Thesis (M. Phil.)--University of Hong Kong, 1978. / Xeorx copy of typescript.

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The purpose was to determine the effect of Naproxen in attenuating the symptoms (muscle soreness level) and signs (plasma CK activity and muscular strength decrement) of delayed onset muscle soreness (DOMS). Twenty subjects were randomly assigned Naproxen (500 mg BID) or placebo in a double-blind, crossover design. Two testing phases, each 8 days in duration, were separated by a washout period of 7 days. Eccentric single-leg exercises were performed on Days 1, 3 and 4 to induce DOMS in the quadriceps muscles. Perception of muscle soreness, plasma CK, and knee extensor torque were evaluated throughout each phase. Following the eccentric exercise, plasma CK levels were similarly elevated in both Naproxen and placebo conditions. After DOMS had developed, Naproxen reduced the perception of soreness on Day 3 when muscle soreness was highest. Following treatments with Naproxen, peak quadriceps torque during leg extension at 60$ sp circ$/s was higher compared to placebo, however at higher velocity (180 and 300$ sp circ$/s) peak muscle torques were similar. The data indicate that therapeutic doses of Naproxen do not prevent CK release into the plasma but decreases the perception of muscle soreness and positively influences quadriceps peak torque.

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Proteins comprise approximately 80 per cent of the solid matter of muscle tissue and in the living animal are called upon to perform many varied functions. Proteins are present in muscle tissue which are capable of rapid contraction and relaxation, together with a complex system of enzymes to supply these elements with energy, a surrounding network of connective tissue to bind them into place and to bear the stress of their movements, and an intricate blood supply and nervous system. [...]

During C. elegans embryogenesis, myoblasts initially form two rows along the left and right lateral midlines and at ~290 min of development migrate dorsally and ventrally to form the four muscle quadrants present upon hatching (Sulston et al, 1983). As the myoblasts migrate they are still dividing, as are many other cells in their immediate environment. This means the cell-cell contact of cells during migration is dynamic and can vary from animal to animal (Schnabel et al, 1997). This situation creates an environment where the extracellular matrix (ECM) and cell surface contacts are in constant flux, which begs the questions as to how these cells navigate unerringly to their final destination. In an attempt to identify genes mediating these migrations, I performed an RNAi based screen targeting 776 genes predicted to be members of the extracellular matrix (ECM), or one of its receptors. Using both feeding and injection based RNAi, I was able to identify three genes of interest. Knockdowns of F56B3.2 resulted in paralyzed animals with detached muscle, making it a good candidate for a new component of the muscle attachment complex. F33G12.4 knockdowns resulted in an embryonic arrest phenotype with an abnormal muscle lineage, possibly stemming from polarity defects. The only knockdown that resulted in muscle migration defects was that for lam-2, which encodes for the laminin gamma subunit. Analysis of the lam-2 knockdown, as well as knockdowns for the other laminin subunits, revealed dorsal/ventral migration defects as well as a posterior displacement of the anterior-most ventral muscle cells. Investigation of this posterior displacement has led to the identification of a previously un-described anterior muscle migration event and its dependency upon the extension of muscle processes from the leading cells.

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