The rise of thawing drip: Freezing rate effects on ice crystallization and myowater dynamics changes.

To better reveal the formation of thawing drip, this study investigated the ice crystallization and myowater dynamics changes in frozen bovine Longissimus dorsi muscle. In ultra-fast freezing a narrow distribution of ice crystals size was observed together with higher solubility, lower surface hydrophobicity and stable second structure of myofibrillar protein. Accordingly, ultra-fast freezing samples exhibited significantly lower thaw loss (4.35 %) than slow freezing (8.22 %) after 48 h of freezing. Upon thawing, 2D T1-T2 relaxation spectra indicated a myowater redistribution, in which slow freezing led to major migration of water from immobile water to free water. Besides, T1 and T2 relaxation times showed an increasing trend with freezing process. The proton density images displayed major free water seep from myofibrils to the surface of muscle. Consequently, the water from the "reservoir" (free water) flowed into the "channel" (the widened spaces between muscle fibres), and formed into the thawing drip.

Contribution of calpain to protein degradation, variation in myowater properties and the water-holding capacity of pork during postmortem ageing.

To investigate calpain's effect on protein degradation, myowater properties, and the water-holding capacity (WHC), porcine longissimus muscles were incubated with control buffer, PD150,606 (calpain-specific inhibitor) and MG-262 (multiple-protease inhibitor) and assigned to an ageing period of 1, 4 or 7 d. Over 7 d of storage, no significant differences (P > 0.05) were observed in desmin or integrin expression between the MG-262 and PD150,606 groups, which indicated that calpain played a major role in protein proteolysis. Compared to those in the control group, muscle samples subjected to PD150,606 and MG-262 exhibited higher water mobility and a poorer WHC. Additionally, there were no significant differences in myowater properties or the WHC between the two groups at 1 d postmortem (P > 0.05). Calpain regulated the distribution and mobility of myowater, which contributed to a higher WHC in the early postmortem period (before 4 d), but other proteases tended to take over at a later stage.