In 1923 a very important meeting was held at the Edgewater Beach Hotel in Chicago. Attending this meeting were 10 of the world's most successful business men and financiers. Those present were the president of the largest independent steel company, the president of the national city bank, the president of the largest utility company, the president of the largest gas company, the greatest wheat speculator, the president of the New York Stock Exchange, a member of the President's Cabinet, the greatest 'bear' in Wall Street, head of the world's greatest monopoly, President of the Bank of International Settlement. I must admit there here were gathered a group of the world's most successful businessmen; men in the business of making money, at least, men who had found the secret of making money. But 25 years later, let's see where these men ended up.
The president of the largest independent steel company, Charles Schwab, died a bankrupt and lived on borrowed money for 5 years before his death. The president of the greatest utility company, Samuel Insull, died a fugitive from justice and penniless in a foreign land. The president of the largest gas company, Howard Rapson, went insane. The greatest wheat speculator, Arthur Cutten, died abroad insolvent. The president of the New York Stock Exchange (at that time,) Richard Whitney, was later released from Sing Sing penitentiary. The member of the President's Cabinet, Albert B. Fall, was pardoned from prison so that he could die at home. The greatest 'bear' in Wall Street, Jesse Livermore, died a suicide. The head of the greatest monopoly, Ivor Krueger, died a suicide; the president of the Bank of International Settlement, Leon Frazer, died a suicide. Fast forward to the current times and history repeats itself with Bernie Madoff starting a long list..........
All these men learned well the art of making money, but NONE of the learned how to live. What an achievement. All they learned was the art of making money; and generally when a man makes money, he thinks he has achieved that which is greater than any other thing on earth.
Money is, of course, very necessary; it is a necessary evil and I wish I had more of it. But I would rather know how to live and have ideas and ideals to live to, than acquire wealth because I know that when my turn comes, it doesn't matter how much I have since I can't take it with me.
I share with you now an alternative story. The story of Michael Dowling. Great Great Grandpa Dowling was a young man who fell from a wagon in a blizzard in Michigan when he was 14 years old. Before his parents had discovered he had fallen from the rear of the wagon, he had been frostbitten. His right leg was amputated almost to the hip, his left leg just above the knee; his right arm was amputated; his left hand was amputated. Not much future for a young man like that. He learned to focus on what he controlled, on what he could do and went to the board of county commissioners and told them that if they would educate him he would pay back every cent. During World War I, Grandpa Dowling, who at the time was the president of one of the largest banks in St. Paul, went to Europe to visit the soldiers - to visit those who were wounded. I read in his diary, that upon one occasion, he was in a large hotel in London, and he had before him the wounded soldiers in their wheelchairs. They were in the lobby and he was up on the mezzanine floor. As he started to speak, he minimized the seriousness of their wounds, the fact that they had lost one eye, another had lost an arm, etc. were no grounds for complaint. Well, he got them so wrought up that they started to boo him. Then he walked over to the stairway and down the stairs towards the lobby telling them as he walked how fortunate they were, and they continued booing him. Finally, he sat down on one of the steps and took off his right leg. And he kept talking and telling them how well off they were. They calmed down a little bit but still resented his remarks. Then he took off his left leg. Well, the booing stopped. But before he had arrived at the bottom of the stairs, he had taken off his right arm and flipped off his left hand and there he sat - just the stump of a body! Grandpa Dowling was the president of one of the largest banks in St. Paul. He had married and was the father of 5 children. He knew how to live and he knew how to rear a family - and he finally died as a result of the strength he gave in encouraging the wounded soldiers of World War I.
My point is, he used his talents and everything is his control to help those around him become better and want to be better than they otherwise would have been and lived life to fullest in the process, refusing to accept barriers, obstacles or challenges as limiting factors. I admire those same qualities in Chris Gleason.
A sincere wish to you and all of your families for the best Thanksgiving ever this year as we all internalize how very much we have to be thankful for and the opportunities that yet lie ahead only limited by what we cannot dream.............
"Being physically fit, whatever that means to you, is always healthier for your heart than a sedentary lifestyle."
Totally agree. But for me it's not about doing nothing it's about the extremeness of the events that needs balancing. 40 mile runs, multiple marathons in a week. While those things were fun to see if I can "push myself" and they make for great stories and forum fodder but did they make me healthier? Maybe....?? long term i'm sure but my body was wrecked after those stunts.
1. There is a strong link between endurance sports and major heart arrhythmias. That's a fact. Period. It's true for swimming, cycling, and running (among other endeavors). Trust me, developing an arrhythmia WILL change your life, and not for the better. I wish it on no one.
2. No matter what we say here, most will carry on. People often see and take in only what they want to know. I am not immune from the same. But this discussion has made me know that I will redouble my efforts to figure out what is truly driving me. I must answer why and should I continue. So thanks, everyone, for helping me see that.
Q:
3. An EN friend ended up in the med tent after a recent IM. This athlete's cardiac enzyme levels were equal to that of someone who had a heart attack. Does that mean the same damage was done? I hope a doc can answer this, b/c that is something very important to know. Is is possible that we all experience scary enzyme levels after an IM or marathon? I don't know.
Q:
4. Maybe it would be healthier to back off from the endurance lifestyle after a major event? Maybe a few years between IMs with NO marathons and the like picking up the slack? Musing here. I am beginning to think that ongoing, frequent endurance training and racing may, in the end, be detrimental to our cardiac and physical health--not to mention the performance plateaus that often come, as well as injuries.
Great discussion...thanks to everyone. All I know is Chris Gleason--my friend and someone I grew to love--is being waked today and will be buried tomorrow. That wonderful man is gone. He would never want us to risk life and limb because of what he called, "stupid human tricks." He would be glad we're talking about all of this.
Linda, regarding your enzyme question, Dean Karnazes is the only genetic freak that I've heard of that reportedly does not have enzyme abnormalities after a marathon. As someone stated in an earlier post, liver function tests and CK are commonly out of whack, and not considered concerning unless they reach a certain point. TroponinI, a cardiac specific enzyme, should not be elevated due to an athletic event, and could be indicative of heart damage. How much damage can only be quantified by further testing, and cardiac imaging. I've not heard that they test for troponin in a medical tent, although I'm curious to hear if others know that for certain. I would imagine that if your cardiac enzymes were elevated after an IM, you would guarantee yourself a trip to the local hospital and a full cardiac workup. What happened to your friend following the event?
Thanks to you and others for bringing up some tough questions, and points to consider. I feel completely inadequate and unable to respond to those in any reasonable way at this point. I'm so sorry you all have lost a friend.
@ Linda - I don't know wht they may test for exactly, but the body's muscle cells have an enzyme called CPK. It's found in skeletal muscle as well as heart muscle. There is a way to test for the heart specific subtype of the enzyme (CPK-MB) which is one way they look for heart muscle damage from a heart attack. If I had to guess, my suspicion would be that they check for total CPK which would be an indication of general muscle damage. As a test that would be most applicable to athletes ending up in medical tents, this would be most appropriate. You can understand why it would be abnormally elevated in virtually anyone after a long-distance endurance event and how it could be very high like it often is in heart attacks. The heart is a muscle, being overworked all day long like the other muscles in the body, so I'm sure the -MB subtype would be elevated in most people after such an event. But just like I would assume that CPK's would be elevated in most IM athletes at the finish line due to ongoing pounding and damage, not because of an occlusion of blood flow to them, I would also assume the same of CPK-MB. In addition, let's remember that it is those ending up in medical tents that would be the ones receiving these tests. The main reason a general CPK level would be checked is that very high levels, especially combined with dehydration, can lead to acute kidney failure.
Looking at the big picture here. Are there labs that can indicate heart damage after an endurance event and are they likely high in most, if not all people? Yes. Does that translate to clinically significant heart damage such that heart function deteriorates over time due to progressive heart muscle cell death? There is no evidence whatsoever to support that. There are people who have done hundreds of marathons, dozens of ironmans, etc. Certainly plenty of people out there that someone would have made a connection by now and it hasn't happened.
Bottom line....everyone knows that doing an ironman hurts the body and that it needs to recover afterward. It seems to make sense that multiple endurance events done close to each other can hinder recovery from previous ones and therefore compromise the body even further. But how many events, what type of events, how close together, and most importantly, the body of the person doing them, all have an influence on whether there is a potential for long-term, or even permanent, bodily injury.
Finally, it is true that statistics can be manipulated to prove a point, but only in how they are portrayed. The numbers are the numbers. For instance (remember I'm making these numbers up), your risk of getting in a car accident driving on Los Angeles is 2 in 1000 (0.2%) and is 1 in 1000 (0.1%) in Portland. So you can say you are half as likely to get into a car accident in Portland (or you are twice as likely to get into one in LA). That sounds bad when you say it like that and that is often how statistics are advertised. But the numbers are the numbers. In the worst case scenario here, you still have a 99.8% vs. 99.9% chance of not getting in an accident. The numbers say there really isn't any real safety benefit driving in Portland. It is very easy to count up the number of people starting marathons in the US each year (or ironmans, or triathlons, or centuries, etc.), and dividing the number of people that die during them. And if someone did that, and says that your risk of dying in a marathon is 1 in 50,000 (or 100,000 or 200,000) then statistically that is the risk. It's up to you if that risk is too high for you. Me....I'll take my chances.
From what I was able to dig up on pubmed, elevation of cardiac specific Troponin levels is pretty common in Ironman athletes and in one study was detectable in 9% of finishers in Kona (though I don't know how many they actually sampled, I can't imagine everyone gave blood). Interestingly, troponin levels were more apt to be elevated in faster finishers so the fitter, faster athletes also had the higher enzyme bumps. Even more interesting, in the exact same study done on Western States 100-miler finishers, absolutely none of the athletes had troponin bumps.
Now while this may sound alarming and almost certainly indicates some degree of myocardial injury, stress, etc, I don't think it necessarily has the same connotation as troponin elevation does in the setting of ischemic cardiac disease. To make an analogy, most athletes finishing an Ironman will have elevated creatine kinase levels, CK, a marker for skeletal muscular injury. The blood CK levels can be alarming and in other settings would be considered consistent with life threatening rhabdomyolysis, liver and kidney failure. But these bad things basically never happen to Ironman athletes despite the elevated CK levels. In short the elevation of CK post Ironman just doesn't mean the same thing it does when we see elevated CK after a prolonged resuscitation, reperfusion injury, etc. I think the same may be true here. The troponin elevation from exercise doesn't carry the same negative meaning as elevation from ischemia. I don't know this for sure mind you (nor does anyone ), but looking at what happens in situations of true rhabdomyolysis (limb ischemia, etc) where the muscle basically dies and is permanently damaged and weaker vs IM where the muscle emerges unscathed (sore for a bit, but then pretty much back to business); I think the same is true here. Troponin elevations in the setting of ischemia/vascular occlusion indicate permanent damage to myocardium whereas after IM, it indicates an inflammation in the heart muscle that reverses. What the long term implications of this are I don't know, but given that the people with the highest levels of enzymes are the fastest pros and they seem to bounce back to compete again and again, I think any damage must be minimal. Patients who experience a myocardial infarction frequently require significant rehab to regain function.
Again, the data on this are out, and the elevated enzymes certainly indicate some level of cardiac muscular irritation, inflammation, etc; but it clearly doesn't mean the same thing as when we see these levels go up from a true MI.
Kevin, thanks for the info! It was my understanding that the troponin bumps seen in those studies were not consistent with the levels you would see in a true MI. What have you found? I appreciate your diligence with the Pubmed searches. I'm also curious if you've read the studies about abnormal echo findings after ultra events. Those also appeared to be transient abnormalities, but with uncertain long term consequences.
Haven't read the echo studies and could only get abstracts on the troponin stuff so far since I'm on my home computer (no call and an awesome 4-days off rights now!) and not linked into the University where I can download most articles for free. Based on the abstracts though, I think you are right the bumps are not as high as would be expected with real MI's.
Fwiw, I developed an arythmia during IM Moo 2008 and took 9 months without raising my HR above aerobic. Occasionally I would push too hard up a hill and set it off and just get off the bike until it went away. I reduced caffeine also as I was consuming 8+ espresso shots/day during my ramp up.
I had a hormone panel performed (as part of my exam) and discovered I had low testosterone. I went on supplemental Test (brought me to 600 ng/dl from 230 ng/dl...high normal value is 1100) and after a month or two started to feel good again. During 2010 I could push myself up a hill hard enough to develop tunnel vision and upper extremity numbness and tingling then back off and sit down. The visual field would return and n/t would instantly disappear. No arythmia. Last year I raced bikes only and couldn't even get the tunnel vision or N/T to return.
I realize this is n=1 stuff but did some reading and low Test levels have been associated with increased risk of cardiac episodes in a VA study. I'm not sure how this pans out for a woman but there may be a balance of hormones that needs to be considered. Again, FWIW.
@Vince. Can I ask your age? Did you also test thyroid? Just curious as an endocrinologist friend and I were discussing overtraining/under recovery and effects on pituitary and hormone levels. Can happen in younger guys who are really pushing it but obviously a lot more common as we age up.
After some research it appears to me that there is some debate as to what causes the c-Tn elevations following an endurance event > 3hrs. One group suggests that there is actual cell death (like a heart attack) another group suggests that it is due to leakage associated with damage to the cell membrane. Though a 2009 study suggests that the latter is likely the cause based on MRI assessment. I suspect catecholamine’s play a role as does level of dehydration.
Most echo studies seem to show significant decreases in diastolic (Resting) and systolic (pumping) function of both ventricles following an endurance event. These changes are no different between young or old participants and the diastolic as well as systolic changes were still present at 4 weeks based on spectral tissue Doppler assessment. The changes were also present at 1 week based on MRI findings. Changes seemed to be associated with training volume, at least for age group marathoners with greater changes seen at lower volume (< 35 miles/wk average).
Regarding long term effects Olympic endurance athletes followed for an average of 5 years had no change in cardiac function or morphology. One athlete was followed for 17 years. However, a study in age group endurance athletes (Wilson et al, Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes) show at least some older endurance athletes have increased myocardial fibrosis based on MRI studies as well as changes in cardiac size when compared to an age matched cohort and a control group. Granted that was a small study of 12 athletes and there is no long term follow-up.
I also found 2 fairly good reviews on this subject ( http://www.pponline.co.uk/encyc/heart-attack-risks-are-greater-for-athletes-who-compete-in-endurance-sports-263 ) and (http://mdredux.blogspot.com/2011/01/does-endurance-exercise-damage-heart.html ). The later was written by an MD that is also a marathoner and both cite sources. Bottom line from my assessment is that there is an increased risk of cardiac related death associated with an endurance event. That risk is ~ 1:50,000 during the event and for ~ 24 hours after. However, endurance athletes have ~ a 60% less change of cardiac related death outside of that window. There may be some lasting effects from endurance training and /or events on the heart but the jury is still out on what that translates to as regards to risk. Also some cardiac enzymes (cTn and BNP) are elevated following an event and the faster you complete the event the higher the levels in general. The cause of theses elevation in not known.
Also a recent article (Heart Nov/2011 "Cardiac adaptation to acute and chronic participation in endurance sports") may shed some light on this discussion but I do not have access to this journal. If anyone does and can e-mail me a copy I would appreciated it.
Sorry to jump in on this late & to repeat anything that may have been asked before. I've tried to attach the article that Dewey referenced. I'm also coming at this from the medical end (surgeon) but not from the in-depth Cardiology background. Richard Shea touched on this a little but I want to be sure I understand correctly. My question is does endurance training and racing create an environment to trigger arrythmia in someone WITHOUT a history of arrhythmia? My gut feeling (and please set me straight if I'm clueless) is that during training/racing, we're always in sinus tach and if one hasn't developed an arrythmia after a few years, they probably don't have the predisposition to do so? I've asked a few of my cardiology friends and they tend to agree. I personally haven't done a stress test (I'm 44) but I feel if you can do a marathon, IM, etc., a stress test is meaningless. I appreciate any response and sorry if I'm repeating.
I am a clinical perfusionist and have worked as a physician assistant in cardiac surgery for nearly 23 years. A perfusionist is the person who operates the heart lung machine in open heart surgery. I have been doing triathlons for about 3 years know, although I have been running and cycling for more than 15 years.
About 10 years ago, at an ironman distance event near my home, A 33 year old man was half way through his marathon. At mile 15 he began to experience crushing chest pain and nausea. He was loaded into an ambulance and brought to my hospital. I was on call and we rushed him to the OR after he was found to have severe coronary artery disease. His history? Only a father who had a coronary bypass at age 55. His lipid profile was reasonable, although his HDL was a little low. Laying on the OR bed, it was obvious this young man was in the prime shape of his life. After the surgery we spoke about his training and he had no symptoms whatsoever leading up to the race. He was a very competitive athlete and his splits up to that point were excellent.
A few years ago, a study, which I unfortunately can not find, was done on triathletes. In a race simulated Olympic distance atmosphere, each athlete had a baseline echocardiogram. Following the race, they each had a post race echocardiogram. Findings: A large percent of the contestants had moderate mitral regurgitation and reduced heart function. What is mitral regurgitation? A leaking leaking valve between the left atrium and ventricle. Why was it leaking? It was leaking because of coronary ischemia or reduced coronary blood flow to the heart. Why was the blood flow to the heart reduced? Coronary blood flow occurs when the heart is relaxed ... in diastole. When your heart rate is elevated, the time for coronary filling is reduced significantly. When you are doing this for 1,2 3 or up to 15 hours. That is a long time. If you have underlying coronary disease... 30 minutes may be too long. Compound this with dehydration and the risk is significant. Cardiac output is stroke volume (amount of blood in the heart when it beats) times the heart rate. If you reduce your blood volume from dehydration and the heart rate stays the same, cardiac output is reduced. If a 150-180 pound man or woman loses 3, 4 or 5 pounds during a race and most of it is fluid loss.... not so good. Now, lets compound this with fluid selection during a race. As I demonstrated to my children who run cross country and train in a very hot and humid climate, take a glass of water and add food coloring to it so that the water is significantly darkened. Poor a few ounces out of the glass and add an equal amount of water back to it. Notice after a few repetitions that the water begins to lose its color intensity. If you consider the food coloring to be critical electrolytes in your blood and you have only replenished yourself with water or an insufficient amount of electrolytes, you have dangerously reduced your magnesium, sodium and potassium- in addition to being dehydrated with a heart rate of 140-180 beats per minute.
Studies have also been done on the inflammatory effects of endurance training on coronary disease. The inflammatory mediators released from zone 4 or 5 training attacks the endothelium (inner layer of tissue that lines the blood vessels) and causes irregular surfaces to form. This unfortunately is a great site for platelets to attach to and cause a plaque or obstruction to form. Chronic inflammation may cause concentric narrowing of the blood vessels as well. A ruptured plaque is dangerous and life threatening, often the cause of sudden death in cardiac patients.
Most people wouldn't pay money to do this to themselves as my wife has suggested to me. The problem for many of triathletes is that it has become an outlet for the midlifers. What do I do myself now? I think I will take my recreational biking and running to the next level.... at the age of 40......50.... and even 60. While many of the athletes who suffer cardiac arrest are very competitive accomplished athletes, the bulk of the competitors are not and I am not surprised more people don't have poor outcomes.
As others have spoken here about arrhythmias, like atrial fibrillation, I can only say that it is nothing to play with. As mentioned previously, stroke is a common side effect of A fib and most patients are encouraged to avoid the triggers. I have been caffeine free for years, except for the rare diet coke (once or twice a year after a race). However, at Augusta 70.3 I saw so many people drinking caffeine loaded drinks like red bull and 5 hour energy drinks. I bought one before the race thinking I may give it a try. Keeping the mantra don't try anything new on a race, I threw it out. The other reason was the concern of the caffeine load on my system. I have heard people talking about Ironman being done at a lower heart rate. Maybe in the smartest of racers, but if you are taking caffeine levels like that, I assure you it is impacting your heart rate.
In the end, I too an pretty upset about Chris. I didn't know him either, but I did know a heart surgeon who was doing a sprint a few years ago in New Jersey when he had a heart attack in the water. He was older, but also had hiked to 18 k feet that year as well. He was in excellent shape. I have a VERY strong family history of CAD. By the way, family history of heart disease is considered strong only if it occurs in women 65 years of age or less and 62 or less in men.
If you are concerned, look into getting a cardiac MRI. It isn't definitive, but it is non-invasive and may provide a little assurance in those people with a strong family history. Understand though, that electrolyte abnormalities can be just as deadly as coronary disease. I tend to agree with the other posters here about life in general. I have 2 beautiful children and a lovely wife. The idea of leaving this world due to a race is inconceivable to me. I love to compete, but I have a lot of balance in my work and personal life outside triathlon. Don't get me wrong, I workout pretting f-ing hard, but I have seen a few marriages destroyed by passionate midlife crisis triathletes... I am not one of those It is not my life... Having seen tragedy in my profession, I realized a long time ago that my family is my life.
Thanks Michael. Do you think cardiac deaths in endurance events are ischemia related or arrhythmia related? If ischemia related, I can't imagine that many long term endurance athletes have significant CAD. I have to believe it's more plaque rupture, etc. If so, what can you really do prevent/predict? If deaths are really from underlying CAD, without symptoms, fam hx, etc., how do you know you have coronary artery disease. Along the same lines, if you've trained/raced etc., and you have not had any unusual heart rhythms, how likely are you to have an arrhythmia?
From your experience (and others), other than listening to your body and not doing something really stoopid (ie not drinking, etc.), what else should one to minimize/know one's risk?
You said statistics can be misleading, but the numbers are the numbers. Let me ask you this: of any group of 10,000 marathoners, how many push the pace at any point to subject themselves to a level of discomfort beyond the baseline minimal discomfort required of taking that many steps? Then, how many of these deaths occur in that population? Can you say with total confidence that the distribution is the same? What if the risk in the population of goal-oriented folks trying for a PR is actually 1/10,000 instead of 1/50,000? Does that make you feel differently?
As for the earlier point that there's no reason to believe that you can't sprint the last 400 yards if you've been going that hard for that long, I'd suggest leaving that conclusion for each individual to draw. It's presumptuous to assume that you actually understand all of the physiological demands to picking up the pace after 3 hours of exertion. Is it possible that vulnerable plaque will rupture based on a combination of blood flow rate, and the plasticity of the vessels, which can change after 3 hours of exertion and moderate deyhdration? I don't know, but I do know that I can't say categorically that it doesn't.
I don't have any answers (that's part of the whole process that's difficult, isn't it?). I'd feel a lot better if I knew exactly what it was that caused him to die. I will say that of all the possibilities, most of them would have gotten him at some point or another (some sort of underlying something). There's very few plausible explanations where marathon was going to get him, but general life (lifting weights, raking leaves, running to catch a plane on a short connection) wouldn't have at some point. So, we continue on.
Troponin is a very specific marker (protein) for cardiac muscle and it's release is indicative of muscle damage. There are instances of when it might be elevated, like after heart surgery when the muscle is being operated on, but in general....elevated troponin would indicative of cardiac muscle damage. Many times after a major heart attack the muscle will "leak" troponin according to cardiologists. If you have a heart attack and proceed to have a stent placed, many times the troponin will sharply rise afterwards. Cardiologists always say " it is just leaking from the tissue"- no big deal. That couldn't be any further from the truth, it is most likely due to cell death during the MI and implant of the stent. The kidney's can "leak" troponin as well, mostly in patients with chronic renal failure on dialysis. Patients in chronic congestive heart failure also will have a low level elevated troponin. However, most physicians will say that an elevated troponin is indicative of cell damage or death.
The question of whether I think it is ischemic or a ruptured plaque? I am not sure. The studies would suggest that there is an ischemic insult to the heart after a triathlon. The chronic inflammatory effects of training most likely results in a plaque formation or acceleration of the atherosclerotic process, that seems most likely the cause of sudden death. A rupture plaque is lethal in most circumstances.
Either way, I think the majority of people are safe with participation in triathlon. However, like anything, there is a risk assumed or they wouldn't ask for a waiver. That being said, it might be worthy of seeing a physician for clearance if you are new to the sport and haven't seen a physician in years. Do not fool yourself, age is not always a factor. A number of years ago, a male figure skater collapsed on the ice with his partner (also his wife). Autopsy showed that the 26 yo had a very tight occlusion of his left anterior descending coronary artery. He probably ruptured a plaque. So do not assume if you are 30 that it won't happen to you....
Fwiw, I developed an arythmia during IM Moo 2008 and took 9 months without raising my HR above aerobic. Occasionally I would push too hard up a hill and set it off and just get off the bike until it went away. I reduced caffeine also as I was consuming 8+ espresso shots/day during my ramp up.
I had a hormone panel performed (as part of my exam) and discovered I had low testosterone. I went on supplemental Test (brought me to 600 ng/dl from 230 ng/dl...high normal value is 1100) and after a month or two started to feel good again. During 2010 I could push myself up a hill hard enough to develop tunnel vision and upper extremity numbness and tingling then back off and sit down. The visual field would return and n/t would instantly disappear. No arythmia. Last year I raced bikes only and couldn't even get the tunnel vision or N/T to return.
I realize this is n=1 stuff but did some reading and low Test levels have been associated with increased risk of cardiac episodes in a VA study. I'm not sure how this pans out for a woman but there may be a balance of hormones that needs to be considered. Again, FWIW.
Vince
Hi Vince!
I am SO glad that sorted itself out for you. That is luck-y!
About a year before the A-fib began I was disgnosed with hypothyroid, but at the time the arrythmia developed all was well and calibrated for a long period of time. I also see a hormone doc regularly, and am also on top of that issue. Interesting, though, that both things you mentioned were factors for me even though the arrythmia was no where in sight at the time. When the Afib began I was functioning on all cylinders, as far as I know.
Gang--Thought the docs might be intereted in this... FWIW, I am also part of a clinical trial as part of my ablation. It's through Agility Research, and I carry around a little device by Braemar where I record my heart if I have "symptoms" and send the reading in over the phone. So far every reading I have sent in is normal sinus rhythm, so I am doing very well. I take the readings more from my sense of uncertainty, rather than feeling anything is "wrong." I am still a freaked out that the Afib will return. The study involves a new ablation catheter, although I don't know if they used the new one my EP is so hot on during my procedure. In any case, I felt participating in the study was a way to give back and help out.
Thanks to everyone for sharing all this info. The heart enzyme reading is fascinating.
So I have a marathon this weekend and I'm going to go home tonight and think about writing a will. One thing I've never done is gotten any stress testing done. The doctors at Kaiser wouldn't let me do it since I had no risk factors. Now, I'm kinda upset about that. I HAVE had cholesterol checked and it's low, but after reading about LPP testing, I'm not sure that means as much as I thought.
I'm going to go on with my marathon and go for a PR, but at least at a minimum I will know that my insurance and will are in order. All things considered, this is still unsettling to me. I feel the need to get stress tested and look into LPP blood testing, but I don't want to obsess about it too.
Thanks everyone for contributing to the discussion.
It is time for me to add my $0.02 from an MD, clincial researcher, spouse, father, team member, philosopher perspective. I suck as a philosopher, so I may ramble, but I think it will be personally therapeutic.
One month ago, Jerry Friesen, a local race director, running series organiser, and friend to World Endurance Canada died suddenly, and alone, while out for his morning run.Rumor has it that he had some symptoms in the weeks preceding his death (more on this below). Last week, when Brenda reposted the Facebook message and John posted Chris’s obituary link, I sat in my office and sobbed.Although I never met Chris, I always read what he had to say.
Peering inward, I realize that I am very similar to Chris – 3 kids of the same age, near the top of my game professionally, competitive (albeit a few notches below Chris), and striving to improve.This leaves me, and obviously many others, wondering at what cost and what risk?
I won’t talk about the data much.I think the estimates are probably accurate, but our understanding of the pathophysiology lacking.I accept that this can happen, and it hurts badly when it happens to someone we know.
The definition of a “full life” is very personal.Many dimensions interact to make our lives complete.If I stopped pushing, something will be lacking, and other parts of my life would be adversely affected.My definition of happiness or living life to the fullest today includes training hard and competing as best I can.I am in the camp of Al T, Chris G and Jeff B. If I can go doing what I love, then that is fine.I will accept that it is my time. But, quite frankly, I am not ready to go in my 40s.I would prefer for that scenario to occur in my 80s.
I don’t know how to mitigate risk but I do have strong opinions (not necessarily supported by data):
·A significant proportion of coronary artery disease can present as sudden cardiac death – I am not sure we can do much about this;
·Anybody with a family history of arrhythmic death/near death or hypertrophic cardiomyopathy must be checked out;
·If you ever develop any sort of symptom between your chin, bellybutton, arms or back, STOP EXERCISING immediately and in the future until everyone is sure that it is not your heart.It is not a bad burrito that you ate yesterday. It is not gastroesophageal reflux.It is your heart until proven otherwise.Don’t even do easy workouts.
May Chris rest in peace and his family find the strength to carry on.Train smart everyone, and listen to your body.
While researching the causes of sudden death in endurance events I became interested in trying to determine if I, though my training and racing, was damaging my heart and/or predisposing myself to an increased risk of sudden death. What follows in a summary of some relevant articles, both research and review, on the topic. I would love to say that I have read all the articles on this topic but sadly I have not and most of my review has been limited to reading abstracts due to my inability to obtain the full text articles. However, I do feel like this is a representative review of the current knowledge on the subject primarily fueled by the most recent review article titled “Cardiac adaptation to acute and chronic participation in endurance sports”.
1. Short Term Response
a. “Exercise induced cardiac fatigue” which is a decrease in pumping and resting functions of the heart associated with ultra- endurance events
i. Decrease in pumping function is variable and seems to be associated with duration of event and training status.
ii. Not all studies report a decrease in pumping function.
iii. Decreased resting function is more consistent and repeatable.
iv. Exercise induced cardiac fatigue seems to be more prevalent in the right ventricle (lower chamber) and may lead to remolding (changes within the heart muscle) in some athletes that might predispose them to the development of ventricular arrhythmias.
v. The decrease in pumping and resting function appear to be transient and resolve within 48 hours but may persist up to 1-4 weeks.
b. Elevations in troponin (c-Tn)
i. Overall rate of c-TnT elevation in endurance events is 47%. However, single blood draws post event may underestimate the overall number of post event elevations in c-TnT.
ii. Most studies have shown no correlation between elevations in c-TnT with altered function in the left ventricle but many have linked c-TnT elevation with dysfunction of the right ventricle.
iii. The cause of c-TnT elevation is also unknown but leakage of unbound protein across the cell membranes is suspected. Myocardial damage (ischechemic injury) and death of the heart muscle cells is the other possibility.
iv. Bottom line it is unknown if the elevation results from reversible or irreversible damage to the heart muscle cells
2. Long Term Effects
a. Change to heart structure and function (these changes are expected and are not considered to raise health concerns)
i. Eccentric hypertrophy is an adaptive response to endurance training
1. This is dilation of the cardiac chamber to improve stroke volume or the amount of blood the heart pumps every time it beats.
2. Finding is well documented and balanced between the right and left ventricles.
ii. Changes result in an increased maximal stroke volume with exercise which raises cardiac output during exercise
b. Other changes
i. Studies overall show that endurance exercise decreases cardiovascular risk. However, a 1995 study hints that a high dose of physical activity (>4000 kcal/week) may lead to a small increase in risk.
ii. Greater incidence of atrial fibrillation/atrial flutter in endurance athletes.
iii. Two studies have shown an increase in asymptomatic ventricular arrhythmias in endurance athletes and another has shown 25% of those with ventricular arrhythmia’s have inducible non-sustained ventricular tachycardia. The studies differ on the impact of decreasing training volume of stopping training on the development of the arrhythmia.
iv. Studies have also suggested that there may be a link between the right ventricular changes mentioned above and the development of ventricular arrhythmias that is termed “Exercise Induced Right Ventricular Cardiomyopathy”. This process is not seen in all study participants and I stress that this is not a proven entity.
v. Some endurance athletes have fibrosis (scarring) of their heart muscle noted on MRI that is not consistent with coronary artery disease. This fibrosis can lead to the development of ventricular arrhythmia’s but no link or risk information is available on athletes with scarring of there heart.
3. My Conclusions:
a. Overall endurance training leads to healthy changes to the heart that promotes long life with a decreased risk of death from all causes.
b. There is a slight increase in the risk of death during and for ~ 24 hours following an endurance event. That risk is about 1:50,000 at the highest but may actually be lower.
c. For a small subset of endurance athletes there may be an increased risk for the development of ventricular arrhythmias that may increase the risk of sudden death whether engaged in activity or not. At this time, there is no screening method known to identify the population at risk for arrhythmia development, though evaluation with a Holter and/or contrast MRI may identify athletes with a potential increased risk.
d. Bottom-line the risk seems to be very small that exercise induces changes to the heart could lead to sudden death. This does not take into account the presence of coronary artery disease, or a congenital/genetic cardiac disease that might predispose to sudden death with physical exertion.
e. If you have concerns or experience any unexplained chest or upper body ( back, arm, jaw or stomach) pain, palpitation, unusually high heart rate, or feel faint or light headed during or after exercise stop the activity and please consult with your physician and/or cardiologist for further guidance as soon as possible.
In the interest of full disclosure I am not an MD but I am a veterinary cardiologist. I have 3 years of advance training in comparative cardiology and have been a boarded and practicing veterinary cardiologist for ~ 7 years.
@Dewey This is a great synopsis! Must have taken you some time to compile. I think it'll be helpful to many who have concerns after recent events.
I've long suspected ultra endurance events are not the healthiest thing we can do to our bodies. Hey, if a little is good, a ton must be better right? I've read same studies suggesting more than 4000 kcal/wk MAY be increasing the risk somewhat. I accept that and chose to continue.
Nice work Dewey. That is about as concise and informative a summary that I have seen on the topic. Ignoring the statement that you have made in bold-type is where I believe risk increases.
Comments
A Thanksgiving message:
Wow Shaughn, powerful message!! Thanks!
Shaughn,
Thanks for sharing this. Perspective we can all use when the call of "what" we get in return for something is louder than the "why" we do it.
Totally agree. But for me it's not about doing nothing it's about the extremeness of the events that needs balancing. 40 mile runs, multiple marathons in a week. While those things were fun to see if I can "push myself" and they make for great stories and forum fodder but did they make me healthier? Maybe....?? long term i'm sure but my body was wrecked after those stunts.
Some takeaways and questions from my POV:
1. There is a strong link between endurance sports and major heart arrhythmias. That's a fact. Period. It's true for swimming, cycling, and running (among other endeavors). Trust me, developing an arrhythmia WILL change your life, and not for the better. I wish it on no one.
He would be glad we're talking about all of this.
2. No matter what we say here, most will carry on. People often see and take in only what they want to know. I am not immune from the same. But this discussion has made me know that I will redouble my efforts to figure out what is truly driving me. I must answer why and should I continue. So thanks, everyone, for helping me see that.
Q:
3. An EN friend ended up in the med tent after a recent IM. This athlete's cardiac enzyme levels were equal to that of someone who had a heart attack. Does that mean the same damage was done? I hope a doc can answer this, b/c that is something very important to know. Is is possible that we all experience scary enzyme levels after an IM or marathon? I don't know.
Q:
4. Maybe it would be healthier to back off from the endurance lifestyle after a major event? Maybe a few years between IMs with NO marathons and the like picking up the slack? Musing here. I am beginning to think that ongoing, frequent endurance training and racing may, in the end, be detrimental to our cardiac and physical health--not to mention the performance plateaus that often come, as well as injuries.
Great discussion...thanks to everyone. All I know is Chris Gleason--my friend and someone I grew to love--is being waked today and will be buried tomorrow. That wonderful man is gone. He would never want us to risk life and limb because of what he called, "stupid human tricks."
Thanks to you and others for bringing up some tough questions, and points to consider. I feel completely inadequate and unable to respond to those in any reasonable way at this point. I'm so sorry you all have lost a friend.
Looking at the big picture here. Are there labs that can indicate heart damage after an endurance event and are they likely high in most, if not all people? Yes. Does that translate to clinically significant heart damage such that heart function deteriorates over time due to progressive heart muscle cell death? There is no evidence whatsoever to support that. There are people who have done hundreds of marathons, dozens of ironmans, etc. Certainly plenty of people out there that someone would have made a connection by now and it hasn't happened.
Bottom line....everyone knows that doing an ironman hurts the body and that it needs to recover afterward. It seems to make sense that multiple endurance events done close to each other can hinder recovery from previous ones and therefore compromise the body even further. But how many events, what type of events, how close together, and most importantly, the body of the person doing them, all have an influence on whether there is a potential for long-term, or even permanent, bodily injury.
Finally, it is true that statistics can be manipulated to prove a point, but only in how they are portrayed. The numbers are the numbers. For instance (remember I'm making these numbers up), your risk of getting in a car accident driving on Los Angeles is 2 in 1000 (0.2%) and is 1 in 1000 (0.1%) in Portland. So you can say you are half as likely to get into a car accident in Portland (or you are twice as likely to get into one in LA). That sounds bad when you say it like that and that is often how statistics are advertised. But the numbers are the numbers. In the worst case scenario here, you still have a 99.8% vs. 99.9% chance of not getting in an accident. The numbers say there really isn't any real safety benefit driving in Portland. It is very easy to count up the number of people starting marathons in the US each year (or ironmans, or triathlons, or centuries, etc.), and dividing the number of people that die during them. And if someone did that, and says that your risk of dying in a marathon is 1 in 50,000 (or 100,000 or 200,000) then statistically that is the risk. It's up to you if that risk is too high for you. Me....I'll take my chances.
Now while this may sound alarming and almost certainly indicates some degree of myocardial injury, stress, etc, I don't think it necessarily has the same connotation as troponin elevation does in the setting of ischemic cardiac disease. To make an analogy, most athletes finishing an Ironman will have elevated creatine kinase levels, CK, a marker for skeletal muscular injury. The blood CK levels can be alarming and in other settings would be considered consistent with life threatening rhabdomyolysis, liver and kidney failure. But these bad things basically never happen to Ironman athletes despite the elevated CK levels. In short the elevation of CK post Ironman just doesn't mean the same thing it does when we see elevated CK after a prolonged resuscitation, reperfusion injury, etc. I think the same may be true here. The troponin elevation from exercise doesn't carry the same negative meaning as elevation from ischemia. I don't know this for sure mind you (nor does anyone ), but looking at what happens in situations of true rhabdomyolysis (limb ischemia, etc) where the muscle basically dies and is permanently damaged and weaker vs IM where the muscle emerges unscathed (sore for a bit, but then pretty much back to business); I think the same is true here. Troponin elevations in the setting of ischemia/vascular occlusion indicate permanent damage to myocardium whereas after IM, it indicates an inflammation in the heart muscle that reverses. What the long term implications of this are I don't know, but given that the people with the highest levels of enzymes are the fastest pros and they seem to bounce back to compete again and again, I think any damage must be minimal. Patients who experience a myocardial infarction frequently require significant rehab to regain function.
Again, the data on this are out, and the elevated enzymes certainly indicate some level of cardiac muscular irritation, inflammation, etc; but it clearly doesn't mean the same thing as when we see these levels go up from a true MI.
Fwiw, I developed an arythmia during IM Moo 2008 and took 9 months without raising my HR above aerobic. Occasionally I would push too hard up a hill and set it off and just get off the bike until it went away. I reduced caffeine also as I was consuming 8+ espresso shots/day during my ramp up.
I had a hormone panel performed (as part of my exam) and discovered I had low testosterone. I went on supplemental Test (brought me to 600 ng/dl from 230 ng/dl...high normal value is 1100) and after a month or two started to feel good again. During 2010 I could push myself up a hill hard enough to develop tunnel vision and upper extremity numbness and tingling then back off and sit down. The visual field would return and n/t would instantly disappear. No arythmia. Last year I raced bikes only and couldn't even get the tunnel vision or N/T to return.
I realize this is n=1 stuff but did some reading and low Test levels have been associated with increased risk of cardiac episodes in a VA study. I'm not sure how this pans out for a woman but there may be a balance of hormones that needs to be considered. Again, FWIW.
Vince
@Vince. Can I ask your age? Did you also test thyroid? Just curious as an endocrinologist friend and I were discussing overtraining/under recovery and effects on pituitary and hormone levels. Can happen in younger guys who are really pushing it but obviously a lot more common as we age up.
Most echo studies seem to show significant decreases in diastolic (Resting) and systolic (pumping) function of both ventricles following an endurance event. These changes are no different between young or old participants and the diastolic as well as systolic changes were still present at 4 weeks based on spectral tissue Doppler assessment. The changes were also present at 1 week based on MRI findings. Changes seemed to be associated with training volume, at least for age group marathoners with greater changes seen at lower volume (< 35 miles/wk average).
Regarding long term effects Olympic endurance athletes followed for an average of 5 years had no change in cardiac function or morphology. One athlete was followed for 17 years. However, a study in age group endurance athletes (Wilson et al, Diverse patterns of myocardial fibrosis in lifelong, veteran endurance athletes) show at least some older endurance athletes have increased myocardial fibrosis based on MRI studies as well as changes in cardiac size when compared to an age matched cohort and a control group. Granted that was a small study of 12 athletes and there is no long term follow-up.
I also found 2 fairly good reviews on this subject ( http://www.pponline.co.uk/encyc/heart-attack-risks-are-greater-for-athletes-who-compete-in-endurance-sports-263 ) and (http://mdredux.blogspot.com/2011/01/does-endurance-exercise-damage-heart.html ). The later was written by an MD that is also a marathoner and both cite sources.
Bottom line from my assessment is that there is an increased risk of cardiac related death associated with an endurance event. That risk is ~ 1:50,000 during the event and for ~ 24 hours after. However, endurance athletes have ~ a 60% less change of cardiac related death outside of that window. There may be some lasting effects from endurance training and /or events on the heart but the jury is still out on what that translates to as regards to risk. Also some cardiac enzymes (cTn and BNP) are elevated following an event and the faster you complete the event the higher the levels in general. The cause of theses elevation in not known.
Also a recent article (Heart Nov/2011 "Cardiac adaptation to acute and chronic participation in endurance sports") may shed some light on this discussion but I do not have access to this journal. If anyone does and can e-mail me a copy I would appreciated it.
Hi Everyone,
Sorry to jump in on this late & to repeat anything that may have been asked before. I've tried to attach the article that Dewey referenced. I'm also coming at this from the medical end (surgeon) but not from the in-depth Cardiology background. Richard Shea touched on this a little but I want to be sure I understand correctly. My question is does endurance training and racing create an environment to trigger arrythmia in someone WITHOUT a history of arrhythmia? My gut feeling (and please set me straight if I'm clueless) is that during training/racing, we're always in sinus tach and if one hasn't developed an arrythmia after a few years, they probably don't have the predisposition to do so? I've asked a few of my cardiology friends and they tend to agree. I personally haven't done a stress test (I'm 44) but I feel if you can do a marathon, IM, etc., a stress test is meaningless. I appreciate any response and sorry if I'm repeating.
Appreciate the perspective and always good to hear from all the docs!
About 10 years ago, at an ironman distance event near my home, A 33 year old man was half way through his marathon. At mile 15 he began to experience crushing chest pain and nausea. He was loaded into an ambulance and brought to my hospital. I was on call and we rushed him to the OR after he was found to have severe coronary artery disease. His history? Only a father who had a coronary bypass at age 55. His lipid profile was reasonable, although his HDL was a little low. Laying on the OR bed, it was obvious this young man was in the prime shape of his life. After the surgery we spoke about his training and he had no symptoms whatsoever leading up to the race. He was a very competitive athlete and his splits up to that point were excellent.
A few years ago, a study, which I unfortunately can not find, was done on triathletes. In a race simulated Olympic distance atmosphere, each athlete had a baseline echocardiogram. Following the race, they each had a post race echocardiogram. Findings:
A large percent of the contestants had moderate mitral regurgitation and reduced heart function.
What is mitral regurgitation? A leaking leaking valve between the left atrium and ventricle.
Why was it leaking? It was leaking because of coronary ischemia or reduced coronary blood flow to the heart.
Why was the blood flow to the heart reduced? Coronary blood flow occurs when the heart is relaxed ... in diastole.
When your heart rate is elevated, the time for coronary filling is reduced significantly. When you are doing this for 1,2 3 or up to 15 hours. That is a long time. If you have underlying coronary disease... 30 minutes may be too long. Compound this with dehydration and the risk is significant. Cardiac output is stroke volume (amount of blood in the heart when it beats) times the heart rate. If you reduce your blood volume from dehydration and the heart rate stays the same, cardiac output is reduced. If a 150-180 pound man or woman loses 3, 4 or 5 pounds during a race and most of it is fluid loss.... not so good.
Now, lets compound this with fluid selection during a race. As I demonstrated to my children who run cross country and train in a very hot and humid climate, take a glass of water and add food coloring to it so that the water is significantly darkened. Poor a few ounces out of the glass and add an equal amount of water back to it. Notice after a few repetitions that the water begins to lose its color intensity. If you consider the food coloring to be critical electrolytes in your blood and you have only replenished yourself with water or an insufficient amount of electrolytes, you have dangerously reduced your magnesium, sodium and potassium- in addition to being dehydrated with a heart rate of 140-180 beats per minute.
Studies have also been done on the inflammatory effects of endurance training on coronary disease. The inflammatory mediators released from zone 4 or 5 training attacks the endothelium (inner layer of tissue that lines the blood vessels) and causes irregular surfaces to form. This unfortunately is a great site for platelets to attach to and cause a plaque or obstruction to form. Chronic inflammation may cause concentric narrowing of the blood vessels as well. A ruptured plaque is dangerous and life threatening, often the cause of sudden death in cardiac patients.
Most people wouldn't pay money to do this to themselves as my wife has suggested to me. The problem for many of triathletes is that it has become an outlet for the midlifers. What do I do myself now? I think I will take my recreational biking and running to the next level.... at the age of 40......50.... and even 60. While many of the athletes who suffer cardiac arrest are very competitive accomplished athletes, the bulk of the competitors are not and I am not surprised more people don't have poor outcomes.
As others have spoken here about arrhythmias, like atrial fibrillation, I can only say that it is nothing to play with. As mentioned previously, stroke is a common side effect of A fib and most patients are encouraged to avoid the triggers. I have been caffeine free for years, except for the rare diet coke (once or twice a year after a race). However, at Augusta 70.3 I saw so many people drinking caffeine loaded drinks like red bull and 5 hour energy drinks. I bought one before the race thinking I may give it a try. Keeping the mantra don't try anything new on a race, I threw it out. The other reason was the concern of the caffeine load on my system. I have heard people talking about Ironman being done at a lower heart rate. Maybe in the smartest of racers, but if you are taking caffeine levels like that, I assure you it is impacting your heart rate.
In the end, I too an pretty upset about Chris. I didn't know him either, but I did know a heart surgeon who was doing a sprint a few years ago in New Jersey when he had a heart attack in the water. He was older, but also had hiked to 18 k feet that year as well. He was in excellent shape. I have a VERY strong family history of CAD. By the way, family history of heart disease is considered strong only if it occurs in women 65 years of age or less and 62 or less in men.
If you are concerned, look into getting a cardiac MRI. It isn't definitive, but it is non-invasive and may provide a little assurance in those people with a strong family history.
Understand though, that electrolyte abnormalities can be just as deadly as coronary disease. I tend to agree with the other posters here about life in general. I have 2 beautiful children and a lovely wife. The idea of leaving this world due to a race is inconceivable to me. I love to compete, but I have a lot of balance in my work and personal life outside triathlon. Don't get me wrong, I workout pretting f-ing hard, but I have seen a few marriages destroyed by passionate midlife crisis triathletes... I am not one of those
Venkatesh thanks for the paper I will read it an report back if there is any new info.
From your experience (and others), other than listening to your body and not doing something really stoopid (ie not drinking, etc.), what else should one to minimize/know one's risk?
You said statistics can be misleading, but the numbers are the numbers. Let me ask you this: of any group of 10,000 marathoners, how many push the pace at any point to subject themselves to a level of discomfort beyond the baseline minimal discomfort required of taking that many steps? Then, how many of these deaths occur in that population? Can you say with total confidence that the distribution is the same? What if the risk in the population of goal-oriented folks trying for a PR is actually 1/10,000 instead of 1/50,000? Does that make you feel differently?
As for the earlier point that there's no reason to believe that you can't sprint the last 400 yards if you've been going that hard for that long, I'd suggest leaving that conclusion for each individual to draw. It's presumptuous to assume that you actually understand all of the physiological demands to picking up the pace after 3 hours of exertion. Is it possible that vulnerable plaque will rupture based on a combination of blood flow rate, and the plasticity of the vessels, which can change after 3 hours of exertion and moderate deyhdration? I don't know, but I do know that I can't say categorically that it doesn't.
I don't have any answers (that's part of the whole process that's difficult, isn't it?). I'd feel a lot better if I knew exactly what it was that caused him to die. I will say that of all the possibilities, most of them would have gotten him at some point or another (some sort of underlying something). There's very few plausible explanations where marathon was going to get him, but general life (lifting weights, raking leaves, running to catch a plane on a short connection) wouldn't have at some point. So, we continue on.
The question of whether I think it is ischemic or a ruptured plaque? I am not sure. The studies would suggest that there is an ischemic insult to the heart after a triathlon. The chronic inflammatory effects of training most likely results in a plaque formation or acceleration of the atherosclerotic process, that seems most likely the cause of sudden death. A rupture plaque is lethal in most circumstances.
Either way, I think the majority of people are safe with participation in triathlon. However, like anything, there is a risk assumed or they wouldn't ask for a waiver. That being said, it might be worthy of seeing a physician for clearance if you are new to the sport and haven't seen a physician in years. Do not fool yourself, age is not always a factor. A number of years ago, a male figure skater collapsed on the ice with his partner (also his wife). Autopsy showed that the 26 yo had a very tight occlusion of his left anterior descending coronary artery. He probably ruptured a plaque. So do not assume if you are 30 that it won't happen to you....
Hi Vince!
I am SO glad that sorted itself out for you. That is luck-y!
About a year before the A-fib began I was disgnosed with hypothyroid, but at the time the arrythmia developed all was well and calibrated for a long period of time. I also see a hormone doc regularly, and am also on top of that issue. Interesting, though, that both things you mentioned were factors for me even though the arrythmia was no where in sight at the time. When the Afib began I was functioning on all cylinders, as far as I know.
Gang--Thought the docs might be intereted in this... FWIW, I am also part of a clinical trial as part of my ablation. It's through Agility Research, and I carry around a little device by Braemar where I record my heart if I have "symptoms" and send the reading in over the phone. So far every reading I have sent in is normal sinus rhythm, so I am doing very well. I take the readings more from my sense of uncertainty, rather than feeling anything is "wrong." I am still a freaked out that the Afib will return. The study involves a new ablation catheter, although I don't know if they used the new one my EP is so hot on during my procedure. In any case, I felt participating in the study was a way to give back and help out.
Thanks to everyone for sharing all this info. The heart enzyme reading is fascinating.
Hello,
So I have a marathon this weekend and I'm going to go home tonight and think about writing a will. One thing I've never done is gotten any stress testing done. The doctors at Kaiser wouldn't let me do it since I had no risk factors. Now, I'm kinda upset about that. I HAVE had cholesterol checked and it's low, but after reading about LPP testing, I'm not sure that means as much as I thought.
I'm going to go on with my marathon and go for a PR, but at least at a minimum I will know that my insurance and will are in order. All things considered, this is still unsettling to me. I feel the need to get stress tested and look into LPP blood testing, but I don't want to obsess about it too.
Thanks everyone for contributing to the discussion.
It is time for me to add my $0.02 from an MD, clincial researcher, spouse, father, team member, philosopher perspective. I suck as a philosopher, so I may ramble, but I think it will be personally therapeutic.
One month ago, Jerry Friesen, a local race director, running series organiser, and friend to World Endurance Canada died suddenly, and alone, while out for his morning run. Rumor has it that he had some symptoms in the weeks preceding his death (more on this below). Last week, when Brenda reposted the Facebook message and John posted Chris’s obituary link, I sat in my office and sobbed. Although I never met Chris, I always read what he had to say.
Peering inward, I realize that I am very similar to Chris – 3 kids of the same age, near the top of my game professionally, competitive (albeit a few notches below Chris), and striving to improve. This leaves me, and obviously many others, wondering at what cost and what risk?
I won’t talk about the data much. I think the estimates are probably accurate, but our understanding of the pathophysiology lacking. I accept that this can happen, and it hurts badly when it happens to someone we know.
The definition of a “full life” is very personal. Many dimensions interact to make our lives complete. If I stopped pushing, something will be lacking, and other parts of my life would be adversely affected. My definition of happiness or living life to the fullest today includes training hard and competing as best I can. I am in the camp of Al T, Chris G and Jeff B. If I can go doing what I love, then that is fine. I will accept that it is my time. But, quite frankly, I am not ready to go in my 40s. I would prefer for that scenario to occur in my 80s.
I don’t know how to mitigate risk but I do have strong opinions (not necessarily supported by data):
· A significant proportion of coronary artery disease can present as sudden cardiac death – I am not sure we can do much about this;
· Anybody with a family history of arrhythmic death/near death or hypertrophic cardiomyopathy must be checked out;
· If you ever develop any sort of symptom between your chin, bellybutton, arms or back, STOP EXERCISING immediately and in the future until everyone is sure that it is not your heart. It is not a bad burrito that you ate yesterday. It is not gastroesophageal reflux. It is your heart until proven otherwise. Don’t even do easy workouts.
May Chris rest in peace and his family find the strength to carry on. Train smart everyone, and listen to your body.
While researching the causes of sudden death in endurance events I became interested in trying to determine if I, though my training and racing, was damaging my heart and/or predisposing myself to an increased risk of sudden death. What follows in a summary of some relevant articles, both research and review, on the topic. I would love to say that I have read all the articles on this topic but sadly I have not and most of my review has been limited to reading abstracts due to my inability to obtain the full text articles. However, I do feel like this is a representative review of the current knowledge on the subject primarily fueled by the most recent review article titled “Cardiac adaptation to acute and chronic participation in endurance sports”.
1. Short Term Response
a. “Exercise induced cardiac fatigue” which is a decrease in pumping and resting functions of the heart associated with ultra- endurance events
i. Decrease in pumping function is variable and seems to be associated with duration of event and training status.
ii. Not all studies report a decrease in pumping function.
iii. Decreased resting function is more consistent and repeatable.
iv. Exercise induced cardiac fatigue seems to be more prevalent in the right ventricle (lower chamber) and may lead to remolding (changes within the heart muscle) in some athletes that might predispose them to the development of ventricular arrhythmias.
v. The decrease in pumping and resting function appear to be transient and resolve within 48 hours but may persist up to 1-4 weeks.
b. Elevations in troponin (c-Tn)
i. Overall rate of c-TnT elevation in endurance events is 47%. However, single blood draws post event may underestimate the overall number of post event elevations in c-TnT.
ii. Most studies have shown no correlation between elevations in c-TnT with altered function in the left ventricle but many have linked c-TnT elevation with dysfunction of the right ventricle.
iii. The cause of c-TnT elevation is also unknown but leakage of unbound protein across the cell membranes is suspected. Myocardial damage (ischechemic injury) and death of the heart muscle cells is the other possibility.
iv. Bottom line it is unknown if the elevation results from reversible or irreversible damage to the heart muscle cells
2. Long Term Effects
a. Change to heart structure and function (these changes are expected and are not considered to raise health concerns)
i. Eccentric hypertrophy is an adaptive response to endurance training
1. This is dilation of the cardiac chamber to improve stroke volume or the amount of blood the heart pumps every time it beats.
2. Finding is well documented and balanced between the right and left ventricles.
ii. Changes result in an increased maximal stroke volume with exercise which raises cardiac output during exercise
b. Other changes
i. Studies overall show that endurance exercise decreases cardiovascular risk. However, a 1995 study hints that a high dose of physical activity (>4000 kcal/week) may lead to a small increase in risk.
ii. Greater incidence of atrial fibrillation/atrial flutter in endurance athletes.
iii. Two studies have shown an increase in asymptomatic ventricular arrhythmias in endurance athletes and another has shown 25% of those with ventricular arrhythmia’s have inducible non-sustained ventricular tachycardia. The studies differ on the impact of decreasing training volume of stopping training on the development of the arrhythmia.
iv. Studies have also suggested that there may be a link between the right ventricular changes mentioned above and the development of ventricular arrhythmias that is termed “Exercise Induced Right Ventricular Cardiomyopathy”. This process is not seen in all study participants and I stress that this is not a proven entity.
v. Some endurance athletes have fibrosis (scarring) of their heart muscle noted on MRI that is not consistent with coronary artery disease. This fibrosis can lead to the development of ventricular arrhythmia’s but no link or risk information is available on athletes with scarring of there heart.
3. My Conclusions:
a. Overall endurance training leads to healthy changes to the heart that promotes long life with a decreased risk of death from all causes.
b. There is a slight increase in the risk of death during and for ~ 24 hours following an endurance event. That risk is about 1:50,000 at the highest but may actually be lower.
c. For a small subset of endurance athletes there may be an increased risk for the development of ventricular arrhythmias that may increase the risk of sudden death whether engaged in activity or not. At this time, there is no screening method known to identify the population at risk for arrhythmia development, though evaluation with a Holter and/or contrast MRI may identify athletes with a potential increased risk.
d. Bottom-line the risk seems to be very small that exercise induces changes to the heart could lead to sudden death. This does not take into account the presence of coronary artery disease, or a congenital/genetic cardiac disease that might predispose to sudden death with physical exertion.
e. If you have concerns or experience any unexplained chest or upper body ( back, arm, jaw or stomach) pain, palpitation, unusually high heart rate, or feel faint or light headed during or after exercise stop the activity and please consult with your physician and/or cardiologist for further guidance as soon as possible.
In the interest of full disclosure I am not an MD but I am a veterinary cardiologist. I have 3 years of advance training in comparative cardiology and have been a boarded and practicing veterinary cardiologist for ~ 7 years.
@Dewey This is a great synopsis! Must have taken you some time to compile. I think it'll be helpful to many who have concerns after recent events.
I've long suspected ultra endurance events are not the healthiest thing we can do to our bodies. Hey, if a little is good, a ton must be better right?
I've read same studies suggesting more than 4000 kcal/wk MAY be increasing the risk somewhat. I accept that and chose to continue.
Heard this report on the BBC this morning. Here's a print version.
Doing extreme endurance exercise, like training for a marathon, can damage the heart, research reveals.
@Linda I've seen several studies that suggest something similar. Wondering about this quote:
"The researchers told the European Heart Journal how these changes might cause heart problems like arrhythmia"
Curious if they refer to something like A FIB which many endurance athletes may experience or something more serious like a V TACH.