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Skeletal muscle reactive oxygen species: a target of good cop/bad cop for exercise and disease

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Version 1 2015-01-08, 15:26
journal contribution
posted on 2024-06-06, 09:28 authored by S Mason, Glenn WadleyGlenn Wadley
Metabolic stresses associated with disease, ageing, and exercise increase the levels of reactive oxygen species (ROS) in skeletal muscle. These ROS have been linked mechanistically to adaptations in skeletal muscle that can be favourable (i.e. in response to exercise) or detrimental (i.e. in response to disease). The magnitude, duration (acute versus chronic), and cellular origin of the ROS are important underlying factors in determining the metabolic perturbations associated with the ROS produced in skeletal muscle. In particular, insulin resistance has been linked to excess ROS production in skeletal muscle mitochondria. A chronic excess of mitochondrial ROS can impair normal insulin signalling pathways and glucose disposal in skeletal muscle. In contrast, ROS produced in skeletal muscle in response to exercise has been linked to beneficial metabolic adaptations including mitochondrial biogenesis and muscle hypertrophy. Moreover, unlike insulin resistance, exercise-induced ROS appears to be primarily of non-mitochondrial origin. The present review summarizes the diverse ROS-targeted metabolic outcomes associated with insulin resistance versus exercise in skeletal muscle, thus, presenting two contrasting perspectives of pathologically harmful versus physiologically beneficial ROS. Here, we discuss the key sites of ROS production during exercise and the effect of ROS in skeletal muscle of people with type 2 diabetes.

History

Journal

Redox report

Volume

19

Pagination

97-106

Location

Leeds, England

Open access

  • Yes

ISSN

1351-0002

eISSN

1743-2928

Language

eng

Publication classification

C Journal article, C1 Refereed article in a scholarly journal

Copyright notice

2014, Maney Publishing

Issue

3

Publisher

Maney Publishing