Date of this Version
1995 Poultry Science 74:176-186
This study was conducted to elucidate the mechanism of action of two selected rigor mortis-accelerating treatment systems employed in the prevention of the toughness associated with early-harvested (1 h post-mortem) broiler Pectoralis muscle. The treatments included 14 min of low voltage electrical stimulation (110 V, 1 A, pulsing 1 s on and 1 s off) combined with high temperature conditioning (39 C) and muscle tensioning (LV + HTC + MT); a 15-s high voltage stimulation (440 V, 1 A pulsing 2 s on and 1 s off) combined with muscle tensioning (HV + MT); and a control simulating commercial broiler processing practices. The rigor-accelerating treatments reduced pH and increased R-value (inosine:adenosine ratio) at 1 h post-mortem, but only the LV + HTC + MT treatment reduced sarcomere shortening. Both rigor treatments reduced the amount of measurable myofibrillar fragmentation. Cathepsin B and B + L activities were not affected by the rigor treatments. Calpain I activity was not detectable in any 24-h post-mortem sample. Calpain II activity at 24 h post-mortem was greater in muscles receiving HV + MT than from the LV + HTC + MT or control carcasses, but was reduced in all muscles by 24 h postmortem. An SDS-PAGE indicated a 30-kDa polypeptide that was absent at death and appeared in control and LV + HTC + MT muscles but to a lesser extent in HV + MT muscles. These results suggested that the LV + HTC + MT treatment has a greater tenderizing effect than the HV + MT treatment because the former achieves a better balance between reduced sarcomere shortening and myofibrillar fragmentation.