Abstract
Skeletal muscle possesses a remarkable ability to adapt to various physiologic conditions. AMPK is a sensor of intracellular energy status that maintains energy stores by fine-tuning anabolic and catabolic pathways. AMPK’s role as an energy sensor is particularly critical in tissues displaying highly changeable energy turnover. Due to the drastic changes in energy demand that occur between the resting and exercising state, skeletal muscle is one such tissue. Here, we review the complex regulation of AMPK in skeletal muscle and its consequences on metabolism (e.g., substrate uptake, oxidation, and storage as well as mitochondrial function of skeletal muscle fibers). We focus on the role of AMPK in skeletal muscle during exercise and in exercise recovery. We also address adaptations to exercise training, including skeletal muscle plasticity, highlighting novel concepts and future perspectives that need to be investigated. Furthermore, we discuss the possible role of AMPK as a therapeutic target as well as different AMPK activators and their potential for future drug development.—Kjøbsted, R., Hingst, J. R., Fentz, J., Foretz, M., Sanz, M.-N., Pehmøller, C., Shum, M., Marette, A., Mounier, R., Treebak, J. T., Wojtaszewski, J. F. P., Viollet, B., Lantier, L. AMPK in skeletal muscle function and metabolism.
Highlights
One fundamental function of skeletal muscle is to generate mechanical force to support body posture and to facilitate a wide variety of movements
Numerous studies have highlighted the role of AMPK as a mediator of cell signaling pathways that are intrinsically linked to muscle function and metabolism
These observations are consistent with the idea that AMPK is essential for a healthy muscle phenotype, a lack of AMPK in skeletal muscle in general only leads to mild alterations in the muscle/whole-body phenotype
Summary
One fundamental function of skeletal muscle is to generate mechanical force to support body posture and to facilitate a wide variety of movements. AICAR appears to induce comparable activation of a1- and a2-containing AMPK complexes and increases glucose uptake in an AMPK a2b2g3 complex–dependent manner [125, 145, 146]. Later observations in the AMPKa2 kinase dead mouse model provided genetic evidence to support a role of AMPK in regulating muscle glucose uptake but not fatty acid oxidation in response to AICAR stimulation [196, 197].
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