| Description: |
Despite the end of the COVID-19 pandemic, many patients continue to experience adverse sequelae of the disease, including cardiometabolic disturbances. The spectrum of symptoms associated with long COVID is broad and heterogeneous, necessitating a deeper understanding of the underlying mechanisms. One of the proposed mechanisms contributing to long COVID is transient postviral mitochondrial dysfunction. It is hypothesized that SARS-CoV-2, either directly or indirectly via systemic inflammation, induces metabolic reprogramming of cells, leading to impaired oxidative phosphorylation, reduced ATP production, and increased generation of reactive oxygen species (ROS). Under conditions of metabolic reprogramming, cells preferentially rely on glycolysis for lactate production. Elevated blood lactate levels at low exercise intensity are indicative of mitochondrial dysfunction. Cardiorespiratory fitness is directly related to the integrated function of multiple physiological systems and is considered a reflection of overall health status. The most objective and accurate measure of cardiorespiratory fitness is the direct assessment of maximal oxygen uptake (VO₂max) using cardiopulmonary exercise testing (CPET). Accordingly, monitoring blood lactate levels in conjunction with peak oxygen consumption assessed by CPET may be effectively used in the design of future research studies. The search, selection, and analysis of relevant sources were conducted using scientific databases including cyberleninka.ru, elibrary.ru, link.springer.com, frontiersin.org, pubmed.ncbi.nlm.nih.gov, Google Scholar, and others, with the aim of systematizing current evidence supporting mitochondrial dysfunction as a key pathogenetic mechanism of long COVID. |