AFib caused by endurance exercise (studies)

To all,

I've been reading studies (mostly done in Europe) that afib can be caused by endurance exercise, and when it is caused by too much endurance exercise, it often shows up in younger people. Here's a link to a bunch of studies:

[eurheartj.oxfordjournals.org]

I have done a lot of long-distance bike rides, especially over the last 10 years. I'm 52 now and was diagnosed with
AFib September of 2011. I have regularly done distances of 50-100 miles on the weekends, and for a few years did a week-long long-distance organized bike tour of about 400 miles each year (all with lots of hills). I have also done weightlifting since my 20's, but no more than an hour at a time, and no more than 3 days a week (it's been hard to motivate myself to do it).

So this brings up questions I have for the forum:

1. How many of you have a history of intense exercise, what type and for how long each session?

2. For those who answer "yes" how tall are you and what is your gender? The studies are showing that taller than average people are at much higher risk for this (6" of height above average gives you 50% more risk of Afib). I'm 5'10" tall. Another interesting thing: I read last week that there is a lot of AFib showing up in professional basketball players. Larry Bird (of the Boston Celtics) has it. A member of our local Blazers team has it (and he's only in his 30's). They are obviously very tall.

3. I am a member of two bicycle clubs (one for recumbents in Portland, and one for regular bikes in Vancouver) so am part of a wide social network of bike riders. I also know a lot of long-distance runners. Many are in their 50's and 60's. Yet none of them have AFib. The only people I've met with AFib are over 70 and inactive. A theory as to why I don't know anyone with AFib is, at least here in Portland, the vast majority (I'd say 95%) of the endurance athletes I know are less than average height for their genders (for men less than 5'10" and for women, less than 5'4". I don't know why that is, but around here (and maybe this is a U.S. phenomenon) endurance exercise just doesn't seem to attract tall people. And famous extreme endurance athletes I've read about (Scott Jurek, Mark Allen, Dave Scott) are, I believe, around 5'10" (I think Scott Jurek the famous ultradistance runner, is actually quite a bit shorter). Interestingly, I have met several long-distance bike riders from Holland who have come here either to do tours or participate in a bike race in Battle Mountain, NV (I was just a spectator) and most of them are very tall (over 6'4" for the men, and a woman who's come here to race is my height). They are about 10 years younger than me, so maybe AFib hasn't had time to show up in them yet, but this goes to show that endurance athletes (and people in general) in Europe are often taller than here in the U.S. (it is well known that people in the Netherlands are the tallest people, and there's a lot of tall people in Germany as well, as I noticed when I was travelling there). This may explain why doctors don't know about the connection between AFib and endurance exercise in this country, because maybe it doesn't really exist in most people here, due to shorter people doing it. Just a theory.

4. Why would tall people have more problems with AFib due to performing endurance exercise? Is it due to the fact that our hearts are the size of the hearts of normal people but have to pump blood for much larger bodies? And by doing endurance exercise, are we burdening our hearts too much? I wish someone had warned me about this before I took up long-distance bike riding, because I've really pushed myself hard over the years (more than I think I needed to). If I had gone slower, and not pushed myself, would I have AFib now?

5. Here's a chicken and egg question that maybe someone knows the answer to: Fibrosis is seen in the hearts of people with lone AFib. Did the fibrosis get their first (say, due to overexercise or some other cause) and cause the AFib, or did AFib cause the fibrosis? If anyone has an answer, I'd love to hear it.

Thanks for any answers people have.

Diane,

This is how God penalizes you for all that good exercise over the years (a little gallows humor):

To answer your questions:

1. I took up running in College, over 35 years average running 3-5 times per week, 3-5 miles per run. I also took up mountain biking in the 90s, we would do "bi-athlelons" consisting of an hour on the mountain bike followed by a 4 miles run. A good workout. My first afib episode was at age 53.

2. I am a male, 6' 1" tall.

3. I recall seeing a study done on a European cross country ski team from the 70s (it was either the Swedish or Norwegian team, can't recall). Thirtry years later something like 30% of them have afib. Statistically way out of the norm.

4-5. I had a procedure in January this year, the Five Box TTM (a more specialized type of Mini-maze) and I have been afib free since the surgery. Post-op, my surgeon, Dr. John Sirak, noted the fibrotic nature of my LA and told me that it was not unusual for chronic exercisers like me to have fibrosis. The implication was that the extended periods of high heart rate exercise caused the fibrosis (I did not ask him about the height angle).

I did ask him whether I should stop all cardio and he said absolutely not, the benefits of cardio out weigh the risks of fibrosis development (however I shouldn't try to run any marathons.)

So welcome to the club.

EB

EB,

Thanks so much for the reply. I'm seeing a new EP next week and will ask him the same question, about fibrosis and exercise, and how much I should scale back.

Just out of curiosity, why did you get the Five-Box TTB instead of an ablation? Based on my reading, ablation appears to be the best procedure so far (although by no means perfect). Isn't the Mini-Maze kind of invasive, and don't you need a pacemaker afterwards?

Diane

Diane,

I had a PVI ablation in September 2009; it reduced my afib burden slightly for a short period but did not correct the problem. I chose the Five Box as the next step due to Dr. Sirak's high success rate (90+%). Based on what he found (the fibrosis) my problem would have been an extremely complicated CA procedure. The fibrosis scatters the electrical signals and the EP is faced with multiple rogue electrical paths. The Five Box handles this by creating concentric "boxes"; multiple ablation lines to cut off the current. It is a similar effect to the COX Maze cut and sew procedure.

Regarding pacemakers, as I understand it, 4-6% have a temporary pacemaker and about 2% of Five Box patients end up with a permanent pacemaker; these individuals typically have sick sinus or some other co-morbidity.

So the order of treatment (my opinion)- 1) drugs, diets, supplements: 2) CA with an experienced EP (most people require 2 procedures); 3) Five Box or Mini-Maze.

If you knew your heart was fibrotic, you could make an argument to go straight to the Five Box after failing drug therapy. This has been debated/ discussed in the past. Another factor in this decision is the FIRM procedure which looks promising but is still a ways out.

Regarding de-training, I am now jogging 4X per week, keeping my heart rate under 145, for 20 minutes per session. Contrast this with 4 years ago, my exercise rate was in the 170s for extended periods of exercise.

Best of luck,

EB

Diane,

I was a competitive swimmer for 14 years and ended my career by competing in two events in the 1968 Olympic games. I am 6' 1".

I was not a distance swimmer, but between 1962 & 1968, I averaged about 2 hours a day in the water, 5-6 days a week (range from 1-3.5 hrs a day). I think the time is more a factor than mileage, but during the heaviest training in the summers, I covered between 6000-9000 meters a day.

Since 1968, I have stayed very fit, but no more swimming and no endurance work beyond 5 K runs. Weights, jogging, walking golf, hiking and a lot of windsurfing.

I am now 67 and had a successful ablation 6 years ago.

The one BIG benefit of a high level of fitness for those with afib, is that afib is more of an inconvenience than a handicap. For the10 years I had afib, the only things I didn't do was run or do weights while in afib, so 99.99% of the time, I lead a normal life, just a little more out of breath when going up a few flights of stairs and occasionally a little dizzy when standing up. I also didn't sleep on my left side while in afib because of the physical sensation of the rapid, irregular heart rate. I averaged about 3 episodes of afib a month that lasted from 2-50 hours each.

If I had known that my swimming would eventually cause afib, I would NOT have done anything differently.

Diane,

I wanted to echo something Ken said- if I had known that my running might cause afib, I still would not have done anything differently. Heart disease runs in my family; my father died of congestive heart failure and every one of his siblings has either passed away from heart related complications or had multiple bypass procedures related to heart disease. Structurally my heart is in very good condition.

It is perhaps a little OCD but I have always felt the benefits outweighed the risks. And I know how good I felt after a big workout (and I still feel good after my smaller workouts today).

So anybody who says "I am not exercising because I might get afib;" is doing some fibbing of their own.

EB

My afib onset began when I was about 52. I had been into longer endurance exercises since I turned thirty - running (for a couple of years), road bicycling in hilly terrain, and mountain biking...all so I could compete in off-road motorcycle races. The most demanding was the off-road motorcycling, which I would do for 1 to 2 hours without breaks, several time a week. I did not understand proper training and used to push hard aerobically for hours at a time. Would I have changed anything? Sure - I wish I knew to moderate a bit more...but I wouldn't have changed anything else.
I'm headed for an ablation in a couple of weeks, and I'm hoping for a one-time fix, but now that I turned persistent, that is less likely to happen.
Tom

Edit: I turn 65 this month.



Edited 1 time(s). Last edit at 10/05/2012 10:59AM by Tom B.

Dianne,

You may be interested in my report Endurance Exercise - Is it worth it? [afibbers.org].

As far as the question "Does afib cause fibrosis or does fibrosis cause afib?" my money would be on "afib causes fibrosis" although just like the question "Does afib cause inflammation or does inflammation cause afib" the answer is not entirely clear. Nevertheless I think it is clear that increasing presence of fibrosis is associated with faster progression from paroxysmal to persistent and permanent afib.

Hans

Diane

1. I played intercollegiate football (US) in college. After that I ran, played raquetball, hiked, biked & etc. For 10 years before I had afib I competed in a race that was 13.3 miles long and topped out at 14,110'. The elevation gain was about 7,850'. I was 49 when I had first episode, now am 57.

2. Male, 6'

3. Around 2005, we did an informal poll here and all the men were athletic and all but two were tall (out of 19). The women were mostly athletic, but not as universally tall as the men. Unfortunately the link to the original survey is broken.

M/F           #Responding  Athletic  Tall  Both
Female              15         11     7      7
Male                19         19    17     17
Total               34         30    24     24

I've controlled my afib pretty well with K+, Mg++ and Taurine supps for 8 years. I use PIP flec when this fails. In the first 7 1/2 years, I used maybe 10 doses of flec (I had a 2.5 month episode, terminated with 300 mg Flec in 20 hours prior to starting the supps). This year has been more difficult. I've had the stress of divorce to contend with - lack of sleep & etc. So I've used maybe 10 doses of Flec in the last 7 months. I recently started an experiment with an enzyme (trade name Vitalzym) to see if I can do something about the fibrosis. It seems to be helping, but it also could be that I'm sleeping and emotionally much better (always hard to control all the variables). I've remained active, however I don't train for endurance activities now. Most of my training is ultra high intensity, short duration (Tabata style). Mostly body weight exercises to failure. This and my ketogenic diet allow me to keep up very easily with my friends who train for marathons when we go hike 14ers' & the like. I don't even breathe hard on top of the mountain. I also rock climb, ski, backpack, hike & etc., so am not a couch potato. I just don't compete or train for endurance.

George

I'm 55 soon to be 56 diagnosed at 52 which seems to be the norm here with athletic types?
My whole life I was working out or playing sports from a young kid biking long distances to the beach, running long distances races my friends and I created to compete with each other., playing basketball literally 24 hours a day from after school centers, night centers,college, High School, every basketball league CYO, PAL etc I could find and pickup games around the city I could find, roller hockey, baseball then would hit the gym for heavy workouts. Last 10 years I concentrated mostly on weights lifting 4 days a week eventually Benching 405 lbs at 50 years old was proud of that. No steroids ever too. I was told by some friends I got to know to slow up before I'd get a heart attack....HA! Soon after afib hit! I'm 5'11' weigh about 205 lbs. Hmmmmm me sees a pattern here.........

Intracellular Mg deficiency (IC MgD) --> cardiac fibrosis --> AF --> more fibrosis --> more AF --> more fibrosis --> etc...
Aerobic exercise --> oxidative stress --> cardiac inflammation --> furthering the MgD / fibrosis / AF process.

Source:

Magnesium deficiency and fibrosis in AF [www.afibbers.org]

Proarrhythmic potential of fibrosis [spo.escardio.org]



Edited 2 time(s). Last edit at 10/06/2012 02:24PM by Erling.

Thanks for all your replies. Let me respond:

1. There is little heart disease in my family (none whatsoever in my mother's side of the family, she had 7 siblings all with very healthy hearts, many who lived into their 80's and 90's and one, who's still alive in his mid 90's (albeit with Parkinson's disease). She died at 81. My dad was skipping heartbeats so at age 72 they installed a pacemaker on him (the diagnosis is brachycardia), but had no other symptoms at the time other than noticing a skipped heartbeat here and there. His father died of a heart attack at age 56, but other than that there's not a lot of heart disease on his side of the family.

However no relatives on either side have done endurance exercise the way I have.

2. I read the article "Endurance Exercise - Is it worth it?" Thanks for the article. I'm glad it gives advice about what to do if you're an endurance athlete diagnosed with AFib, and mentions that "deconditioning" should help. Interestingly, I took two vacations this year (one 5 days, one 9 days, during which I did no endurance exercise) and my AFib mostly went away during those trips. At the time I attributed it to not being stressed at work, but now I realize that taking a break from the long bike rides might have something to do with it.

3. For me, if I'd known the long-distance bike rides could cause AFib, I'm not sure what I'd do. At the very least I never would have pushed myself as hard as I have. I ride with my husband, and in the past, he'd get on my case if I rode to slow (he's faster than me) and would frequently complain I was too slow (he liked us to stay together). If I had to do it over again, I would have insisted we ride separately, when participating in group rides or bike tours (like a lot of other married couples we know do) so he could ride at his speed and I could ride at mine. It's possible I wouldn't have gotten AFib if I hadn't pushed myself as much as I did over the years. Another thing I definitely would have done differently if I had it to do over again would be to take regular magnesium supplements and get my RBC magnesium checked annually. I'm sure it was low (I'm on magnesium supplements now, but with the likely fibrosis I have, it probably won't stop my AFib).

4. This brings up a question: Does endurance exercise cause AFib because endurance exercisers let their magnesium levels get low? If you do hard endurance exercise over the decades, but take magnesium supplements regularly and don't let your RBC magnesium get low (get it checked) can you avoid AFib and other heart problems completely? I suspect you can. But it would require research to know for sure.

I sure wish I had known about the importance of having my magnesium checked and, at least, taking supplements. It could have saved me a lot of trouble.

Hans, thank-you for an extremely thorough and interesting article. After reading it, I am still wondering just precisely WHAT would be a vigorous & or prolonged run that might make my lone AF worse, and WHAT would be a moderate run that would help me avoid other heart and health problems (and have fun!) However, I suspect no-one has attempted to research this 100 dollar question. I am reluctant to scale back my already modest running too much, as I have kept long-term records and I can find NO link between my training sessions or races and my AF incidents, which with one exception have always taken place on waking from sleep, quite often after a couple of days without training. Also, I have recorded my waking and resting HR for many years and again there is NO correlation between HR and AF incidents.

How do I weigh up the possible damage done by a 5K where I try to run my fastest (not actually very fast at all) against 10 miles run more slowly? Is the damage in the time spent on my feet or the HR reached / sustained? Is perceived effort / distress a good guide to what is happening to my heart? I would very much appreciate any comments.

Hello, Diane, I haven't any answers for you but I'm very grateful to you for raising this topic, which is very important to me. I am 70, 5'9-10". My running training is rather modest - 20 miles is a very good week for me - but it is extremely important to me. I also weight train ideally 3 times a week for an hour, but that unfortunately gets neglected in the Summer when I do more mountain walking.

You might like to look at Dr John Mandrola's blog, if you haven't already.
[www.drjohnm.org]
I imagine he is summarising many studies you have already read. Elsewhere he more often emphasises the heart- unhealthiness of obesity and inactivity, and he is a keen racing cyclist who has himself experienced one episode of AF (and written about it).
I would like to set against all these rather frightening studies the work of Paffenbarger, who found in his very long-term studies that exercisers lived much longer than non-exercisers. I don't think he separated out the "excessive" exercisers from the moderate. Perhaps we could do with reminding ourselves that AF doesn't often kill people (yes, I know our risk of stroke is higher than normal), whereas heart attacks and heart disease frequently do

Diane,

" Does endurance exercise cause AFib because endurance exercisers let their magnesium levels get low?"

This is probably part, but may not be all of the equation. There is also the issue of genetics. There was a Cleveland Clinic study done in 2003. They looked at cadavers with and without a history of afib. My recollection from a more detailed version of the study is that 4/4 afibers had pacing cells in the pulmonary veins and the non-afibber did not. Not a huge study, but telling. This may explain why not all endurance exercisers get afib.

Certainly for me, keeping my Mg levels up is an important strategy. However, I can exercise long and hard enough to override my supplementation. I try to avoid doing this, now.

George

George,

Patrick Chambers, MD discussed the Cleveland findings in his article P cells and potassium [afibbers.org]

Hans

IMO we are focussing too much on the possible ill effects of exercise here. Because I am 70, most electrophysiologists would automatically put me immediately on to Warfarin and beta blockers. The fact that when I take even a modest one off dose (5mg) of Bisoprolol my HR for the 2 succeeding days is stuck at about 77bpm, so that it is uncomfortable for me even to walk upstairs, would interest them not at all. However, because I run regularly and performed well on 2 exercise stress tests my cardiologist felt justified in risking putting me onto Flecainide. It is early days yet, but so far I feel normal, have had no further AF episodes, and am able to exercise. I don't know if my AF is linked to exercise. Lots of inactive people also get it. I do know that being reasonably fit has won me a more acceptable treatment.

Exercise and Arrhythmia

I’d like to direct you to a report titled “Correcting Magnesium May Prolong Life” by William J. Rowe, MD, that was referenced in a magnesium thread (General Health Forum) not long ago and to share with you excerpts from several of many very important observational articles by Dr. Rowe.

Last February, when that observational report first circulated, I began following the various related links related not only to that report but to the many exercised-induced, heart-related problems reported Dr. Rowe which then link to a wider scope of other informative links.
[www.femsinspace.com]

Since so often we have new readers looking for arrhythmia help who also report they are endurance runners or exercisers, Dr. Rowe’s research reports investigating magnesium deficiencies in world-class athletes are highly informative and relevant to this thread as well.

Dr. Rowe is a physician involved in research studying the detrimental effects of space travel for both humans and animals and is not only an MD, but a Fellow British Interplanetary Society (FBIS) member. (Bio link follows)

The entire original report is definitely worth reading since, once again, it confirms the important role of magnesium and which segues right into all the previous Conference Room discussions on fibrosis formation being the result of magnesium deficiency and a cause for not only arrhythmia but other heart function problems as well.

Dr. Rowe says, “Since microgravity accelerates the aging process, the loss of the functional capacity of the cardiovascular system in open space flight is over ten times faster which not only means specific care and attention to space travelers, but also a type of ‘fast forward’ look at what eventually happens to us here on Earth at a much slower, but inevitable pace. It takes a huge amount of effort and medical detail to ensure that those in space remain healthy.”

Dr. Rowe’s microgravity observations confirm the strong need for magnesium’s protective properties as an antioxidant and calcium channel blocker against the adverse effects in space; i.e., oxidative stress, insulin resistance, inflammatory conditions in space with animals showing significant endothelial injuries and mitochondrial damage…..not all that different from what we encounter here in everyday life.

Following are a few quotes/clips from many of the very interesting observational reports. Hopefully, you’ll be inspired to continue reading.

Jackie

Each Marathoner is Different
William J. Rowe M.D.
Daily Progress, Charlottesville, Virginia, Jan. 25, 2012

The recent encouraging article in the Sunday issue (Jan 15, 2012) citing a New England J. of Medicine paper, I believe, is somewhat misleading with the concluding statement that since the incidence of sudden death is very low among those participating in marathons, it follows that this is a reasonably safe proposition.

My concern is this: although the incidence of sudden death during this single event is extremely low, might there not be recurring asymptomatic injuries, during or immediately after such events? “ Silent ischemia “ (an imbalance between oxygen supply and demand ) is a huge problem in Cardiology and provides a rationale for example for performing exercise stress and invasive tests.

Granted we have the genes for long distance running based on the fact that the Navajo, Tarahumara Indians, Bushmen of the Kalahari desert, and the Aborigines all have the capability of chasing an antelope for up to 2 days until the animal drops from exhaustion. But with my having published in 1992 a LANCET study of Sy Mah, the Guinness Book of Records holder for having completed 524 marathons, free of any cardiac symptoms despite findings at autopsy consistent with permanent injury to the normal heart , I am concerned that prospective marathoners will develop a false sense of security.
Continue: [femsinspace.com]

Extraordinary unremitting endurance exercise and permanent injury to normal heart
WILLIAM J. ROWE, MD
The Lancet, Vol 340 VOL 340: SEPT 19, 1992, pp. 712-714

(selected quotes)
This hypothesis is that permanent cardiac injury could develop in some endurance athletes despite the absence of coronary atherosclerosis and ventricular hypertrophy. The proposed mechanism by which this injury could arise involves two physiological "vicious cycles". The first vicious cycle would occur between severe ischaemia and high catecholamines, the second would be between coronary vasospasm (induced by high catecholamines) and endothelial injury. The likelihood of the injury becoming permanent might increase if there is insufficient time between bouts of endurance exercise for regression of ischaemia and endothelial repair. Furthermore, magnesium ion deficiency, which can be induced by exercise, could exacerbate these vicious cycles and also contribute to catecholamine-induced thrombogenesis. In addition to ischaemia, there are several mechanisms, including the effect of free fatty acids liberated by the lipolytic effect of high catecholamines, that could cause direct myocardial injury.

Introduction
Early man's survival before the development of even the crudest of weapons probably depended on his capacity for great endurance. This capacity is exemplified today by the Tarahumara Indians of northern Mexico who can chase a deer for up to 2 days until the animal drops from exhaustion.[1] Primitive hunting societies follow a "Palaeolithic rhythm" of 1 or 2 days of hunting, 6 to 8 hours a day, followed by 1 or 2 days of rest.[2] Could some endurance athletes benefit by this restraint? In the past 2 decades, there has been a sharp increase in the number of extremely challenging endurance events. Such events include the world's longest annual ultramarathon (over 1000 km) in Australia, and in the USA the most arduous yearly marathon, to Pike's Peak (4300 m). The cavalier attitude to the potential cardiac risk may result partly from the popular belief promulgated by Karvonen and cited in a widely circulated textbook of the heart,[3] that there is no evidence that strenuous athletic activity in a trained individual with a normal heart increases the risk of early death or morbidity from cardiovascular disease.

Morbidity related to endurance exercise
The case of a fatal myocardial infarction in the absence of significant coronary atherosclerosis reported by Green et al[4] in a runner nearing the end of a marathon was complicated since the athlete probably also had heat stroke.[5] Acute pulmonary oedema developed in 2 apparently healthy participants near the end of the 90 km Comrades Ultramarathon in South Africa. Follow-up studies revealed that the athletes' coronary arteries were angiographically normal and that there were no other apparent confounding factors[6]
With regard to a permanent cardiac injury, Sy Mah, who set a world record of 524 marathons, was shown by stress tests to have probable exercise-induced coronary vasospasm with circadian variation 9 months before death from lymphoma at age 62 years. There was no history of heat stroke,[4,5] nor were any other confounding factors found at necropsy, which revealed focal fibrosis of the left ventricular papillary muscles. It was postulated[7] that these findings were related to exercise induced high concentrations of catecholamines.[8]

Magnesium deficiency and thrombogenesis
Magnesium ion deficiency is a further possible complication of long exercise,[18-20] some deficiency may still be present 3 months later.[18] The mechanism is not clear, but may be partly due to removal of free magnesium ions from the circulation by chelation with catecholamine-induced free fatty acids.[19]

Exposure to heat also contributes to magnesium ion deficiency.[20] This deficiency increases release of catecholamines,[21] increases the potential for coronary vasospasm,[22] potentiates the vasoconstrictor action of catecholamines,[22] and—in combination with catecholamine infusions or stress—sensitises animals to myocardial necrosis.[23]

Magnesium ion deficiency may precipitate a hypercoagulable state,[23] which may be aggravated by residual increased catecholamines (conducive to platelet aggregation and thrombin generation),[24] the increase in catecholamine concentration may persist until the second day after a marathon.[25] It is noteworthy that in a group of 20 patients with vasospastic (variant) angina Goto et al [26] showed that almost half had magnesium ion deficiency that is often unrecognised.[19,21,26]
Continue reading: [www.femspace.com] for this report and the many other related articles at these links: [www.femsinspace.com]

A World Record Marathon Runner with Silent lschemia without
Coronary Atherosclerosis*
William Rowe, M.D.
A 62-year-old world record marathon runner was found to
have silent ischemia manifested by a very abnormal stress
test, whereas at autopsy nine months later, there was
virtually no coronary atherosclerosis nor other disease of
the coronary microvasculature. However, there was focal
fibrosis of the papillary muscles consistent with remote
ischemia secondary to possible CV. It is postulated that
endurance-related high catecholamine levels might have
been responsible.
(the pdf version of this article has a graphic color photo of fibrosis in the ventricle.) [journal.publications.chestnet.org]

American J. Cardiology 86:256, 2000
Our Ancestors Had It Right
William J. Rowe, MD
Swanton, Ohio 28 March 2000
The absorption of just the right amount of iron through the intestine (duodendum) might have provided significant cardiovascular advantages to early man, the Masai of today, and conceivably has been advantageous to an extraordinary urban athlete. Excess iron may be more detrimental than iron deficiency, because high iron levels can lead to the formation of highly reactive hydroxyl radicals and lipid peroxidation, conducive to early atherosclerosis. Furthermore, there must be enough protein in the diet to sequester iron.(1)
But can we, with our modem diet and often iron supplements, establish a proper balance?
Continue: [www.femsinspace.com]

Potential Myocardial Injuries to Normal Heart with Prolonged Space Missions
Selected quotes:
(Animal) Studies by the Russians, of experimental animals in space, demonstrated pronounced impaired microcirculation and serious myocardial pathology, even on space flights of only a few weeks. Edema of the endothelium was demonstrated, with altered endothelial permeability, and some of the coronary vessels were completely occluded. There was also noted atrophy of the cardiac muscle. Other studies suggested the possibility that some of these changes were stress-related, since there was significant increase in the concentration of norepinephrine in cardiac tissue. Finally, in addition to decreased activity of enzymes with injury of the mitochondria, there was evidence of impairment in the repair mechanism.5 These animal studies suggest that even relatively brief space missions, may predispose to a myocardial infarction in the absence of coronary artery disease prior to the space flight.

Mechanisms for Endothelial Injury
Too much or too little exercise may damage the endothelium through similar mechanisms.4

High shear stress and turbulence, precipitated by catecholamine-induced coronary vasospasm may injure the endothelium and in turn lead to further vasospasm by a vicious cycle. High catecholamines, with release of high levels of free fatty acids, which bind magnesium ions, may persist by ongoing vicious cycles as well. A third vicious cycle can be precipitated by elevations of catecholamines related to ischemia. These mechanisms can injure the normal heart from extraordinary unremitting endurance exercise.2,3
Continue:[www.bad-radkersburg-online.at]
William J. Rowe, M.D.
Former Clinical Assistant
Professor of Medicine
Medical College of Ohio at Toledo

(as reported in CR 74 on fibrosis)
Fibrosis in heart disease: understanding the role of transforming growth factor-beta in cardiomyopathy, valvular disease and arrhythmia.
Khan R, Sheppard R.
Source Immunology. 2006 May;118(1):10-24.
McGill University, Faculty of Medicine, Montreal, Quebec, Canada.
Abstract
The importance of fibrosis in organ pathology and dysfunction appears to be increasingly relevant to a variety of distinct diseases. In particular, a number of different cardiac pathologies seem to be caused by a common fibrotic process. Within the heart, this fibrosis is thought to be partially mediated by transforming growth factor-beta1 (TGF-beta1), a potent stimulator of collagen-producing cardiac fibroblasts. Previously, TGF-beta1 had been implicated solely as a modulator of the myocardial remodelling seen after infarction. However, recent studies indicate that dilated, ischaemic and hypertrophic cardiomyopathies are all associated with raised levels of TGF-beta1. In fact, the pathogenic effects of TGF-beta1 have now been suggested to play a major role in valvular disease and arrhythmia, particularly atrial fibrillation. Thus far, medical therapy targeting TGF-beta1 has shown promise in a multitude of heart diseases. These therapies provide great hope, not only for treatment of symptoms but also for prevention of cardiac pathology as well. As is stated in the introduction, most reviews have focused on the effects of cytokines in remodeling after myocardial infarction. This article attempts to underline the significance of TGF-beta1 not only in the post-ischaemic setting, but also in dilated and hypertrophic cardiomyopathies, valvular diseases and arrhythmias (focusing on atrial fibrillation). It also aims to show that TGF-beta1 is an appropriate target for therapy in a variety of cardiovascular diseases.
PMID:16630019
[www.ncbi.nlm.nih.gov]


REFERENCES:

Original Report:
Correcting magnesium deficiencies may prolong life.
Rowe WJ.
Clin Interv Aging. 2012;7:51-4. Epub 2012 Feb 16.
Source: Medical University of Ohio at Toledo, Ohio, USA.
[www.ncbi.nlm.nih.gov]

Short Biography of Dr Rowe
William J. Rowe M.D. FBIS (Fellow British Interplanetary Society ) is a board certified specialist in Internal Medicine. He received his M.D. at the University of Cincinnati and was in private practice in Toledo, Ohio for 34 years. During that time he supervised over 5000 symptom – limited maximum hospital-based treadmill stress tests. He is a former Assistant Clinical Professor of Medicine at the University of Ohio, School of Medicine at Toledo. He studied 3 world class extraordinary endurance athletes and published their exercise –related magnesium deficiencies. This triggered an 18 year pursuit of the cardiovascular complications of Space flight. He has published in LANCET that extraordinary, unremitting endurance exercise can injure a perfectly normal heart and in CIRCULATION a description of only the second Space-related Syndrome. He has been listed in the Marquis Who’s Who of the World from 2002-2009, 2013. [www.femsinspace.com]

Jackie, if Sy Mah did not die of a heart related condition and was not suffering heart related symptoms when he died, can it be that the fibrosis found in his heat was not such a problem after all?

Two more data points:

1. The famous marathon runner, Alberto Salazar, collapsed from ventricular fibrillation when it was reported he had a heart attack a few years ago (I read his book). There was some atheriosclerosis (cardiovascular disease runs in his family) but not nearly enough to explain his heart stopping. It was likely a ventricular arrhythmia.

2. Caballo Blanco, an American who essentially joined the Tarahumara tribe and ran like they did, recently was found dead. They did an autopsy and found he likely died of a heart problem. He ate like the Tarahumara (very healthy, mostly plant-based diet).

Interestingly some of those articles mention the possibility of valve problems from endurance exercise. That happened to a good friend of mine, who can't be any older than his early 60's. He just had to have a heart valve replaced, which involves open heart surgery and a very long recovery time (at least a year). He was very unhappy about that, as he liked to go on long bike rides. He'd had the surgery about 6 months ago when I last saw him, and he'd put on a bunch of weight because he wasn't able to bike ride. I asked him if the doctor said that bike riding could have caused his valve to fail, and he said No. But from reading the articles (and others I've read) that does seem possible.

Interestingly, the doctor told him his arteries were clearer than anyone else he'd seen at that age so he had no trace of cardiovascular (artery clogging) disease.

Alexandra...

Fibrosis in any organ is not good. The more fibrosis, the more functional interference--.not only the heart, but kidney, lungs, liver, breasts, uterus, skin, intestines, joints, etc. Just because Mah died at 62 from another cause (cancer) doesn’t mean that had he lived longer, that the fibrotic buildup would not have eventually caused significant problems. Fibrosis is aptly called The Enemy of Life since it increases with age without preventive measures. Further, chronic inflammation and oxidative stress is a major cause of age-related disease and cancer

The main point here is what’s predictable over time--thanks to that fast-forward look at the negative impact of microgravity on astronauts which gives us a preview of what happens to us here on earth at a much slower but inevitable rate. So, from the Fibrosis Conference Room discussions, the science says magnesium deficiency promotes fibrosis. Therefore, the title of Dr. Rowe’s report meshes nicely with what’s important for everyone (especially afibbers) at all levels of activity, but most specifically, heavy exercisers. We all should welcome the potential to lengthen a healthy aging process. Keeping fibrosis out of the heart should be everyone’s goal. But, first, it takes awareness.

Jackie


This reference list has some interesting links....
[1] Vilenchik MM, Knudson AG. Endogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer. Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12871-6. [pmid.us].
[2] Cooper MB et al. The effect of marathon running on carnitine metabolism and on some aspects of muscle mitochondrial activities and antioxidant mechanisms. J Sports Sci. 1986 Autumn;4(2):79-87. [pmid.us].
[3] Neubauer O et al. Exercise-induced DNA damage: is there a relationship with inflammatory responses? Exerc Immunol Rev. 2008;14:51-72. [pmid.us].
[4] Braidy N et al. Age related changes in NAD+ metabolism oxidative stress and sirt1 activity in wistar rats. PLoS One. 2011 Apr 26;6(4):e19194. [pmid.us].
[5] Sipos I et al. Quantitative relationship between inhibition of respiratory complexes and formation of reactive oxygen species in isolated nerve terminals. J Neurochem. 2003 Jan;84(1):112-8. [pmid.us].
[6] Safiulina D et al. Dehydroepiandrosterone inhibits complex I of the mitochondrial respiratory chain and is neurotoxic in vitro and in vivo at high concentrations. Toxicol Sci. 2006 Oct;93(2):348-56. [pmid.us]
[7] Gastman B et al. A novel apoptotic pathway as defined by lectin cellular initiation. Biochem Biophys Res Commun. 2004 Mar 26;316(1):263-71. [pmid.us].
[8] Ambros-Rudolph CM et al. Malignant melanoma in marathon runners. Arch Dermatol. 2006 Nov;142(11):1471-4. [pmid.us].

Diane - as discussed in CR 74, fibrosis is a natural, protective response to the inflammation and oxidative stress that accompanies endurance exercise and if it forms in the heart, it certainly has the potential to affect valve function.
Jackie