from Laura Schwecherl