Redox Signalling and Exercise

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (29 February 2020) | Viewed by 129181

Special Issue Editor

1. Research Institute of Sport Science, University of Physical Education, 1123 Budapest, Hungary
2. Faculty of Sport Sciences, Waseda University, Tokorozawa 2-579-15, Japan
Interests: exercise; aging; epigenetics; hormesis; systemic adaptation; microbiome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Exercise can increase the metabolism of many biochemical pathways that are associated with the enhanced generation of reactive oxygen species (ROS). It is known that ROS are important, necessary regulators of cellular function and metabolism. It is under debate whether antioxidant treatment can attenuate or eliminate exercise-induced adaptive responses in skeletal muscle and in other tissues. It has been reported that antioxidant supplementation, for example, vitamin C, reduced the peroxisome proliferator-activated receptor gamma coactivator 1 nuclear-respiratory factors  activation, and the whole adaptive response was knocked out. On the other hand, the results of a number of papers suggest that the adaptive response is much more complex and is regulated by multi-protein pathways. Some studies also indicate that antioxidant treatment does not eliminate the adaptive response to regular exercise.  Exercise has systemic effects, and a significant part of the adaptive response is mediated by redox signaling. The effects of exercise on skeletal muscle, the brain, and the liver are quite well studied, but further investigation is necessary in order to elucidate  the exercise-induced redox regulation in the kidney, gut, and reproductive organs.

This Special Issue of Redox Signalling and Exercise welcomes top quality original research papers and reviews so as to expand on our understanding and perspective on all aspects of redox homeostasis related adaptation, redox signalling, oxidative damage, and the repair process. Papers on the redox sensitive housekeeping process are very welcomed. We are very much looking forward to receiving papers on redox mediated epigenetics as a result of physical exercise.

Prof. Zsolt Radak
Guest Editor

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Keywords

  • Antioxidants
  • Exercise
  • Oxidative damage
  • Redox signaling
  • Systemic adaptation
  • Mitochondria
  • Housekeeping systems

Published Papers (10 papers)

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Research

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22 pages, 3394 KiB  
Article
Reversible Oxidative Modifications in Myoglobin and Functional Implications
by Mark H. Mannino, Rishi S. Patel, Amanda M. Eccardt, Blythe E. Janowiak, David C. Wood, Fahu He and Jonathan S. Fisher
Antioxidants 2020, 9(6), 549; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9060549 - 24 Jun 2020
Cited by 13 | Viewed by 4342
Abstract
Myoglobin (Mb), an oxygen-binding heme protein highly expressed in heart and skeletal muscle, has been shown to undergo oxidative modifications on both an inter- and intramolecular level when exposed to hydrogen peroxide (H2O2) in vitro. Here, we show that [...] Read more.
Myoglobin (Mb), an oxygen-binding heme protein highly expressed in heart and skeletal muscle, has been shown to undergo oxidative modifications on both an inter- and intramolecular level when exposed to hydrogen peroxide (H2O2) in vitro. Here, we show that exposure to H2O2 increases the peroxidase activity of Mb. Reaction of Mb with H2O2 causes covalent binding of heme to the Mb protein (Mb-X), corresponding to an increase in peroxidase activity when ascorbic acid is the reducing co-substrate. Treatment of H2O2-reacted Mb with ascorbic acid reverses the Mb-X crosslink. Reaction with H2O2 causes Mb to form dimers, trimers, and larger molecular weight Mb aggregates, and treatment with ascorbic acid regenerates Mb monomers. Reaction of Mb with H2O2 causes formation of dityrosine crosslinks, though the labile nature of the crosslinks broken by treatment with ascorbic acid suggests that the reversible aggregation of Mb is mediated by crosslinks other than dityrosine. Disappearance of a peptide containing a tryptophan residue when Mb is treated with H2O2 and the peptide’s reappearance after subsequent treatment with ascorbic acid suggest that tryptophan side chains might participate in the labile crosslinking. Taken together, these data suggest that while exposure to H2O2 causes Mb-X formation, increases Mb peroxidase activity, and causes Mb aggregation, these oxidative modifications are reversible by treatment with ascorbic acid. A caveat is that future studies should demonstrate that these and other in vitro findings regarding properties of Mb have relevance in the intracellular milieu, especially in regard to actual concentrations of metMb, H2O2, and ascorbate that would be found in vivo. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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14 pages, 1983 KiB  
Article
One-Week High-Intensity Interval Training Increases Hippocampal Plasticity and Mitochondrial Content without Changes in Redox State
by Jonathas Rodrigo dos Santos, Mariza Bortolanza, Gustavo Duarte Ferrari, Guilherme Pauperio Lanfredi, Glauce Crivelaro do Nascimento, Ana Elisa Calereiro Seixas Azzolini, Elaine Del Bel, Alline Cristina de Campos, Vitor Marcel Faça, Anderson Vulczak and Luciane Carla Alberici
Antioxidants 2020, 9(5), 445; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9050445 - 21 May 2020
Cited by 8 | Viewed by 4065
Abstract
Evidence suggests that physical exercise has effects on neuronal plasticity as well as overall brain health. This effect has been linked to exercise capacity in modulating the antioxidant status, when the oxidative stress is usually linked to the neuronal damage. Although high-intensity interval [...] Read more.
Evidence suggests that physical exercise has effects on neuronal plasticity as well as overall brain health. This effect has been linked to exercise capacity in modulating the antioxidant status, when the oxidative stress is usually linked to the neuronal damage. Although high-intensity interval training (HIIT) is the training-trend worldwide, its effect on brain function is still unclear. Thus, we aimed to assess the neuroplasticity, mitochondrial, and redox status after one-week HIIT training. Male (C57Bl/6) mice were assigned to non-trained or HIIT groups. The HIIT protocol consisted of three days with short bouts at 130% of maximum speed (Vmax), intercalated with moderate-intensity continuous exercise sessions of 30 min at 60% Vmax. The mass spectrometry analyses showed that one-week of HIIT increased minichromosome maintenance complex component 2 (MCM2), brain derived neutrophic factor (BDNF), doublecortin (DCX) and voltage-dependent anion-selective channel protein 2 (VDAC), and decreased mitochondrial superoxide dismutase 2 (SOD 2) in the hippocampus. In addition, one-week of HIIT promoted no changes in H2O2 production and carbonylated protein concentration in the hippocampus as well as in superoxide anion production in the dentate gyrus. In conclusion, our one-week HIIT protocol increased neuroplasticity and mitochondrial content regardless of changes in redox status, adding new insights into the neuronal modulation induced by new training models. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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15 pages, 2869 KiB  
Article
Protective Effects of Sulforaphane on Exercise-Induced Organ Damage via Inducing Antioxidant Defense Responses
by Ruheea Taskin Ruhee, Sihui Ma and Katsuhiko Suzuki
Antioxidants 2020, 9(2), 136; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9020136 - 04 Feb 2020
Cited by 43 | Viewed by 5992
Abstract
Regular exercise is beneficial to maintain a healthy lifestyle, but the beneficial effects are lost in the case of acute exhaustive exercise; this causes significant inflammation, oxidative stress along with organ damage. Recently, sulforaphane (SFN), an indirect antioxidant, has drawn special attention for [...] Read more.
Regular exercise is beneficial to maintain a healthy lifestyle, but the beneficial effects are lost in the case of acute exhaustive exercise; this causes significant inflammation, oxidative stress along with organ damage. Recently, sulforaphane (SFN), an indirect antioxidant, has drawn special attention for its potential protective effect against inflammation and oxidative stress. However, no studies have been performed regarding acute exhaustive exercise-induced organ damage in association with SFN administration. Therefore, the aim of this study was to investigate the effects of SFN on acute exhaustive exercise-induced organ damage and the mechanisms involved. To perform the study, we divided mice into four groups: Control, SFN, exercise, and SFN plus exercise. The SFN group was administered orally (50 mg/kg body wt) 2 h before the running test. We measured plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), and acute exhaustive exercise significantly increased these biomarkers. In addition, the mRNA expression of pro-inflammatory cytokines, IL-6, IL-1β, and TNF-α, were significantly increased in the liver of exercise group. However, the SFN plus exercise group showed a significant reduction in the expression of cytokines and blood biomarkers of tissue damage or cell death. Furthermore, we measured mRNA expression of Nrf2, heme oxygenase (HO)-1, and antioxidant defense enzymes expression, i.e., superoxide dismutase (SOD1), catalase (CAT), and glutathione peroxidase (GPx1) in the liver. The expression of all these biomarkers was significantly upregulated in the SFN plus exercise group. Collectively, SFN may protect the liver from exhaustive exercise-induced inflammation via inducing antioxidant defense response through the activation of Nrf2/HO-1 signal transduction pathway. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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16 pages, 1535 KiB  
Article
Strenuous Acute Exercise Induces Slow and Fast Twitch-Dependent NADPH Oxidase Expression in Rat Skeletal Muscle
by Juliana Osório Alves, Leonardo Matta Pereira, Igor Cabral Coutinho do Rêgo Monteiro, Luiz Henrique Pontes dos Santos, Alex Soares Marreiros Ferraz, Adriano Cesar Carneiro Loureiro, Crystianne Calado Lima, José Henrique Leal-Cardoso, Denise Pires Carvalho, Rodrigo Soares Fortunato and Vânia Marilande Ceccatto
Antioxidants 2020, 9(1), 57; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9010057 - 08 Jan 2020
Cited by 30 | Viewed by 3825
Abstract
The enzymatic complex Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidase (NOx) may be the principal source of reactive oxygen species (ROS). The NOX2 and NOX4 isoforms are tissue-dependent and are differentially expressed in slow-twitch fibers (type I fibers) and fast-twitch fibers (type II fibers) [...] Read more.
The enzymatic complex Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidase (NOx) may be the principal source of reactive oxygen species (ROS). The NOX2 and NOX4 isoforms are tissue-dependent and are differentially expressed in slow-twitch fibers (type I fibers) and fast-twitch fibers (type II fibers) of skeletal muscle, making them different markers of ROS metabolism induced by physical exercise. The aim of this study was to investigate NOx signaling, as a non-adaptive and non-cumulative response, in the predominant fiber types of rat skeletal muscles 24 h after one strenuous treadmill exercise session. The levels of mRNA, reduced glycogen, thiol content, NOx, superoxide dismutase, catalase, glutathione peroxidase activity, and PPARGC1α and SLC2A4 gene expression were measured in the white gastrocnemius (WG) portion, the red gastrocnemius (RG) portion, and the soleus muscle (SOL). NOx activity showed higher values in the SOL muscle compared to the RG and WG portions. The same was true of the NOX2 and NOX4 mRNA levels, antioxidant enzymatic activities, glycogen content. Twenty-four hours after the strenuous exercise session, NOx expression increased in slow-twitch oxidative fibers. The acute strenuous exercise condition showed an attenuation of oxidative stress and an upregulation of antioxidant activity through PPARGC1α gene activity, antioxidant defense adaptations, and differential gene expression according to the predominant fiber type. The most prominent location of detoxification (indicated by NOX4 activation) in the slow-twitch oxidative SOL muscle was the mitochondria, while the fast-twitch oxidative RG portion showed a more cytosolic location. Glycolytic metabolism in the WG portion suggested possible NOX2/NOX4 non-regulation, indicating other possible ROS regulation pathways. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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20 pages, 1370 KiB  
Article
Impact of ApoE Polymorphism and Physical Activity on Plasma Antioxidant Capability and Erythrocyte Membranes
by Rebecca Piccarducci, Simona Daniele, Jonathan Fusi, Lucia Chico, Filippo Baldacci, Gabriele Siciliano, Ubaldo Bonuccelli, Ferdinando Franzoni and Claudia Martini
Antioxidants 2019, 8(11), 538; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox8110538 - 09 Nov 2019
Cited by 11 | Viewed by 3053
Abstract
The allele epsilon 4 (ε4) of apolipoprotein E (ApoE) is the strongest genetic risk factor for Alzheimer’s disease (AD). ApoE protein plays a pivotal role in the synthesis and metabolism of amyloid beta (Aβ), the major component of the extracellular plaques that constitute [...] Read more.
The allele epsilon 4 (ε4) of apolipoprotein E (ApoE) is the strongest genetic risk factor for Alzheimer’s disease (AD). ApoE protein plays a pivotal role in the synthesis and metabolism of amyloid beta (Aβ), the major component of the extracellular plaques that constitute AD pathological hallmarks. Regular exercise is an important preventive/therapeutic tool in aging and AD. Nevertheless, the impact of physical exercise on the well-being of erythrocytes, a good model of oxidative stress and neurodegenerative processes, remains to be investigated, particularly depending on ApoE polymorphism. Herein, we evaluate the oxidative status, Aβ levels, and the membrane’s composition of erythrocytes in a cohort of human subjects. In our hands, the plasma antioxidant capability (AOC), erythrocytes membrane fluidity, and the amount of phosphatidylcholine (PC) were demonstrated to be significantly decreased in the ApoE ε4 genotype and non-active subjects. In contrast, erythrocyte Aβ content and lipid peroxidation increased in ε4 carriers. Regular physical exercise was associated with an increased plasma AOC and membrane fluidity, as well as to a reduced amount of erythrocytes Aβ. Altogether, these data highlight the influence of the ApoE genotype on erythrocytes’ well-being and confirm the positive impact of regular physical exercise. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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17 pages, 1426 KiB  
Article
Moderate Intensity Resistive Training Reduces Oxidative Stress and Improves Muscle Mass and Function in Older Individuals
by Alessandra Vezzoli, Simona Mrakic-Sposta, Michela Montorsi, Simone Porcelli, Paola Vago, Ferdinando Cereda, Stefano Longo, Marcello Maggio and Marco Narici
Antioxidants 2019, 8(10), 431; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox8100431 - 26 Sep 2019
Cited by 29 | Viewed by 4157
Abstract
An innovative moderate-intensity resistive exercise-training (RT) program was tested in thirty-five sarcopenic elders (SAR). The subjects were randomized into two groups: SAR training (SAR-RT), n = 20, 73.0 ± 5.5 years, or SAR non-training (SAR-NT), n = 15, 71.7 ± 3.4 years. The [...] Read more.
An innovative moderate-intensity resistive exercise-training (RT) program was tested in thirty-five sarcopenic elders (SAR). The subjects were randomized into two groups: SAR training (SAR-RT), n = 20, 73.0 ± 5.5 years, or SAR non-training (SAR-NT), n = 15, 71.7 ± 3.4 years. The training consisted of 12-week progressive RT, thrice/week, at 60% one-repetition maximum (1RM), 3 sets, 14–16 repetitions for both upper and lower limbs. The pre and post intervention measurements included: the skeletal muscle index (SMI%); strength (1RM); stair-climbing power (SCP); muscle thickness (MT) of vastus lateralis (VL) and elbow flexors (EF), VL pennation angle (PA), rectus femoris (RF) anatomical cross-sectional area (ACSA); reactive oxygen species (ROS), total antioxidant capacity (TAC), protein carbonyls (PC), thiobarbituric acid-reactive substances (TBARS), 8-isoprostane (8-iso-PGF2-α), 8-OH-2-deoxyguanosine (8-OH-dG), as markers of oxidative stress/damage (OxS). In SAR-RT, SCP increased by 7.7% (P < 0.01), MT increased by 5.5% for VL, 10.4% for EF and PA increased by 13.4% for VL (P < 0.001 for all). The RF ACSA increased by 14.5% (P < 0.001). 1RM significantly increased by at least 67% for all muscles tested. Notably muscle strength (1RM) positively correlated (P < 0.001) with TAC and negatively with PC (P < 0.001). In conclusion, moderate intensity RT is an effective strategy to increase muscle mass and strength in SAR, while minimizing OxS. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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Review

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41 pages, 739 KiB  
Review
Exercise-Induced Regulation of Redox Status in Cardiovascular Diseases: The Role of Exercise Training and Detraining
by Tryfonas Tofas, Dimitrios Draganidis, Chariklia K. Deli, Kalliopi Georgakouli, Ioannis G. Fatouros and Athanasios Z. Jamurtas
Antioxidants 2020, 9(1), 13; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9010013 - 23 Dec 2019
Cited by 38 | Viewed by 5665
Abstract
Although low levels of reactive oxygen species (ROS) are beneficial for the organism ensuring normal cell and vascular function, the overproduction of ROS and increased oxidative stress levels play a significant role in the onset and progression of cardiovascular diseases (CVDs). This paper [...] Read more.
Although low levels of reactive oxygen species (ROS) are beneficial for the organism ensuring normal cell and vascular function, the overproduction of ROS and increased oxidative stress levels play a significant role in the onset and progression of cardiovascular diseases (CVDs). This paper aims at providing a thorough review of the available literature investigating the effects of acute and chronic exercise training and detraining on redox regulation, in the context of CVDs. An acute bout of either cardiovascular or resistance exercise training induces a transient oxidative stress and inflammatory response accompanied by reduced antioxidant capacity and enhanced oxidative damage. There is evidence showing that these responses to exercise are proportional to exercise intensity and inversely related to an individual’s physical conditioning status. However, when chronically performed, both types of exercise amplify the antioxidant defense mechanism, reduce oxidative stress and preserve redox status. On the other hand, detraining results in maladaptations within a time-frame that depends on the exercise training intensity and mode, as high-intensity training is superior to low-intensity and resistance training is superior to cardiovascular training in preserving exercise-induced adaptations during detraining periods. Collectively, these findings suggest that exercise training, either cardiovascular or resistance or even a combination of them, is a promising, safe and efficient tool in the prevention and treatment of CVDs. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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15 pages, 1064 KiB  
Review
Effects of Resistance Exercise on Cerebral Redox Regulation and Cognition: An Interplay Between Muscle and Brain
by Ricardo A. Pinho, Aderbal S. Aguiar, Jr. and Zsolt Radák
Antioxidants 2019, 8(11), 529; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox8110529 - 06 Nov 2019
Cited by 27 | Viewed by 9365
Abstract
This review highlighted resistance training as an important training type for the brain. Most studies that use physical exercise for the prevention or treatment of neurodegenerative diseases have focused on aerobic physical exercise, revealing different behavioral, biochemical, and molecular effects. However, recent studies [...] Read more.
This review highlighted resistance training as an important training type for the brain. Most studies that use physical exercise for the prevention or treatment of neurodegenerative diseases have focused on aerobic physical exercise, revealing different behavioral, biochemical, and molecular effects. However, recent studies have shown that resistance training can also significantly contribute to the prevention of neurodegenerative diseases as well as to the maintenance, development, and recovery of brain activities through specific neurochemical adaptations induced by the training. In this scenario we observed the results of several studies published in different journals in the last 20 years, focusing on the effects of resistance training on three main neurological aspects: Neuroprotective mechanisms, oxidative stress, and cognition. Systematic database searches of PubMed, Web of Science, Scopus, and Medline were performed to identify peer-reviewed studies from the 2000s. Combinations of keywords related to brain disease, aerobic/resistance, or strength physical exercise were used. Other variables were not addressed in this review but should be considered for a complete understanding of the effects of training in the brain. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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27 pages, 891 KiB  
Review
Antioxidant and Adaptative Response Mediated by Nrf2 during Physical Exercise
by Nancy Vargas-Mendoza, Ángel Morales-González, Eduardo Osiris Madrigal-Santillán, Eduardo Madrigal-Bujaidar, Isela Álvarez-González, Luis Fernando García-Melo, Liliana Anguiano-Robledo, Tomás Fregoso-Aguilar and José A. Morales-Gonzalez
Antioxidants 2019, 8(6), 196; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox8060196 - 25 Jun 2019
Cited by 86 | Viewed by 9753
Abstract
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a powerful nuclear transcription factor that coordinates an antioxidant cytoprotector system complex stimulated by the increase in inoxidative stress (OS). In the present manuscript, we conduct a review on the evidence that shows the effect [...] Read more.
Nuclear factor erythroid 2-related factor 2 (Nrf2) is a powerful nuclear transcription factor that coordinates an antioxidant cytoprotector system complex stimulated by the increase in inoxidative stress (OS). In the present manuscript, we conduct a review on the evidence that shows the effect different modalities of physical exercise exert on the antioxidant metabolic response directed by Nrf2. During physical exercise, the reactive oxygen species (ROS) are increased; therefore, if the endogenous and exogenous antioxidant defenses are unable to control the elevation of ROS, the resulting OS triggers the activation of the transcriptional factor Nrf2 to induce the antioxidant response. On a molecular basis related to physical exercise, hormesis maintenance (exercise preconditioning) and adaptative changes in training are supported by a growing body of evidence, which is important for detailing the health benefits that involve greater resistance to environmental aggressions, better tolerance to constant changes, and increasing the regenerative capacity of the cells in such a way that it may be used as a tool to support the prevention or treatment of diseases. This may have clinical implications for future investigations regarding physical exercise in terms of understanding adaptations in high-performance athletes but also as a therapeutic model in several diseases. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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Other

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15 pages, 740 KiB  
Hypothesis
Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage
by Balazs Sonkodi, Istvan Berkes and Erika Koltai
Antioxidants 2020, 9(3), 212; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9030212 - 05 Mar 2020
Cited by 42 | Viewed by 77732
Abstract
According to our hypothesis, delayed onset muscle soreness (DOMS) is an acute compression axonopathy of the nerve endings in the muscle spindle. It is caused by the superposition of compression when repetitive eccentric contractions are executed under cognitive demand. The acute compression axonopathy [...] Read more.
According to our hypothesis, delayed onset muscle soreness (DOMS) is an acute compression axonopathy of the nerve endings in the muscle spindle. It is caused by the superposition of compression when repetitive eccentric contractions are executed under cognitive demand. The acute compression axonopathy could coincide with microinjury of the surrounding tissues and is enhanced by immune-mediated inflammation. DOMS is masked by sympathetic nervous system activity at initiation, but once it subsides, a safety mode comes into play to prevent further injury. DOMS becomes manifest when the microinjured non-nociceptive sensory fibers of the muscle spindle stop inhibiting the effects of the microinjured, hyperexcited nociceptive sensory fibers, therefore providing the ‘open gate’ in the dorsal horn to hyperalgesia. Reactive oxygen species and nitric oxide play a cross-talking role in the parallel, interlinked degeneration–regeneration mechanisms of these injured tissues. We propose that the mitochondrial electron transport chain generated free radical involvement in the acute compression axonopathy. ‘Closed gate exercises’ could be of nonpharmacological therapeutic importance, because they reduce neuropathic pain in addition to having an anti-inflammatory effect. Finally, DOMS could have an important ontogenetical role by not just enhancing ability to escape danger to survive in the wild, but also triggering muscle growth. Full article
(This article belongs to the Special Issue Redox Signalling and Exercise)
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