Figure 4.

Acute muscle-specific deletion impairs glycogen synthesis following exercise and abrogates the ability for glycogen supercompensation following exercise. A novel mouse model with acute genetic deletion of AMPK catalytic activity in skeletal muscle was generated. Deletion of the catalytic subunits AMPK α1 and α2 and reduced signaling of the downstream targets TBC1D1 and ACC was verified by immunoblotting (A). Protein expression of mitochondrial complex proteins (Complex I-V) in quadriceps muscle was investigated by use of specific antibodies (B). In vivo glycogen synthesis rate (C), glucose uptake (D) and muscle glycogen concentration (E) were assessed in quadriceps muscle from WT mice and mice with acute inducible deletion of AMPK catalytic activity (imdKO). Glycogen synthesis rate and glucose uptake was investigated in vivo in response to oral glucose gavage (2 g/kg body wt) in the rested state (Rest + 1 h Glucose) and exercised state (Exercise + 1 h Glucose). Muscle glycogen content in quadriceps muscle was measured in the basal state and 5 h post exercise with glucose gavage (2 g/kg body wt) given immediately after 1½ h exercise and again following 1 h recovery. ^###p ≤ 0.001 for different from corresponding resting value. ^†p ≤ 0.005 and ^††p ≤ 0.01 for effect of genotype. Data are presented as means ± SEM (n = 4–8).