Abstract
Increased reactive oxygen species (ROS) production is crucial to the remodelling that occurs in skeletal muscle in response to both exercise training and prolonged periods of disuse. This review discusses the redox-sensitive signalling pathways that are responsible for this ROS-induced skeletal muscle adaptation. We begin with a discussion of the sites of ROS production in skeletal muscle fibres. This is followed by an overview of the putative redox-sensitive signalling pathways that promote skeletal muscle adaptation. Specifically, this discussion highlights redox-sensitive kinases, phosphatases and the transcription factor nuclear factor-κB. We also discuss the evidence that connects redox signalling to skeletal muscle adaptation in response to increased muscular activity (i.e. exercise training) and during prolonged periods of muscular inactivity (i.e. immobilization). In an effort to stimulate further research, we conclude with a discussion of unanswered questions about redox signalling in skeletal muscle.
Highlights
During the 1980s and 1990s it was widely assumed that muscular activity- or inactivity-induced reactive oxygen species (ROS) production was cytotoxic to skeletal muscle fibres
The first segment of this review identifies the potential sites of ROS production in skeletal muscle
Many signalling molecules are manipulated by ROS, including redox-sensitive kinases, phosphatases and the transcription factor nuclear factor-κB (NF-κB)
Summary
Increased reactive oxygen species (ROS) production is crucial to the remodelling that occurs in skeletal muscle in response to both exercise training and prolonged periods of disuse. We begin with a discussion of the sites of ROS production in skeletal muscle fibres This is followed by an overview of the putative redox-sensitive signalling pathways that promote skeletal muscle adaptation. It was later discovered that ROS generation increases in skeletal muscle fibres following prolonged periods of disuse (e.g. immobilization; Kondo et al 1991). Growing evidence indicates that increased ROS production plays an important role in the regulation of signalling pathways that are required to promote skeletal muscle adaptation in response to both exercise and muscle inactivity. We conclude with a discussion of the voids in our knowledge about redox control of muscle adaptation in the hope of stimulating future research in this field
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