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

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.

Relationship between Eccentric-Exercise-Induced Loss in Muscle Function to Muscle Soreness and Tissue Hardness

It is well-known that unusual exercise, especially eccentric contraction (ECC), could cause delayed-onset muscle soreness. However, the factors related to the loss of muscle strength and range of motion (ROM) caused by eccentrically damaged muscle, such as increases in muscle soreness, tissue hardness, and pain threshold, have not been investigated in detail. Thus, this study was conducted to investigate the factors related to the loss of muscle strength and ROM caused by eccentrically damaged muscle in a large sample. Fifty-six sedentary healthy young male volunteers were instructed to perform 60 repetitions of ECC exercise. The outcome variables were measured before and 48 h after the ECC exercise. The results showed that a decrease in ROM was correlated to an increase in tissue hardness, whereas a decrease in muscle strength was correlated to an increase in muscle soreness. Our results suggested that tissue hardness must be controlled for ROM loss, and muscle soreness must be controlled for muscle-strength loss.

Sound generation mechanism of compressible vortex reconnection

We study the sound generation mechanism of initially subsonic viscous vortex reconnection at vortex Reynolds number $Re~(\equiv \text {circulation}/\text {kinematic viscosity})=1500$ through decomposition of Lighthill's acoustic source term. The Laplacian of the kinetic energy, flexion product, enstrophy and deviation from the isentropic condition provide the dominant contributions to the acoustic source term. The overall (all time) extrema of the total source term and its dominant hydrodynamic components scale linearly with the reference Mach number $M_o$ ; the deviation from the isentropic condition shows a quadratic scaling. The significant sound arising from the flexion product occurs due to the coiling and uncoiling of the twisted vortex filaments wrapping around the bridges, when a rapid strain is induced on the filaments by the repulsion of the bridges. The spatial distributions of the various acoustic source terms reveal the importance of mutual cancellations among most of the terms; this also highlights the importance of symmetry breaking in the sound generation during reconnection. Compressibility acts to delay the start of the sequence of reconnection events, as long as shocklets, if formed, are sufficiently weak to not affect the reconnection. The delayed onset has direct ramifications for the sound generation by enhancing the velocity of the entrained jet between the vortices and increasing the spatial gradients of the acoustic source terms. Consistent with the near-field pressure, the overall maximum instantaneous sound pressure level in the far field has a quadratic dependence on $M_o$ . Thus, reconnection becomes an even more dominant sound-generating event at higher $M_o$ .

Successful Use of Neurovascular Plug for Embolization of Scalp Arteriovenous Fistula: A Novel Technique

Purpose: We report a case of a pediatric patient developing a delayed-onset scalp arteriovenous fistula (AVF) and pseudoaneurysm managed with a new technique. Technique: A 10-year-old boy presented to the outpatient clinic complaining of a growing pulsatile mass in the right side of the skull after head trauma 6 months ago. He had no neurological deficits. Imaging studies revealed scalp AVF with pseudoaneurysm. The arterial feeding was from the right temporal artery, while the blood was drained into the superior sagittal sinus and the facial vein. The fistula was occluded successfully by a microvascular plug (MVP). Follow-up angiography 1 year later showed that the AVF was no longer seen with complete embolization of pseudoaneurysm, total occlusion of the abnormal vessels, and the absence of MVP migration. Conclusion: To the best of our knowledge, we report the first case of successfully using MVP to treat scalp AVF. The MVP is a novel technique with its unique ability to achieve rapid, safe, effective, and permanent vascular occlusion through a single device. Besides, the possibility of delayed-onset traumatic vascular injuries should be considered in a patient with head or facial trauma.

Dietary Supplementation for Attenuating Exercise-Induced Muscle Damage and Delayed-Onset Muscle Soreness in Humans

Dietary supplements are widely used as a nutritional strategy to improve and maintain performance and achieve faster recovery in sports and exercise. Exercise-induced muscle damage (EIMD) is caused by mechanical stress and subsequent inflammatory responses including reactive oxygen species and cytokine production. Therefore, dietary supplements with anti-inflammatory and antioxidant properties have the potential to prevent and reduce muscle damage and symptoms characterized by loss of muscle strength and delayed-onset muscle soreness (DOMS). However, only a few supplements are considered to be effective at present. This review focuses on the effects of dietary supplements derived from phytochemicals and listed in the International Olympic Committee consensus statement on muscle damage evaluated by blood myofiber damage markers, muscle soreness, performance, and inflammatory and oxidative stress markers. In this review, the effects of dietary supplements are also discussed in terms of study design (i.e., parallel and crossover studies), exercise model, and such subject characteristics as physical fitness level. Future perspectives and considerations for the use of dietary supplements to alleviate EIMD and DOMS are also discussed.