Skeletal muscle tissue is characterized by an extraordinary phenotypic plasticity. Using specific training interventions massive functional changes in strength or endurance in untrained subjects can be induced in weeks. These functional gains are the result of muscle structural modifications which have been well characterized over the last 30 years. Molecular tools enable us now to study the mechanisms of muscle plasticity. It has become clear recently that many of the structural and functional consequences of typical exercise regimes are controlled by changes in gene expression and or changes in translation.

During exercise muscle cells are subjected to mechanical, metabolic, neuronal and metabolic signals which are transduced over multiple pathways to the muscle genome. Exercise thus activates a range of signaling cascades, the individual characteristic of the stress leading to a specific response of a network of signaling pathways. Signaling typically results in the transcription of multiple early genes among those of the well known fos and jun family as well as many other transcription factors. These bind to the promoter regions of downstream genes initiating the structural response of muscle tissue. While signaling is a matter of minutes, early genes are activated over hours leading to modifications of structure genes that are then effective over days. Repeated exercise sessions lead to concerted accretions of multiple mRNAs which upon translation result in a stepwise increase of proteins of related functional entities. On the structural level the protein accretion manifests itself for instance as an increase in mitochondrial and capillary volume upon endurance training and myofibrils and associated proteins upon strength training. The molecular response to strength training (i.e. the accretion of myofibrillar proteins) is less established. We find a transient depression of transcription over 24 hours. It looks as if the main actors in strength training are the mTOR pathway and the S6 Kinase both influencing translation. It is likely that a single exercise stimulus carries a molecular signature which is typical both for the type of stimulus (i.e. endurance vs. strength) as well as the actual condition of muscle tissue (i.e. untrained vs. trained). It therefore seems feasible to use molecular tools to judge the properties of an exercise stimulus earlier and at a much finer level than is possible with conventional functional or structural techniques which require weeks of exercise before a training response can be detected reliable.

The current molecular techniques begin to paint a very detailed picture of the modulatory events involved in muscle malleability indicating distinctly different molecular reaction patterns for endurance and strength type exercise.