. Increased muscle proteolysis after local trauma mainly reflects macrophage-associated lysosomal proteolysis. Am J Physiol Endocrinol Metab 282: E326-E335, 2002; 10.1152/ajpendo.00345.2001.-Rat gastrocnemius showed increased protein degradation (ϩ75-115%) at 48 h after traumatic injury. Injured muscle showed increased cathepsin B activity (ϩ327%) and mRNA encoding cathepsin B (ϩ670%), cathepsin L (ϩ298%), cathepsin H (ϩ159%), and cathepsin C (ϩ268%). In in situ hybridization, cathepsin B mRNA localized to the mononuclear cell infiltrate in injured muscle, and only background levels of hybridization were observed either over muscle cells in injured tissue or in uninjured muscle. Immunogold/electron microscopy showed specific staining for cathepsin B only in lysosome-like structures in cells of the mononuclear cell infiltrate in injured muscle. Muscle cells were uniformly negative in the immunocytochemistry. Matrix metalloproteinase-9 (granulocyte-macrophage gelatinase) mRNA and activity were not present in uninjured muscle but were expressed after trauma. There was no activation of the ATP-ubiquitinproteasome-dependent proteolytic pathway in injured muscle, by contrast to diverse forms of muscle wasting where the activity of this system and the expression of genes encoding ubiquitin and proteasome elements rise. These results suggest that proteolytic systems of the muscle cells remain unstimulated after local injury and that lysosomal enzymes of the inflammatory infiltrated cells are likely to be the major participant in protein catabolism associated with local trauma. injury; protein degradation IN A MODEL OF BLUNT TRAUMA TO MUSCLE, we demonstrated a period of degeneration lasting ϳ3 days, characterized by gross disruption of muscle cells, hemorrhage, inflammation, invasion of the injured site by mononuclear cells, and a 26% loss of previously existing muscle protein (12). A large increase in the process of protein catabolism occurs in injured muscle; however, it is not known which of the several distinct intracellular pro-

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Abstract. The cellular effects of pulsed and continuous ultrasound on the protein content of muscle after trauma were determined in this study. Rats were subjected to a single impact trauma to the gastrocnemius. Six major treatment groups were employed: (1) uninjured control, (2) injured control, (3) & (4) uninjured ultrasound treated, and (5) & (6) injured ultrasound treated. The ultrasound treated groups were subdivided into continuous ultrasound, and pulsed ultrasound treatments (dosage = 1.0 watts/cm 2 × 5 min), which were given from day 2 to day 7 post-trauma once daily. Animals were sacrificed at 1, 3 and 7 days, the medial gastrocnemius muscle being dissected and solubilized for protein content determination. On day 7 the control injured group had a statistically greater mean protein content than the injured continuous ultrasound treatment group, and the mean protein content of the injured pulsed ultrasound treatment group was statistically greater than both the injured control or the injured continuous ultrasound treatment groups (one way ANOVA, P<0.05). The means of all three uninjured control groups were not significantly different at day 1 or 7. Within each group, only the control injured (18% or 44 mg increase ± 17 mg) and the injured pulsed ultrasound treatment (7% or 22 mg increase ± 9 mg) groups showed statistically significant changes (95% Confidence Interval) in protein content from day 1 to day 7. All other treatment groups showed no statistically significant increases.

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