Other metabolic state and existing conditions of muscle often direct the extent of pH decline in postmortem muscle.
Many studies have reported the effect of treatment to decrease glycogen content in muscle to minimize lactate accumulation in postmortem muscle (reviewed by Rosenvold & Andersen, 2003).
Genetic factors influencing basal metabolism clearly have the potential to
similarly affect lactate accumulation and extent of pH decline.
The discovery (Milan et al., 2000) of a non-conserved substitution in protein kinase adenosine monophosphate- activated c3-subunit gene (PRKAG3) has
explained the dominant mutation (denoted RN) that accounted for large differences in meat quality and processing yield in the Hampshire pig breed (Monin & Sellier,
1985).
The substitution (R200Q) in the PRKAG3 gene causes a 70% increase in muscle glycogen in RN homozygous and heterozygous pigs. This increase in
glycogen directly results in greater production of lactate in postmortem muscle, a lower ultimate pH and poorer water holding capacity in fresh pork.