Muscle-derived ROS and thiol regulation in muscle fatigue.

@article{Ferreira2008MusclederivedRA,
  title={Muscle-derived ROS and thiol regulation in muscle fatigue.},
  author={Leonardo F. Ferreira and Michael B. Reid},
  journal={Journal of applied physiology},
  year={2008},
  volume={104 3},
  pages={
          853-60
        }
}
Muscles produce oxidants, including reactive oxygen species (ROS) and reactive nitrogen species (RNS), from a variety of intracellular sources. Oxidants are detectable in muscle at low levels during rest and at higher levels during contractions. RNS depress force production but do not appear to cause fatigue of healthy muscle. In contrast, muscle-derived ROS contribute to fatigue because loss of function can be delayed by ROS-specific antioxidants. Thiol regulation appears to be important in… 
View on PubMed
jap.physiology.org
214 Citations
Highly Influential Citations
14
Background Citations
109
Methods Citations
2
Results Citations
3

Figures from this paper

214 Citations

Mediators of Physical Activity Protection against ROS-Linked Skeletal Muscle Damage

To elucidate the complex role of ROS in exercise, the literature dealing on sources of ROS production and concerning the most important redox signaling pathways are reviewed, including MAPKs that are involved in the responses to acute and chronic exercise in the muscle, particularly those involving in the induction of antioxidant enzymes.

Protein carbonylation in skeletal muscles: impact on function.

The observation that the levels of oxidant-derived posttranslational protein modifications, including protein carbonylation, are elevated inside skeletal muscle fibers when oxidative stress develops suggest that these modifications play important roles in regulating muscle function.

Potential molecular mechanisms underlying muscle fatigue mediated by reactive oxygen and nitrogen species

This review highlights some of the recent efforts which have the potential to offer uniquely precise information on the underlying molecular basis of fatigue, including the regulatory protein troponin and the actin binding region of myosin.

Exercise-induced oxidative stress in humans: cause and consequences.

Effectiveness of sulfur-containing antioxidants in delaying skeletal muscle fatigue.

It is concluded that NACA and ERGO are unlikely to improve human exercise performance and should not be evaluated for effects on muscle fatigue in vitro.

Nicorandil improves post-fatigue tension in slow skeletal muscle fibers by modulating glutathione redox state

The results suggest that nicorandil improves the muscle function reversing fatigue in slow skeletal muscle fibers of chicken through its effects not only as a mitoKATP channel opener but also as NO donor and as an antioxidant.

Iron injections in mice increase skeletal muscle iron content, induce oxidative stress and reduce exercise performance

Iron accumulation in skeletal muscle may play a significant role in the reduced exercise capacity seen in iron overload disorders and in ageing, and may play an underlying role in skeletal Muscle atrophy.

Protein carbonylation and muscle function in COPD and other conditions.

The review summarizes the effects of protein carbonylation on muscles in several models and conditions such as COPD, disuse muscle atrophy, cancer cachexia, sepsis, and aging.

L-2-Oxothiazolidine-4-carboxylate reverses glutathione oxidation and delays fatigue of skeletal muscle in vitro.

It is demonstrated that OTC modulates the muscle GSH pool and opposes fatigue under the current experimental conditions.

Po2 cycling protects diaphragm function during reoxygenation via ROS, Akt, ERK, and mitochondrial channels.

This current investigation has discovered a correlation between KATP and mPTP and the Po2 cycling pathway in diaphragmatic skeletal muscle and identified a unique signaling pathway that may involve ROS, Akt, ERK, and mitochondrial channels responsible for Po1 cycling protection during reoxygenation conditions in the diaphagm.
...

References

SHOWING 1-10 OF 134 REFERENCES

Oxidant activity in skeletal muscle fibers is influenced by temperature, CO2 level, and muscle-derived nitric oxide.

  • S. ArbogastM. Reid
  • Biology
    American journal of physiology. Regulatory, integrative and comparative physiology
  • 2004
It is concluded that net oxidant activity in resting muscle fibers is decreased at subphysiological temperatures, increased by CO(2) exposure, and influenced by muscle-derived ROS and NO derivatives to similar degrees.

Reactive oxygen in skeletal muscle. I. Intracellular oxidant kinetics and fatigue in vitro.

It is concluded that diaphragm fiber bundles produce reactive oxygen intermediates, including O2-.

Dietary antioxidants and exercise

There is limited evidence that dietary supplementation with antioxidants will improve human performance, and it is currently unclear whether regular vigorous exercise increases the need for dietary intake of antioxidants.

Glutathione homeostasis in response to exercise training and nutritional supplements

  • C. Sen
  • Biology
    Molecular and Cellular Biochemistry
  • 2004
Results show that sprint training may also have a beneficial effect on tissue GSH homeostasis against exercise induced oxidative stress and an improved form of LA, a positively charged analogue (LA-Plus), has been discovered.

N-acetylcysteine enhances muscle cysteine and glutathione availability and attenuates fatigue during prolonged exercise in endurance-trained individuals.

NAC improved performance in well-trained individuals, with enhanced muscle cysteine and GSH availability a likely mechanism.

Free radical generation by skeletal muscle of adult and old mice: effect of contractile activity

Contractile activity increased skeletal muscle ROS generation in both adult and old mice with no evidence for an age‐related exacerbation of ROS generation.

Hypoxia-induced reactive oxygen species formation in skeletal muscle.

  • T. Clanton
  • Biology
    Journal of applied physiology
  • 2007
Drawing general conclusions that hypoxia-induced ROS may be a normal physiological response to imbalance in oxygen supply and demand or environmental stress and may play a yet undefined role in normal response mechanisms to these stimuli are drawn.

Free radicals and tissue damage produced by exercise.

Nitric oxide in skeletal muscle

It is shown that rat skeletal muscle expresses neuronal-type NO synthase and that activity varies among several respiratory and limb muscles, and that two physiological functions of NO in skeletal muscle are supported.

Respiratory loading intensity and diaphragm oxidative stress: N-acetyl-cysteine effects.

Results suggest that high-intensity respiratory loading-induced oxidative stress may be neutralized by N-acetyl-cysteine treatment during IRB in the canine diaphragm.
...