Abstract
PURPOSE: Although the development of respiratory muscle fatigue has been well documented, its molecular basis is poorly understood. We wished to characterize the development of fatigue in rats subjected to severe inspiratory resistive loading (IRL) and identify IRL-induced changes to the diaphragmatic myofilament proteome. We hypothesized that inspiratory resistive loading (IRL) would elicit diaphragmatic fatigue (a decrease in the ratio of transdiaphragmatic pressure to integrated phrenic; Pdi/|MiPhr) due, in part, to modifications to myofilament proteins.
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