Similar Patterns of Dysautonomia in Myalgic Encephalomyelitis/Chronic Fatigue and Post-COVID-19 Syndromes.
Ryabkova, Varvara A, Rubinskiy, Artemiy V, Marchenko, Valeriy N et al. · Pathophysiology : the official journal of the International Society for Pathophysiology · 2024 · DOI
Quick Summary
This study found that people with ME/CFS and those with long COVID have similar problems with how their autonomic nervous system (the system that controls heart rate, blood pressure, and other automatic body functions) works. Researchers measured heart rate variability and blood pressure patterns in 34 ME/CFS patients, 29 long COVID patients, and 32 healthy controls. Both patient groups showed reduced autonomic function compared to healthy people, and these problems were linked to their fatigue—but not to depression or anxiety.
Why It Matters
This research provides objective physiological evidence that ME/CFS and long COVID share common autonomic nervous system dysfunction, which helps validate these conditions and suggests they may benefit from similar autonomic-focused treatments. Understanding that autonomic dysfunction—not psychiatric illness—drives fatigue could shift clinical approaches and improve recognition of these diseases.
Observed Findings
HRV total power and low/high-frequency components were significantly lower in both ME/CFS and PCC patients compared to controls at rest.
Baroreflex sensitivity was significantly reduced in both patient groups.
During slow breathing, HRV parameters normalized in PCC patients but remained abnormal in ME/CFS patients.
Autonomic parameters (HRV, BPV, baroreflex sensitivity) correlated strongly with fatigue severity in both groups.
Neither HRV nor baroreflex parameters correlated with depression/anxiety scores on HADS scale.
Inferred Conclusions
ME/CFS and post-COVID-19 condition share a similar pattern of autonomic nervous system dysfunction characterized by reduced heart rate and blood pressure variability and baroreflex failure.
The autonomic dysfunction represents an accelerated, pathological version of age-related autonomic decline in both conditions.
Autonomic dysregulation in ME/CFS and PCC is mechanistically linked to fatigue rather than to psychiatric comorbidities, suggesting a primary physiological basis for symptom burden.
The differential response to slow breathing (normalization in PCC but not ME/CFS) may indicate distinct mechanisms or disease stages between the two conditions.
Remaining Questions
What This Study Does Not Prove
This study cannot establish causation or determine whether autonomic dysfunction causes fatigue or results from it. Cross-sectional design means it captures a single moment in time and cannot track how autonomic function changes over disease course. The findings do not prove that all ME/CFS and long COVID cases have identical mechanisms or that autonomic dysfunction is the sole pathophysiological driver of these conditions.
Why do ME/CFS and PCC patients show different responses to slow breathing, and what does this difference reveal about underlying disease mechanisms?
Can objective autonomic measures be used as biomarkers to track disease progression and treatment response over time?
What causes the autonomic dysfunction in these conditions—is it primarily vascular, neurological, inflammatory, or multifactorial?
Could treatments specifically targeting autonomic function (such as physical conditioning, medication, or pacing strategies) improve outcomes in ME/CFS and PCC patients?