The plasticity of skeletal muscle, whether an increase in size, change in metabolism, or alteration in structural properties, is in a continuous state of flux largely dependent upon physical activity. Much of the past research has expounded upon these ever-changing aspects of the muscle fiber following exercise. Specifically, endocrine and paracrine signaling have been heavily investigated lending to much of the past literature comprised of such endocrinological dynamics following muscle activity. Mechanotransduction, the ability of a cell to convert a mechanical stimulus into an intracellular biochemical response, has garnered much less attention. Recent work, however, has demonstrated the physical continuity of the muscle fiber, specifically demonstrating a continuous physical link between the extracellular matrix (ECM), cytoskeleton, and nuclear matrix as a means to rapidly regulate gene expression following a mechanical stimulus. Similarly, research has shown mechanical stimuli to directly influence cytoplasmic signaling whether through oxidative adaptations, increased muscle size, or enhanced muscle integrity. Regrettably, minimal research has investigated the role that exercise may play within the mechanotransducing signaling cascades. This proposed line of study may prove paramount as muscle-related diseases greatly impact one's ability to lead an independent lifestyle along with contributing a substantial burden upon the economy. Thus, this review explores both biophysical and biochemical mechanotransduction, and how these signaling pathways may be influenced following exercise.
Keywords: Exercise; Hypertrophy; Integrin; Mechanotransduction; Muscle; mTOR.