The Heart - Swimmer vs. Runner and Athletic Heart Syndrom

The Heart of a Swimmer  vs. Runner

Regular exercise changes the look and workings of the human heart. And researchers are discovering that different sports affect the heart differently.

Reprinted from Gretchen Reynolds and related articles in Wikipedia

Do world-class swimmers’ hearts function differently than the hearts of elite runners?

A new study finds that the answer may be yes, and the differences, although slight, could be telling and consequential, even for those of us who swim or run at a much less lofty level. 

Cardiologists and exercise scientists already know that regular exercise changes the look and workings of the human heart. The left ventricle, in particular, alters with exercise. This chamber of the heart receives oxygen-rich blood from the lungs and pumps it out to the rest of the body, using a rather strenuous twisting and unspooling motion, as if the ventricle were a sponge being wrung out before springing back into shape.

Exercise, especially aerobic exercise, requires that considerable oxygen be delivered to working muscles, placing high demands on the left ventricle. In response, this part of the heart in athletes typically becomes larger and stronger than in sedentary people and functions more efficiently, filling with blood a little earlier and more fully and untwisting with each heartbeat a bit more rapidly, allowing the heart to pump more blood more quickly.

While almost any exercise can prompt remodeling of the left ventricle over time, different types of exercise often produce subtly different effects. A 2015 study found, for instance, that competitive rowers, whose sport combines endurance and power, had greater muscle mass in their left ventricles than runners, making their hearts strong but potentially less nimble during the twisting that pumps blood to muscles.

These past studies compared the cardiac effects of land-based activities, though, with an emphasis on running. Few have examined swimming, even though it is not only a popular exercise but unique. Swimmers, unlike runners, lie prone, in buoyant water and hold their breaths, all of which could affect cardiac demands and how the heart responds and remakes itself.

So, for the new study, which was published in November in Frontiers in Physiology, researchers at the University of Guelph in Canada and other institutions set out to map the structure and function of elite swimmers’ and runners’ hearts.

The researchers focused on world-class performers because those athletes would have been running or swimming strenuously for years, presumably exaggerating any differential effects of their training, the researchers reasoned.

Eventually they recruited 16 national-team runners and another 16 comparable swimmers, male and female, some of them sprinters and others distance specialists.

They asked the athletes to visit the exercise lab after not exercising for 12 hours and then, when on site, to lie quietly. They checked heart rates and blood pressures and finally examined the athletes’ hearts with echocardiograms, which show both the structure and functioning of the organ.

It turned out, to no one’s surprise, that the athletes, whether runners or swimmers, enjoyed enviable heart health. Their heart rates hovered around 50 beats per minute, with the runners’ rates slightly lower than the swimmers’. But all of the athletes’ heart rates were much lower than is typical for sedentary people, signifying that their hearts were robust.

The athletes also had relatively large, efficient left ventricles, their echocardiograms showed.

But there were interesting if small differences between the swimmers and runners, the researchers found. While all of the athletes’ left ventricles filled with blood earlier than average and untwisted more quickly during each heartbeat, those desirable changes were amplified in the runners. Their ventricles filled even earlier and untwisted more emphatically than the swimmers’ hearts did.

In theory, those differences should allow blood to move from and back to the runners’ hearts more rapidly than would happen inside the swimmers’.

But these differences do not necessarily show that the runners’ hearts worked better than the swimmers’, says Jamie Burr, a professor at the University of Guelph and director of its human performance lab, who conducted the new study with the lead author, Katharine Currie, and others.

Since swimmers exercise in a horizontal position, he says, their hearts do not have to fight gravity to get blood back to the heart, unlike in upright runners. Posture does some of the work for swimmers, and so their hearts reshape themselves only as much as needed for the demands of their sport.

The findings underscore how exquisitely sensitive our bodies are to different types of exercise, Dr. Burr says.

They also might provide a reason for swimmers sometimes to consider logging miles on the road, he says, to intensify the remodeling of their hearts.

Of course, the athletes here were tested while resting, not competing, he says, and it is not clear whether any variations in their ventricles would be meaningful during races.

The study also was cross-sectional, meaning it looked at the athletes only once. They might have been born with unusual cardiac structures that somehow allowed them to excel at their sports, instead of the sports changing their hearts.

Dr. Burr, however, doubts that. Exercise almost certainly remakes our hearts, he says, and he hopes future experiments can tell us more about how each activity affects us and which might be best for different people.

In other articles summarized here from Wikipedia (https://en.wikipedia.org/wiki/Athletic_heart_syndrome) 

We find discussion of Athletic heart syndrome (AHS), also known as athlete's heart, athletic bradycardia, or exercise-induced cardiomegaly is a non-pathological condition commonly seen in sports medicine, in which the human heart is enlarged, and the resting heart rate is lower than normal.

The athlete's heart is associated with physiological remodeling as a consequence of repetitive cardiac loading. Athlete's heart is common in athletes who routinely exercise more than an hour a day, and occurs primarily in endurance athletes, though it can occasionally arise in heavy weight trainers. The condition is generally considered benign, but may occasionally hide a serious medical condition, or may even be mistaken for one. 

Athlete's heart most often does not have any physical symptoms, although an indicator would be a consistently low resting heart rate. Athletes with AHS often do not realize they have the condition unless they undergo specific medical tests, because athlete's heart is a normal, physiological adaptation of the body to the stresses of physical conditioning and aerobic exercise. People diagnosed with athlete's heart commonly display three signs that would usually indicate a heart condition when seen in a regular person: bradycardia, cardiomegaly, and cardiac hypertrophy. Bradycardia is a slower than normal heartbeat, at around 40–60 beats per minute. Cardiomegaly is the state of an enlarged heart, and cardiac hypertrophy the thickening of the muscular wall of the heart, specifically the left ventricle, which pumps oxygenated blood to the aorta. Especially during an intensive workout, more blood and oxygen are required to the peripheral tissues of the arms and legs in highly trained athletes' bodies. A larger heart results in higher cardiac output, which also allows it to beat more slowly, as more blood is pumped out with each beat. 

Another sign of athlete's heart syndrome is an S3 gallop, which can be heard through a stethoscope. This sound can be heard as the diastolic pressure of the irregularly shaped heart creates a disordered blood flow. However, if an S4 gallop is heard, the patient should be given immediate attention. An S4 gallop is a stronger and louder sound created by the heart, if diseased in any way, and is typically a sign of a serious medical condition. 

#heartofswimmer

#athleteheart

Young Hearts 4 Life - ECG Screening of active children and young adults Program

There are some things you cannot place an economic value on, a child’s life if one of them

Dr. Marek, an internationally recognized cardiologist, here with Ultra marathon open water swimmer Don Macdonald, has taught physicians across America how to run screenings for students and athletes. Over 10,000 community volunteers.

Young Hearts for Life® (YH4L) and One Stroke at a Time supported a recent Barrington High School (Chicagoland) Cardiac Screening Program Event, YH4L nationally known for its unique model, has screened over 110,000 students for conditions that cause sudden cardiac death.  This milestone is a first for any heart screening program of this kind in the United States.

Each week, sudden cardiac death claims the lives of more than 60 young adults in the United States.  YH4L has been a leader the medical community to address this problem in the Chicago area.

The YH4L screening program was founded by Dr. Joseph Marek in 2006 and is well known for its unique model that uses trained community volunteers to deliver a low cost, efficient screening program.

To date, over 1,900 students screened through YH4L have been identified as “at risk” students.  Of those, hundreds were found to have life threatening conditions, including Hypertrophic Cardiomyopathy, Long QT Syndrome, Wolff-Parkinson- White Syndrome (WPW), Brugada Syndrome, and Arrhythmogenic Right Ventricular Dysplasia.

Living proof (one of the 1%er's) to the value of finding these hidden health challenges. I encourage you to consider having your kids screened every two years and while your at it yourself.

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.

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.

Endurance Athletes - Nutrition Matters and corn products are not healthy for you long term

Corn is not a vegetable

Reprinted from The natural nutritionist

Endurance Athletes, pay attention to what you are eating as 'false' energy from corn products can adversely affect your cardiovascular system, causing inflammation long term. As an endurance athlete we eat lots of food but processed foods such as GU gels, snack bars, Gatorade, smoothies, the list goes on and on...carry very poor nutritrients and for some of us with genetic family traits, this can be harmful long term.

Parents, with kids in school and athletics. Please engage with your school and coaches to learn exactly what your kids are being fed. 

Just like peanuts are legumes and not nuts, corn is a grain, not a vegetable. But (whole)grains are good for me aren’t they? No. 

The truth is that we’ve been fed that lie to support industry. (Just like how the food pyramid was created by the agricultural industry!) Corn in particular, is the perfect industrial crop. According to Toby A.A. Heaps, author of The Killer Kernel, it has an abundant source of cheap interchangeable calories, and with a large amount of fertilizer, can be grown rapidly and predictably often on a one-person, one-machine farm enterprise.

Before I continue, let me get one thing straight. I’m not talking about the occasional corn on the cob at your family barbecue, but rather the reliance on corn as an every day food. Cornflakes for breakfast. Corn cakes and Vegemite as your afternoon snack. Cornbread. Corn starch, a common gluten free substitution; often found in low-fat products. ANYTHING containing high fructose corn syrup (HFCS). It’s simply not real food. All you are doing is jumping on the blood sugar-insulin roller coaster, which leads to chronic hunger, energy peaks and troughs, and the all-too-common 3.30-it is. Significantly, chronically elevated insulin levels are the enemy to sustainable weight loss, lean muscle mass development and weight maintenance.

Why corn is not part of my daily food pyramid

1. Corn is a sugary, starchy, low-nutrient grain.
2. While gluten is by far the worst culprit, grains can still be inflammatory and are high in phytic acid, substances that can inhibit nutrient absorption. The problem with high levels of phytate is mostly relevant when gut health is sub-optimal, and the overall nutrition is deficient in micro nutrients and essential food sources. Something you will definitely need to consider if you have been following our traditional food pyramid.
3. The over consumption of grains decreases the release of our major digestive and satiety hormone cholecystokinin, or CCK.  This is known to be one of the major causes of insulin resistance, the precursor to obesity.
4. There is not a single nutrient, vitamin or mineral present in grains that you cannot obtain from natural, wholefoods.
5. Corn is used to fatten pigs, cows and other livestock, and is the key ingredient in HFCS, the leading cause of obesity in America. Enough said?

Is corn GMO?

Overseas, corn, otherwise known as maize, is genetically modified (GM) for greater resistance to pests and viruses, higher nutritional value and longer shelf life. In Australia, imported GM corn is predominately used as cattle feed and thankfully, has not been approved for farming. 

However, GM corn may have entered our market through imported foods like bread and cereals, corn chips, gravy mixes and sports drinks. Avoid these products like the plague.

On a positive note, before any of these products are sold in Australia, they are checked for safety by Food Standards Australia and New Zealand (FSANZ). According to Australia’s Chief Scientist, the law in Australia requires that food labels must show if food has been GM, or contains GM ingredients, or whether GM additives or processing aids remain in the final food product. Please avoid GM foods, but that’s another story all together.

The moral of the story?

There are far better choices than corn. Focus on nutrient dense, real food. And if you do buy food products with a label, read them carefully. 

References

Genetically Modified Foods. Food Standards Australia and New Zealand. Available: http://www.foodstandards.gov.au/consumerinformation/gmfoods/.

Genetically modified food explained. Australia’s Chief Scientist. Available: http://www.chiefscientist.gov.au/2011/11/genetically-modified-food-explained/.

Haros M, Bielecka M, Honke J, & Sanz Y. (2007). Myo-inositol hexakisphosphate degradation by Bifidobacterium infantis ATCC 15697. International Journal of Food Microbiology, 117(1), 76-84.

Heaps TAA. The Killer Kernal. Corporate Knights. Available: http://www.corporateknights.com/article/killer-kernel.