Redox Control of Signalling Responses to Contractile Activity and Ageing in Skeletal Muscle
Malcolm J. Jackson,
Natalie Pollock,
Caroline Staunton,
Samantha Jones,
Anne McArdle
Affiliations
Malcolm J. Jackson
MRC-Versus Arthritis Centre for Integrated Research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool L7 8TX, UK
Natalie Pollock
MRC-Versus Arthritis Centre for Integrated Research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool L7 8TX, UK
Caroline Staunton
MRC-Versus Arthritis Centre for Integrated Research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool L7 8TX, UK
Samantha Jones
MRC-Versus Arthritis Centre for Integrated Research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool L7 8TX, UK
Anne McArdle
MRC-Versus Arthritis Centre for Integrated Research into Musculoskeletal Ageing (CIMA), Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, Liverpool L7 8TX, UK
Research over almost 40 years has established that reactive oxygen species are generated at different sites in skeletal muscle and that the generation of these species is increased by various forms of exercise. Initially, this was thought to be potentially deleterious to skeletal muscle and other tissues, but more recent data have identified key roles of these species in muscle adaptations to exercise. The aim of this review is to summarise our current understanding of these redox signalling roles of reactive oxygen species in mediating responses of muscle to contractile activity, with a particular focus on the effects of ageing on these processes. In addition, we provide evidence that disruption of the redox status of muscle mitochondria resulting from age-associated denervation of muscle fibres may be an important factor leading to an attenuation of some muscle responses to contractile activity, and we speculate on potential mechanisms involved.
