Long COVID is a multisystem condition that comprises a set of symptoms following a
SARS-CoV-2 infection. At least 65 million people around the world present symptoms
associated with persistent COVID, an incidence of 10% of infected people is estimated1.
The incidence is estimated at 10-30% of non-hospitalized cases, 50-70% of hospitalized
cases2,3, and 10-12% of vaccinated cases4,5. Persistent COVID is associated with all ages
and severity of illness in the acute phase, with the highest percentage of diagnoses
between the ages of 36 and 50 years, and the majority of cases of persistent COVID are
found in non-hospitalized patients with a mild acute illness6, as this population
represents the majority of overall COVID-19 cases. The most prevalent symptoms in
persistent COVID are fatigue, dyspnea and weakness7.

In our first published study the investigators observed that patients with fatigue after
SARS CoA2 infection behaved very similarly to COPD patients, observing a decrease in
mechanical efficiency (ME) at the first threshold, second threshold and at maximum
consumption. of oxygen during an incremental test8. (Figure 1).

Mechanical efficiency (ME) refers to the ability of an individual to transform oxygen
consumption into effective work. In other words, poorer efficiency will increase the
percentage of maximum oxygen uptake (VO2max) needed to sustain a given mechanical work. A
decrease in ME, indicating that more energy is expended in a given work output, could
represent an increased energy cost of respiration during exercise, an altered efficiency
in ATP production (ATP produced per O2 consumed), or a higher ATP cost of contraction
(ATP consumed by work production)9. Patients with a decreased ME would decrease their
performance and, therefore, could be limited in terms of physical activity9.

In our second study, the investigators observed that patients recovered from SARS-CoV-2
but with symptoms of fatigue presented significant muscle dysfunction compared to healthy
women with similar characteristics. These findings were corroborated by detecting an
increase in VO2sc and a deterioration in ME and ventilatory efficiency during the
constant load test10. These results guide us towards a problem of oxygen diffusion in the
muscle cell that the investigators are confirming with the findings currently obtained in
quadriceps muscle biopsies. The hypothesis of causing an increase in the dilation of
muscle capillaries to improve oxygen diffusion made us think about the vasodilator and
ergogenic effects of beets.

Beet juice (BRJ) has become increasingly popular among athletes looking to improve sports
performance. BRJ contains high concentrations of nitrate, which can be converted to
nitric oxide (NO) after consumption. NO has several functions in the human body,
including a vasodilatory effect, which reduces blood pressure and increases the delivery
of oxygen and nutrients to various organs. BRJ consumption also has an impact on oxygen
delivery to skeletal muscles, muscle efficiency, tolerance and endurance and can
therefore have a positive impact on sports performance12.

Once ingested, NO3- is reduced to nitrite (NO2-) by anaerobic bacteria in the oral cavity
through the action of nitrate reductase enzymes13 and then to nitric oxide (NO) in the
stomach14. This physiological mechanism depends on the entero-salivary circulation of
inorganic nitrate without involving the activity of NOS. Once in the stomach (at an
acidic pH), nitrite is instantly decomposed to become NO and other nitrogen oxides that
perform crucial physiological functions. The remaining nitrate and nitrite are absorbed
from the intestine into the circulation, which can be converted to bioactive NO in
tissues and blood under conditions of physiological hypoxia14. NO induces several
physiological mechanisms that influence O2 utilization during contraction of the
intestine. skeletal muscle. The physiological mechanisms for NO2- reduction are
facilitated by hypoxic conditions, therefore NO is produced in those parts of the muscle
that consume or need more O2. This mechanism would allow local blood flow to adapt to the
O2 requirement, providing an adequate homogeneous distribution within the skeletal
muscle. This physiological response could be positive in terms of muscle function,
although it would not explain the reduction in O2 expenditure during exercise15. Another
probable mechanism is related to NO2- and NO as regulators of cellular O2 utilization15.