scholarly journals Intense Acute Swimming Induces Delayed-Onset Muscle Soreness Dependent on Spinal Cord Neuroinflammation

2022 ◽  
Vol 12 ◽  
Author(s):  
Sergio M. Borghi ◽  
Sylvia K. D. Bussulo ◽  
Felipe A. Pinho-Ribeiro ◽  
Victor Fattori ◽  
Thacyana T. Carvalho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Muscle Soreness ◽  
Nuclear Factor Κb ◽  
Delayed Onset Muscle Soreness ◽  
Pyrrolidine Dithiocarbamate ◽  
Peripheral Tissues ◽  
Delayed Onset ◽  
Tnf Α ◽  
And Oxidative Stress

Unaccustomed exercise involving eccentric contractions, high intensity, or long duration are recognized to induce delayed-onset muscle soreness (DOMS). Myocyte damage and inflammation in affected peripheral tissues contribute to sensitize muscle nociceptors leading to muscle pain. However, despite the essential role of the spinal cord in the regulation of pain, spinal cord neuroinflammatory mechanisms in intense swimming-induced DOMS remain to be investigated. We hypothesized that spinal cord neuroinflammation contributes to DOMS. C57BL/6 mice swam for 2 h to induce DOMS, and nociceptive spinal cord mechanisms were evaluated. DOMS triggered the activation of astrocytes and microglia in the spinal cord 24 h after exercise compared to the sham group. DOMS and DOMS-induced spinal cord nuclear factor κB (NFκB) activation were reduced by intrathecal treatments with glial inhibitors (fluorocitrate, α-aminoadipate, and minocycline) and NFκB inhibitor [pyrrolidine dithiocarbamate (PDTC)]. Moreover, DOMS was also reduced by intrathecal treatments targeting C-X3-C motif chemokine ligand 1 (CX3CL1), tumor necrosis factor (TNF)-α, and interleukin (IL)-1β or with recombinant IL-10. In agreement, DOMS induced the mRNA and protein expressions of CX3CR1, TNF-α, IL-1β, IL-10, c-Fos, and oxidative stress in the spinal cord. All these immune and cellular alterations triggered by DOMS were amenable by intrathecal treatments with glial and NFκB inhibitors. These results support a role for spinal cord glial cells, via NFκB, cytokines/chemokines, and oxidative stress, in DOMS. Thus, unveiling neuroinflammatory mechanisms by which unaccustomed exercise induces central sensitization and consequently DOMS.

Effect of 4-Week Ingestion of Tomato-Based Carotenoids on Exercise-Induced Inflammation, Muscle Damage, and Oxidative Stress in Endurance Runners

2018 ◽  
Vol 28 (3) ◽  
pp. 266-273 ◽  
Author(s):  
David C. Nieman ◽  
Courtney L. Capps ◽  
Christopher R. Capps ◽  
Zack L. Shue ◽  
Jennifer E. McBride
Keyword(s):  
Oxidative Stress ◽  
Creatine Kinase ◽  
Muscle Damage ◽  
Muscle Soreness ◽  
Delayed Onset Muscle Soreness ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Delayed Onset ◽  
Reducing Ability ◽  
And Oxidative Stress

This double-blind, randomized, placebo-controlled crossover trial determined if ingestion of a supplement containing a tomato complex with lycopene, phytoene, and phytofluene (T-LPP) and other compounds for 4 weeks would attenuate inflammation, muscle damage, and oxidative stress postexercise and during recovery from a 2-hr running bout that included 30 min of −10% downhill running. Study participants ingested the T-LPP supplement or placebo with the evening meal for 4 weeks prior to running 2 hr at high intensity. Blood samples and delayed onset muscle soreness ratings were taken pre- and post-4-week supplementation, and immediately following the 2-hr run, and then 1-hr, 24-hr, and 48-hr postrun. After a 2-week washout period, participants crossed over to the opposite treatment and repeated all procedures. Plasma lycopene, phytoene, and phytofluene increased significantly in T-LPP compared with placebo (p < .001 for each). Significant time effects were shown for serum creatine kinase, delayed onset muscle soreness, C-reactive protein, myoglobin, 9- and 13-hydroxyoctadecadienoic acids, ferric reducing ability of plasma, and six plasma cytokines (p < .001 for each). The pattern of increase for serum myoglobin differed between T-LPP and placebo (interaction effect, p = .016, with lower levels in T-LPP), but not for creatine kinase, delayed onset muscle soreness, C-reactive protein, the six cytokines, 9- and 13-hydroxyoctadecadienoic acids, and ferric reducing ability of plasma. No significant time or interaction effects were measured for plasma-oxidized low-density lipoprotein or serum 8-hydroxy-2′-deoxyguanosine. In summary, supplementation with T-LPP over a 4-week period increased plasma carotenoid levels 73% and attenuated postexercise increases in the muscle damage biomarker myoglobin, but not inflammation and oxidative stress.

scholarly journals Effect of curcumin supplement or placebo in delayed onset muscle soreness: a systematic review and meta-analysis

2021 ◽  
Vol 45 (1) ◽  
Author(s):  
Natthanichar Rattanaseth ◽  
Patteera Panyarapeepat ◽  
Janisa Andrea Muljadi ◽  
Kornkit Chaijenkij ◽  
Jatupon Kongtharvonskul
Keyword(s):  
Muscle Soreness ◽  
Meta Analysis ◽  
Delayed Onset Muscle Soreness ◽  
Main Body ◽  
Level Of Evidence ◽  
Post Exercise ◽  
Multiple Strategies ◽  
Delayed Onset ◽  
Tnf Α ◽  
Exercise Induced

Abstract Background There are multiple strategies that have been suggested to attenuate delayed onset muscle soreness (DOMS). Curcumin has been shown to reduce exercise-induced oxidative stress (OS) and inflammation. However, currently, there is still controversy. Main body of the abstract We conduct this meta-analysis according to the PRISMA guidelines. Relevant studies were included from Medline and Scopus from the date of inception to May 04th, 2021 that reported VAS score, blood markers (creatinine kinese (CK), tumor necrotic factor (TNF)-α and interleukin (IL)-6) and range of motion of either group. There were total of 13 studies including 202 and 176 persons in curcumin and placebo group. The unstandardized mean difference (UMD) of VAS muscle soreness in post-exercise, 1, 2, 3 and 4 days was − 0.12 (95% CI − 0.46, 0.22), − 0.38 (− 0.83, 0.08), − 0.67 (− 1.19, − 0.16), − 0.86 (− 1.38, − 0.34), − 0.81 (− 1.27, − 036) and − 1.24 (− 1.50, − 0.99) scores lower in curcumin when compared to placebo. The UMD of CK was − 11.07 (95% CI − 24, 1.86), − 37.51 (− 68.04, − 6.97), − 45.40 (− 95.67, 4.86), − 53.33 (− 128.11, 21.45), − 90.98 (− 173.45, − 8.51) and 117.84 (− 338.69, 574.37) lower in curcumin when compared to placebo. No statistically significantly differences were noted for IL-6, TNF-α and ROM between two groups. Short conclusion This meta-analysis suggested that curcumin supplement reduced delayed onset muscle soreness and CK after exercise in 1, 2, 3, and 4 days when compared to placebo. However, TNF and IL were not affected by curcumin ingestion. Level of evidence I.

Effect of 1-week Calendula officinalis consumption before high-intensity interval exercise on some delayed onset muscle soreness (DOMS) elements in male rowers

2021 ◽  
pp. 1-8
Author(s):  
B. Mohammadi ◽  
L. Anoosheh ◽  
S. Rahmati-Ahmadabad
Keyword(s):  
High Intensity ◽  
Muscle Soreness ◽  
Pain Perception ◽  
Delayed Onset Muscle Soreness ◽  
Calendula Officinalis ◽  
Interval Exercise ◽  
Delayed Onset ◽  
Tnf Α ◽  
High Intensity Interval ◽  
Experimental Group

Previous studies showed that some medicinal herbs can prevent delayed onset muscle soreness (DOMS). The present study investigates the effect of Calendula officinalis supplementation on DOMS elements on male rowers. Thirty healthy adult male rowers were randomly chosen and equally divided into experimental and control groups. Blood samples, Sargent jumps (SJ), and pain perception tests were measured at the starting point. The experimental group consumed (twice a day, 200 μl each time) C. officinalis extract for a week while the control group received a placebo. After consuming the supplementations for a week, the second samples and tests were taken. All the athletes participated in the high-intensity interval exercise (HIIE – a muscle soreness protocol). Third, fourth, and fifth samples/tests were executed immediately, 24 and 48 h after HIIE. Statistical analysis was conducted and P≤0.05 was considered as the significant level. The results showed that HIIE induced a significant increase in the serum tumour necrosis factor-alpha (TNF-α) and creatine kinase-MB (CK-MB) values as well as the pain perception in both groups. TNF-α and pain perception were significantly lower in the experimental group immediately, 24 and 48 h after HIIE. CK-MB activity was significantly decreased in the experimental group during next 24 and 48 h after HIIE. The muscle soreness protocol and its preceding supplementation had no significant effect on SJ. The present study suggests that the consumption of C. officinalis based on the present study dose and timespan may be effective to attenuate inflammation and pain induced by HIIE in male rowers and probably has no functional impact on muscle.

scholarly journals Role of TNF-α/TNFR1 in intense acute swimming-induced delayed onset muscle soreness in mice

2014 ◽  
Vol 128 ◽  
pp. 277-287 ◽  
Author(s):  
Sergio M. Borghi ◽  
Ana C. Zarpelon ◽  
Felipe A. Pinho-Ribeiro ◽  
Renato D.R. Cardoso ◽  
Marli C. Martins-Pinge ◽  
...  
Keyword(s):  
Muscle Soreness ◽  
Delayed Onset Muscle Soreness ◽  
Delayed Onset ◽  
Tnf Α

Pyrrolidine dithiocarbamate inhibits superoxide anion-induced pain and inflammation in the paw skin and spinal cord by targeting NF-κB and oxidative stress

2016 ◽  
Vol 24 (2-3) ◽  
pp. 97-107 ◽  
Author(s):  
Felipe A. Pinho-Ribeiro ◽  
Victor Fattori ◽  
Ana C. Zarpelon ◽  
Sergio M. Borghi ◽  
Larissa Staurengo-Ferrari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Superoxide Anion ◽  
Pyrrolidine Dithiocarbamate ◽  
And Oxidative Stress

scholarly journals miRNA-221 Regulates Spinal Cord Injury-Induced Inflammatory Response through Targeting TNF-α Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Feng Sun ◽  
Haiwei Zhang ◽  
Tianwen Huang ◽  
Jianhui Shi ◽  
Tianli Wei ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Luciferase Reporter ◽  
Spinal Cord Tissue ◽  
Tnf Α ◽  
Cord Injury ◽  
And Oxidative Stress

Objectives. To investigate the roles of miR-221 in spinal cord injury (SCI) as well as the underlying mechanism. Methods. A mouse model of SCI was generated and used to examine dynamic changes in grip strength of the mouse upper and lower limbs. The expression of miR-221 and tumor necrosis factor-α (TNF-α) was detected by RT-qPCR and Western blot. Levels of inflammation and oxidative stress in microglia cells of the injured mice overexpressing miR-221 were then measured by ELISA. Bioinformatics analysis and dual-luciferase reporter assay were conducted to identify the miR-221 target. Results. We successfully constructed SCI mouse model. The results of qRT-PCR showed that miR-221 was gradually upregulated in the spinal cord tissue of mice in the SCI group with the prolonged injury time. At the same time, the mRNA and protein of TNF-α gradually decreased. We further confirmed through cell experiments that the inflammatory factors TNF-α and IL-6, as well as iNOS and eROS, were upregulated in spinal cord microglia cells of SCI mice, and upregulation of miR-122 can inhibit their expression. Finally, the luciferase reporter experiment confirmed that miR-122 targeted TNF-α. Conclusions. We present evidence that miR-221 promotes functional recovery of the injured spinal cord through targeting TNF-α, while alleviating inflammatory response and oxidative stress.

The cross-talk between NF-κB and HIF-1: further evidence for a significant liaison

2008 ◽  
Vol 412 (3) ◽  
pp. e17-e19 ◽  
Author(s):  
Agnes Görlach ◽  
Steve Bonello
Keyword(s):  
Oxidative Stress ◽  
Cellular Response ◽  
Distinct Element ◽  
Hypoxia Inducible Factor ◽  
Nuclear Factor Κb ◽  
Proximal Promoter ◽  
Α Subunit ◽  
Hypoxic Conditions ◽  
Tnf Α ◽  
And Oxidative Stress

HIF-1 (hypoxia-inducible factor-1) has been shown to essentially control the cellular response to hypoxia. Hypoxia stabilizes the inducible α-subunit, preventing post-translational hydroxylation and subsequent degradation via the proteasome. In recent years, clear evidence has emerged that HIF-1α is also responsive to many stimuli under normoxic conditions, including thrombin, growth factors, vasoactive peptides, insulin, lipopolysaccharide and cytokines such as TNF-α (tumour necrosis factor-α), and in many cases reactive oxygen species are involved. One important mechanism underlying these responses is the transcriptional regulation of HIF-1α by the redox-sensitive transcription factor NF-κB (nuclear factor κB), which binds at a distinct element in the proximal promoter of the HIF-1α gene. More recently, NF-κB binding to this site in the HIF-1α promoter has been shown also under hypoxic conditions. Thus these two major pathways regulating the responses to inflammation and oxidative stress on the one hand, and hypoxia on the other hand, appear to be intimately linked. In this issue of the Biochemical Journal, a study by van Uden et al. has supported these findings further, in which they have confirmed the binding of several proteins of the NF-κB family at the previously identified consensus site in the HIF-1α promoter and shown that TNF-α can also transcriptionally induce HIF-1α by this previously described pathway. The identification of HIF-1α as a target gene of NF-κB will have important implications for a variety of disorders related to hypoxia–ischaemia and/or inflammation and oxidative stress.

Inhibition of the nuclear factor—κB activation with pyrrolidine dithiocarbamate attenuating inflammation and oxidative stress after experimental spinal cord trauma in rats

2004 ◽  
Vol 1 (3) ◽  
pp. 311-321 ◽  
Author(s):  
Giovanni La Rosa ◽  
Salvatore Cardali ◽  
Tiziana Genovese ◽  
Alfredo Conti ◽  
Rosanna Di Paola ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nuclear Factor Κb ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor ◽  
Mobility Shift ◽  
Content Type ◽  
Cord Injury ◽  
Mobility Shift Assay ◽  
And Oxidative Stress ◽  
Fine Print

Object. The nuclear factor—κB (NF-κB) is a transcription factor that plays a pivotal role in the induction of genes involved in physiological processes and in the response to inflammation. The authors of recent studies have demonstrated that NF-κB and oxidative stress contribute to secondary injury after impact-induced spinal cord injury (SCI) in the rat. Dithiocarbamates are antioxidants that are potent inhibitors of NF-κB. The authors postulated that pyrrolidine dithiocarbamate (PDTC) would attenuate NF-κB—related inflammatory and oxidative events that occur after SCI. Methods. Spinal cord injury was induced by the application of vascular clips (force of 50 g) to the dura mater after a four-level T5–8 laminectomy. The authors investigated the effects of PDTC (30 mg/kg administered 30 minutes before SCI and 6 hours after SCI) on the development of the inflammatory response associated with SCI in rats. Levels of myeloperoxidase activity were measured as an indicator of polymorphonuclear infiltration; malondialdehyde levels in the spinal cord tissue were determined as an indicator of lipid peroxidation. The following studies were performed: immunohistochemical analysis to assess levels of inducible nitric oxide synthase (iNOS), nitrotyrosine formation, poly([adenosine diphosphate]-ribose) polymerase (PARP) activity; Western blot analysis to determine cytoplasmic levels of inhibitory—κB-α (IκB-α); and electrophoretic mobility-shift assay to measure the level of DNA/NF-κB binding. The PDTC treatment exerted potent antiinflammatory effects with significant reduction of polymorphonuclear cell infiltration, lipid peroxidation, and iNOS activity. Furthermore, administration of PDTC reduced immunohistochemical evidence of formation of nitrotyrosine and PARP activation in the spinal cord section obtained in the SCI-treated rats. Additionally, PDTC treatment significantly prevented the activation of NF-κB (electrophoretic mobility-shift assay and immunoblot analysis). Conclusions. Overall, the results clearly demonstrate that PDTC-related prevention of the activation of NF-κB reduces the development of some secondary injury events after SCI. Therefore, inhibition of NF-κB may represent a novel approach in the treatment of SCIs.

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