Does POTS cause excessive sweating?

It can, but not always. POTS affects the autonomic nerves that control sweat glands, so sweating may be increased, reduced, or uneven. In one large cohort about half of patients had reduced sweating in the legs on testing, while other patients report excessive sweating and heat intolerance.

Why do some people with POTS sweat less?

In the neuropathic subtype, postganglionic sympathetic nerves are damaged in a length-dependent way, which blunts or removes sweating in the feet and lower legs first. This shows up as an abnormal quantitative sudomotor axon reflex test (QSART) or thermoregulatory sweat test.

Is abnormal sweating enough to diagnose POTS?

No. POTS is defined by a sustained heart-rate rise of at least 30 beats per minute (40 in those under 19) within 10 minutes of standing, without a drop in blood pressure, plus chronic orthostatic symptoms. Sweating changes are a supporting feature, not a diagnostic test.

How common is POTS and who does it affect?

Expert reviews estimate that roughly 1 to 3 million people in the United States have POTS. It disproportionately affects women of reproductive age; in the Mayo Clinic cohort, 86.8% of patients were female with a mean age near 30.

What tests measure sweating in POTS?

Autonomic testing can include the quantitative sudomotor axon reflex test (QSART), which measures postganglionic sweat responses, and the thermoregulatory sweat test (TST), which maps whole-body sweating. Reduced distal sweating supports a neuropathic pattern of POTS.

Is this page medical advice?

No. It is a summary of verified figures from published sources. Only a clinician can evaluate orthostatic symptoms and determine whether an individual's sweating relates to POTS or another cause.

Research

POTS and Sweating: What the Research Shows

Postural orthostatic tachycardia syndrome (POTS) is a disorder of the autonomic nervous system in which standing up produces an excessive rise in heart rate without a drop in blood pressure. Because the same autonomic pathways that regulate heart rate and blood vessels also control the sweat glands, many people with POTS notice changes in sweating. The pattern is not uniform: in a landmark Mayo Clinic study of 152 patients, about half had reduced or absent sweating on formal testing (a neuropathic pattern), while other patients describe excessive sweating and heat intolerance. This page summarizes what the peer-reviewed literature reports about sweating in POTS. It is educational only and is not a diagnosis or medical advice.

By the Sweat Explained Editorial Team · Published 2026-07-20 · Last reviewed 2026-07-20 · Educational information, not medical advice.

Key statistics at a glance

≥30 bpm
sustained heart-rate rise within 10 minutes of standing (≥40 bpm for those under 19), without orthostatic hypotension, defines POTS
Sheldon 2015 HRS consensus; Vernino 2021
~50%
of a 152-patient POTS cohort had sudomotor (sweating) abnormalities on QSART and thermoregulatory sweat testing, indicating distal postganglionic denervation
Thieben 2007 (Mayo Clin Proc)
86.8%
of that POTS cohort were female, with a mean age of about 30 years
Thieben 2007 (Mayo Clin Proc)
44 bpm
mean orthostatic heart-rate increment recorded in the cohort
Thieben 2007 (Mayo Clin Proc)
~1 to 3 million
estimated number of people in the United States living with POTS
Vernino 2021 (Auton Neurosci); Raj 2013

What POTS is

POTS is defined by a sustained increase in heart rate of at least 30 beats per minute (or 40 beats per minute in people under 19) within 10 minutes of standing or head-up tilt, in the absence of a fall in blood pressure that would define orthostatic hypotension, together with chronic symptoms of orthostatic intolerance lasting at least three months. Common symptoms include lightheadedness, palpitations, fatigue, brain fog, and exercise intolerance. The diagnostic thresholds come from the 2015 Heart Rhythm Society expert consensus and are reiterated in the 2019 National Institutes of Health consensus review (Vernino et al., 2021).

POTS is not a single disease but a final common pathway with several overlapping mechanisms, often grouped as neuropathic (a partial autonomic neuropathy affecting peripheral nerves), hyperadrenergic (excess standing noradrenaline), and hypovolemic (low blood volume). It disproportionately affects women of reproductive age. In the Mayo Clinic series, 86.8% of patients were female with a mean age near 30, and expert reviews estimate that roughly 1 to 3 million people in the United States are affected.

Why sweating is affected in POTS

Eccrine sweat glands are driven by sympathetic cholinergic nerves that are part of the same autonomic system disrupted in POTS. When those postganglionic fibers are damaged, the sweating response can be blunted or lost in a length-dependent way, meaning the feet and lower legs are affected first. This is the sudomotor abnormality measured by the quantitative sudomotor axon reflex test (QSART) and the thermoregulatory sweat test (TST).

Not everyone with POTS sweats less. Many patients report the opposite, describing excessive sweating, flushing, and marked heat intolerance, and some report patchy or asymmetric sweating. Reviews of the autonomic symptom burden in POTS note that secretomotor complaints are common and can run in either direction (Vernino et al., 2021). In other words, POTS can be associated with reduced sweating, increased sweating, or both in different body regions, and the sweating change reflects the underlying autonomic disturbance rather than a primary sweat-gland disease.

What the Mayo Clinic cohort found

Thieben and colleagues reviewed 152 patients with POTS evaluated with a full autonomic reflex screen, including QSART and thermoregulatory sweat testing (Mayo Clin Proc 2007).

Selected findings from a 152-patient POTS cohort (Thieben 2007)
Finding	Value	Interpretation
Female sex	86.8%	Strong female predominance, mean age about 30 years
Mean orthostatic heart-rate rise	44 bpm	Well above the 30 bpm diagnostic threshold
Sudomotor abnormalities (QSART + TST)	~50%	Distal postganglionic sympathetic denervation, a neuropathic pattern
Significant adrenergic impairment	34.9%	Overlap of autonomic deficits in many patients
Ganglionic AChR antibody detected	14.6%	Suggests an autoimmune contribution in a subset

This is a referral-clinic cohort at a specialized autonomic center, so the proportion with measurable nerve involvement may be higher than in the general POTS population.

Why sweating differs from person to person

Several factors help explain why sweating in POTS is reduced in some people and increased in others:

Subtype. The neuropathic pattern, present in roughly half of the Mayo cohort, tends to reduce sweating in the feet and legs. The hyperadrenergic pattern, with elevated standing noradrenaline, is more often linked to reports of excessive sweating and flushing.
Distribution. Because autonomic neuropathy is often length-dependent, reduced sweating can appear distally (feet and lower legs) while other areas sweat normally or excessively, producing an uneven picture.
Compensation. When distal sweating is impaired, other regions can sweat more to maintain heat loss, so a person may feel they sweat too much in some places and too little in others.
Overlapping conditions. POTS frequently coexists with small-fiber neuropathy, Ehlers-Danlos syndrome, and other autonomic disorders, each of which can independently affect sweating.
Triggers. Heat, standing, deconditioning, and dehydration all worsen orthostatic symptoms and can change how sweating is experienced day to day.

The neuropathic pattern and sweat testing

The finding that stood out in the Mayo series was that thermoregulatory sweat test results and QSART results were significantly correlated, supporting peripheral postganglionic sympathetic denervation in the legs. On that basis the authors concluded that at least half of the cases had a neuropathic basis. This is why formal autonomic testing in POTS often includes sudomotor measurement: reduced distal sweating is one of the more objective signs of the peripheral nerve involvement that characterizes the neuropathic subtype.

It is worth emphasizing that abnormal sweat testing is a marker of autonomic involvement, not a treatment target in itself. Sweating changes in POTS are managed as part of the overall condition by the clinician coordinating care, not as an isolated symptom.

What this means in plain terms

Sweating changes are a recognized part of POTS because the disorder affects the autonomic nerves that control the sweat glands. The research does not point to a single sweating pattern: reduced sweating (especially in the feet and legs) is common in the neuropathic subtype, while excessive sweating and heat intolerance are also frequently reported. On its own, a change in sweating cannot diagnose POTS, which is defined by the heart-rate response to standing and confirmed with orthostatic testing.

If sweating changes come with the core features of POTS, such as a racing heart on standing, lightheadedness, fatigue, and exercise intolerance, those symptoms are worth discussing with a clinician. This page describes an association reported in the literature; it is educational and cannot determine the cause of any individual's sweating.

Methodology and limitations

This page draws on the Thieben et al. 2007 Mayo Clinic cohort of 152 POTS patients (Mayo Clin Proc 82:308-313), the 2015 Heart Rhythm Society expert consensus statement on postural tachycardia syndrome (Sheldon et al.), the 2019 National Institutes of Health expert consensus review (Vernino et al., Auton Neurosci 2021), and the Raj 2013 Circulation review of POTS. Each figure (30 bpm diagnostic threshold, ~50% sudomotor abnormality, 86.8% female, 44 bpm mean increment, and the 1 to 3 million US estimate) was traced to those sources.

Limitations: the ~50% sudomotor figure comes from a single specialized autonomic referral center and may overstate nerve involvement in milder community cases. POTS is heterogeneous, and the proportion of patients with reduced versus excessive sweating has not been established with a single reliable percentage; the literature describes both. Prevalence figures for POTS are estimates rather than measured population counts. Nothing here is a diagnosis or medical advice; anyone with orthostatic symptoms should be evaluated by a clinician.

Frequently asked questions

Does POTS cause excessive sweating?: It can, but not always. POTS affects the autonomic nerves that control sweat glands, so sweating may be increased, reduced, or uneven. In one large cohort about half of patients had reduced sweating in the legs on testing, while other patients report excessive sweating and heat intolerance.
Why do some people with POTS sweat less?: In the neuropathic subtype, postganglionic sympathetic nerves are damaged in a length-dependent way, which blunts or removes sweating in the feet and lower legs first. This shows up as an abnormal quantitative sudomotor axon reflex test (QSART) or thermoregulatory sweat test.
Is abnormal sweating enough to diagnose POTS?: No. POTS is defined by a sustained heart-rate rise of at least 30 beats per minute (40 in those under 19) within 10 minutes of standing, without a drop in blood pressure, plus chronic orthostatic symptoms. Sweating changes are a supporting feature, not a diagnostic test.
How common is POTS and who does it affect?: Expert reviews estimate that roughly 1 to 3 million people in the United States have POTS. It disproportionately affects women of reproductive age; in the Mayo Clinic cohort, 86.8% of patients were female with a mean age near 30.
What tests measure sweating in POTS?: Autonomic testing can include the quantitative sudomotor axon reflex test (QSART), which measures postganglionic sweat responses, and the thermoregulatory sweat test (TST), which maps whole-body sweating. Reduced distal sweating supports a neuropathic pattern of POTS.
Is this page medical advice?: No. It is a summary of verified figures from published sources. Only a clinician can evaluate orthostatic symptoms and determine whether an individual's sweating relates to POTS or another cause.

Sources

Primary peer-reviewed studies and official sources first, then reviews and institutional framing (secondary).

Thieben MJ, Sandroni P, Sletten DM, et al. Postural orthostatic tachycardia syndrome: the Mayo Clinic experience. Mayo Clin Proc. 2007;82(3):308-313. 152 patients; ~50% with sudomotor abnormalities on QSART and thermoregulatory sweat testing; 86.8% female; mean orthostatic heart-rate increment 44 bpm. Journal
Vernino S, Bourne KM, Stiles LE, et al. Postural orthostatic tachycardia syndrome (POTS): state of the science and clinical care from a 2019 National Institutes of Health Expert Consensus Meeting, Part 1. Auton Neurosci. 2021;235:102828. Diagnostic criteria, epidemiology (estimated 1 to 3 million in the US), and autonomic symptom profile including sudomotor complaints. PubMed
Sheldon RS, Grubb BP, Olshansky B, et al. 2015 Heart Rhythm Society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm. 2015;12(6):e41-e63. Defines the ≥30 bpm (≥40 bpm for age <19) orthostatic heart-rate criterion for POTS. PubMed
Raj SR. Postural tachycardia syndrome (POTS). Circulation. 2013;127(23):2336-2342. Clinical review of mechanisms and epidemiology. (secondary) Full text
Low PA, Sandroni P, Joyner M, Shen WK. Postural tachycardia syndrome (POTS). J Cardiovasc Electrophysiol. 2009;20(3):352-358. Review describing neuropathic, hyperadrenergic, and hypovolemic patterns. (secondary) Full text
Pintér A, Cseh D, Sárközi A, Illigens BM, Siepmann T. Autonomic dysregulation in multiple sclerosis (sudomotor testing methods). Int J Mol Sci. 2015;16(8):16920-16952. Background on QSART and thermoregulatory sweat testing as measures of sudomotor function. (secondary) Full text

How to cite this page

Sweat Explained. POTS and Sweating: What the Research Shows. Published 2026-07-20; last reviewed 2026-07-20. Available at: https://sweatexplained.com/research/pots-and-sweating

Please cite the original studies for the underlying figures. Journalists are welcome to link to this page; the charts are original renderings of the cited data.