As noted above, our studies have in

As noted above, our studies have indicated that differences in the rate and extent of postmortem tenderization are responsible for variation in tenderness of aged beef. Furthermore, our results have demonstrated that the calpain enzyme system is responsible for the changes that result in meat tenderization. Thus, our approach to tenderness prediction has been to identify a trait that measures the capacity of this enzyme system. The principal regulator of the calpain enzyme system, in postmortem muscle, is its endogenous and specific inhibitor called calpastatin. In several studies designed to determine the biological reason for differences in meat tenderness between Bos indicus and Bos taurus cattle, it was determined that calpastatin activity at 24 hours postmortem would explain a greater proportion of the variation in aged beef tenderness than any other trait measured in those experiments. In a subsequent experiment , postrigor calpastatin was shown to be highly heritable . Furthermore, the genetic correlation between postrigor calpastatin and Warner-Bratzler shear force was 0.50. Collectively, these results demonstrate that selection against postrigor calpastatin activity could result in improved meat tenderness. Furthermore, it suggests that postrigor calpastatin activity could be used as a predictor of beef tenderness. Unfortunately, current methods of calpastatin quantification are laborious and time consuming. We have just developed a rapid method for quantification of calpastatin using an Enzyme-Linked Immunosorbant Assay . We are now in the process of determining the efficacy of postrigor calpastatin as a predictor of beef tenderness using the ELISA.