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Muscle-derived ROS and thiol regulation in muscle fatigue.
- Source :
-
Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2008 Mar; Vol. 104 (3), pp. 853-60. Date of Electronic Publication: 2007 Nov 15. - Publication Year :
- 2008
-
Abstract
- 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 this biology. Fatigue causes oxidation of glutathione, a thiol antioxidant in muscle fibers, and is reversed by thiol-specific reducing agents. N-acetylcysteine (NAC), a drug that supports glutathione synthesis, has been shown to lessen oxidation of cellular constituents and delay muscle fatigue. In humans, NAC pretreatment improves performance of limb and respiratory muscles during fatigue protocols and extends time to task failure during volitional exercise. These findings highlight the importance of ROS and thiol chemistry in fatigue, show the feasibility of thiol-based countermeasures, and identify new directions for mechanistic and translational research.
- Subjects :
- Animals
Antioxidants metabolism
Antioxidants pharmacology
Glutathione metabolism
Humans
Muscle, Skeletal drug effects
Oxidation-Reduction
Oxidative Stress
Reactive Nitrogen Species metabolism
Research Design
Exercise
Muscle Contraction drug effects
Muscle Fatigue drug effects
Muscle, Skeletal metabolism
Reactive Oxygen Species metabolism
Sulfhydryl Compounds metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 8750-7587
- Volume :
- 104
- Issue :
- 3
- Database :
- MEDLINE
- Journal :
- Journal of applied physiology (Bethesda, Md. : 1985)
- Publication Type :
- Academic Journal
- Accession number :
- 18006866
- Full Text :
- https://doi.org/10.1152/japplphysiol.00953.2007