Post-translational modification of myofilament proteins in the regulation of skeletal muscle contraction.

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Muscle contraction is the result of the complex interactions of many proteins. It is, ultimately, the interplay between the contractile proteins, in a calcium dependent manner, which produces force at the expense of ATP hydrolysis. Protein alterations (e.g., phosphorylation) are common mechanisms regulating or 'fine tuning' critical cellular processes. Alterations in one or more of the myofilament proteins, the proteins directly responsible for contraction, have the potential to affect force production and/or contractile economy. Exercise-induced fatigue can be characterized by temporary reductions in the ability to produce force. The goal of my research is to identify changes in myofilament proteins that occur in response to fatigue. Each protein alteration could be an adaptive or compensatory response to fatigue. There are no studies examining the time-related effects of fatiguing exercise on alterations to myofilament proteins. The is the first step in determining the significance of each myofilament alteration and delineating the molecular pathways which were activated to cause each specific alteration. The proposed studies, therefore, will generate new information about how alterations in skeletal myofilament proteins contribute to muscle fatigue. These studies have the potential to provide new insights into unappreciated aspects of how myofilament proteins contribute to fatigue. With a clearer understanding of the basic mechanisms regulating skeletal myofilament function, we will be in a better position to understand the regulation of skeletal muscle function.