Re: Aerobic Exercise

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Posted by steve giddings on October 26, 2002 at 13:21:48:

In Reply to: Re: Aerobic Exercise posted by L. Paul Teague on October 25, 2002 at 20:26:16:

"that increased pressure in the heart's chambers stretches the upper chambers of the heart, the same way that blowing into a balloon makes it exand. As the heart muscles stretches, fibers that conduct electrical impulses may fray of break, setting the stage for the electrical chaos known as atrial fibrillation." Steady state exercise causes the heart to expand, so this may explain the unusual frequency of lone AF in aerobic exercisers."

There are several statements here that are not particulary well documented. The heart enlarges in different ways in response to different stimuli. Atrial enlargement in the diseased heart occurs because the ventricular heart wall becomes thickened and stiff, either because it is pumping against an increased pressure load (hypertension), a limiting orifice (valvular heart disease or is damaged by lack of blood flow (ishemic heart disease). These are the most common causes, there are others. The end diastolic (between beats) pressure in the ventricle rises as a result, passive diastoic filling is compromised (in the mnormal heart, when the ventricle relaxes actively during early diastole it actually sucks blood into it from the atrium) and the atrium has to work harder in turn to push blood into the ventricle against a pressure load. Ventricular stiffening also occurs with aging and the atrial "Kick" becomes more important. This is one reason why af is more common in older people and why old people are more symptomatic with a fib, their hearts work less efficiently with af.

Aerobic exercise does not increase end diastolic pressure. If anything, it decreases and passive filling becomes proprotionally greater. The ventricular volume increases, but the heart muscle itself does not become thicker. As the ventricle enlarges in this setting, blood flow to it increases, the number of capillaries per muscle fiber if anything increase, and the ability of the heart muscle to extract oxygen from the blood and convert it into energy also increases. The atria increase in size modestly, to deliver an increased amount of blood per contraction to the ventricles. There is no evidence anywhere that atrial fibers fray or break in this setting. Scarring and alteration in electrical conductivity, the substrate for atrial fibriallation occurs as a result of ishemia, inflammation or other insult. Free radicals may play a roll in these processes, but lots of folks have been working many years to prove this and have not been able to. The recent HOPE trial, which looked at the effects of vitamin E (a free radicle scavenger) had no benefit on cardiac endpoints in this huge study.

The increase in atrial size alone, however, may make a fib more likely to occur in response to some other insult.

I basically agree that af may be more likely to occur in folks with hearts that are larger because of chronic endurance training. Remember, however, that the risk is much greater for af in folks with hypertension (the most common putative cause) and ischemic heart disease. Both of these occur more frequently in non-exwercisers.

The only reason I make such an issue of all this is because I don't think that we are doing anyone a favor by encouraging a sedentary lifestyle for fear of A fib.

I also had the MAZE procedure about 4 years ago, and don't regret it for a minute. It had a profound effect on my well-being and I am most grateful to Dr. Cox and all the folks at Georgetown who helped me through the process.

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