In situ investigation of the calcium-induced proteolytic and salting-in mechanisms causing tenderization in calcium-enhanced muscle

The objective of this experiment was to explore the mechanism(s) of calcium-induced tenderization in calcium-enhanced beef muscle. At 72 h postmortem, beef strip loins (n=15) were injected (9% by weight) with 0.0, 0.05, 0.1, 0.2, or 0.4 M calcium chloride (CaCl2) with and without 0.05 M zinc chloride (ZnCl2), and aged until 15 days postmortem. Warner–Bratzler shear force peak values indicated that addition of ZnCl2 drastically inhibited tenderization; however, enhancement with CaCl2 still tended to reduce shear values (P=0.07; 0.55 kg) when ZnCl2 was present. In the absence of ZnCl2, the 0.2 and 0.4 M CaCl2 treatments were 18.9 and 32.1% more (P<0.05) tender than the 0.0 M CaCl2 treatment. SDS-PAGE indicated that addition of zinc reduced breakdown of troponin-T into ∼31 and ∼28 kDa components. Transmission electron micrographs indicated that addition of CaCl2 without ZnCl2 caused more frequent Z-line fractures and increased lateral spreading of myofibrils. These results suggest that both calcium-activated enzymatic activity and a non-enzymatic salting-in effect contributed to tenderization of calcium-enhanced muscle. However, the enzymatic mechanism reduced toughness 2.9- to 7.5-fold more than the non-enzymatic mechanism. Calcium-activated enzymatic degradation appears to be the major tenderization mechanism and non-enzymatic salting-in of calcium ions appears to be a minor tenderization mechanism, even at high calcium concentrations.