What is the clinical evidence from this study?

Study design: Case-Control. Population: Long COVID (n=21). Intervention: Long COVID vs. Controls. Primary outcome: Peak V̇O2 (mL·kg−1·min−1) (p=0.04).

What question did this study set out to answer?

To determine whether persistent endothelial dysfunction or altered myocardial work underlies ongoing exercise intolerance three years after SARS-CoV-2 infection.

October 1, 2026Physiological ReportsOpen Access

Persistent endothelial dysfunction is associated with exercise intolerance in adults despite preserved myocardial work 3 years after SARS‐CoV‐2 infection

Q: What are the key findings of this study?

Long COVID 3 years post-infection was associated with lower peak V̇O2 (19.6 vs 24.3 mL/kg/min, p=0.04) and impaired endothelial function (p<0.001) despite preserved myocardial work.

Q: What does this research mean for the field?

Persistent exercise intolerance in Long COVID approximately three years post-infection is associated with peripheral endothelial dysfunction rather than impaired myocardial work. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

Long COVID at 3 years linked to ~19% lower peak VO2 and impaired endothelial function.

P=0.04
n=21

Why the study?

The relative contributions of peripheral vascular dysfunction and myocardial function to persistent exercise intolerance in Long COVID remain unclear.

Is persistent exercise intolerance in adults 3 years after SARS-CoV-2 infection associated with endothelial dysfunction or altered myocardial work?

Comparison

Long COVID vs controls

Design

Case-control study

Follow-up

Approximately 3 years after SARS-CoV-2 infection

Authors

CACarla Cristina de AraújoUniversidade de Brasília CGCássia da Luz GoulartUniversidade de Brasília LDLuciana Bartolomei Orru D’ÁvilaUniversidade de Brasília

Discussion

Member takes

Overview

Endothelial dysfunction may drive persistent Long COVID exercise intolerance; hypothesis-generating for vascular-targeted trials in larger cohorts.

Key Points

To determine whether persistent endothelial dysfunction or altered myocardial work underlies ongoing exercise intolerance three years after SARS-CoV-2 infection.
Conducted a case–control study comparing adults with Long COVID (n = 10) to healthy controls (n = 11) approximately 3 years post-infection.
Assessed exercise performance via cardiopulmonary exercise testing (CPET), cardiac mechanics via echocardiography with global longitudinal strain and myocardial work indices, and peripheral vascular function via brachial artery flow-mediated dilation (FMD).
Long COVID participants showed lower peak V̇O2 (19.6 ± 2.5 vs. 24.3 ± 6.5 mL·kg−1·min−1, p = 0.04) and percent-predicted peak V̇O2 (61.1 ± 8.3 vs. 77.0 ± 14.2%, p = 0.006).
Conventional echocardiographic markers and myocardial work indices showed no significant differences between groups (all p > 0.05).
Vascular endothelial function was significantly reduced in Long COVID with lower FMD (p < 0.001) and peak shear rate (p = 0.01), with FMD correlating positively with peak V̇O2 (r = 0.68, p = 0.03).

Study Design

Type

Case-Control (n=21)

Structured PICO

Is persistent exercise intolerance in adults 3 years after SARS-CoV-2 infection associated with endothelial dysfunction or altered myocardial work?

Population

21 adults (10 with Long COVID and 11 controls) evaluated for exercise intolerance and endothelial dysfunction approximately 3 years after SARS-CoV-2 infection.

Exposure

Long COVID (prior SARS-CoV-2 infection approximately 3 years prior)

Comparator

Controls without Long COVID

Outcome

Exercise capacity (peak V̇O2, percent-predicted peak V̇O2, V̇O2 at first ventilatory threshold), myocardial work (MW) via echocardiography, and endothelial function via brachial artery flow-mediated dilation (FMD)surrogate

Main Result

Absolute Event Rate: 19.6% vs 24.3%

p-value: p=0.04

Persistent exercise intolerance in Long COVID 3 years post-infection is associated with peripheral endothelial dysfunction rather than impaired myocardial work.

Cite This Study

Araújo et al. (2026) conducted a case-control in Long COVID (n=21). Long COVID vs. Controls was evaluated on Peak V̇O2 (mL·kg−1·min−1) (p=0.04). Long COVID 3 years post-infection was associated with lower peak V̇O2 (19.6 vs 24.3 mL/kg/min, p=0.04) and impaired endothelial function (p<0.001) despite preserved myocardial work.

synapsesocial.com/papers/6abda8ff4d657f10339f95b5 https://doi.org/10.14814/phy2.71103

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October 1, 2026Physiological ReportsOpen Access

Persistent endothelial dysfunction is associated with exercise intolerance in adults despite preserved myocardial work 3 years after SARS‐CoV‐2 infection

View Full Paper

Ask AI

Bookmark

Key result

Long COVID at 3 years linked to ~19% lower peak VO2 and impaired endothelial function.

P=0.04
n=21

Why the study?

The relative contributions of peripheral vascular dysfunction and myocardial function to persistent exercise intolerance in Long COVID remain unclear.

Is persistent exercise intolerance in adults 3 years after SARS-CoV-2 infection associated with endothelial dysfunction or altered myocardial work?

Comparison

Long COVID vs controls

Design

Case-control study

Follow-up

Approximately 3 years after SARS-CoV-2 infection

Authors

CACarla Cristina de AraújoUniversidade de Brasília CGCássia da Luz GoulartUniversidade de Brasília LDLuciana Bartolomei Orru D’ÁvilaUniversidade de Brasília

Discussion

Member takes

Overview

Endothelial dysfunction may drive persistent Long COVID exercise intolerance; hypothesis-generating for vascular-targeted trials in larger cohorts.

Key Points

To determine whether persistent endothelial dysfunction or altered myocardial work underlies ongoing exercise intolerance three years after SARS-CoV-2 infection.
Conducted a case–control study comparing adults with Long COVID (n = 10) to healthy controls (n = 11) approximately 3 years post-infection.
Assessed exercise performance via cardiopulmonary exercise testing (CPET), cardiac mechanics via echocardiography with global longitudinal strain and myocardial work indices, and peripheral vascular function via brachial artery flow-mediated dilation (FMD).
Long COVID participants showed lower peak V̇O2 (19.6 ± 2.5 vs. 24.3 ± 6.5 mL·kg−1·min−1, p = 0.04) and percent-predicted peak V̇O2 (61.1 ± 8.3 vs. 77.0 ± 14.2%, p = 0.006).
Conventional echocardiographic markers and myocardial work indices showed no significant differences between groups (all p > 0.05).
Vascular endothelial function was significantly reduced in Long COVID with lower FMD (p < 0.001) and peak shear rate (p = 0.01), with FMD correlating positively with peak V̇O2 (r = 0.68, p = 0.03).

Study Design

Type

Case-Control (n=21)

Structured PICO

Is persistent exercise intolerance in adults 3 years after SARS-CoV-2 infection associated with endothelial dysfunction or altered myocardial work?

Population

21 adults (10 with Long COVID and 11 controls) evaluated for exercise intolerance and endothelial dysfunction approximately 3 years after SARS-CoV-2 infection.

Exposure

Long COVID (prior SARS-CoV-2 infection approximately 3 years prior)

Comparator

Controls without Long COVID

Outcome

Main Result

Absolute Event Rate: 19.6% vs 24.3%

p-value: p=0.04

Persistent exercise intolerance in Long COVID 3 years post-infection is associated with peripheral endothelial dysfunction rather than impaired myocardial work.

Cite This Study

synapsesocial.com/papers/6abda8ff4d657f10339f95b5 https://doi.org/10.14814/phy2.71103

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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