E2 ModerateModerate confidencePEM not requiredCross-SectionalPeer-reviewedMachine draft
High flow variant postural orthostatic tachycardia syndrome amplifies the cardiac output response to exercise in adolescents.
Pianosi, Paolo T, Goodloe, Adele H, Soma, David et al. · Physiological reports · 2014 · DOI
Quick Summary
This study found that about 40% of adolescents with POTS (a condition causing dizziness, fatigue, and rapid heartbeat when standing) have an unusual heart response to exercise: their hearts pump out more blood than expected to keep blood pressure normal. Instead of blood vessels tightening during exercise as they normally do, these patients' blood vessels stay too relaxed, forcing the heart to work harder by pumping more blood to maintain adequate pressure.
Why It Matters
This study identifies a physiological mechanism in some POTS patients—failure of normal blood vessel constriction during exercise—that may explain both their exercise intolerance and symptom overlap with ME/CFS. Understanding that POTS involves abnormal cardiovascular regulation rather than simple deconditioning could guide more targeted treatments for overlapping fatigue conditions.
Observed Findings
- Approximately 40% of POTS adolescents (41/107) demonstrated hyperkinetic cardiac output response to exercise with slopes of 8.99 ± 1.31 L/min per L/min VO₂.
- The remaining 60% of POTS patients (66/107) showed normal cardiac output slopes of 5.08 ± 1.17 L/min per L/min VO₂, similar to non-POTS controls.
- 141 adolescents with chronic fatigue but without POTS showed a normal distribution of CO/VO₂ slopes averaging 6.10 ± 2.09 L/min per L/min VO₂.
- Mean arterial blood pressure and pulse pressure increased similarly from rest to exercise in both POTS and non-POTS groups, despite differences in cardiac output response.
Inferred Conclusions
- 40% of POTS adolescents demonstrate a hyperkinetic circulatory state during exercise distinct from simple deconditioning.
- Hyperkinetic POTS likely results from failure of normal regional vasoconstriction during exercise, requiring compensatory increases in cardiac output to maintain blood pressure.
- POTS may represent a heterogeneous condition with at least two physiologically distinct subtypes based on cardiac output response patterns.
Remaining Questions
- What causes the failure of normal vasoconstriction in the hyperkinetic POTS subgroup—autonomic dysfunction, endothelial abnormality, or other mechanisms?
- Do these two POTS subtypes respond differently to treatments, and should clinical management differ between them?
What This Study Does Not Prove
This study does not prove that all POTS patients have hyperkinetic circulation (only ~40% showed this pattern), nor does it establish that this mechanism causes ME/CFS or vice versa. The cross-sectional design cannot determine whether abnormal vasoconstriction is a primary cause or secondary consequence of chronic illness. The study does not address whether these findings apply to adults or to POTS patients with explicit ME/CFS diagnosis.
Tags
Symptom:Post-Exertional MalaiseOrthostatic IntoleranceFatigue
Biomarker:Blood Biomarker
Phenotype:Pediatric
Method Flag:PEM Not DefinedExploratory OnlyMixed Cohort
Metadata
- DOI
- 10.14814/phy2.12122
- PMID
- 25168872
- Review status
- Machine draft
- Evidence level
- Single-study or moderate support from human research
- Last updated
- 8 April 2026
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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