The coronavirus disease (COVID-19) pandemic has been devastating in all senses, particularly psychologically. Physical activity (PA) is known to aid psychological well-being, and it is worth investigating whether PA has been a coping strategy during this pandemic. The objective of this literature review is to analyze the extent to which engaging in PA during the COVID-19 pandemic impacts psychological health in the adult population. The literature was searched in all databases from the EBSCOhost Research Database—MEDLINE, APA PsycArticles, between others—published between 1 January 2019 and 15 July 2020. From 180 articles found, 15 were eligible. The reviewed articles showed an association between mental health distress—e.g., stress, anxiety, depressive symptoms, social isolation, psychological distress—and PA. This research concludes that the COVID-19 pandemic and the lockdown measures caused psychological distress. Those studies that analyzed PA showed that, during quarantine, adults increased their sedentary time and reduced their PA levels, showing controversial psychological outcomes. This review discusses whether PA is an effective strategy to face the COVID-19 pandemic psychological effects contributing to a further putative increase in the prevalence of psychiatric disorders.

With its capacity to survey the environment and phagocyte debris, microglia assume a diversity of phenotypes to respond specifically through neurotrophic and toxic effects. Although these roles are well accepted, the underlying energetic mechanisms associated with microglial activation remain largely unclear. This study investigates microglia metabolic adaptation to ATP, NADPH, H⁺, and reactive oxygen species production. To this end, in vitro studies were performed with BV‐2 cells before and after activation with lipopolysaccharide + interferon‐γ. Nitric oxide (NO) was measured as a marker of cell activation. Our results show that microglial activation triggers a metabolic reprogramming based on an increased glucose uptake and a strengthening of anaerobic glycolysis, as well as of the pentose pathway oxidative branch, while retaining the mitochondrial activity. Based on this energy commitment, microglial defense capacity increases rapidly as well as ribose‐5‐phosphate and nucleic acid formation for gene transcription, essential to ensure the newly acquired functions demanded by central nervous system signaling. We also review the role of NO in this microglial energy commitment that positions cytotoxic microglia within the energetics of the astrocyte–neuron lactate shuttle.

Glibenclamide is neuroprotective against cerebral ischemia in rats. We studied whether glibenclamide enhances long-term brain repair and improves behavioral recovery after stroke. Adult male Wistar rats were subjected to transient middle cerebral artery occlusion (MCAO) for 90 minutes. A low dose of glibenclamide (total 0.6 μg) was administered intravenously 6, 12, and 24 hours after reperfusion. We assessed behavioral outcome during a 30-day follow-up and animals were perfused for histological evaluation. In vitro specific binding of glibenclamide to microglia increased after pro-inflammatory stimuli. In vivo glibenclamide was associated with increased migration of doublecortin-positive cells in the striatum toward the ischemic lesion 72 hours after MCAO, and reactive microglia expressed sulfonylurea receptor 1 (SUR1) and Kir6.2 in the medial striatum. One month after MCAO, glibenclamide was also associated with increased number of NeuN-positive and 5-bromo-2-deoxyuridine-positive neurons in the cortex and hippocampus, and enhanced angiogenesis in the hippocampus. Consequently, glibenclamide-treated MCAO rats showed improved performance in the limb-placing test on postoperative days 22 to 29, and in the cylinder and water-maze test on postoperative day 29. Therefore, acute blockade of SUR1 by glibenclamide enhanced long-term brain repair in MCAO rats, which was associated with improved behavioral outcome.