Introduction

Cells in the body are subjected to both static and dynamic physical forces. In the musculoskeletal system, cells are constantly under the stress of gravity, as well as to tension resulting from muscular contractions of widely varying intensities. Hypertrophy of cardiac, skeletal and arterial smooth muscle and increased bone density are commonly described adaptation to increased mechanical stress. Interest in the mechanical load is transduced not only into such elevated cellular growth but also into modulation of phenotype in a variety of cell types has increased greatly over the last few years as indicated by increasing numbers of articles and reviews (Komuro & Yazaki, 1993; Morgan & Baker, 1991; Watson, 1991; Davies, 1995). The role of mechanical strain in the determination of cardiac muscle phenotype has received considerable attention, but the effect on skeletal muscle is less well documented. This may be due, in part, to a traditional emphasis on neural regulation of skeletal muscle phenotype. It is clear that both active and passive mechanical forces can induce skeletal muscle enlargement and this increase in the adult animal is due solely to fibre hypertrophy. This is a product of elevated protein synthesis which outweighs parallel increases in protein degradation (Loughna, Goldspink & Goldspink, 1986).

There are a number of in vivo and in vitro models that have been employed to investigate the actions of active and passive tension upon skeletal muscle including tenotomy, pinning of joints, centrifugation and weights attached to avian wings (Alway et al, 1989; Morgan & Loughna, 1989; Sola, Christensen & Martin, 1973).