Physiological significance of elevated levels of lactate by exercise training in the brain and body.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic concepts without systematic search or original human data.
PubMed 36681523 · doi:10.1016/j.jbiosc.2022.12.001
What was done
This narrative review summarizes literature regarding the metabolic and signaling roles of exercise-induced lactate, focusing on its functions across skeletal muscle, heart, liver, kidneys, and the brain, as well as its relationship to metabolic acidosis and chronic disease prevention.
What was found
The abstract provides no empirical data, numbers, or effect sizes. It qualitatively describes that the lactate dehydrogenase reaction consumes protons (delaying metabolic acidosis), accumulated lactate serves as a substrate for hepatic glucose synthesis and direct oxidation, and lactate promotes expression of vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF), with potential implications for hippocampal mitochondrial regulation, depression, and Alzheimer's disease.
Why it matters
It highlights the conceptual shift in exercise physiology from viewing lactate strictly as a fatigue-inducing waste product to recognizing it as a systemic signaling metabolite and fuel source.
Limits
The abstract describes a broad narrative overview without systematic review methods, meta-analytic data, or original experimental results. It provides no quantitative metrics, sample characteristics, or critical appraisals of the underlying primary studies.
Cited by
- supports During vigorous exercise, muscles synthesize lactate and myokines that enter circulation and signal to tissues to stimulate the synthesis of brain-derived neurotrophic factor (BDNF).