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]