Fibromyalgia and Heat Intolerance

• About
• Latest Posts

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.

Latest posts by Adam Foster (see all)

• Hypermobile hip exercises we use, and why clamshells aren’t one of them - 17 October 2026
• Is Fibromyalgia a Disability in the UK, and Can You Claim PIP? - 14 October 2026
• Fibromyalgia and Central Sensitisation, What Is It in Plain English? - 8 October 2026

Heat flattens some people with fibromyalgia in a way it plainly doesn’t flatten everybody else. The afternoon that has everyone outside with a cold drink, leaves you sat in a car with the air conditioning on full, sweating, lightheaded, and quietly working out how to get out of the thing you agreed to.

So, here’s the answer up front, and it isn’t drink more water. Heat intolerance in fibromyalgia is rarely one problem. It’s usually two, and often a third that’s sitting in your bathroom cabinet. The first is what heat does to your blood pressure when you’re upright. The second is your sweating, which goes wrong in two ways, and the third is medication. Those three want different things done about them, which is exactly why the standard hot weather advice, does so very little for you.

Working out which of them is yours, is most of the job, and it’s actually less complicated than it sounds. The blood pressure version is caused when you’re upright, and eases when you get your head down. The sweating version builds while you stay hot, and it doesn’t much mind what position you’re in. And the medication one, you can check against a list.

Is it actually the fibromyalgia?

In part, yes. The more useful question though, is what else is sitting underneath the label, because the pain itself isn’t whats making a warm rooms unbearable.

Your autonomic nervous system is the part that runs everything you don’t think about: heart rate, how wide your blood vessels are, sweating, gut movement, pupil size. It’s also your thermostat, and it’s the thing that can catch you out when you stand up. In fibromyalgia, it doesn’t come out abnormal sitting still, it comes out slow to react. The short term cardiovascular adjustments to standing up and lying back down, come out blunted, with smaller changes in heart rate, blood pressure, cardiac output and peripheral resistance, meaning how tightly the small vessels squeeze, and the weaker those adjustments are, the worse the pain tends to be ^[1].

Tilt table testing, where you’re strapped to a table that tips you upright while your heart rate and blood pressure are recorded, points the same way. On tilt, what turns up is usually orthostatic intolerance, which is the clinical name for feeling dreadful on standing, or a POTS-like response, meaning the heart rate climbs steeply upright, rather than outright failure at rest ^[2]. Widen it out to chronic musculoskeletal pain generally, and pool the studies, and it puts some degree of dysautonomia, which just means an autonomic system not doing its job properly, in around two thirds of people ^[3].

So, the thermostat and the thing that catches you out when you stand up are the same equipment. If it’s slow about a change in position, there’s no good reason to expect it to be quick about a change in temperature.

When the overlap is hypermobility or POTS

Fibromyalgia can sit alongside two other conditions that bring their own autonomic problems, and plenty of people carry more than one label, without anyone having joined them up.

Hypermobility is the big one. Autonomic symptom burden in hypermobile Ehlers-Danlos syndrome comes out markedly higher than in healthy controls, and roughly on a par with fibromyalgia, with orthostatic and gut complaints the most prominent ^[4]. Looking from the other side, in one large hypermobility clinic cohort, over half the people with hEDS or hypermobility spectrum disorder also had fibromyalgia, and the ones who did, carried a heavier multisystem symptom load ^[5]. There’s even a signal that the hypermobility is doing some of the work. In one tilt table study, people with fibromyalgia had a higher baseline and maximal heart rate on tilt and more autonomic symptoms, and joint hypermobility statistically accounted for the whole of the relationship between fibromyalgia and that maximal tilt heart rate in the group tested ^[6]. One cohort, reported briefly, so hold it loosely.

Then there’s POTS, postural orthostatic tachycardia syndrome, where the heart rate jumps on standing and stays jumped. Reviews put 20 to 30 per cent of people with POTS as meeting hEDS or HSD criteria, and 35 to 50 per cent of people with hypermobility disorders as having orthostatic intolerance or tachycardia ^[7]. And heat is a recognised trigger for orthostatic symptoms in both hypermobility and POTS ^[7], with POTS itself commonly bringing heat intolerance, abnormal sweating and a clear worsening in hot environments ^[8].

So, if heat is doing this to you, orthostatic intolerance is worth ruling in or out properly rather than filing under fibromyalgia and moving on. It’s the one strand here with actual treatment attached to it.

The people who find heat helps

Not everybody with fibromyalgia hates the heat. Some find warmth is the thing that helps, and cold is the thing that ruins them. If that’s you, you’ll have noticed your support group mostly says the opposite.

Cold often worsens symptoms, while warmth relieves them, a pattern described repeatedly in the mechanistic and experimental work on fibromyalgia ^[9]. Cold is also the single most reliably abnormal thing in the thermal testing literature: all seventeen studies in one systematic review reported numerically lower cold pain thresholds in fibromyalgia, with the difference reaching statistical significance in fourteen ^[10]. Meaning cold starts hurting at temperatures that wouldn’t bother anyone else.

Heat sensitivity and cold sensitivity aren’t opposite ends of one dial, and plenty of people have both. But if your version of this is that a warm bath is the best part of your day, and a cold snap wipes you out, the medication question and the orthostatic one are still yours to check.

What’s going on when you overheat

Two separate things, and the current evidence genuinely does split them rather than running them together. One is an orthostatic problem: heat worsens blood pooling, drops the volume getting back to your heart, and cuts the blood flow to your brain ^[11]. The other is a thermoregulatory one, where impaired sweating limits how much heat can actually leave you ^[11].

They feel similar from the inside and they want different things done about them.

Heat moves your blood to the wrong place

Getting hot makes your blood vessels open up, which is the whole point, because moving warm blood out to the skin is how you dump heat. The cost is that a lot of your circulating volume is now sat in the vessels of your skin and your legs rather than coming back up to your heart. Stand still in it, and more of it pools downwards. Your heart has less to pump, and your blood pressure now has to be held up by something. When it’s working, that something is a fast autonomic correction, the vessels squeezing down and the heart speeding up, and it happens without you ever knowing.

If that correction is blunted, as it measurably is in a good proportion of people with fibromyalgia ^[1], you get the version of this you’ll recognise. Vision greying at the edges in a hot shop. Heart racing while you’re stood doing nothing. The sudden need to crouch down in the supermarket aisle. That’s presyncope, the run up to a faint, and it’s a blood pressure and brain blood flow event rather than anything your muscles are doing. It’s also why heat plus standing is so much worse than heat alone ^[11].

The sweating part, too much and too little

Some people sweat buckets at nothing. Some hardly sweat at all and just cook. Both are sudomotor problems, which is the word for whatever your sweat glands and the nerves running them are up to.

Sweating is the main way humans lose heat, once the air gets near body temperature. Below that you can shed heat by radiating it off warm skin. Above it, the air is no longer colder than you are, and evaporation off wet skin is essentially the only tool left. Which is why the sweating question is not a cosmetic one.

On the measured side, the direction in fibromyalgia leans towards less. Electrodermal testing, which reads sweating off how well the skin conducts a tiny current, found lower resting skin conductance, smaller responses to breathing manoeuvres, and loss of the normal link between sweating and body temperature, all of which point to reduced sympathetic output to the sweat glands and a system that’s lost some of its flexibility ^[12]. That last one is worth a second: losing the link means the sweating is no longer keeping step with your temperature, which is a different fault from the glands simply not working.

There’s a structural finding underneath that in a subgroup. Skin biopsies in people with fibromyalgia and small fibre pathology, meaning damage to the thinnest nerves in the skin, showed reduced nerve supply to the sweat glands and the hair erector muscles, so the damage isn’t confined to the sensory fibres ^[13]. Small fibre impairment of some kind turns up in roughly half of people with fibromyalgia across the pooled studies ^[14].

On the symptom side, what gets reported is both. The standard autonomic questionnaires ask about sweating with exertion, inability to tolerate heat and dry mouth and eyes, and people with fibromyalgia endorse those items often ^[15]. Those are the lived descriptions of two different faults, and a questionnaire can’t tell them apart, so keep that in mind.

If you sweat heavily, the thing sitting under your heat intolerance is volume and salt, because you’re losing both. If you barely sweat, it’s your core temperature, because your main cooling route is partly out of order.

Why your tests came back normal

You’ve probably had the tests, been told everything looks fine, and come away feeling like the problem must be you. There’s a decent explanation for that gap, and it isn’t that you were wrong.

Symptoms consistently outrun what the objective testing picks up. On the standard autonomic questionnaire, the secretomotor scores, the ones asking about sweating and dryness, came out much higher in fibromyalgia than in controls, while the testing itself showed only mild adrenergic differences, meaning on the blood pressure side, and no difference at all on the sudomotor subscore ^[16]. That isn’t unique to fibromyalgia. In large autonomic datasets, questionnaires agree well with other questionnaires and objective tests agree well with other objective tests, and the two barely correlate with each other, so the authors of ^[17] say questionnaires shouldn’t be used as a replacement for testing.

Thermal imaging is the other one worth knowing about, because people ask for it all the time. Resting skin temperature comes out with no clinically meaningful difference between fibromyalgia and controls, and infrared thermography isn’t useful as a supplementary assessment ^[18]. So a normal thermal scan tells you very little about what happens to you in a heatwave.

None of that means the measurement is the truth and you’re the error. The tests you were given measure you sitting still. Your problem is a response problem.

Could it be your medication?

Possibly, and it’s the question most likely to change somebody’s summer.

Fibromyalgia is treated, very often, with drugs that interfere with one half or the other of your cooling system. Nobody mentions it, because the side effect that gets listed is dry mouth and the side effect that gets lived is a ruined July. None of this is a reason to stop a tablet. It’s a reason to ask a question at your next appointment, ideally before the weather turns.

Anticholinergics, and amitriptyline in particular

Sweat glands run on acetylcholine. That’s the main signal your nervous system sends to those glands, and anything that blocks muscarinic receptors, which is what anticholinergic means in practice, blocks that signal, which directly impairs evaporative cooling ^[19]. The same receptor type dominates in your salivary glands, so dry mouth and reduced sweating tend to arrive together ^[19]. A d ry mouth is the clue, and it rarely gets joined up.

Strongly anticholinergic drugs raise core temperature during heat stress, by around four tenths of a degree at air temperatures of thirty degrees and above, with reduced sweating alongside it, on moderate quality evidence ^[20]. That was measured in heat rather than in a cool room, which is the part that makes it matter. Drugs with weaker anticholinergic properties showed no thermoregulatory effect at all, which tells you something useful: it’s the anticholinergic load that counts, not the name of the drug class ^[20].

Amitriptyline is the one to check first. It’s consistently rated as strongly anticholinergic, and randomised trials across multiple conditions show a large excess of anticholinergic side effects compared with placebo ^[21]. Those trials mostly recorded dry mouth and sedation rather than anything to do with heat, so they establish that the drug does this sort of thing rather than measuring what it does to you in August ^[21]. There is direct volunteer work though: amitriptyline suppressed chemically evoked sweating in healthy volunteers, and in a separate study amitriptyline and doxepin both significantly reduced finger sweating against placebo ^[22].

There are gaps in that. Amitriptyline itself still needs direct thermoregulation studies, and the experimental work leans heavily on atropine in young healthy adults ^[20]. Tricyclics are awkward too, because they can cause more sweating as well as less, which is why they turn up on both the reduced sweating and the excess sweating lists in the pharmacology reviews ^[19].

So the question for your GP isn’t is amitriptyline bad. It’s what my total anticholinergic load is across everything I’m taking, and whether the summer version of my prescription should look different from the winter one: which no body asks, and I wish they would.

Duloxetine, venlafaxine and the ones that make you sweat more

SNRIs do the opposite thing, and it’s a common enough effect to have been measured properly. Pooling seventy six randomised trials, the risk of hyperhidrosis, meaning sweating well beyond what the situation calls for, came out around three times that of placebo, with no clear relationship to dose ^[23]. The mechanism appears to be central, a thermoregulatory and sympathetic effect rather than anything happening at the sweat gland itself ^[23].

That puts these drugs in a different category. The risk isn’t that you can’t shed heat, it’s dehydration and salt loss from shedding it enthusiastically, which matters a great deal if you’re also trying to hold your blood volume up for orthostatic reasons. Antidepressants as a whole showed no evidence of altering core temperature during heat stress, so these are not interchangeable with the anticholinergics ^[20].

Beta blockers

Beta blockers mostly interfere with the other cooling route, which is skin blood flow rather than sweat.

The split that matters is selective against non-selective. Non-selective beta blockers raised core temperature during heat stress by about a tenth of a degree, while selective ones showed no core temperature effect ^[20]. The physiology behind that is straightforward enough: during exercise in the heat, propranolol reduced forearm blood flow and raised vascular resistance, meaning less warm blood reaching the skin where it could be dumped ^[24].

It isn’t a closed case though, and the counterweight is worth having. In middle aged and older adults with stage 1 hypertension, there was no difference in the critical environmental limits people could tolerate, meaning the hottest conditions they could still cope with, according to whether they were on antihypertensive medication, as long as they were properly hydrated ^[25]. That last condition is not a small one. But it does argue against writing yourself off as heat intolerant purely because of what’s on your repeat prescription.

What actually helps

Two levers, matched to the two mechanisms. If your problem is orthostatic, you’re aiming at blood volume and at the position your body is in. If your problem is heat loss, you’re aiming at getting heat off your skin by a route that doesn’t depend on your own sweat glands.

Cooling, and which sort

Skin cooling genuinely improves orthostatic tolerance during heat stress, and the way it does it is by propping up blood pressure and brain blood flow rather than by cooling you down in any deep sense ^[26]. Which means a cold flannel on the back of your neck when you feel the grey-out coming is doing something real and specific.

What it is not doing is lowering your core temperature much. Broad area cooling outperforms small local devices for that. In a hot humid chamber test, a fan cooling jacket lowered skin temperature, armpit temperature and sweat volume more than a thermoelectric neck cooler, which mainly delivered a transient feeling of comfort ^[27]. Comfort and safety are not the same measurement, and the device that makes you feel coolest fastest is often the one doing least.

So, in order of likely return. Get wet and stay wet, because evaporation off skin works whether or not your own sweat glands are cooperating. Cover a lot of surface area rather than one strategic spot. Keep the cold flannel on the neck for the orthostatic wobble, which is what it’s good at, rather than as your heat plan. The authors of ^[28] suggest these as plausible countermeasures in hot environments, and say that direct trials of cooling in POTS are still lacking. And sit down early, because reversing presyncope is easier than recovering from it.

Fluid and salt

This is the best supported thing here that doesn’t come in a blister pack, and it’s aimed squarely at the orthostatic half of the problem.

The typical dysautonomia clinic regimen is roughly 2.5 to 3 litres of fluid a day with 7 to 10 g of salt, alongside compression and trigger avoidance ^[28]. The reason it’s salt and not just water is that sodium is what makes you hold onto the fluid. More sodium means more retained water, which means more circulating volume, which means an easier time being upright. When it was tested directly, a high sodium diet in POTS increased plasma volume, lowered standing noradrenaline and reduced upright tachycardia compared with a low sodium one ^[29].

Keep the expectations calibrated though. Pool the salt loading trials for orthostatic intolerance and what comes out is low quality, mostly short term evidence, with very little on the outcomes that matter most, like syncope burden, falls or heat illness ^[30]. That isn’t a finding that it doesn’t work. It means nobody can tell you precisely how much, for how long, or for whom.

Which is why it’s worth getting this matched to you rather than taken on faith. The people with low 24 hour urinary sodium look the most likely to benefit, and measuring it has been suggested rather than prescribing high salt to everyone ^[31]. High salt isn’t free either: it needs monitoring if you have high blood pressure, fluid retention, kidney or heart problems ^[32]. Salt tablets also upset a lot of stomachs, which is its own argument for getting it from food and electrolyte drinks instead.

If you’re the heavy sweating sort, this matters more rather than less, because you’re losing sodium out through your skin as well as needing it in your circulation.

The fan, and the water

A fan is conditional, which is not what the hot weather advice sheet says. Fans helped in some hot humid conditions and made thermal and cardiovascular strain worse in very hot dry conditions and at very high temperatures ^[33]. The reason is simple: a fan helps by speeding evaporation off wet skin, and if the air is hotter than you are and your skin is dry, you’ve built a convection oven. Later reviews caution specifically against relying on a fan above 35°C if your sweating capacity is impaired ^[34], which is precisely the group with the most to lose here. Wet your skin first, then the fan has something to work with.

And more water is not automatically safer. Across the exercise and wilderness heat literature, overdrinking causes hyponatraemia, meaning the sodium in your blood falls too low, which can mimic heat exhaustion and gets dangerously worse if it’s treated with more plain water ^[35]. You can see how that happens: feeling awful in the heat, told repeatedly to hydrate, drinking more, feeling worse, drinking more again. If you’re drinking a lot, the sodium has to come with it.

When it is more than a bad day

There’s a line where this stops being miserable and turns into something that can hurt you, and it’s worth knowing where it is before you’re the far side of it.

The strongest evidence for direct heat injury risk sits with the conditions involving genuine sweating failure rather than with chronic pain syndromes on their own ^[36]. Widespread anhidrosis, meaning an inability to sweat across a large area of skin, causes heat intolerance and can put someone at risk of heat stroke under heat stress ^[36]. The clinical picture of it is documented and reads uncomfortably close to what people describe: in chronic idiopathic anhidrosis, people became hot, flushed, dizzy, breathless and weak in heat or with exercise, while failing to sweat ^[37].

So the thing to watch for isn’t how awful you feel. It’s whether you’ve stopped sweating while still getting hotter, and whether your thinking has gone. Confusion, slurred or muddled speech, not making sense, skin that’s hot and dry when it ought to be damp, vomiting, or a temperature that keeps climbing after you’ve got out of the heat: that’s an emergency and it needs 999, not a lie down. Get cold water on the skin while you wait.

Nothing about having fibromyalgia makes that likelier to be a false alarm. If anything, years of being told you’re exaggerating makes people wait too long.

So, four things. Get the orthostatic side looked at properly rather than filed under fibromyalgia. Take your prescription list to your GP before the weather turns, not after. Get wet rather than just getting a fan. And put the salt in with the water.

Adam

References

[1] Contreras-Merino, A.M., Davydov, D.M., Galvez-Sánchez, C.M. and Reyes del Paso, G.A. (2022) ‘Blunted short-term autonomic cardiovascular reactivity to orthostatic and clinostatic challenges in fibromyalgia as an indicator of the severity of chronic pain’, International Journal of Psychophysiology. https://doi.org/10.1016/j.ijpsycho.2022.03.001

[2] Staud, R. (2008) ‘Autonomic dysfunction in fibromyalgia syndrome: Postural orthostatic tachycardia’, Current Rheumatology Reports. https://doi.org/10.1007/s11926-008-0076-8

[3] Almutairi, N.A., Greenwood, D.C. and Sivan, M. (2026) ‘The prevalence of dysautonomia in chronic musculoskeletal pain: a systematic review and meta-analysis’, Rheumatology Advances in Practice. https://doi.org/10.1093/rap/rkag034