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Skeletal muscle ageing is characterised by atrophy, a deficit in specific force generation, increased susceptibility to injury, and incomplete recovery after severe damage. The hypothesis that increased generation of reactive oxygen species (ROS) in vivo plays a key role in the ageing process has been extensively studied, but remains controversial. Skeletal muscle generates ROS at rest and during exercise. ROS can cause oxidative damage particularly to proteins. Indeed, products of oxidative damage accumulate in skeletal muscle during ageing and the ability of muscle cells to respond to increased ROS becomes defective. The aim of this review is to examine the evidence that ROS manipulation in peripheral nerves and/or muscle modifies mechanisms of proteostasis in skeletal muscle and plays a key role in initiating sarcopenia. [ABSTRACT FROM AUTHOR]

An increasingly sophisticated array of approaches are now available for the study of the activities of reactive oxygen species and oxidative modifications in skeletal muscle, but the most up-to-date techniques are not readily available to many researchers in this field due to their requirement for sophisticated mass spectrometry, imaging or other high cost technologies. Most papers published therefore rely on a number of established approaches although the choice of approach is also clearly dependent upon the experimental model and access to skeletal muscle that is available to the investigator, how much detail is required and the overall question to be addressed. Numerous reports have described the problems associated with some of the popular approaches that are widely followed, including measurement of thiobarbituric acid substances and the sole use of fluorescence-based probes such as dichlorodihydrofluorescein. This brief review reports the areas in which methods are improving to allow valid assessments to made in this area and indicates some of the more recent developments that provide alternative ways to assess the activity of individual species and endpoints in the various experimental models that may be examined. [ABSTRACT FROM AUTHOR]

Chronic exercise improves endurance and skeletal muscle oxidative capacity. Despite the potential importance of reactive oxygen species (ROS) generated during exercise as regulators of these adaptations, the effect of repeated bouts of aerobic exercise on ROS generation by skeletal muscles during contractions has not been examined. Our aim was to establish the impact of repeated treadmill running exercise on muscle ROS generation and activation of redox-sensitive transcription factors. Following 8 weeks of treadmill running, mice displayed an improvement in running speed that was associated with an enhanced ability of gastrocnemius (GTN) muscles to maintain force during a protocol of isometric contractions. In contrast to GTN muscles of cage-sedentary (Sed) mice, muscles from exercised (Exer) mice did not release superoxide or nitric oxide during the isometric contractions. For male mice, basal levels of nuclear factor kappaB (NFkappaB) and activator protein-1 (AP-1) DNA binding were increased by treadmill running, and the contraction-induced activation of NFkappaB and AP-1 observed in muscles of Sed mice was absent in Exer muscles. Also in contrast to Sed muscles, Exer muscles displayed no reductions in glutathione or protein thiol levels in response to contraction. Our observations of decreases for Exer compared with Sed muscles in contraction-induced (i) ROS generation, (ii) activation of redox-sensitive signalling pathways, and (iii) ROS stress suggest that exercise conditioning enhances the ability of skeletal muscle to readily and rapidly detoxify ROS and/or reduces ROS generation, providing protection from ROS-induced damage and reducing signals that might act to mediate further unnecessary adaptations.