ArticleRedox biology2019
Adaptations to high-intensity interval training in skeletal muscle require NADPH oxidase 2.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.
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Who cites it
45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.
- Is low-volume high intensity interval training a time-efficient strategy for improving body composition and cardiovascular health in children and adolescents? Evidence from a systematic review and three-level meta-analysis.Frontiers in physiology · 2025Pooled it
- Effects of Mitoquinone (MitoQ) Supplementation on Aerobic Exercise Performance and Oxidative Damage: A Systematic Review and Meta-analysis.Sports medicine - open · 2024Pooled it
- Resistance-based training improves mitochondrial capacity and redox balance in aging adults, independent of polyphenol supplementation.Redox biology · 2026Trial
- MitoQ supplementation does not impact redox responses to acute exercise in skeletal muscle of older individuals.Redox biology · 2025Trial
- Trial
- Carbohydrate restriction following strenuous glycogen-depleting exercise does not potentiate the acute molecular response associated with mitochondrial biogenesis in human skeletal muscle.European journal of applied physiology · 2021Trial
- Systems modelling of mitochondrial dynamics in different exercise regimes.The Journal of physiology · 2026Article
- A decline in skeletal muscle NOX4 abrogates exercise-induced adaptive homeostasis and exacerbates biological aging.Science advances · 2026Article
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Reactive oxygen species in health and disease.Molecular biomedicine · 2026Review
- Skeletal muscle knockout of NAD(P)H oxidase 2 delays the development of isotonic diaphragm fatigue in mice.Free radical biology & medicine · 2025Article
- Redox-regulated signalling of adaptations to contractile activity in skeletal muscle: Implications for age-related muscle weakness.Experimental physiology · 2025Review
- Effects and moderator of high-intensity interval training and moderate-intensity continuous training among children and adolescents with overweight or obese: a systematic review and meta-analysis.Frontiers in physiology · 2025Review
- Redox Control of Skeletal Muscle Function and Adaptations to Exercise.Advances in experimental medicine and biology · 2025Review
- Minutes that matter: time-efficient high-intensity interval training improves cardiac function with transcriptomic evidence in post-myocardial infarction mice.Frontiers in cell and developmental biology · 2025Article
- Normobaric hypoxia accelerates high-intensity intermittent training-induced mitochondrial biogenesis (PGC-1α)- and dynamics (OPA1)-related protein expressions in rat gastrocnemius muscle.Journal of physiology and biochemistry · 2024Article
- Reactive oxygen species promote endurance exercise-induced adaptations in skeletal muscles.Journal of sport and health science · 2024Review
- Identification of the serum metabolomic profile for acute ischemic preconditioning in athletes.Frontiers in physiology · 2024Article
- Genetically Encoded Biosensors for the Fluorescence Detection of OSensors (Basel, Switzerland) · 2023Review
- NOX2 deficiency exacerbates diet-induced obesity and impairs molecular training adaptations in skeletal muscle.Redox biology · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveReactive oxygen species (ROS) have been proposed as signaling molecules mediating exercise training adaptation, but the ROS source has remained unclear. This study aimed to investigate if increased NADPH oxidase (NOX)2-dependent activity during exercise is required for long-term high-intensity interval training (HIIT) in skeletal muscle using a mouse model lacking functional NOX2 complex due to absent p47phox (Ncf1) subunit expression (ncf1* mutation).
methodsHIIT was investigated after an acute bout of exercise and after a chronic intervention (3x/week for 6 weeks) in wild-type (WT) vs. NOX2 activity-deficient (ncf1*) mice. NOX2 activation during HIIT was measured using an electroporated genetically-encoded biosensor. Immunoblotting and single-fiber microscopy was performed to measure classical exercise-training responsive endpoints in skeletal muscle.
resultsA single bout of HIIT increased NOX2 activity measured as p47-roGFP oxidation immediately after exercise but not 1 h or 4 h after exercise. After a 6-week HIIT regimen, improvements in maximal running capacity and some muscle training-markers responded less to HIIT in the ncf1* mice compared to WT, including superoxide dismutase 2, catalase, hexokinase II, pyruvate dehydrogenase and protein markers of mitochondrial oxidative phosphorylation complexes. Strikingly, HIIT-training increased mitochondrial network area and decreased fragmentation in WT mice only.
conclusionThis study suggests that HIIT exercise increases NOX2 activity in skeletal muscle and shows that NOX2 activity is required for specific skeletal muscle adaptations to HIIT relating to antioxidant defense, glucose metabolism, and mitochondria.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.