Muscle damage and inflammation during recovery from exercise

Unaccustomed exercise consisting of eccentric (i.e., lengthening) muscle contractions often results in muscle damage characterized by ultrastructural alterations in muscle tissue, clinical signs, and symptoms (e.g., reduced muscle strength and range of motion, increased muscle soreness and swelling, efflux of myocellular proteins). The time course of recovery following exercise-induced muscle damage depends on the extent of initial muscle damage, which in turn is influenced by the intensity and duration of exercise, joint angle/muscle length, and muscle groups used during exercise. The effects of these factors on muscle strength, soreness, and swelling are well characterized. By contrast, much less is known about how they affect intramuscular inflammation and molecular aspects of muscle adaptation/remodeling. Although inflammation has historically been viewed as detrimental for recovery from exercise, it is now generally accepted that inflammatory responses, if tightly regulated, are integral to muscle repair and regeneration. Animal studies have revealed that various cell types, including neutrophils, macrophages, mast cells, eosinophils, CD8 and T-regulatory lymphocytes, fibro-adipogenic progenitors, and pericytes help to facilitate muscle tissue regeneration. However, more research is required to determine whether these cells respond to exercise-induced muscle damage. A large body of research has investigated the efficacy of physicotherapeutic, pharmacological, and nutritional interventions for reducing the signs and symptoms of exercise-induced muscle damage, with mixed results. More research is needed to examine if/how these treatments influence inflammation and muscle remodeling during recovery from exercise.

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Stimuli and sensors that initiate skeletal muscle hypertrophy following resistance exercise

Journal of Applied Physiology ◽

10.1152/japplphysiol.00685.2018 ◽

2019 ◽

Vol 126 (1) ◽

pp. 30-43 ◽

Cited By ~ 45

Author(s):

Henning Wackerhage ◽

Brad J. Schoenfeld ◽

D. Lee Hamilton ◽

Maarit Lehti ◽

Juha J. Hulmi

Keyword(s):

Skeletal Muscle ◽

Resistance Exercise ◽

Muscle Damage ◽

Muscle Hypertrophy ◽

Muscle Protein ◽

Large Body ◽

Focal Adhesions ◽

Indirect Evidence ◽

Skeletal Muscle Hypertrophy ◽

Exercise Induced

One of the most striking adaptations to exercise is the skeletal muscle hypertrophy that occurs in response to resistance exercise. A large body of work shows that a mammalian target of rapamycin complex 1 (mTORC1)-mediated increase of muscle protein synthesis is the key, but not sole, mechanism by which resistance exercise causes muscle hypertrophy. While much of the hypertrophy signaling cascade has been identified, the initiating, resistance exercise-induced and hypertrophy-stimulating stimuli have remained elusive. For the purpose of this review, we define an initiating, resistance exercise-induced and hypertrophy-stimulating signal as “hypertrophy stimulus,” and the sensor of such a signal as “hypertrophy sensor.” In this review we discuss our current knowledge of specific mechanical stimuli, damage/injury-associated and metabolic stress-associated triggers, as potential hypertrophy stimuli. Mechanical signals are the prime hypertrophy stimuli candidates, and a filamin-C-BAG3-dependent regulation of mTORC1, Hippo, and autophagy signaling is a plausible albeit still incompletely characterized hypertrophy sensor. Other candidate mechanosensing mechanisms are nuclear deformation-initiated signaling or several mechanisms related to costameres, which are the functional equivalents of focal adhesions in other cells. While exercise-induced muscle damage is probably not essential for hypertrophy, it is still unclear whether and how such muscle damage could augment a hypertrophic response. Interventions that combine blood flow restriction and especially low load resistance exercise suggest that resistance exercise-regulated metabolites could be hypertrophy stimuli, but this is based on indirect evidence and metabolite candidates are poorly characterized.

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Sand training: Exercise-induced muscle damage and inflammatory responses to matched-intensity exercise

European Journal of Sport Science ◽

10.1080/17461391.2017.1304998 ◽

2017 ◽

Vol 17 (6) ◽

pp. 741-747 ◽

Cited By ~ 3

Author(s):

Henry Brown ◽

Brian Dawson ◽

Martyn J. Binnie ◽

Hugh Pinnington ◽

Marc Sim ◽

...

Keyword(s):

Muscle Damage ◽

Inflammatory Responses ◽

Training Exercise ◽

Exercise Induced

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Amoebae in Chronic, Polymicrobial Endodontic Infections Are Associated with Altered Microbial Communities of Increased Virulence

Journal of Clinical Medicine ◽

10.3390/jcm9113700 ◽

2020 ◽

Vol 9 (11) ◽

pp. 3700

Author(s):

Garrit Koller ◽

Federico Foschi ◽

Philip Mitchell ◽

Elizabeth Witherden ◽

Kenneth Bruce ◽

...

Keyword(s):

Microbial Communities ◽

High Throughput Sequencing ◽

Inflammatory Responses ◽

Clinical Signs ◽

Signs And Symptoms ◽

Resistant Bacteria ◽

Low Grade ◽

Taxonomic Assignment ◽

Microbial Composition ◽

Endodontic Infections

Background: Infections of the root canal space involve polymicrobial biofilms and lead to chronic, low grade inflammatory responses arising from the seeding of microbes and by-products. Acute exacerbation and/or disseminating infections occur when established microbial communities undergo sudden changes in phenotypic behaviour. Methods: Within clinical endodontic infections, we assessedcategorical determinants comprising, and changing microbial composition of, chronic polymicrobial infections and their association with amoebae. After standardised assessment, primary or secondary infections underwent sampling and DNA processing, targeting bacteria, fungi and amoebae, including 16S high-throughput sequencing. After taxonomic assignment, community composition was correlated with clinical signs and symptoms. Diversity and abundance analyses were carried out in relation to the presence of non-bacterial amplicons. Results: Clinical specimens revealed two distinct community clusters, where specific changes correlated with clinical signs. An association between the compositions of microbiomes was found between these groups and the presence of Entamoeba gingivalis in 44% of cases. When amoebae were present in endodontic infections, we demonstrate changes in microbial community structure that mirror those observed in treatment-resistant or recurrent infections. Conclusions: Amoeba are present in endodontic infections at a high prevalence, and may promote increased virulence by enrichment for phagocytosis-resistant bacteria.

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Time Course of Change in Critical Torque following Exercise-Induced Muscle Damage

Medicine & Science in Sports & Exercise ◽

10.1249/01.mss.0000563201.19473.2f ◽

2019 ◽

Vol 51 (Supplement) ◽

pp. 902

Author(s):

Robert E. Hight ◽

Darshit S. Patel ◽

Jessica A. Peterson ◽

Cameron Lohman ◽

Jason A. Campbell ◽

...

Keyword(s):

Muscle Damage ◽

Time Course ◽

Exercise Induced

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The effects of tart cherry juice with whey protein on the signs and symptoms of exercise-induced muscle damage following plyometric exercise

Journal of Functional Foods ◽

10.1016/j.jff.2016.12.026 ◽

2017 ◽

Vol 29 ◽

pp. 185-192 ◽

Cited By ~ 4

Author(s):

Angela R. Hillman ◽

Bryna C.R. Taylor ◽

Diahnn Thompkins

Keyword(s):

Muscle Damage ◽

Whey Protein ◽

Signs And Symptoms ◽

Tart Cherry ◽

Plyometric Exercise ◽

Cherry Juice ◽

Exercise Induced

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Time Course of Muscle Damage and Inflammatory Responses to Resistance Training with Eccentric Overload in Trained Individuals

Mediators of Inflammation ◽

10.1155/2013/204942 ◽

2013 ◽

Vol 2013 ◽

pp. 1-6 ◽

Cited By ~ 3

Author(s):

Bernardo Neme Ide ◽

Lázaro Alessandro Soares Nunes ◽

René Brenzikofer ◽

Denise Vaz Macedo

Keyword(s):

Resistance Training ◽

Muscle Damage ◽

Initial Phase ◽

Time Course ◽

Inflammatory Responses ◽

White Blood Cells ◽

C Reactive Protein ◽

Reactive Protein ◽

High Magnitude ◽

Eccentric Overload

The purpose of this study was to observe the time course of muscle damage and inflammatory responses following an eccentric overload resistance-training (EO) program. 3 females (23.8 ± 2.6 years; 70.9 ± 12.7 kg; 1.6 ± 0.08 m) and 5 males (23.8 ± 2.6 years; 75.1 ± 11.2 kg; 1.8 ± 0.1 m) underwent thirteen training sessions (4 × 8–10 eccentric-only repetitions—80% of eccentric 1RM, one-minute rest, 2x week−1, during 7 weeks, for three exercises). Blood samples were collected prior to (Pre) and after two (P2), seven (P7), nine (P9), eleven (P11), and thirteen (P13) sessions, always 96 hours after last session. The reference change values (RCV) analysis was employed for comparing the responses, and the percentual differences between the serial results were calculated for each subject and compared with RCV95%. Four subjects presented significant changes for creatine kinase at P2, and another two at P13; six for C-reactive protein at P2, and three at P11; two for neutrophils at P2, P4, and P13, respectively; and only one for white blood cells at P2, P4, P7, and P9, for lymphocyte at P7, P9, and P13, and for platelet at P4. We conclude that EO induced high magnitude of muscle damage and inflammatory responses in the initial phase of the program with subsequent attenuation.

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Time-course of recovery of peak oxygen uptake after exercise-induced muscle damage

Respiratory Physiology & Neurobiology ◽

10.1016/j.resp.2015.06.008 ◽

2015 ◽

Vol 216 ◽

pp. 70-77 ◽

Cited By ~ 5

Author(s):

Christopher D. Black ◽

Alexander R. Gonglach ◽

Robert E. Hight ◽

Jessica B. Renfroe

Keyword(s):

Oxygen Uptake ◽

Muscle Damage ◽

Time Course ◽

Peak Oxygen Uptake ◽

Exercise Induced

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The cytokine response to strenuous exercise

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y98-055 ◽

1998 ◽

Vol 76 (5) ◽

pp. 505-511 ◽

Cited By ~ 135

Author(s):

Bente Klarlund Pedersen ◽

Kenneth Ostrowski ◽

Thomas Rohde ◽

Helle Bruunsgaard

Keyword(s):

Muscle Damage ◽

Eccentric Exercise ◽

Time Course ◽

Close Association ◽

Serum Levels ◽

Strenuous Exercise ◽

Necrosis Factor Alpha ◽

Sequential Release ◽

Systemic Endotoxemia ◽

Exercise Induced

Strenuous exercise is accompanied by an increase in circulating proinflammatory and inflammation responsive cytokines, having some similarities with the response to sepsis and trauma. The sequential release of tumour necrosis factor-alpha, interleukin (IL)1beta, IL-6, and IL-1 receptor antagonist (IL-1ra) in the blood is comparable to that observed in relation to bacterial diseases. Eccentric exercise is associated with an increase in serum IL-6 concentrations and is significantly correlated with the concentration of creatine kinase (CK) in the following days, whereas no changes are found after the concentric exercise; this demonstrates a close association between exercise-induced muscle damage and increased serum levels of IL-6. The time course of cytokine production, the close association with muscle damage, and the finding of mRNA-IL-6 in skeletal muscle biopsies after intense exercise all support the idea that during eccentric exercise myofibers are mechanically damaged and that this process stimulates the local production of inflammatory cytokines. It remains to be shown whether systemic endotoxemia during exercise is also a cause of elevated levels of cytokines in the plasma. The present review also discusses the possible roles of protein breakdown, delayed onset muscle soreness, and clinical implications of the acute-phase response following exercise.Key words: exercise, sport, trauma, sepsis, cytokines, interleukin, muscle.

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Can Exercise-Induced Muscle Damage Be a Good Model for the Investigation of the Anti-Inflammatory Properties of Diet in Humans?

Biomedicines ◽

10.3390/biomedicines9010036 ◽

2021 ◽

Vol 9 (1) ◽

pp. 36

Author(s):

Spyridon Methenitis ◽

Ioanna Stergiou ◽

Smaragdi Antonopoulou ◽

Tzortzis Nomikos

Keyword(s):

Muscle Damage ◽

Dietary Patterns ◽

Inflammatory Responses ◽

Low Grade ◽

Inflammatory Stimuli ◽

Methodological Approaches ◽

Anti Inflammatory ◽

Exercise Induced ◽

Low Grade Inflammation ◽

Inflammatory Effect

Subclinical, low-grade, inflammation is one of the main pathophysiological mechanisms underlying the majority of chronic and non-communicable diseases. Several methodological approaches have been applied for the assessment of the anti-inflammatory properties of nutrition, however, their impact in human body remains uncertain, because of the fact that the majority of the studies reporting anti-inflammatory effect of dietary patterns, have been performed under laboratory settings and/or in animal models. Thus, the extrapolation of these results to humans is risky. It is therefore obvious that the development of an inflammatory model in humans, by which we could induce inflammatory responses to humans in a regulated, specific, and non-harmful way, could greatly facilitate the estimation of the anti-inflammatory properties of diet in a more physiological way and mechanistically relevant way. We believe that exercise-induced muscle damage (EIMD) could serve as such a model, either in studies investigating the homeostatic responses of individuals under inflammatory stimuli or for the estimation of the anti-inflammatory or pro-inflammatory potential of dietary patterns, foods, supplements, nutrients, or phytochemicals. Thus, in this review we discuss the possibility of exercise-induced muscle damage being an inflammation model suitable for the assessment of the anti-inflammatory properties of diet in humans.

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