A qualitative study exploring postpartum patients' experiences with remote blood pressure monitoring.

Lactate was long considered merely a waste product of metabolism and its presence only viewed as a hallmark of incomplete respiration and oxygen deprivation. This view drastically changed when the ability of neurons to use lactate as an energy substrate was discovered and the astrocyte-neuron lactate shuttle hypothesis was proposed. Glial cells and the vascular system provide lactate to neurons that use monocarboxylate transporters (MCTs) for its uptake. While the interstitial brain lactate concentration lies in the low millimolar range at rest, a 2-fold increase can be observed during synaptic activity. Furthermore, intense physical exercise raises plasma lactate concentration up to 10–20 mM, favoring lactate entrance into the brain by crossing the blood-brain barrier. Strong evidence supports the shuttling of energy-rich substrates such as lactate between glia and neurons in the cerebellum, where transport and metabolism of glucose are preferentially attributed to Bergmann glial (BG) over Purkinje cells (PCs). Cerebellar interstitial lactate is increased by 30% during climbing fiber (CF) stimulation, whereas glucose remains constant. The expression of transporters responsible for the release of lactate by BG (MCT4) and its uptake by PCs (MCT2) further supports the existence of a lactate shuttle in the healthy cerebellum. Interestingly, in humans, NMR spectroscopy in patients with ataxia revealed elevated cerebellar lactate levels possibly linked to mitochondrial disorders. It became evident that lactate also serves as a signaling molecule when its specific receptor was identified. Lactate activates a Gi-protein-coupled receptor (GPCR) known as hydroxycarboxylic acid receptor 1 (HCAR1, formerly GPR81), initially identified in adipocytes.