Altered central and peripheral hemodynamics during rhythmic handgrip exercise in young adults with SARS-CoV-2, 2021, Stute et al

[Andy]

Abstract

New Findings

• What is the central question of this study?

• This study sought to investigate whether central and peripheral hemodynamics during handgrip exercise were different in young adults 3–4 weeks following infection with of SARS-CoV-2 compared with young healthy adults.

• What is the main finding and its importance?

• The main findings are that exercising heart rate was higher while brachial artery blood flow and vascular conductance were lower in the SARS-CoV-2 compared with the control group. These findings provide evidence for peripheral impairments to exercise among adults with SARS-CoV-2, which may contribute to exercise limitations.

Abstract

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can have a profound impact on vascular function. While exercise intolerance may accompany a variety of symptoms associated with SARS-CoV-2 infection, the impact of SARS-CoV-2 on exercising blood flow (BF) remains unclear.

Methods
: Central (photoplethysmography) and peripheral (Doppler ultrasound) hemodynamics were determined at rest and during rhythmic handgrip exercise at 30% and 45% of maximal voluntary contraction (MVC) in young adults with mild symptoms 25 days after testing positive for SARS-CoV-2 (SARS-CoV-2: n = 8M/5F; Age: 21±2yrs; Height: 176±11cm; Mass: 71±11kg) and were cross-sectionally compared with control subjects (Control: n = 8M/5F; Age: 27±6yrs; Height: 178±8cm; Mass: 80±25kg).

Results
: Systolic blood pressure, end systolic arterial pressure, and rate pressure product were higher in the SARS-CoV-2 group during exercise at 45%MVC compared with Controls. Brachial artery BF was lower in the SARS-CoV-2 group at both 30%MVC (Control: 384.8±93.3ml·min–1; SARS-CoV-2: 307.8±105.0ml·min–1; p = 0.041) and 45%MVC (Control: 507.4±109.9ml·min–1; SARS-CoV-2: 386.3±132.5ml·min–1; p = 0.002). Brachial artery vascular conductance was lower at both 30%MVC (Control: 3.93±1.07ml·min–1·mmHg–1; SARS-CoV-2: 3.11±0.98ml·min–1·mmHg–1; p = 0.022) and 45%MVC (Control: 4.74±1.02ml·min–1·mmHg–1; SARS-CoV-2: 3.46±1.10ml·min–1·mmHg–1; p<0.001) in the SARS-CoV-2 group compared to Control group. The shear-induced dilation of the brachial artery increased similarly across exercise intensities in the two groups, suggesting the decrease in exercising blood flow may be due to microvascular impairments.

Conclusion
: Brachial artery BF is attenuated during handgrip exercise in young adults recently diagnosed with mild SARS-CoV-2, which may contribute to diminished exercise capacity among those recovering from SARS-CoV-2 like that seen in severe cases.

Open access, https://physoc.onlinelibrary.wiley.com/doi/10.1113/EP089820

 

[alktipping]

: Brachial artery BF is attenuated and did they find a reason for this attenuation and presumably reduced blood flow ?

 

[Hutan]

Finally, when examining the shear-induced brachial artery vasodilation, both groups had similar brachial artery diameter responses to two sustained shear stimuli at 30% and 45% MVC, suggesting the impairment in exercising BF may be due to microvascular impairments downstream of the conduit vessel. Taken together, these findings demonstrate an impaired hyperemic response, but a preservation of conduit vessel endothelial function during small muscle mass exercise in young adults recovering from SARS-CoV-2.

It's sounding like the artery is doing what it should, dilating to allow more blood through in response to exercise. In the post-Covid cohort, heart rate increased, so the heart was trying to pump the blood though. The authors seem to think there is a blockage down stream - so the capillaries or the venules aren't working right.

It's notable that a large number of the post-Covid cohort had mild fatigue.

It would be nice to see the same study done in people with overt Long Covid, and with ME/CFS.

 

[Milo]

It would be nice to see the same study done in people with overt Long Covid, and with ME/CFS

Comparison studies are essential. At this point in the game, the 2 diseases should not work in silos. But then it seems to me that they need to define ‘Long-COVID’, what symptoms are typical and what symptom is actually organ damage or other pathologic process.