Exercise signalling to glucose transport in skeletal muscle.
Level 5 - mechanism / opinion, no new human data
Narrative review of molecular mechanisms without systematic review methods or new human data
PubMed 15294032 · doi:10.1079/PNS2004343
What was done
Narrative review summarizing the molecular signaling mechanisms responsible for contraction-induced, insulin-independent GLUT4 translocation and glucose transport in skeletal muscle.
What was found
The abstract reports no numerical findings. It identifies multiple putative regulatory pathways for exercise-stimulated glucose uptake, including calcium-sensitive pathways (Ca2+/calmodulin-dependent protein kinase II and protein kinase C isoforms), metabolic status sensors (5'AMP-activated protein kinase), and activation pathways such as p38 mitogen-activated protein kinase, alongside muscle fiber type differences.
Why it matters
Highlights the intracellular signaling networks mediating exercise-induced glucose transport independent of insulin action, clarifying molecular targets involved in muscle energy metabolism.
Limits
Contains no original empirical data, quantitative meta-analysis, or systematic literature search criteria. Signaling interactions and the role of fiber type heterogeneity remain incompletely characterized.
Cited by
- supports Muscle contraction triggers glucose transporter translocation to muscle cell surfaces independently of insulin.