The problem of atrial fibrillation is found to be aggravated by obesity.
Obesity contributes to hypertension but also to cardiac load. If one weighs 200 pounds the heart has to circulate more blood and there is also an increase in total vascular resistance. More pipes, longer pipes, more load than if one weighs 150, so cardiac problems like heart failure and cardiac rhythm disturbances can be expected to increase.
Here’s a link to a study that makes sense.
http://acsh.org/2013/11/drug-free-way-reduce-palpitations-dangers-fib/
Venous return doesn’t have much if any impact on cardiac status. It’s a passive, low pressure return on the order of 10 cm of water pressure in the major veins entering the heart. Can cause dilatation of the right atrium which will increase the chance of atrial rhythm problems. However muscle and condition increases in return normally doesn’t cause right sided increases in pressure, usually caused by pulmonary congestion from left side failure or a valve problem on the right side of the heart, or essential pulmonary hypertension, that can develop for no known reason, intrinsic lung disease , and even from sleep apnea, which is a sneaky pete disease.
The big work is done by the left side ventricle (lower chamber) against arterial circulation, which is high pressure. If the left side isn’t working well causes pulmonary congestion and hypertension, also results in dilated heart from cardiomyopathy or hypertrophy from adaptation. Dilated hearts are prone to arrhythmias. Hypertrophic (muscle over development) hearts are also prone to rhythm problems and relative hypoxia (inadequate oxygen).
The coronary artery disease that causes myocardial infarctions is not so much related to stress and demand except that it becomes symptomatic when the heart is working harder and can’t get enough oxygen. The coronary lesions are caused by a different process. Make sense?
Right you are, and I don’t know how big his heart was.
I was wrong.
Glenn Cunningham was a remarkable US runner in the thirties and came close to 4 minutes, never under, except maybe one performance in high school that was not official.
He had burned legs as a child and was a candidate for amputation, but rehabilitated them and overcame the handicap/disability by running, eventually becoming the best middle distance runner in America for a period of years in the 30s. Great story, big heart.
Roger Bannister was a wonderful story and a classy guy for sure. I didn’t disturb his legacy with my mistake, but thanks for correcting me.
I thought that Rodger Bannister was the first 4 minute miller.
Theoretically there would be an increased work load, more resistance but there is a genetic/hormonal predisposition to hypertension and probably hypertrophy. for example Glenn Cunningham, the first 4 minute miler had a very big heart that went very slow. There is an adaptive cardiomegaly/hypertrophy that causes an increase in stroke volume.
However hypertension is not consistently a result of increased body mass since it is multi factoral, so it is hormonally affected by the renin angiotensin kidney cotrol system that is not caused by obesity or increased body mass. There are other autonomic factors that have to do with adrenergic receptors, for example some people are what we call hot reactors, their blood pressure jumps up or their circulation fails with stress or fright–some get red and hypertensive, some faint.
My experience and the experience of cardiolgists I talk to is that for more than one reason obesity results in congestive heart failure and hypertension and obesity related cardiomyopathy is probably hormonally affected in addition to the systemic vascular load problems and the effects of hypo ventilation, which is, in its extreme forms, enough to cause pulmonary hypertension (hi blood pressure in the pulmonary vessels, and chronic hypoxia. Such things will result in cardiac disease just from bad oxygen at night.
Obesity definitely impacts glucose metabolism so there’s a diabetes factor too.
Don’t you just love all the uncertainties in medicine. Great hiding place for a imprecise thinker like myself.
“….body builders are in danger as well, yes?”
Unless more muscles also assist the heart in some way, by perhaps squeezing veins in the correct direction? Just Guessing…
If more arteries and vessels increase load and stress, then body builders are in danger as well, yes?
output demands don’t cause valve disease, but they can make valve disease more symptomatic.
as for the question of what causes more problems, muscle or fat, the heart don’t know nothing, just pumping.
if your body mass is made by muscle you can still suffer from relative increases in output demand, with other factors unknown like xoygenation from stronger muscles and ability to inhale, as a simple example.
stupid tissues and muscles don’t say–wow we inhabit a well conditioned body—-unless the well conditioned body provides a more favorable environment for stupid tissues.
It’s hard to know if a greater body mass contributes to problems like valve disease or rhythm disease, or if greater body mass just makes the symptoms and maybe the outcomes worse.
Note I used “greater body mass.” Muscles and their related structures also have blood vessels and we can probably argue quite a lot about the difference in circulatory situations between a 200lb 18% body-fat man and a 200lb 7% body fat man.