The Role of AMPK in the Regulation of Skeletal Muscle Size, Hypertrophy, and Regeneration

Abstract

AMPK (5’-adenosine monophosphate-activated protein kinase) is heavily involved in skeletal muscle metabolic control through its regulation of many downstream targets. Because of their effects on anabolic and catabolic cellular processes, AMPK plays an important role in the control of skeletal muscle development and growth. In this review, the effects of AMPK signaling, and those of its upstream activator, liver kinase B1 (LKB1), on skeletal muscle growth and atrophy are reviewed. The effect of AMPK activity on satellite cell-mediated muscle growth and regeneration after injury is also reviewed. Together, the current data indicate that AMPK does play an important role in regulating muscle mass and regeneration, with AMPKα1 playing a prominent role in stimulating anabolism and in regulating satellite cell dynamics during regeneration, and AMPKα2 playing a potentially more important role in regulating muscle degradation during atrophy.

Heat-Killed Bifidobacterium breve B-3 Enhances Muscle Functions: Possible Involvement of Increases in Muscle Mass and Mitochondrial Biogenesis

“…Indeed, in the present study, we found that daily administration of B-3 to rats for a prolonged period tended to increase muscle mass and activate AMPK, a well-known master metabolic regulator, in the soleus [22,23]. Furthermore, the gene expression of PGC-1α and CCO was higher in the B-3 administration group than in the control group.…”

“…In general, AMPK is well known to inhibit protein synthesis through the suppression of the mTOR, a critical regulator of anabolic pathways [22,23], which indicates that the co-activation of both anabolic and catabolic pathways does not occur in the skeletal muscle at the same time. However, we observed the co-activation of Akt and AMPK in response to B-3HK by western blotting analysis.…”

“…We then examined the effects of B-3 administration on muscle metabolism, which is related to energy productivity and consumption [21]. B-3HK significantly promoted the activation of AMPK ( Figure 4A,B), which regulates energy balance at both the cellular and physiological levels as a master regulator of metabolism [22,23]. No change was observed in the group treated with leucine, a well-known muscle hypertrophy-promoting nutrient.…”

Muscle atrophy and regeneration associated with behavioural loss and recovery of function after sciatic nerve crush

“…The atrophy is executed mainly by regulated proteolysis of contractile proteins through the proteasome but also autophagy‐lysosomal breakdown of other redundant myofibre constituents occur in parallel . The signalling pathways governing contractile protein breakdown is normally active and balanced by stimuli to increase myosins to enlarge myofibre size and muscle mass . Originating from theory that the DNA of a nucleus can support but a limited cellular volume and that this relationship sets a ceiling for growth (; myonuclear domain, MND), major alteration in fibre size should be accompanied by either a reduction of total number of myonuclei or the recruitment and incorporation of de novo formed myonuclei deriving from the regional stem cell niche, ie, Satellite cell (SC) niche .…”

“…[28][29][30] The signalling pathways governing contractile protein breakdown is normally active and balanced by stimuli to increase myosins to enlarge myofibre size and muscle mass. [30][31][32][33][34][35][36] Originating from theory that the DNA of a nucleus can support but a limited cellular volume and that this relationship sets a ceiling for growth (37)(38)(39) ; myonuclear domain, MND), major alteration in fibre size should be accompanied by either a reduction of total number of myonuclei or the recruitment and incorporation of de novo formed myonuclei deriving from the regional stem cell niche, ie, Satellite cell (SC) niche. [40][41][42][43][44] As currently debated, more recent data suggest that both significant atrophy and hypertrophy can occur without changes to number of myonuclei 39,41 or replenishment of myonuclei from the SC cell niche.…”