Prior beetroot juice ingestion offsets endothelial dysfunction following prolonged sitting, 2022, Takuma Morishima et al

[Mij]

For the record, I drank tons of beetroot juice when I was juicing in the 90s. I'm still 'here'.


Abstract

Nutritional strategies to prevent endothelial dysfunction following prolonged sitting remain largely unknown. Given that beetroot juice (BRJ) ingestion enhances nitric oxide (NO) bioavailability, we aimed to evaluate whether prior BRJ ingestion would prevent sitting-induced endothelial dysfunction in the leg.

Eleven healthy young males (n = 7) and females (n = 4) underwent two experimental trials of prolonged sitting with prior: 1) placebo ingestion (PL trial) and 2) BRJ ingestion (BRJ trial). All subjects ingested 140 ml of PL or BRJ (~0.0055 or ~12.8 mmol of nitrate, respectively) immediately before 3 h of sitting.

Pre and post-sitting measurement of popliteal artery flow-mediated dilation (FMD) and blood pressure, and blood collection were undertaken. During the sitting period, an hourly assessment of popliteal artery diameter and blood velocity, blood pressure, and blood collection was performed. Popliteal artery blood flow and shear rate were significantly and similarly reduced during the sitting period in both trials (p < 0.001).

Plasma nitrate and NOx (total nitrite and nitrate) concentrations were significantly increased relative to baseline in the only BRJ trial, and the overall concentrations were significantly higher in the BRJ trial (p < 0.001). Popliteal artery FMD was significantly reduced after the sitting period in the PL trial (p < 0.05), whereas no reduction was observed in the BRJ trial. Therefore, prior BRJ ingestion would prevent sitting-induced leg endothelial dysfunction via enhancing NO bioavailability.


https://journals.physiology.org/doi/abs/10.1152/japplphysiol.00200.2022

 

[Hutan]

I haven't seen the full article.

Comparing 3 hours of sitting after drinking a glass of beetroot juice to 3 hours sitting after drinking a placebo - in healthy young people:

Regardless of which drink they had, there was a similar reduction in leg artery blood flow and shear rate.
Through thick and thin: The interdependence of blood viscosity, shear stress and endothelial function

Shear rate is often estimated from ultrasound-derived arterial diameter and blood velocity (shear rate = blood velocity/diameter).

Flow-mediated dilation - was reduced with placebo + sitting, but not after beetroot juice + sitting
Flow-mediated dilation is measured by cutting off the blood supply for a moment e.g. with a blood pressure cuff, and then letting the blood flow, and measuring the widening of the artery when the blood flow increases.

The beetroot juice did seem to increase plasma nitrate and total nitrites and nitrate in the blood. (Which is relevant because endothelial cells make blood vessels dilate by releasing nitric oxide.)

So, they conclude that beetroot juice prevents sitting-induced endothelial dysfunction.

I'm not entirely sure that a reduction in flow-mediated dilation after sitting (as occurred with the placebo) is 'endothelial dysfunction'. Remember, these are healthy young volunteers who are sitting. There isn't a high demand for oxygen by leg tissue while they are sitting. A brief interruption in blood supply during the FMD measurement makes it more important to get a small amount of blood to all of the tissues quickly, rather than a large amount of blood to the tissues slowly. So, it's better to keep the pipes narrow when the blood supply re-starts during the FMD measurement.

So, maybe the beetroot juice actually stops endothelial function which is normal during prolonged sitting occurring in these healthy young people.

 

[Hutan]

Endothelial dysfunction and FMD responses to nitric oxide are of interest in ME/CFS e.g
from Fluge, Mella and Tronstad's 'Pathomechanisms and possible interventions in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)' paper.

There is growing evidence for endothelial dysfunction in ME/CFS, affecting large arteries, assessed by flow-mediated dilation (FMD), and small arteries, assessed by postocclusive reactive hyperemia (refs. 9, 10, and Figure 1). FMD mainly reflects the release of nitric oxide (NO) from endothelial cells in response to shear stress in vessel walls. However, patients had intact ability to dilate adequately from endothelium-independent vasodilation when given sublingual nitroglycerin. The endothelial dysfunction was not associated with laboratory markers of endothelial dysfunction seen in cardiovascular disease, which argues for a different mechanism, possibly related to an abnormal immune response (10).