A cascading series of control systems is developed which incorporates the molecular events that are currently thought to cause a muscular contraction. The model is developed with the hypothesis that a series of disturbing signals (or inputs) simply propagate faster than the respective controlling signals can correct for them. Transfer functions for each system are developed, with quantification derived for the excitation and the excitation-contraction coupling control systems. These latter systems include the release of acetylcholine into the synapse, the depolarization of the muscle membrane, and the release of calcium ions into the sarcoplasm. Expressions involving the energy processes, as well as the exact mechanism of the power stroke, are also developed. The systems involved are the Krebs cycle, thick and thin filament regulation, and the generation of a cross-bridge power stroke. / Master of Science