I experienced the same condition of reduced heart rate while exercising during a time when I was taking beta blockers. In my case, I was able to sustain the same power output with an average heart rate of 120 that would usually require a heart rate of around 140. What was lost, however, was the upper end power. My sustainable heart rate for over 30 minutes was 157. With beta blockers I could never reach the same power output.
I suspect that with the lower heart rate, there is more complete filling of the heart chambers or more blood volume per stroke which helps to compensate for the reduced rate.
Last July I completed a catheter ablation and have not had any symptoms since the procedure. I have discontinued all meds and returned to my former level of exercise. The EP told me not to worry about elevated heart rate (over 170 in my case) but that does not answer your question about enlargement or structural problems.
Thanks for the reply. Excellent news on your ablation. My cardio has mentioned the possibility of ablation but he says the results are far from guaranteed and suggests I stay with the drug therapy as it seems to be working well.
I don't know why your are taking both Sotalol (an anti-arrhythmic drug) and a beta blocker. Do you suffer from high blood pressure?
When I was still on a work-out program I found that sinus rhythm and anti-arrhythmic drugs resulted in may HR being very predictable and reasonable... I was working typically up to 150 bpm, but tried not to sustain a HR that high. During these times I was in NSR, no AFib. When I go into AFib it is full-time/permanent. That's where I am at the moment, and I am on Metoprolol now (a BB) to lower my HR. I don't push (run) my HR and haven't in the last two years+.
Some years back I was in NSR with just Toprol (a BB) and while my overall HR was lower, it was not real low. Best I can recall it was 60+ at rest and would run fine at 150 if I was working at a constant level. I was a runner/jogger, so I had regular experience with holding a target HR for a half hour or so, I usually quite/slowed-down at 3 miles.
No sure I have helped, but maybe my questioning why you are on a BB is worth something.
Jerry, thanks for your response. I'm taking only Sotalol, nothing else. Sotalol is actually a non-selective beta blocker. It is also a potassium channel blocker and is therefore a class III anti-arrhythmic agent. I was originally on Bisoprolol, a pure beta blocker, but it controlled the rate but not the arrhythmia. Both suppress my heart rate. In fact, the Sotalol, even at the low dosage I am on, puts me into the mid 40s during the day. Feels kind of plodding at times but my blood pressure stays normal and I have no dizziness so I guess it's ok.
I believe this might be what you're looking for, Bob:
Oxygen Uptake Kinetics and
Cardiopulmonary Performance in Lone
Atrial Fibrillation and the Effects of
"As oxygen pulse (which reflects stroke volume) is normalized after
sotalol; this suggests that our patients without signifi¬
cant structural heart disease are able to utilize the
stroke volume reserve to compensate the negative
inotropic and chronotropic effect of sotalol."
So, it's as smconorm says. And that would seem to allay any concern about LVH, since the heart is not contractong harder (which wouldn't t increase stroke volume anyway) - and besides they specifically mention the inotropic effects of sotalol.
Hope that might help.
Thanks NTB. Interesting article and it does alleviate my concerns about the potential for LVH due to the inotropic effect of Sotalol and beta blockers in general. That's good to know. That said, the study doesn't exactly address my situation as it was done on people who were actually in a-fib during the tests (two of them actually cardioverted during the study - lucky them). My question about training levels actually relates more to the effect of Sotalol on heart efficiency in people like me whose afib is controlled (or who don't suffer from it at all) and who are in NSR during their workouts. As an aside, I really can't exercise during a-fib episodes and I actually find it difficult to imagine doing so as my heart rate would go through the roof.
From my standpoint, as an a-fib sufferer, one of the study's conclusions - that "Despite an exaggerated exercise heart rate, Vo2 kinetics, cardio pulmonary performance, and maximal exercise capacity are impaired in patients with AF even without significant underlying heart disease..." - seems self-evident. :)