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

ABSTRACT: 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.

SUBMITTER: Borghi SM

PROVIDER: S-EPMC8776654 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Histamine contributes to elevations in skeletal muscle blood flow following exercise, which raises the possibility that histamine is an important mediator of the inflammatory response to exercise. We examined the influence of antihistamines on postexercise blood flow, inflammation, muscle damage, and delayed-onset muscle soreness (DOMS) in a model of moderate exercise-induced muscle damage. Subjects consumed either a combination of fexofenadine and ranitidine (blockade, n = 12) or nothing (control, n = 12) before 45 min of downhill running (-10% grade). Blood flow to the leg was measured before and throughout 120 min of exercise recovery. Markers of inflammation, muscle damage, and DOMS were obtained before and at 0, 6, 12, 24, 48, and 72 h postexercise. At 60 min postexercise, blood flow was reduced ~29% with blockade compared with control (P < 0.05). Markers of inflammation were elevated after exercise (TNF-ɑ, IL-6), but did not differ between control and blockade. Creatine kinase concentrations peaked 12 h after exercise, and the overall response was greater with blockade (18.3 ± 3.2 kU·l-1·h-1) compared with control (11.6 ± 2.0 kU·l-1·h-1; P < 0.05). Reductions in muscle strength in control (-19.3 ± 4.3% at 24 h) were greater than blockade (-7.8 ± 4.8%; P < 0.05) and corresponded with greater perceptions of pain/discomfort in control compared with blockade. In conclusion, histamine-receptor blockade reduced postexercise blood flow, had no effect on the pattern of inflammatory markers, increased serum creatine kinase concentrations, attenuated muscle strength loss, and reduced pain perception following muscle-damaging exercise.NEW & NOTEWORTHY Histamine appears to be intimately involved with skeletal muscle during and following exercise. Blocking histamine's actions during muscle-damaging exercise, via common over-the-counter antihistamines, resulted in increased serum creatine kinase, an indirect marker of muscle damage. Paradoxically, blocking histamine's actions attenuated muscle strength loss and reduced perceptions of muscle pain for 72 h following muscle-damaging exercise. These results indicate that exercise-induced histamine release may have a broad impact on protecting muscle from exercise-induced damage.

Project description:Background There is limited information about perfusion in exercise-induced muscle injuries such as delayed-onset muscle soreness (DOMS) and the effect of compression garments as a therapeutic strategy during the regeneration phase. The purpose of this prospective, explorative study was to evaluate muscle perfusion in DOMS and to assess the effect of compression garments at resting conditions and during DOMS by magnetic resonance (MR) arterial spin labeling (ASL). Methods DOMS was induced from 03/2021 to 04/2021 using an eccentric and plyometric exercises targeting the calf muscles in 14 volunteers. A compression garment (21–22 mmHg) was worn during and for 6 h after exercise on one randomized leg. Magnetic resonance imaging (MRI) including ASL of both lower legs was performed before and directly after the exercise as well as after 6 h, and 48 h using a 3 Tesla MRI system. Perfusion analyses of the gastrocnemius muscle (GM) and the tibialis anterior muscle (TA) were performed and results were compared to baseline measurements. T2-weighted images and creatine kinase levels were acquired at baseline and after 48 h. Results All volunteers presented a successful induction of DOMS in the GM after 48 h. Arterial muscle perfusion in the GM increased from baseline to measurements taken directly after the exercise (4.97±5.59 mL/100 g/min, P<0.001). No significant alteration in perfusion compared to baseline was observed at 6 h (P=0.16) and 48 h (P=1.0) after the induction of DOMS. Compression garments did not elicit a significant alteration in ASL parameters in the GM (P=0.65) or the TA (P=0.05) at any time point. No adverse events occurred during the study. Conclusions After an initial exercise-associated increase in arterial muscle perfusion, a normalization of blood supply was observed at 6 and 48 h after the exercise intervention inducing DOMS. Wearing a compression garment (21–22 mmHg) during and after the induction of DOMS did not affect muscle perfusion at rest, nor did it have any significant effect on muscle perfusion during the regeneration phase. The results can help to better understand the pathophysiological properties of DOMS and may have implications for diagnostic and therapeutic strategies.

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

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