Afib and exercising

[www.washingtonpost.com]

As the paper [academic.oup.com] that PC links in his post in the thread below this one notes, exercise helps most people with afib. However those, especially males, who are at the far end of the intensity/volume spectrum can be damaged by exercise. As I've posted before, for me the trigger is the product of intensity times duration. I've found that limiting my intensity on exercise sessions of longer duration to Zone 2, MAF (180-age heart rate) or only nasal breathing (described in links in my linked post), seems to mitigate the issue. These 3 limits are qualitatively similar and are designed to keep you in a pure aerobic zone. My doc friend, Mark Cucuzzella, who has used MAF training for 20 years, says he always comes back feeling better, not wiped out, from a workout. He says he always feels like he's "loafing" during a workout.

There seems to be two issues. One, the paper doesn't define "remodeling with intense exercise"., In other words, what is intense and for how long. It assume that athletes that trained at a very high level for years are more susceptible to afib than normal people. I am one of those and maybe that explains why am here sharing information. But what about the recreational exerciser that trains at a moderate to high level and competes in races like biking and running? Are they more susceptible to afib? I guess there aren't any studies that have suggested or defined a point where afib becomes more prevalent when training for recreational type endurance sports.

Two, when I was experiencing afib ( for11 years before my first ablation), I never found intense exercise to be a trigger.

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Ken
There seems to be two issues. One, the paper doesn't define "remodeling with intense exercise"., In other words, what is intense and for how long. It assume that athletes that trained at a very high level for years are more susceptible to afib than normal people. I am one of those and maybe that explains why am here sharing information. But what about the recreational exerciser that trains at a moderate to high level and competes in races like biking and running? Are they more susceptible to afib? I guess there aren't any studies that have suggested or defined a point where afib becomes more prevalent when training for recreational type endurance sports.

Two, when I was experiencing afib ( for11 years before my first ablation), I never found intense exercise to be a trigger.

In PC's linked paper:

"Women showed a more pronounced risk reduction with activity than men, as well as a protective effect over the entire range of physical activity levels examined, with statistically significant reductions in AF risk up to 2500 MET-min/week. For men, however, increasing physical activity was only protective against AF to a level of 1500 MET-min/week; beyond that, the protective effect was lost. Furthermore, there was a statistically significant interaction between sex and vigorous activity effects. In women, a beneficial anti-AF effect was observed for vigorous exercise, whereas for men, there was a progressive increase in AF risk with greater amounts of vigorous physical activity, with a statistically significant 12% risk enhancement at 5000 MET-min/week.

Here is one list of MET's by activity.

What PC posted was an editorial comment. When you look at the original paper, you can see these graphs:


These show the increase for men as you get above 1500 MET-min /week. Women seem to get a pass. Also it appears to be the vigorous activity for the men that do not provide a lot of benefit.

That being said, the risk enhancement, 12%, is not strong. I would hypothesize this is because there is a genetic component to this. If you don't have those risk genes (whatever they are), then heavy exercise isn't a risk.

In my case, though I was chronically fit, I was a recreational athlete and my volume/intensity certainly wasn't at the Olympic level, as yours was, Ken.

One issue with this study is they had people fill out a questionnaire once, then follow them through the UK health system for 7 or 8 years.

In my case, short duration intense exercise has not been a trigger. It has been relatively long duration activity, coupled with intensity. For example, one day I decided to see how many laps I could ski off piste on the steeps. I pushed every turn hard, the lift queue had nobody in it, so I did 35 laps in 7 hours, about 47,000' vertical plus a few laps on another lift. That activity proved to provide me with a delayed parasympathetic afib trigger a few hours later. I can routinely ski 30-35,000' vertical on the same terrain without afib consequences. I can also ski over 60,000' vertical on groomed runs without consequences. I am fortunate in that my volume intensity limit is actually pretty high.

George,

I had to look up MET, and now see how the exercise/activity is being calculated.

I guess this should be obvious, and if so I missed it. Is the study correlating a short period of high MET activity (a few weeks or daily) to initiating an particular afib episode? Or is the correlation between those individuals with years of high MET activity (athletes) being more susceptible to afib during their lifetime?

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Ken
I guess this should be obvious, and if so I missed it. Is the study correlating a short period of high MET activity (a few weeks or daily) to initiating an particular afib episode? Or is the correlation between those individuals with years of high MET activity (athletes) being more susceptible to afib during their lifetime?

My interpretation is it is lifetime.

From the study

"Study design
The UK Biobank cohort includes 502 543 community-dwelling individuals, aged 40–69 years, recruited between April 2007 and December 2010. Participants were invited to attend 1 of 22 assessment centres around the UK, where they completed extensive touch screen questionnaires as well as undertaking physical measurements. In this prospective, population study, self-reported physical activity habits formed the primary exposure variable with sociodemographic factors, lifestyle habits, and comorbidities as covariates. This analysis was restricted to the 402 406 participants who completed physical activity screening at baseline. All participants were followed up for health outcomes through linkage to national electronic health-related data sets.

"Methods and results
We included 402 406 individuals (52.5% female), aged 40–69 years, with over 2.8 million person-years of follow-up who underwent self-reported physical activity assessment computed in metabolic equivalent-minutes per week (MET-min/wk) at baseline, detailed physical assessment and medical history evaluation. Arrhythmia episodes were diagnosed through hospital admissions and death reports. "

"Physical activity assessment
Physical activity was assessed at baseline using the self-reported short-form international physical activity questionnaire (IPAQ). The IPAQ questions participants on three types of activity (walking, moderate, and vigorous-intensity activities). From these questions, the total physical activity volume can be computed in metabolic equivalent-minutes per week (MET-min/wk). Additionally, the MET-min/wk within each type of activity (i.e. walking, moderate-intensity, and vigorous intensity) was calculated.

To assess any potential thresholds for risk, we performed analyses using physical activity dose as a continuous exposure variable. To assess the association between vigorous physical activity and arrhythmia risk, the above analysis was repeated with self-reported vigorous physical activity as a continuous exposure variable."



Edited 1 time(s). Last edit at 06/14/2020 06:40PM by GeorgeN.

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Ken
There seems to be two issues. One, the paper doesn't define "remodeling with intense exercise"., In other words, what is intense and for how long. It assume that athletes that trained at a very high level for years are more susceptible to afib than normal people. I am one of those and maybe that explains why am here sharing information. But what about the recreational exerciser that trains at a moderate to high level and competes in races like biking and running? Are they more susceptible to afib? I guess there aren't any studies that have suggested or defined a point where afib becomes more prevalent when training for recreational type endurance sports.

Two, when I was experiencing afib ( for11 years before my first ablation), I never found intense exercise to be a trigger.

This remains an enigma for me. Both parents afibbers, and I'm bicycling for years. My cardiologist said I'm likely genetically predisposed to afib, and riding my bycicle had brought it to day. Despite of that, my heart is 100% normal. No enlargements, normal thickness.
1 hour of moderate exercise, AM or PM, may give me afib in the night. But it does not always happen. And there's no obvious relation between intensity and afib.

My hypothesis is that there is a lifetime exercise exposure, which includes duration and intensity, coupled with a genetic predisposition to afib that leads to afib in those with chronic fitness. Once the afib threshold has been crossed, then exercise may also be a trigger for a delayed episode for those with vagal triggers.

I also hypothesize that if the lifetime exercise exposure were done in a pure aerobic fashion (i.e. Zone 2), then the initial afib threshold may never be crossed. I don't know how this can ever be tested.

I agree with GeorgeN. What I don't understand is, if there is some damage to the heart from chronic fitness, albeit electrical, why does the afib start at night even though the 'damage' is there during the day as well.
I can over exercise during the day and feel great, but I'll probably wake up in afib sometime during the night or even the next evening. Also while I am throwing questions out there; can the heart heal itself after detraining? I am doing much better by detraining, i.e., heart rate < 60% of max, but will it ever go away?

I am hoping this study will answer that question link.

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MikeN
What I don't understand is, if there is some damage to the heart from chronic fitness, albeit electrical, why does the afib start at night even though the 'damage' is there during the day as well.
I can over exercise during the day and feel great, but I'll probably wake up in afib sometime during the night or even the next evening.

For a vagal trigger, the autonomic nervous system is generally more parasympathetic during sleep, while resting and after meals. These are common times for afib initiation in those who are subject to vagal triggers. The exercise can tilt the autonomic nervous system towards being more parasympathetic. Hence, this is why many athletes have low resting heart rates. Early in my afib career, I could terminate an episode by doing something to activate the sympathetic system. Sometimes, exercising during an episode would terminate it. During the time when I was unknowingly over consuming calcium, I was much more sensitive to being vagal. I could sometimes ward off an episode by doing something more vigorous. During this time, for example, the period immediately after orgasm, when the heart rate was rapidly lowering, was a risk period. If I felt PAC's, if I changed my position to be vertical, or get up and move around, it was enough, many times, to ward off an episode.

{edit} - to clarify - exercise will make the autonomic nervous system (ANS) more sympathetic during the exercise, but the long term effect is to make the ANS more parasympathetic after the exercise. I've posted before that after running a race - like running over 13 miles, climbing 7,800' & topping out over 14,000', my resting heart rate would remain elevated over normal for several days. A sympathetic effect and likely an indication of inflammation. Then the resting heart rate would drop below the normal rate. This drop period was an afib risk period for me.

There is quite a bit here written on the effective refractory period. This is the time after a cell depolarizes that it won't get stimulated to depolarize again. See here. Things like the autonomic nervous system can change and shorten (or lengthen) this period. The shorter it is, the more likely a PAC or afib is to happen. This is a search on our site on atrial refractory period. You can read more about it. PC MD can answer in even more detail.

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MikeN
Also while I am throwing questions out there; can the heart heal itself after detraining? I am doing much better by detraining, i.e., heart rate < 60% of max, but will it ever go away?

In my case, no. As I've posted, my strategy is more than just detraining and includes electrolytes. About 15 years ago, I got this pretty dialed in. I had a run of two years without afib. I concluded I was healed. I stopped my supplements. I had afib in 24 or 48 hours. That disabused me of the idea of being healed. Subsequently, I've had experiences where I realized the "wall" separating NSR and afib for me, was pretty thin. As long as I followed my plan, I stayed in NSR, but when I deviated, afib was very nearby. As mentioned above, there was a time I increased my calcium consumption. This was because I was going through a divorce, was eating low carb/keto and thought stress eating wheels of brie was a free pass. Turns out, the extra calcium was enough to make me much more sensitive to triggers. Took me about 15 months to figure this out (after rereading the literature). When I quit the brie, my control went back to pre divorce levels.

As mentioned above, I'm blessed, my exercise tolerance is actually pretty high. I'm sure this is individual. I have to really push myself to exceed my limit and cause afib. Also, in my case, keeping my electrolytes in balance is key to maintaining this relatively high exercise tolerance. Even so, the electrolytes don't give me a free pass to push myself past my limit. During the excess calcium period, the tolerance level was lower. If I miss taking the electrolytes, it can take little or nothing in the way of activity to trigger afib. So for me, it is a combination of factors.



Edited 1 time(s). Last edit at 06/16/2020 01:05PM by GeorgeN.

It's interesting, George. What you describe about the ANS is what happens to me. Meanwhile, I did never succeed stopping an afib episode with exercise.
It's likely that exercise in the day contributes to some lowering of my resting HR, particularly in the hours after midnight. I often wake up between 1 and 3 AM, and everything seems okay, but with a HR at 60 or slightly below. If I can't get back to sleep within a tenth minutes, ectopics may appear and, sometimes, afib.
Before my first afib episode, my current resting HR was around 50.
Since my ablations, my resting HR is higher : 60-65 BPM. It seems it can sometimes be slower... inviting ectopics.
About digestion :
Quiet exercise after meal may prevent ectopics and afib.

GeorgeN, thanks for your valuable info. Without this forum and contributors, I would be left in the dark. It seems my tolerance for exercise has been falling a bit, but at the same time I've been tapering off the magnesium over the last year. After seeing your post, I might try increasing the Mg a bit and see what happens.

Also, my resting heart rate at the start of my afib 2.5 years ago was around 52. I stopped my vigorous exercise and over the course of 6 months it increased to 57, where it is now. I'm wondering if this small increase of 5 beats per minute is what has lowered my afib burden.

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MikeN
Also, my resting heart rate at the start of my afib 2.5 years ago was around 52. I stopped my vigorous exercise and over the course of 6 months it increased to 57, where it is now. I'm wondering if this small increase of 5 beats per minute is what has lowered my afib burden.

In my case, it doesn't appear to be the heart rate, per se. It has to do with the ANS & I really can't measure it. An example is my heart rate dropping after orgasm example from above. It was the decline in the heart rate, not the absolute value. I could have been at the same absolute heart rate at another time, without issue.

Another example. I've had autoimmune issues my whole life. I got an Oura tracking ring 18 months ago. It showed I was getting 0-3 minutes of deep sleep/night (not good). My lowest heart rate over night was typically in the early morning, just before waking up. The Oura folks said optimal heart rate profile was one where it was a broad valley with the lowest rate in the middle of the night. They said my profile was indicative of eating too much, too close to bed or exercising too much too close to bed. I knew that neither of these were true. I was at my wits end as to how to change this. I came across Dr. Arthur Coca's book, written in 1956. The gist of it is that an elevated pulse after eating something is indicative you are sensitive to it. Specifically he suggests taking your pulse (a minute average, which I found to be better than an instantaneous one provided by a device) before eating & then 30, 60 & 90 minutes after. If you see a pulse elevation of more than 6 BPM, he thinks it is indicative you are sensitive to it. Of course, if you are eating a mixed meal, you have to eat things one by one, to figure out what is causing the elevation. I did this and found some things that I was eating with non-subtle pulse elevations, like 15-25 BPM (he says what foods will cause this is different for each person). In April, 2019, before doing this analysis, my average heart rate during sleep on a random night was 63 BPM. I eliminated the most egregious offenders. In May 2019, I had an average heart rate of 45 BPM, without any change in exercise. I had some nights with the lowest rate in the high 30's. I bring this up as you might think this would be risky from an afib perspective. However, it was not. I think the heart rate drop was due to eliminating inflammation rather than creating inflammation, which some exercise regimes can do. I hypothesize this is why it was not risky for me. That it is the inflammation caused by exercise in some cases, that is the issue. By the way, the Oura now says my deep sleep is 30 - 120 or more minutes. A huge difference. I know these trackers aren't perfectly accurate, but comparing against myself, something is happening. Also, my heart rate profile looks much more optimal. My HRV has increased, also.

George:

Does Steve's Ca reduction protocol effect ANS, as far as less issues with VMLAF?

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The Anti-Fib
George:

Does Steve's Ca reduction protocol effect ANS, as far as less issues with VMLAF?

Good question that I don't know the answer to. In my case, I'm not sure that reducing Ca impacted the ANS, it impacted the atrial sensitivity to ANS changes. For example, I've noted that during my high Ca period, the time immediately after orgasm when the heart rate declines rapidly was a risk period. The rapid heart rate decline still happens, it just doesn't translate into PAC's or afib risk.

Maybe it (Ca) shortens the atrial effective refractory period? " Another feature of the electrical remodeling is the accumulation
of calcium within atrial myocytes leading to a further shortening of the atrial refractory period. " From last paragraph, p2 here.

And from PC, MD in the archives " After all many experts feel that increased intracellular Ca is the final common pathway for
electrical remodeling. And why, more than any other supplement, is Mg so helpful? " From paragraph 5, p25 here.

Though PC, MD hasn't been commenting on afib stuff very much as he's ablated and doing well, he's much more qualified than me to comment. I'll see if this will ping him.

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PC, MD
See above.

George, thanks for the ping.
Aloha TAF
I am not aware of any significant direct effect of calcium intake on the ANS.
When I struggled with VMAF, it was all about magnesium, potassium, and hydration. But I think my main problem was the defective substrate.
IMHO FWIW the calcium to magnesium ratio is very important. They compete with each other like sodium and potassium or lysine and arginine.
High levels of calcium decreased tissue levels of magnesium and exacerbates deficiency and decreases magnesium absorption.
The western diet is high in calcium and most of us suffer from magnesium deficiency.
When you look at the three requirements for atrial fibrillation
1) defective substrate
2) autonomic imbalance
3) electrolyte imbalance
I believe the impact of calcium (and magnesium) rests in number three not number two.

Thanks George and PC.

Wow George you have a good memory as to what was written 15-20 years ago.

PC, have you tried the CA reduction protocol to see if it reduces your PAC's?

TAF
That's an interesting question.
Prior to COVID and recognition of the need for D I was only taking 2000 IU of D3 with a 25 (OH)D level of 78ng/ml.
Since upping it to 5000 my bowel tolerance for Mg has increased and PAC "awareness" has decreased.
So maybe your suggestion is a good one and my experience supports it.

George:

How do you know the Oura Tracking ring is accurate for tracking deep sleep? Is there a brand you can recommend?

Also after you exercise, how long does it take your HR to go back to normal? Mine has been staying elevated until 3-4 hours post exercise. I don't think it was like that in years past.



Edited 1 time(s). Last edit at 06/25/2020 11:53AM by The Anti-Fib.

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The Anti-Fib
How do you know the Oura Tracking ring is accurate for tracking deep sleep? Is there a brand you can recommend?

On one of Berkeley sleep researcher, Matt Walker's interviews with Peter Attia, Walker noted any of these weren't particularly accurate (~60%), especially comparing two different people. However he did say that comparing the same person to themselves over time was likely meaningful. I can see changes in the actual data - heart rate, HRV & etc, not just deep or REM sleep. When I compare nights of zero deep sleep to one of 60 minutes, the heart rate profile is different - not the lowest value at the end of sleep. Lowest and average heart rate are much lower. HRV is higher and so on.

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The Anti-Fib
Also after you exercise, how long does it take your HR to go back to normal? Mine has been staying elevated until 3-4 hours post exercise. I don't think it was like that in years past.

Since I generally stay with the lower heart rate: Zone 2, MAF (180-age), nasal breathing during exercise as I detailed here, it returns quickly. As I'm now 65, my MAF HR is 115. I rarely wear a HR monitor, but did during my daily ~hour long KAATSU exercise class a couple of days ago. It maxed out a few times in the 120's, but still not high. You can see it drops quickly during the session when the exertion drops. The beats that are 2x as long (1/2 the rate) are PVC's - the Polar strap doesn't "see" them, so reports them as a slow beat. I count 11 PVC's and 2 or 3 PAC's. The average for the whole session was 98 BPM.



Also, I will infrequently do 4 minute HIIT Tabatas (20 seconds hard, 10 seconds rest - 8 cycles), which will push my heart rate into the 150's or 160's. It still comes down fast.



Edited 2 time(s). Last edit at 06/25/2020 04:30PM by GeorgeN.

George:

Which Oura tracking ring do you use? I guess for just keeping track of HR and SpO2 levels a cheaper one would suffice. I am seeing them as low as $25 on Amazon.

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The Anti-Fib
George:

Which Oura tracking ring do you use? I guess for just keeping track of HR and SpO2 levels a cheaper one would suffice. I am seeing them as low as $25 on Amazon.

Sadly the ring I use is not $25. I'm not sure what is on Amazon, but this is the Oura site.

I've not been tracking SpO2 during sleep. I do have a device for that, but it has a wrist watch format plus a finger cuff.

The Oura tracks temp during sleep, HR, HR variability & motion (3D accelerometer). It uses these data for its deep/rem/light/total sleep report. It also tracks activity & HR during the day, however I keep it in airplane mode when it is on, so I don't see that except when I download the data.

For beat to beat HR during sleep, I use a Polar H10 strap and the Heart Rate Variability Logger app on my iPhone. If I really want to get a report like I posted, I download the R to R data and import it into an old Polar program on the Windows side of my Mac. I don't typically sleep with the strap on, though do on occasion. I use the Polar data during sleep or meditation to get PAC/PVC counts.

My last HR last night was 115 going into the Gym and walking around, dropped to 95-100 during Cardio using stair machine, then dropped more still to 85-90 during weight training with little to no rest between sets, and afterward stayed around 90 for 4 hours. After this sitting down it was 75, and went down to 58 as I sleep later on. Paranormal cardiology?
HR also slightly lower when I hike if it's on a level surface than compared to before when I start moving.

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The Anti-Fib
My last HR last night was 115 going into the Gym and walking around,
HR also slightly lower when I hike if it's on a level surface than compared to before when I start moving.

How long before the gym does the 115 occur and what are the circumstances?

I need to recheck this before leaving home, and then getting out of my Car in the parking lot. It was 115 as I was walking onto the gym floor. I have noticed also higher reading just as I start a Hike, then it drops down 10-15 BPM.



Edited 1 time(s). Last edit at 07/01/2020 05:02AM by The Anti-Fib.

I'm used to experience some fast HR when moving suddenly after having been quiet for a while.
Typically, I may experience that when leaving my car after a 30 km drive to my workplace. There are eight stairs and about 50m to walk from the parking to the building. It's little, but I may be breathless if I don't start quietly.
I never bothered about such things before afib and ablations, only five years ago, but now I've to remember I must allow my heart some time to get ready to work when needed. After some warming, I'm all right.

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The Anti-Fib
I need to recheck this before leaving home, and then getting out of my Car in the parking lot. It was 115 as I was walking onto the gym floor. I have noticed also higher reading just as I start a Hike, then it drops down 10-15 BPM.

I happened to be in a Zoom meeting yesterday with a university researcher from the UK. He's an exercise physiologist, associated with the IOC (International Olympic Committee) and looks at a lot of wearable devices. He was commenting about how unreliable many of the consumer devices are. He quipped, "My parents take their blood pressure 25 times a day and it varies greatly. This is because they are using a random number generator device. When I take their blood pressure the old fashioned way, it is always the same."

I've used Polar straps for 20+ years and they have a lot of studies suggesting their accuracy. When I've used some other devices, when I compare my radial pulse manually to the device output, many times there is little agreement. So one suggestion would be to check your pulse rate manually against the device output.



Edited 1 time(s). Last edit at 07/02/2020 11:50AM by GeorgeN.

Can I ask what "defective substrate" refers to here?

Hi Sdweller,

That's an excellent question. Unfortunately no one really knows the answer. But generally speaking it's a defective cardiac conduction system. The electrical wiring is problematic so to speak. There has been a long running search for the holy grail on this, looking at dysfunctional ionic channels a.k.a. channelopathies and other mechanisms, which are genetic. Some have been well defined, but the "defective substrate" is very much a mixed bag.

Atrial fibrillation is the most common cardiac arrhythmia. Approximately 1/3 of these individuals also developed atrial flutter. But they may appear in reverse order. The association of these two arrhythmias is so strong that a preventative cavotricuspid isthmus ablation is usually performed on the right side during the typical ablation for atrial fibrillation on the left side.

Although both are triggered by acute changes in atrial effective refractory period (AERP), they are otherwise different. One is typically right sided and orderly while the other left sided and chaotic.

I've had both. IMHO those with hearts capable of developing both are heavy on the defective substrate input and are incapable of controlling their arrhythmias by addressing the other two required inputs for AF - electrolyte imbalance and autonomic imbalance.