Fibromyalgia and Your Heart: Heart Rate, Palpitations and HRV

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Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

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An ECG looks at the pump, It checks whether the heart muscle is damaged and whether the electrical signal is getting through it properly. What an ECG doesn’t look at is the controls, and the controls are where fibromyalgia turns up when anybody actually measures it, at group level rather than in everybody, and not as a general autonomic neuropathy ^[1]. Autonomic neuropathy means the nerves of that control system are themselves damaged, which is a different thing from a control system being driven badly.

The brake on your heart rate

Left to itself, the heart beats at roughly a hundred times a minute. The pacemaker sits inside the heart, a patch of cells in the top right chamber that fire on their own schedule, so the thing carries on quite happily with no instructions at all. The reason your resting pulse is nowhere near a hundred is that the vagus nerve is holding it down continuously, like a hand resting on a dial. That’s the parasympathetic side of the autonomic nervous system, and most of your minute to minute heart rate control is that brake being eased off and reapplied rather than the accelerator being pressed.

The other side is sympathetic: adrenaline, and the nerves that carry the same message, raising both the rate and the force of each beat. People picture those two as a seesaw, and that picture is a bit misleading, because they work on quite different timescales.

The vagal brake can change your heart rate inside a single beat. The sympathetic side takes seconds to get going and seconds to let go, which is why a fright you’ve already stopped thinking about is still sitting in your pulse a minute later. That’s why the gap between your heartbeats isn’t the same twice running. Breathe in and the brake eases, so the beats come closer together. Breathe out and it comes back on, so they space out. Stand up and the pressure sensors in your neck and chest notice the drop and let the brake off within a beat or two. Heart rate variability is the measurement of that and nothing more exotic: how much the gap between one beat and the next differs from the gap before it. A heart keeping perfect time is a heart whose controls have stopped adjusting, which is why high variability is generally the good end.

So, when somebody with fibromyalgia has a resting rate that’s crept up and variability that’s dropped down, the heart is doing exactly what it’s being told to do. What’s changed is the telling.

Why your heart is doing that

Three things come up over and over again: a resting rate that’s crept up, something horrible that happens on standing, and beats you can feel. They’re the same control problem seen from three angles.

A resting rate that sits higher

Set against healthy people of a similar age, resting heart rate in fibromyalgia comes out higher on average. In one study of 51 women with fibromyalgia set against 31 controls, resting rates were 72.3 against 64.5 beats a minute ^[2]. The gap is about eight beats and both of those numbers are perfectly ordinary, which is the part that falls out when the finding gets repeated. It’s a shift in a group average rather than resting tachycardia, meaning a resting pulse fast enough to count as abnormal in its own right, and the distinction matters when you’re sat looking at 88 on a watch face wondering what it says about you.

It’s also far from uniform, and some of the scatter has an explanation. In one controlled comparison the higher heart rates and lower variability showed up in people who had fibromyalgia and depression, and not in people who had fibromyalgia without it ^[3]. Depression alters autonomic regulation in anybody who has it, so that reads as depression turning up inside a fibromyalgia group rather than as something fibromyalgia is doing.

Deconditioning is the other obvious candidate, and it’s genuinely part of this. Cardiorespiratory fitness and neuromuscular function both come out lower in fibromyalgia when they’re measured properly ^[4], and a lower ceiling means ordinary tasks sit at a higher percentage of your maximum. The stairs really do cost you more than they cost the person in front of you.

Fitness doesn’t account for all of it though. When women with fibromyalgia were matched against controls for the maximum workload they could reach on a bike, the autonomic differences were still there ^[5]. And parasympathetic variability came out similarly reduced in moderate and in severe fibromyalgia, even though the severe group was the more deconditioned of the two ^[6]. If being out of condition were the whole story, you’d expect this to track severity, and it doesn’t.

So, a resting rate in the high seventies or the eighties, on its own, in a person with fibromyalgia, isn’t a cardiac finding. What’s worth doing is knowing your own number. Take it sitting, at the same time of day, a few mornings running, and write it down somewhere you’ll find it again. A rate that’s moved a long way from your own baseline is a far more useful thing to put in front of a GP, than a rate that’s simply higher than a generic chart says it should be.

Why standing up is the worst of it

Standing up is the hardest thing your circulation does all day. Blood drops into your legs and abdomen within seconds of getting up, the amount returning to the heart falls, and blood pressure starts to follow it down. Pressure sensors in the neck and in the aorta catch that, the vagal brake comes off, the rate climbs, the vessels in your legs squeeze, and the whole correction has happened before you’ve consciously noticed anything. In fibromyalgia, that correction is reliably less tidy than it should be.

The grey, swimming, tunnelling feeling is what it feels like when the brain is briefly short of its supply. Your head sits at the top of the body, so it goes short first when pressure drops, and vision tends to go before anything else does because the retina is fussy about blood flow. It won’t necessarily arrive the instant you stand, either, because the first correction can hold and then give way, which is why the worst of it can land a minute or two later with the kettle already on. Presyncope is the word for it, meaning the bit before a faint without the faint, and it’s worth borrowing, because telling a GP you get presyncopal on standing gets a different response from telling them you go a bit funny.

Orthostatic intolerance is the other phrase you’ll see on a letter, and it means symptoms brought on by being upright and relieved by lying down. The symptoms are the better established half of this. In a matched comparison, the orthostatic intolerance symptom score came out at 20.4 against 5.2 ^[7].

What the physiology does underneath depends on how you provoke it. Under an active stand test, where you simply get up and somebody measures you, the early cardiovascular adjustments come out smaller and slower than they should be ^[8]. Under other testing, the heart rate rise on standing has come out larger, alongside a bigger fall in blood pressure ^[9]. Those sound contradictory and they aren’t quite, because a weak early correction followed by an exaggerated later one is what a control loop reacting late looks like from the outside.

Then there’s POTS, which stands for postural tachycardia syndrome. What it describes is straightforward enough: you stand, your heart rate climbs a long way and stays climbed, and your blood pressure doesn’t drop enough to account for it. A tilt test is the formal way of catching that, strapped to a table that tips you upright while the kit records what your circulation does, and there’s a set threshold for how big and how sustained the rise has to be before the label applies. Postural tachycardia turns up often enough on tilt testing in fibromyalgia to count as a frequent finding ^[10].

What you’ll see quoted online is a percentage, and it’s usually pointing the wrong way. The figure that exists is that around 21.6% of people with POTS also have fibromyalgia ^[11]. That’s a different claim from the one it gets turned into, which is that the same share of people with fibromyalgia have POTS, and there’s no reason for those two numbers to resemble each other. If somebody quotes you a POTS rate in fibromyalgia, ask which way round the denominator was.

An active stand test takes ten minutes and costs nothing: lie flat for a few minutes, take heart rate and blood pressure, then stand and take them again at intervals over the next ten. A GP can do it in the room. The one thing worth adding is a note of what you actually felt at each reading, because that belongs in the record alongside what the cuff said.

Fluttering and skipped beats

A palpitation is awareness of your own heartbeat, and the commonest thing underneath one is an ectopic, a beat that fires early and out of sequence. The early beat itself is small and slips past you. What you feel is the pause afterwards, while the heart fills for longer than usual, and then the next beat, which lands harder because there’s more blood in the ventricle to shift. That’s the thud. Healthy hearts do this all day, and whether it reaches you at all has more to do with where your attention happens to be pointed than with anything the beat did. The beat is real, the pause is real, and the thud is real.

So the first question is whether anything abnormal is happening to the rhythm at all, and the direct answer is reassuring. A Holter is the test you get sent for: a small box on your belt, sticky pads on your chest, every beat recorded for a day, and no shower. When 90 people with fibromyalgia were compared against 70 controls on 24 hour monitoring, no significant difference in the Holter findings turned up, despite the palpitation complaints that had sent them for it in the first place ^[12]. Looked at from the electrical side, no association between fibromyalgia and confirmed arrhythmia turned up either ^[13].

That’s weaker than it actually sounds. Across more than a million ambulatory recordings, the median time to a first actionable arrhythmia was longer than 48 hours, which is twice as long as the test most people get ^[14]. Symptoms lined up with the recorded rhythm only 18% of the time ^[14]. Stretch the recording out and the picture changes: a fourteen day patch, a plaster sized thing stuck to the chest, picked up atrial fibrillation or flutter, a fast and disorganised rhythm in the heart’s upper chambers, in 6% of people where a 24 hour Holter picked up none ^[15].

Put those together and a normal 24 hour Holter means your rhythm was normal for 24 hours. It isn’t a statement about whatever happened to you at four in the morning the week before, and you’re allowed to say that out loud in the room. What to ask for instead is longer monitoring, or a device you press yourself when it happens, because letting people record at the moment they actually felt something found arrhythmias in 14.9% of them, against 7.7% with standard monitoring ^[16].

The clinical rules of thumb are worth knowing as well, because they’re what a GP is weighing while you talk. Palpitations lasting less than 5 minutes make an arrhythmia less likely. A known history of heart disease, palpitations that affect your sleeping, and palpitations happening at work all push the other way. And a regular rapid pounding felt in the neck is a strong pointer towards one specific rhythm problem, AVNRT, which happens to be very treatable ^[17]. AVNRT is a short circuit: the electrical signal finds a small loop near the top of the heart and goes round and round it, which is why it’s regular rather than chaotic and why it tends to start and stop abruptly.

When to get it looked at properly

Most of this is regulation and most of it isn’t dangerous. Some of it needs somebody with a stethoscope, sooner rather than at the next review.

Fainting, meaning actually losing consciousness, than simply just feeling like you might. Especially if it came without warning, or happened while you were sitting or lying down.

Palpitations with chest pain, or with breathlessness that’s new to you.

A regular, rapid pounding you can feel in your neck, which is the AVNRT pointer, and the reason to know that word ^[17].

Palpitations affected by sleeping, or happening at work, both of which nudge the odds towards an arrhythmia, as does any known history of heart disease ^[17].

Anything at all if you’re over 50, because older age raises the odds that a monitor finds something worth finding ^[18].

Is fibromyalgia damaging your heart?

Now, the thing people are actually frightened of, which is whether fibromyalgia is quietly wrecking out their heart while everybody tells them it’s fine.

Detailed cardiac imaging in fibromyalgia does find small differences against controls, and those measurements sit inside of normal limits ^[19]. Scarring of the heart muscle, which is the mark left behind when heart tissue has been injured and patched with fibrous tissue, wasn’t demonstrated on cardiac MRI ^[19]. So the differences that have been found, are subtle, and they stay inside the range a cardiologist would call normal.

Damage and risk are different questions though, and the risk one has something in it. In 61,612 people followed over time, new coronary heart disease turned up at 15.2 against 9.26 per 1,000 person years, and the gap survived adjustment ^[20]. That unit is just a way of counting new cases: follow a thousand people for a year, and that’s how many of them get it. Data from another country found ischaemic heart disease, which is the same thing under a different name, in 9.2% against 6.2% ^[21]. Stroke risk came out roughly a quarter higher ^[22].

Taking that seriously is a long way from concluding that fibromyalgia causes it. How well those studies accounted for everything else going on has been patchy ^[23], and the competing explanations are sitting right there in plain sight. Cardiorespiratory fitness and neuromuscular function are measurably lower ^[4], and the conditions that arrive alongside fibromyalgia, diabetes in particular, bring their own cardiovascular burden with them ^[20].

Mortality is where the reassurance actually lands. Pooled together, deaths from heart disease in fibromyalgia came out no higher than expected ^[24]. Overall mortality is genuinely disputed, with one pooled estimate showing a modest increase and another showing none ^[25][24].

The cause of death that comes up more reproducibly is suicide rather than anything cardiac ^[25]. That’s a harder sentence to read than anything else on this page and it isn’t here as a statistic. If that’s where you are, it’s the thing to say out loud to a GP ahead of anything about your heart rate, and it’s the part of this that shouldn’t wait for an appointment in three weeks.

What the rest of it adds up to is this. Your risk of coronary disease over decades is somewhat raised, the likeliest mechanism is the ordinary one, and that means the ordinary things are what move it. Blood pressure, cholesterol, smoking, weight, and how much you move. It’s a GP conversation, it’s a boring one, and it’s worth having in your forties rather than in your sixties.

The number on your wrist

Heart rate variability is the measurement that separates fibromyalgia from healthy controls most consistently of anything here. Across chronic pain generally, the measures reflecting vagal activity come out reduced, and the largest effects turn up in fibromyalgia ^[26].

It’s still far from everybody. In one study of 50 people with fibromyalgia set against 50 matched controls, no significant autonomic difference turned up at all ^[27]. When a cohort was tested with proper electrophysiology rather than a questionnaire, objective dysfunction turned up in 46.7% of them ^[28]. So this holds up at group level and misses plenty of individuals on the way, and a normal autonomic test doesn’t make your symptoms less real.

Where it shows up most clearly is overnight. Comparing sleep stages directly, the beat to beat measure came out at 30 against 42 milliseconds in light sleep and 23 against 37 in REM, with no significant difference in the deepest stage ^[29]. Over a whole night recorded at home, overall variability came out at 91.2 against 122.2 milliseconds ^[7]. Those are two different measures with two different names, and they’re worth telling apart, because RMSSD is the beat to beat one and it’s what a ring is most likely putting on your screen, while SDNN is the spread across a whole recording. So if you own a ring, the window it measures in the small hours is the window where the gap is widest.

One warning before you do anything with that. A low reading gets described everywhere as sympathetic overdrive, and the LF/HF ratio, the number people use to make that claim, doesn’t accurately measure the balance between the two branches in the first place ^[30]. Pooled biological markers in fibromyalgia found no significant difference in resting adrenergic activity, which is the adrenaline side measured at rest, alongside a reduced adrenaline response to exercise ^[31]. Low variability means less moment to moment adjustment going on. It doesn’t mean you’re swimming in adrenaline.

Age, sleep and your tablets

Before you read anything at all into your own figure, it’s worth knowing what’s already in it.

Age and sex do most of the work. In 149,205 people, age and sex between them explained roughly 17 to 22% of the differences in one of the main HRV measures, which is more than lifestyle and psychosocial factors managed between them ^[32]. Variability falls with age in everybody, healthy or not, so a woman of 48 and a woman of 24 in identical health will have different numbers, and the app is going to show both of them the same colour.

Sleep is next. Deprive people of sleep and the beat to beat measure drops while the markers of sympathetic predominance climb ^[33]. Carrying insomnia as a standing diagnosis doesn’t reliably do the same thing, where the effect comes out small and too uncertain to call ^[34]. So a genuinely bad night lowers it, and a long standing sleep problem may not.

Then medication, which is where people get caught out. Beta blockers, the drugs that sit on the adrenaline receptors so the sympathetic message doesn’t land, raise HRV, and by a lot: in people with coronary artery disease, two weeks of treatment raised the vagal measures by somewhere around 62 to 70% ^[35]. Tricyclics, the older class of antidepressant handed out at low doses for pain rather than for mood, go the other way and reduce the parasympathetic measures ^[36]. Amitriptyline is one of those, which is why it matters here. SSRIs are inconsistent and mostly don’t shift it ^[37]. And treating the depression doesn’t bring the variability back up, even when the mood itself lifts ^[36].

So if you’re on a beta blocker, part of your number is the drug. If you’re on amitriptyline, part of it is the drug pointing the other way. Neither is a reason to change a medication that’s working for you, and both are reasons to stop reading your ring as a report card on how well you’re coping.

What the ring is actually measuring

Device accuracy is better than the sceptics think and much narrower than the marketing suggests. Measured against ECG overnight, the Oura ring’s beat to beat agreement is very close, with an error of around 6 to 7%, WHOOP sits a little behind it, and Garmin and Polar are further back again ^[38]. Accuracy is at its best when you’re still and asleep, and the frequency based figures that get relabelled as stress or balance have high error rates on most devices ^[39]. The overnight number is the one worth looking at. The daytime stress score is mostly decoration.

Then there’s the noise, which is the part nobody puts on the box. Repeat the same measurement on the same person on different days and the beat to beat measure swings by around 30%, while resting heart rate swings by about 6% ^[40]. Thirty per cent is enormous. It means a single morning’s reading tells you very nearly nothing, and that weekly averages and the direction of travel are what carry the information ^[41].

So, practically: stop looking at today’s number. If you’re going to look at all, look at the seven day average, once a week, and notice whether it’s drifting rather than whether it’s low.

Whether a low number is dangerous

In the general population, low HRV does predict bad outcomes, and the cohorts behind that are large. Across 38,008 people, those in the lowest quarter on the beat to beat measure had a higher risk of dying from any cause, roughly half as high again as everybody else ^[42]. In 51,628 people, those below the twentieth percentile had modestly raised risks of atrial fibrillation, major cardiac events, stroke and death ^[43].

What they don’t establish is that the HRV is doing the damage. Tracked over five years in a large working population, changes in heart rate and HRV had no relationship to later cardiovascular disease or death at all ^[44], which suggests low variability may be a marker of how healthy somebody is rather than a mechanism that shortens life. That distinction is the whole answer to the question. A figure measured across tens of thousands of people in the general population was not a prediction about one person, and nothing in it tells you that variability lowered by living with fibromyalgia carries the same meaning as variability lowered by heart disease.

So if your number is low and you also smoke, or have blood pressure nobody’s treating, or haven’t moved much in three years, those are the things to go at, and they’d be worth going at regardless. If your number is low and everything else is fine, what it’s telling you is how much adjusting your autonomic nervous system is currently doing. Which, in fibromyalgia, is often not very much.

Where we’d put the effort

Exercise is the only thing on this page that moves the symptoms and the measurement. Resistance training improved HRV in women with fibromyalgia ^[45], and so did a programme built around exergames ^[46]. It doesn’t shift it reliably though, and one endurance programme improved aerobic fitness without shifting the autonomic measures at all ^[47]. So train because training is worth doing on its own terms and treat any change in the number as a bonus, and read nothing in the risk figures above as a reason to stop.

Where we’d start is lower and slower than you’d expect, and not with cardio. If standing up is the thing that floors you, the early work is horizontal and supported: strength work lying down or seated, where the circulation isn’t being asked to push uphill at the same time, then the same work sitting, then upright, over weeks rather than sessions. What’s being trained there is tolerance of being upright as much as fitness in the abstract. And if your rate climbs steeply at efforts that used to be nothing, using heart rate as a ceiling rather than going by feel gives you something you can hold to on a bad week, when feel is the least reliable instrument you own.

Breathing based HRV biofeedback is the intervention marketed hardest at this community, and when it was tested properly in fibromyalgia, it didn’t beat the comparison group on its main outcomes ^[48]. It’s free and it won’t hurt you, so if slow breathing makes an evening more bearable, do it for the evening, and don’t judge it by what the smart ring says in the morning.

And sleep. A short night measurably lowers the next day’s variability ^[33], which means a run of bad nights will show up on your ring and you’ll read it as your condition deteriorating. Often it’s the sleep.

So, the answer to the question you came with. Fibromyalgia doesn’t appear to produce a structural heart problem, deaths from heart disease aren’t raised, and the palpitations that frighten people mostly don’t correspond to an abnormal rhythm when somebody records one.

What’s genuinely different is the regulation: a resting rate a few beats higher, less moment to moment adjustment, and a much harder time staying upright than you used to have. Those are real, they’re measurable, and between them they explain nearly everything you’ve been noticing.

Four things worth doing with that:

Know your own resting rate, sitting, same time of day, a few mornings running, because your baseline is the only one that means anything.

Get standing measured if standing is what ruins your days. Ten minutes, a cuff, and somebody writing down what you felt as well as what the numbers did.

Ask for longer monitoring, or a device you press yourself, if you’re getting beats you can feel and the day long tape came back clean.

Read the weekly average and not the morning, if you’re wearing something that hands you a number at all.

And take the dull version of heart health to a GP early rather than late, because over decades that’s the conversation that actually moves anything.

Adam

References

[1] Meeus, M., Goubert, D., De Backer, F., Struyf, F., Hermans, L., Coppieters, I. et al. (2013) ‘Heart rate variability in patients with fibromyalgia and patients with chronic fatigue syndrome: A systematic review’, Seminars in Arthritis and Rheumatism. https://doi.org/10.1016/j.semarthrit.2013.03.004

[2] Zetterman, T., Markkula, R., Miettinen, T. and Kalso, E. (2023) ‘Heart rate variability responses to cognitive stress in fibromyalgia are characterised by inadequate autonomous system stress responses: a clinical trial’, Scientific Reports. https://doi.org/10.1038/s41598-023-27581-9

[3] Reyes del Paso, G.A., Contreras-Merino, A.M. and Duschek, S. (2022) ‘The Role of Depressive Disorders in Autonomic Cardiovascular Dysregulation in Fibromyalgia’, Psychosomatic Medicine. https://doi.org/10.1097/psy.0000000000001097