ArticleThe Journal of physiology2015
Antioxidant treatments do not improve force recovery after fatiguing stimulation of mouse skeletal muscle fibres.
Article in The Journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 84 citations in OpenAlex.
- Trial
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- Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2+ leak after one session of high-intensity interval exercise.Proceedings of the National Academy of Sciences of the United States of America · 2015Trial
- Task Failure in Endurance Sports: A Review.Sports medicine (Auckland, N.Z.) · 2026Review
- Skeletal muscle knockout of NAD(P)H oxidase 2 delays the development of isotonic diaphragm fatigue in mice.Free radical biology & medicine · 2025Article
- Dysferlin and the Regulation of CaCells · 2025Review
- Mitochondrial-targeted plastoquinone therapy prevents early onset muscle weakness that occurs before atrophy during ovarian cancer.Molecular metabolism · 2025Article
- Performance Fatigability at Task Failure and Beyond: Distinct Patterns of Recovery Following Constant Load Versus Intermittent Cycling Exercise.International journal of exercise science · 2025Article
- Stable oxidative posttranslational modifications alter the gating properties of RyR1.The Journal of general physiology · 2024Article
- Acute neuromuscular, cardiovascular, and muscle oxygenation responses to low-intensity aerobic interval exercises with blood flow restriction.Experimental physiology · 2024Article
- From amino-acid to disease: the effects of oxidation on actin-myosin interactions in muscle.Journal of muscle research and cell motility · 2023Review
- Determinants of the maximal functional reserve during repeated supramaximal exercise by humans: The roles of Nrf2/Keap1, antioxidant proteins, muscle phenotype and oxygenation.Redox biology · 2023Article
- Effects of Resveratrol on Muscle Inflammation, Energy Utilisation, and Exercise Performance in an Eccentric Contraction Exercise Mouse Model.Nutrients · 2023Article
- Molecular and biochemical investigations of the anti-fatigue effects of tea polyphenols and fruit extracts ofFrontiers in molecular biosciences · 2023Article
- Mechanisms of eccentric contraction-induced muscle damage and nutritional supplementations for mitigating it.Journal of muscle research and cell motility · 2022Review
- Increasing the resting time between drop jumps lessens delayed-onset muscle soreness and limits the extent of prolonged low-frequency force depression in human knee extensor muscles.European journal of applied physiology · 2022Article
- Redox Signaling and Sarcopenia: Searching for the Primary Suspect.International journal of molecular sciences · 2021Review
- Fast skeletal muscle troponin activator CK-2066260 mitigates skeletal muscle weakness independently of the underlying cause.Journal of cachexia, sarcopenia and muscle · 2020Article
- Targeted Antioxidants in Exercise-Induced Mitochondrial Oxidative Stress: Emphasis on DNA Damage.Antioxidants (Basel, Switzerland) · 2020Review
- Vitamin C and E Treatment Blunts Sprint Interval Training-Induced Changes in Inflammatory Mediator-, Calcium-, and Mitochondria-Related Signaling in Recreationally Active Elderly Humans.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The contractile performance of skeletal muscle declines during intense activities, i.e. fatigue develops. Fatigued muscle can enter a state of prolonged low-frequency force depression (PLFFD). PLFFD can be due to decreased tetanic free cytosolic [Ca(2+) ] ([Ca(2+) ]i ) and/or decreased myofibrillar Ca(2+) sensitivity. Increases in reactive oxygen and nitrogen species (ROS/RNS) may contribute to fatigue-induced force reductions. We studied whether pharmacological ROS/RNS inhibition delays fatigue and/or counteracts the development of PLFFD. Mechanically isolated mouse fast-twitch fibres were fatigued by sixty 150 ms, 70 Hz tetani given every 1 s. Experiments were performed in standard Tyrode solution (control) or in the presence of: NADPH oxidase (NOX) 2 inhibitor (gp91ds-tat); NOX4 inhibitor (GKT137831); mitochondria-targeted antioxidant (SS-31); nitric oxide synthase (NOS) inhibitor (l-NAME); the general antioxidant N-acetylcysteine (NAC); a cocktail of SS-31, l-NAME and NAC. Spatially and temporally averaged [Ca(2+) ]i and peak force were reduced by ∼20% and ∼70% at the end of fatiguing stimulation, respectively, with no marked differences between groups. PLFFD was similar in all groups, with 30 Hz force being decreased by ∼60% at 30 min of recovery. PLFFD was mostly due to decreased tetanic [Ca(2+) ]i in control fibres and in the presence of NOX2 or NOX4 inhibitors. Conversely, in fibres exposed to SS-31 or the anti ROS/RNS cocktail, tetanic [Ca(2+) ]i was not decreased during recovery so PLFFD was only caused by decreased myofibrillar Ca(2+) sensitivity. The cocktail also increased resting [Ca(2+) ]i and ultimately caused cell death. In conclusion, ROS/RNS-neutralizing compounds did not counteract the force decline during or after induction of fatigue.
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