Dataset Information

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.

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 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.

SUBMITTER: Sonkodi B

PROVIDER: S-EPMC7139782 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature

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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.

Sonkodi Balazs B Berkes Istvan I Koltai Erika E

Antioxidants (Basel, Switzerland) 20200305 3

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 ...[more]

PMID: 32150878

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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.

Dataset Information

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.

Publications

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.

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