Cell-cell and intracellular lactate shuttles.
Level 5 - mechanism / opinion, no new human data
Narrative review of physiological and biochemical mechanisms without systematic search methodology or new empirical human data.
PubMed 19805739 · doi:10.1113/jphysiol.2009.178350
What was done
This is a narrative review detailing the conceptual framework and physiological evidence for cell-cell and intracellular lactate shuttles. It examines lactate transport and oxidation across diverse tissues (skeletal muscle, heart, brain, liver, kidneys) and subcellular compartments (mitochondria and peroxisomes) under aerobic conditions.
What was found
The abstract reports no numerical data or statistical effect sizes. Qualitatively, it reports that lactate is continuously produced and utilized aerobically; elevated blood lactate suppresses glucose and free fatty acid oxidation; lactate binding to adipocyte G-protein receptors inhibits lipolysis; lactate generation alters cellular redox state and generates reactive oxygen species; and intracellular lactate upregulates monocarboxylate transporter 1 (MCT1) alongside mitochondrial reticulum genes in skeletal muscle.
Why it matters
It shifts the metabolic paradigm from viewing lactate as a dead-end waste product of anaerobic glycolysis to recognizing it as an essential energy carrier and signaling molecule that coordinates glycolysis with oxidative phosphorylation.
Limits
The abstract describes a narrative review without systematic search protocols, quality assessments, or meta-analytic data. No specific sample sizes, species distinctions (in vitro, animal, or human), or quantitative effect sizes are provided in the abstract.
Cited by
- supports Skeletal muscle produces lactate continuously under fully aerobic conditions.
- supports Lactate released by active skeletal muscle during exercise is taken up and used as a fuel substrate by other organs, including the heart, liver, and brain.