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.

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.

Effects of Acute and Chronic Stretching on Pain Control

ABSTRACT While muscle stretching has been commonly used to alleviate pain, reports of its effectiveness are conflicting. The objective of this review is to investigate the acute and chronic effects of stretching on pain, including delayed onset muscle soreness. The few studies implementing acute stretching protocols have reported small to large magnitude decreases in quadriceps and anterior knee pain as well as reductions in headache pain. Chronic stretching programs have demonstrated more consistent reductions in pain from a wide variety of joints and muscles, which has been ascribed to an increased sensory (pain) tolerance. Other mechanisms underlying acute and chronic pain reduction have been proposed to be related to gate control theory, diffuse noxious inhibitory control, myofascial meridians, and reflex-induced increases in parasympathetic nervous activity. By contrast, the acute effects of stretching on delayed onset muscle soreness are conflicting. Reports of stretch-induced reductions in delayed onset muscle soreness may be attributed to increased pain tolerance or alterations in the muscle's parallel elastic component or extracellular matrix properties providing protection against tissue damage. Further research evaluating the effect of various stretching protocols on different pain modalities is needed to clarify conflicts within the literature.

ANTI-INFLAMMATORIES FOR DELAYED ONSET MUSCLE SORENESS: SYSTEMATIC REVIEW AND META-ANALYSIS

ABSTRACT Objective: To investigate the effectiveness of pharmacological interventions in the treatment of delayed onset muscle soreness (DOMS). Design: A systematic review and meta-analysis of randomized controlled clinical trials (RCTs). Data sources: The PubMed/MEDLINE, EMBASE, SPORTDiscus, Scielo and Cochrane Central Register of Controlled Trials (CENTRAL) databases were searched for RCTs published prior to August 3, 2020. Eligibility criteria for selecting studies: Studies that 1) used an RCT design; 2) evaluated the effectiveness of steroidal or nonsteroidal anti-inflammatory drugs (NSAIDs) in treating DOMS; and 3) therapeutically used drugs after exercise were included. Results: In total, 26 studies (patients = 934) were eligible for inclusion in the qualitative analysis on the treatment of DOMS. The results of the meta-analysis showed no superiority between the use and non-use of NSAIDs in the improvement of late muscle pain, as no statistically significant differences were verified (21 studies, n= 955; standard mean difference (SMD)= 0.02; 95% confidence interval (CI) −0.58, 0.63; p=0.94; I2=93%). The quality of the synthesized evidence was very low according to the Grading of Recommendations Assessment, Development and Evaluation (GRADE) criteria, and there was significant heterogeneity among the included studies. Conclusion: The results demonstrate that NSAIDs are not superior to controls/placebos in treating DOMS. The inclusion of both studies with dose-response protocols and those with exercise protocols may have influenced the results. In addition, the high risk of bias identified reveals that limitations need to be considered when interpreting the results. Level of evidence I; ystematic review of RCT (Randomized and Controlled Clinical Trials).

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

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.

Finishing stationary cycling too early after anterior cruciate ligament reconstruction is likely to lead to higher failure

Background Anterior cruciate ligament injury arises when the knee anterior ligament fibers are stretched, partially torn, or completely torn. Operated patients either end up re-injuring their reconstructed anterior cruciate ligament or majority develop early osteoarthritis regardless of the remarkable improvements of surgical techniques and the widely available rehabilitation best practices. New mechanism theories of non-contact anterior cruciate ligament injury and delayed onset muscle soreness could provide a novel perspective how to respond to this clinical challenge. Main body A tri-phasic injury model is proposed for these non-contact injuries. Mechano-energetic microdamage of the proprioceptive sensory nerve terminals is suggested to be the first-phase injury that is followed by a harsher tissue damage in the second phase. The longitudinal dimension is the third phase and that is the equivalent of the repeated bout effect of delayed onset muscle soreness. Current paper puts this longitudinal injury phase into perspective as the phase when the long-term memory consolidation and reconsolidation of this learning related neuronal injury evolves and the phase when the extent of the neuronal regeneration is determined. Reinstating the mitochondrial energy supply and ‘breathing capacity’ of the injured proprioceptive sensory neurons during this period is emphasized, as avoiding fatigue, overuse, overload and re-injury. Conclusions Extended use, minimum up to a year or even longer, of a current rehabilitation technique, namely moderate intensity low resistance stationary cycling, is recommended preferably at the end of the day. This exercise therapeutic strategy should be a supplementation to the currently used rehabilitation best practices as a knee anti-aging maintenance effort.

Effect of caffeine on delayed-onset muscle soreness: a meta-analysis of RCT

Background There are multiple strategies that have been suggested to attenuate delayed-onset muscle soreness (DOMS). Caffeine has been shown to assist with blocking pain associated with DOMS. However, currently there is still controversy over the effects of caffeine use. Main body We conducted a meta-analysis to compare pain associated with muscle soreness by both the VAS and indirect markers by CK of caffeine and placebo after exercise. The meta-analysis was carried out in accordance with the PRISMA guidelines. Relevant studies from Medline and Scopus published up to May 20, 2021, were included, which resulted in a total of 477 and 132 studies being retrieved from Scopus and Medline, respectively. Seven studies met the inclusion criteria, and in these, there were 68 persons in the caffeine group and 74 persons in the placebo group. A visual analog score of muscle soreness was recorded pre-exercise, immediately post-exercise, and at one to four days post-exercise; the scores at these time points in the caffeine group as compared to those in the placebo group progressed from 0.00 (95% CI − 0.51, 0.50) to − 0.20 (− 1.09, 0.69), − 0.92 (− 2.20, 0.36), − 1.02 (− 1.86, − 0.19), 0.00 (− 0.36, 0.36), and 0.18 (− 0.56, 0.92), respectively. No statistically significant differences were noted for CK between the two groups at 24 h post-exercise. Short conclusion Our meta-analysis results indicate that caffeine supplements reduce delayed-onset muscle soreness when compared to a placebo 48 h after exercise. However, at 24 h post-exercise, caffeine can reduce DOMS only in people who worked on resistant exercise. The CK used in this meta-analysis did not show any differences. Trial registration: PROSPERO CRD42021260248. Level of evidence I.