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Full-Text Articles in Life Sciences
Tropomyosin-Based Effects Of Acidosis On Thin-Filament Regulation During Muscle Fatigue, Brent Scott
Tropomyosin-Based Effects Of Acidosis On Thin-Filament Regulation During Muscle Fatigue, Brent Scott
Masters Theses
Skeletal muscle fatigue is defined as a loss in the force/velocity generating capacity of a muscle. A portion of the loss in function is attributable to effects of acidosis (i.e. low pH) on the regulatory proteins, troponin and tropomyosin (Tm), which regulate the binding of myosin and actin in a calcium (Ca++) dependent manner. However, the relative role of troponin and Tm on myosin-actin function during acidosis is not clear, nor are the mechanisms underlying these effects. PURPOSE: To determine the role of Tm in the acidosis-induced depression of muscle function using isolated muscle proteins in an in …
Observing The Molecular Basis Of Thin Filament Activation With A Three Bead Laser Trap Assay, Thomas Longyear
Observing The Molecular Basis Of Thin Filament Activation With A Three Bead Laser Trap Assay, Thomas Longyear
Doctoral Dissertations
Muscle contracts after calcium (Ca++) is released into the muscle cell, resulting from a cascade of events which result in myosin, the molecular motor of muscle, to produce force and motion. Myosin cyclically binds to a regulated thin filament, using the chemical energy of ATP to produce force and motion. Perturbations in muscle, such as a build-up of metabolic by-products or point mutations in key contractile proteins, can inhibit these functions in both skeletal and cardiac muscle either acutely or chronically. Despite the many years we have studied skeletal and cardiac muscle, we still do not have a clear picture …
Recent Insights Into Muscle Fatigue At The Cross-Bridge Level, Edward Debold
Recent Insights Into Muscle Fatigue At The Cross-Bridge Level, Edward Debold
Edward P. Debold
The depression in force and/or velocity associated with muscular fatigue can be the result of a failure at any level, from the initial events in the motor cortex of the brain to the formation of an actomyosin cross-bridge in the muscle cell. Since all the force and motion generated by muscle ultimately derives from the cyclical interaction of actin and myosin, researchers have focused heavily on the impact of the accumulation of intracellular metabolites [e.g., Pi, H+ and adenosine diphoshphate (ADP)] on the function these contractile proteins. At saturating Ca++ levels, elevated Pi appears to be the primary cause for …