Contribution of the phosphagen system to postmortem muscle metabolism in AMP-activated protein kinase γ3 R200Q pig Longissimus muscle.

Pigs with the AMP-activated protein kinase γ3 R200Q (AMPKγ3(R200Q)) mutation generate pork with low ultimate pH (pHu). We hypothesized that reducing muscle creatine (Cr) and phosphocreatine (PCr) may accelerate postmortem ATP consumption and prevent extended pH decline in AMPKγ3(R200Q) longissimus muscle. Wild type and AMPKγ3(R200Q) pigs were assigned to control diet or diet supplemented with the creatine analog β-guanidinopropionic acid (β-GPA, 1%) for 2 wk. β-GPA reduced muscle PCr (P = 0.006) and total Cr (P<0.0001). In general, AMPKγ3(R200Q)+β-GPA exhibited more rapid metabolism than control, AMPKγ3(R200Q), and β-GPA treatment, evidenced by more rapid loss of ATP, more rapid increase in IMP, and decreased pH during the first 90 min postmortem. Overall, pHu was similar despite elevated glycogen (AMPKγ3(R200Q)), reduced total Cr (β-GPA) or both (AMPKγ3(R200Q)+β-GPA). Thus, reducing muscle phosphagens did not affect pHu in AMPKγ3(R200Q) muscle, but it hastened ATP depletion and pH decline.