Pressure-heat treatment of meat: Changes in myofibrillar proteins and ultrastructure.

The effects on muscle of a combined pressure-heat (P-H) treatment that overcomes myofibrillar toughness have been investigated using SDS gel electrophoresis and electron microscopy. Densitometer scans of polyacrylamide gels of muscle extracts revealed that P-H treatment caused greater degradation of connectin than did heat treatment alone. Breakdown of connection by P-H treatment was reduced in muscle that had been injected with the protease inhibitor pepstatin. However, pepstatin treatment did not reduce the effectiveness of P-H treatment for tenderizing meat, as would be expected if connectin was responsible for myofibrillar toughness. P-H treatment resulted in an increase in the intensity of a peak with M(r) ∼ 150 000, but this peak was also produced by non-tenderizing pressure treatments. The ultrastructural studies revealed that P-H treatment disrupted the thick and the thin filaments, leaving voids at the M-line region. It is suggested that P-H treatment achieves most of its effect by an irreversible disaggregation of the myosin of thick filaments.

Binding of comminuted meat: Effect of high pressure.

Patties prepared from comminuted meat were pressure-treated at up to 150 MPa at 0-3°C and the cohesion between meat particles in the cooked patty investigated from tensile strength measurements. Pressure treatment increased tensile strength, the magnitude of the increase depending upon the intensity and duration of pressure treatment, the concentration of salt in the patty and pH value. The effect was most pronounced in patties of pH 5 to 6 and with 1% salt in the aqueous phase. Under these conditions cooking losses were reduced. When compared with the effect of addition of 0·5% tetrasodium pyrophosphate in a patty with 1% salt, pressure treatment retained its effect at lower pH values.

Pressure-induced pH and length changes in muscle.

The response to increase in pressure of pre- and post-rigor muscle strips supporting a load has been investigated by measuring length changes with application of pressure up to 150 MPa in a windowed pressure vessel. The response of the pre-rigor strips depended on temperature; at 30°C the strips contracted, then, after some minutes, lengthened, presumably because of a breakdown of myofibrillar integrity. At 0°C the cold-shortened muscle lengthened but if pressure was released the strips shortened again. Loaded post-rigor muscle strips lengthened with application of pressure. It is suggested that the conditions that prevail in pre-rigor muscle are not as favourable for disaggregation of the myofilaments as those in post-rigor muscle. Measuresurement of pH changes in pre-rigor pressure-treated muscle showed these were accelerated at 30°C, but completely inhibited by treatment at 0°C for 3 or 24h.

Pressure treatment of meat: Effects on thermal transitions and shear values.

The effects of pressure treatment (150 MN m(-2) for 3 h at 0°C) on the pH, thermal transitions, ultrastructure and Warner-Bratzler shear values of post-rigor beef semimembranosus and longissimus dorsi muscles have been investigated. Pressure treatment resulted in a slight but significant increase in pH. Differential scanning calorimetry revealed large changes in the thermograms of muscle samples as a result of pressure treatment, in particular a transition attributed to F-actin was absent in the pressure-treated sample. Examination of the ultrastructure also revealed extensive change as a result of pressure treatment, particularly in the I-band and M-line region. Pressure treatment either did not change shear values or increased them, according to whether the muscle was in the stretched or contracted state, respectively. The results are thought to support a theory for contraction state toughness proposed by Voyle (1969) in which increasing toughness is caused by an increasing incidence of sarcomeres in which thick filaments have been compressed onto the Z-line, thus removing the I-band as a zone of weakness.