Key result
In subjects adapted to hypoxia, no activation of the succinate-ubiquinone-reductase shunt under hypoxic load was observed, indicating blood lymphocyte reaction can serve as a hypoxia tolerance marker.
Observational
The blood lymphocyte reaction and the absence of succinate-ubiquinone-reductase shunt activation can serve as indicators of tolerance and adaptation to acute hypoxia.
Lymphocyte reaction may mark hypoxia tolerance; hypothesis-generating for biomarker validation in prospective studies.
Activation of respiratory chain complex II during acute hypoxia is an adaptive response that facilitates electron transfer in the respiratory chain when complex I is blocked. Stress induced by acute oxygen deficiency in the body stimulates epinephrine and norepinephrine release into the bloodstream. As a result, compensatory metabolic flows and succinate dehydrogenase and succinate oxidation are activated in the cell. Succinate dehydrogenase activation associated with acute hypoxia exhibits characteristic fluctuations; moreover, stronger stimulation results in oscillations with a shorter period and a higher amplitude. These fluctuations are a consequence of the reciprocal relationship between the sympathetic and parasympathetic systems. In subjects who developed adaptation to hypoxia following repeated sessions of breathing a hypoxic gas mixture, no activation of the succinate–ubiquinone-reductase shunt under hypoxic load was observed. The blood lymphocyte reaction can serve as an indicator of tolerance to acute hypoxia.
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Vasin et al. (2018) conducted an observational in Acute hypoxia. Acute hypoxia was evaluated. In subjects adapted to hypoxia, no activation of the succinate-ubiquinone-reductase shunt under hypoxic load was observed, indicating blood lymphocyte reaction can serve as a hypoxia tolerance marker.
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