Effect of growth promoters on pig muscle structural protein and proteolytic enzyme levels in vivo and in vitro

To elucidate the biochemical mechanism by which the growth hormone porcine somatotrophin (PST) promotes skeletal muscle growth, we have determined the activity of a comprehensive range of protein catabolizing proteolytic enzymes and structural proteins (determined by analytical electrophoresis, SDS-PAGE) in longissimus dorsi muscle from control and PST treated pigs. There was no significant difference in the levels of muscle structural proteins, or in the activity of muscle proteolytic enzymes at point of slaughter in control or PST treated animals. Similarly, in post-mortem muscle proteolysis time course experiments at pH 5.5 or pH 7.5, there was no significant difference in the rate of structural protein degradation by endogenous muscle proteases (determined via SDS-PAGE) using muscle from control or PST treated animals. In addition, investigation of a range of β-agonist related drugs (clenbuterol, salbutamol, pirbuterol, fenoterol) showed no effect (10 −4–10 −8 M) in vitro on the activity of individual protease types in control muscle, or on the degradation rate of muscle structural proteins by endogenous proteases in time course experiments at pH 5.5 or pH 7.5. We conclude that: i) the anabolic action of growth promoters such as PST in promoting skeletal muscle growth in vivo does not occur via simple down-regulation of muscle protease activities, or by alteration in the levels of individual muscle structural proteins; this is supported by the finding that β-agonist drugs do not have any direct effect on the activity of muscle proteases in vitro; ii) PST treatment in vivo does not significantly alter subsequent degradation of structural proteins by endogenous proteases in vitro; similarly the latter process is unaltered in the presence of β-agonist drugs in vitro, suggesting that the potential effect of growth promoters on subsequent meat quality does not operate via the mechanism of post-mortem proteolysis.