Reactive Oxygen Species: Impact on Skeletal Muscle

Powers, Scott K.; Ji, Li Li; Kavazis, Andreas N.; Jackson, Malcolm J.

doi:10.1002/cphy.c100054

Cited by 387 publications

(415 citation statements)

References 424 publications

(597 reference statements)

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“…First, decreasing mitochondrial oxidative capacity with age results from the combination of decreasing mitochondrial volume and increasing mitochondrial dysfunction (Peterson et al ., 2012). Mitochondrial dysfunction creates oxidative stress by generating reactive oxygen species (ROS) that can damage mitochondrial DNA (Peterson et al ., 2012), impair calcium regulation, and affect myofilament structure and function (Powers et al ., 2011). These would all act to decrease skeletal muscle force production.…”

Section: Discussionmentioning

confidence: 99%

Muscle strength mediates the relationship between mitochondrial energetics and walking performance

et al. 2017

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SummarySkeletal muscle mitochondrial oxidative capacity declines with age and negatively affects walking performance, but the mechanism for this association is not fully clear. We tested the hypothesis that impaired oxidative capacity affects muscle performance and, through this mechanism, has a negative effect on walking speed. Muscle mitochondrial oxidative capacity was measured by in vivo phosphorus magnetic resonance spectroscopy as the postexercise phosphocreatine resynthesis rate, kPC r, in 326 participants (154 men), aged 24–97 years (mean 71), in the Baltimore Longitudinal Study of Aging. Muscle strength and quality were determined by knee extension isokinetic strength, and the ratio of knee extension strength to thigh muscle cross‐sectional area derived from computed topography, respectively. Four walking tasks were evaluated: a usual pace over 6 m and for 150 s, and a rapid pace over 6 m and 400 m. In multivariate linear regression analyses, kPC r was associated with muscle strength (β = 0.140, P = 0.007) and muscle quality (β = 0.127, P = 0.022), independent of age, sex, height, and weight; muscle strength was also a significant independent correlate of walking speed (P < 0.02 for all tasks) and in a formal mediation analysis significantly attenuated the association between kPC r and three of four walking tasks (18–29% reduction in β for kPC r). This is the first demonstration in human adults that mitochondrial function affects muscle strength and that inefficiency in muscle bioenergetics partially accounts for differences in mobility through this mechanism.

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Section: Discussionmentioning

confidence: 99%

Muscle strength mediates the relationship between mitochondrial energetics and walking performance

et al. 2017

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“…Hydrogen peroxide (H 2 O 2 ) is a relatively stable molecule with a long half‐life and can diffuse across biomembranes 92. H 2 O 2 has been suggested to be a redox signalling molecule93 that can interact with redox‐sensitive components or pathways, activating various transcription factors in skeletal muscle 94.…”

Section: Chemistry Of Reactive Oxygen and Nitrogen Species Produced Bmentioning

confidence: 99%

“…The chemical reaction of superoxide with NO to generate peroxynitrite has a reaction rate ( k = 7 × 10 9 M −1 s −1 ),70 which is approximately three‐fold higher than the SOD catalysed conversion of superoxide to H 2 O 2 ( k = 2 × 10 9 M −1 s −1 ) as previously discussed. Peroxynitrite can react with thiol compounds to form disulfides123 and, along with its protonated form, peroxynitrous acid, can deplete thiol groups and induce protein, phospholipid oxidation and DNA damage 92, 122. Peroxynitrite leads to nitration of tyrosine residues,124 and S ‐nitrosylation of Cys residues,125 the list of proteins being nitrated and nitrosylated in skeletal muscle, is continuously growing.…”

Section: Chemistry Of Reactive Oxygen and Nitrogen Species Produced Bmentioning

confidence: 99%

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age‐related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this ‘epidemic’ problem, the primary biochemical and molecular mechanisms underlying age‐related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age‐associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age‐related muscle atrophy and weakness.

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“…Hydrogen peroxide in addition to having a relatively long half-life, readily diffuses within or between cells, increasing the likelihood of reacting with other targets. These properties render hydrogen peroxide as an important ROS signalling molecule in skeletal muscle cells which has been shown to activate many "redox sensitive" cascades including growth, differentiation, proliferation and apoptosis (McArdle & Jackson, 2000;Powers et al, 2009;Powers et al, 2011).…”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

Ihsan¹,

Watson²,

Abbiss³

2014

Cell Mol Exerc Physiol

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PGC-1α is regarded as a key regulator of mitochondrial biogenesis due to its central role in regulating the activity of key transcription factors associated with encoding mitochondrial components. Additionally, PGC-1α has shown to mediate adaptations that increase fat metabolism and angiogenesis, contributing to the overall oxidative phenotype of the muscle. While it is well established that exercise is a potent stimulator of PGC-1α, recent evidence indicates that heat and cold exposures may also influence mitochondrial biogenesis through the up-regulation of PGC-1α. This highlights the potential use of these modalities in conjunction with exercise to enhance training adaptations. As such, the purpose of this review is to describe the possible mechanisms and pathways by which exercise, as well as hot and cold exposures may influence mitochondrial biogenesis. It is clear that changes in intracellular calcium, oxidative stress and phosphorylation potential are major up-regulators of PGC-1α during exercise. Moreover, there is evidence implicating calcium signalling, in addition to β-adrenergic activation in cold-induced mitochondrial biogenesis, while PGC-1α during heat exposure is likely triggered by changes in phosphorylation potential and nitric oxide signalling. However, these mechanisms appear to change considerably when cold/heat is administered following exercise, and seem to be dependent on the experimental models used (i.e. in vitro vs. in vivo, rodent vs. human). Understanding the effects heat/cold exposure and its interaction with exercise may lead to the optimisation and development of temperature-related interventions to enhance training adaptations, or aid in the treatment of mitochondrial related diseases.

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Reactive Oxygen Species: Impact on Skeletal Muscle

Cited by 387 publications

References 424 publications

Muscle strength mediates the relationship between mitochondrial energetics and walking performance

Muscle strength mediates the relationship between mitochondrial energetics and walking performance

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

PGC-1α Mediated Muscle Aerobic Adaptations to Exercise, Heat and Cold Exposure

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