Temperature, but not excess of glycogen, regulate post-mortem AMPK activity in muscle of steer carcasses.

Abstract

Post-mortem muscle temperature affects the rate of decline in pH in a linear manner from 37.5 {degrees}C down near 0 {degrees}C, and this pH decline is correlated with the enzymatic degradation of glycogen to lactate. This transformation occurs in an anaerobic context that includes the metabolic splice between glycogenolysis and glycolysis; and both processes are strongly upregulated by AMPK enzyme. In this study we reported changes (0.5 h and 24 h post-mortem) in muscle glycogen concentration, lactate and AMPK activity from 12 samples of Longissimus dorsi from 38 steers that produced high pH (>5.9) and normal pH (<5.8) carcasses at 24 h post-mortem. Moreover, we evaluated changes in AMPK activity in samples from both categories incubated at 37, 25, 17 and 5 {degrees}C and supplemented with exogenous glycogen. Finally, we analysed if there were structural differences between polymers from both categories. Our analyses show that enzymatic AMPK activity was significantly higher at 17 {degrees}C than at 37 {degrees}C or 25 {degrees}C (p<0.0001 and p<0.05 in samples from normal and high pH categories, respectively), and was near zero at 5 {degrees}C. On the other hand, AMPK activity did not change in relation with excess glycogen and we did not detect structural differences in the polymers present in samples from both categories. We concluded that post-mortem AMPK activity level is highly sensitive to temperature and not at in vitro changes in glycogen concentration. Their results suggest that that normal levels of pre-mortem muscle glycogen and an adequate cooling managing of carcasses are relevant to let an efficient glycogenolytic/glycolytic flow required for lactate accumulation and pH decline, trough of post-mortem AMPK signalling pathway.