Muscle Repair Process Research Articles

Effects of myogenic precursor cells (C2C12) transplantation and low-level laser therapy on muscle repair.

The aim of the present study was to evaluate the effects of myoblast inoculation in combination with photobiomodulation therapy (PBMT) on skeletal muscle tissue following injury. Sixty-five Wistar rats were divided into five groups: Control-animals not submitted to any procedure; Injury-cryoinjury of the tibialis anterior muscle; HBSS-animals submitted to cryoinjury and intramuscular Hank's Balanced Salt Solution; Injury + Cells-animals submitted to cryoinjury, followed by myogenic precursor cells (C2C12) transplantation; Injury + Cells + LLLT-animals submitted to cryoinjury, followed by myogenic precursor cells (C2C12) transplantation and PBMT (780 nm, 40 mW, 3.2 J in 8 points). The periods analyzed were 1, 3, and 7 days. The tibialis anterior muscle was harvest for histological analysis, collagen analysis, and immunolabeling of macrophages. No differences were found between the HBSS group and injury group. The Injury + Cells group exhibited an increase of inflammatory cells and immature fibers as well as a decrease in the number of macrophages on Day 1. The Injury + Cells + LLLT group exhibited a decrease in myonecrosis and inflammatory infiltrate at 7 days, but an increase in inflammatory infiltrate at 1 and 3 days as well as an increase in blood vessels at 3 and 7 days, an increase in macrophages at 3 days and better collagen organization at 7 days. Cell transplantation combined with PBMT led to an increase in the number of blood vessels, a reduction in myonecrosis and total inflammatory cells as well as better organization of collagen fibers during the skeletal muscle repair process. Lasers Surg. Med. © 2018 Wiley Periodicals, Inc.

Trichinella spiralis muscle larvae excretory–secretory products induce changes in cytoskeletal and myogenic transcription factors in primary myoblast cultures

Trichinella spiralis infection in skeletal muscle culminates with nurse cell formation. The participation of excretory–secretory products of the muscle larvae has been implicated in this process through different studies performed in infected muscle and the muscle cell line C2C12. In this work, we developed primary myoblast cultures to analyse the changes induced by excretory–secretory products of the muscle larvae in muscle cells. Microarray analyses revealed expression changes in muscle cell differentiation, proliferation, cytoskeleton organisation, cell motion, transcription, cell cycle, apoptosis and signalling pathways such as MAPK, Jak-STAT, Wnt and PI3K-Akt. Some of these changes were further evaluated by other methodologies such as quantitative real-time PCR (qRT-PCR) and western blot, confirming that excretory–secretory products of the muscle larvae treated primary mouse myoblasts undergo increased proliferation, decreased expression of MHC and up-regulation of α-actin. In addition, changes in relevant muscle transcription factors (Pax7, Myf5 and Mef2c) were observed. Taken together, these results provide new information about how T. spiralis could alter the normal process of skeletal muscle repair after ML invasion to accomplish nurse cell formation.

Effect of photobiomodulation on connective tissue remodeling and regeneration of skeletal muscle in elderly rats.

The purpose of this study was to evaluate the effects of low-level laser therapy (LLLT) on morphological aspects, IL-6 and IL-1β expressions, as well as the distribution and organization of collagen in the tibialis anterior (TA) muscle of elderly rats submitted to cryoinjury. Histological photomicrographs were taken of TA muscles stained with HE and picrosirius red. Immunohistochemistry was used for the evaluation of IL-6 and IL-1β. Male Wistar rats, aged 20months, were distributed into three groups: (1) control animals not injured or treated with LLLT (n = 5), (2) cryoinjury without LLLT treatment (n = 15), and (3) cryoinjury treated with infrared LLLT (n = 15). LLLT was applied to the TA 2h after of the injury induction and consisted of daily applications until the sacrifice (1, 3, and 7days). The following parameters were used: λ = 780nm, power density 1W/cm2, output power 40mW, 10s per point, 8 points, and 3.2J of total energy. In the histomorphological analysis, the treated group exhibited a significant decrease in inflammatory infiltrate (p < 0.001) as well as an increase immature fibers and new blood vessels at 7days compared to the untreated group (p < 0.05). Furthermore, treatment induced a better collagen distribution and organization at 7days in comparison to the untreated group (p < 0.05). In conclusion, LLLT demonstrated a modulatory effect on the muscle repair process in elderly animals with regard to the collagen remodeling and morphological aspects of muscle tissue.

Pulsed low-level infrared laser alters mRNA levels from muscle repair genes dependent on power output in Wistar rats

Satellite cells are present in skeletal muscle functioning in the repair and regeneration of muscle injury. Activation of these cells depends on the expression of myogenic factor 5 (Myf5), myogenic determination factor 1(MyoD), myogenic regulatory factor 4 (MRF4), myogenin (MyoG), paired box transcription factors 3 (Pax3), and 7 (Pax7). Low-level laser irradiation accelerates the repair of muscle injuries. However, data from the expression of myogenic factors have been controversial. Furthermore, the effects of different laser beam powers on the repair of muscle injuries have been not evaluated. The aim of this study was to evaluate the effects of low-level infrared laser at different powers and in pulsed emission mode on the expression of myogenic regulatory factors and on Pax3 and Pax7 in injured skeletal muscle from Wistar rats. Animals that underwent cryoinjury were divided into three groups: injury, injury laser 25 Mw, and injury laser 75 mW. Low-level infrared laser irradiation (904 nm, 3 J cm−2, 5 kHz) was carried out at 25 and 75 mW. After euthanasia, skeletal muscle samples were withdrawn and the total RNA was extracted for the evaluation of mRNA levels from the MyoD, MyoG, MRF4, Myf5, Pax3, and Pax7 gene. Pax 7 mRNA levels did not alter, but Pax3 mRNA levels increased in the injured and laser-irradiated group at 25 mW. MyoD, MyoG, and MYf5 mRNA levels increased in the injured and laser-irradiated animals at both powers, and MRF4 mRNA levels decreased in the injured and laser-irradiated group at 75 mW. In conclusion, exposure to pulsed low-level infrared laser, by power-dependent effect, could accelerate the muscle repair process altering mRNA levels from paired box transcription factors and myogenic regulatory factors.

The effect of macadamia oil intake on muscular inflammation and oxidative profile kinetics after exhaustive exercise

In this study, we evaluated the onset and resolution of inflammation in control and macadamia oil‐supplemented rats after a single session of exhaustive exercise. We also analysed the antioxidant enzymes catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS). Rats were supplemented for ten days with macadamia oil (25 mg/kg), which is rich in oleic and palmitoleic acids. On the 10th day, control and macadamia oil‐treated rats exercised to physical exhaustion. Plasma and muscular levels of pro‐inflammatory cytokines (tumour necrosis factor alpha [TNF‐α], interleukin‐1 beta [IL‐1β], IL‐6, cytokine‐induced neutrophil chemoattractant‐3 [CINC‐3], macrophage inflammatory protein‐3‐alpha [MIP‐3α]) and soluble L‐selectin were measured prior to, immediately after, and 2, 24, and 48 h after exercise. Our data revealed increases in the muscle concentrations of IL‐1β, L‐selectin, CINC‐3, and MIP‐3α in the group supplemented with macadamia oil compared with the concentrations in the control group. CAT also increased in the treated group, which is important because pro‐inflammatory cytokines precede growth factor production and might alter the muscle repair process. We concluded that inflammation resulting from exhaustive exercise was greater in animals that received macadamia oil than in control animals.Practical applications: There are potential benefits of using fatty acids in the treatment of injured muscles, and these substances have been used in several types of injured tissues. Macadamia oil intake alters muscle healing signaling by influencing the production of reactive oxygen species and inflammatory mediators. Therefore, it is reasonable to hypothesize that the intake of immunomodulatory supplements would be beneficial to the muscular recovery of an athlete following a strenuous exercise session.The muscle healing process has three phases: inflammation, new tissue formation and tissue remodeling, and these phases might be modulated by fatty acids. After an exhaustive exercise session, muscle inflammatory markers from macadamia oil‐supplemented rats are augmented in comparison to non‐supplemented animals. Our data revealed increases in the muscle concentrations of IL‐1β, L‐selectin, CINC‐3, and MIP‐3α in the group supplemented with macadamia oil compared with the concentrations in the control group.

Molecular alterations in skeletal muscle in rheumatoid arthritis are related to disease activity, physical inactivity, and disability

BackgroundTo identify molecular alterations in skeletal muscle in rheumatoid arthritis (RA) that may contribute to ongoing disability in RA.MethodsPersons with seropositive or erosive RA (n = 51) and control subjects matched for age, gender, race, body mass index (BMI), and physical activity (n = 51) underwent assessment of disease activity, disability, pain, physical activity and thigh muscle biopsies. Muscle tissue was used for measurement of pro-inflammatory markers, transcriptomics, and comprehensive profiling of metabolic intermediates. Groups were compared using mixed models. Bivariate associations were assessed with Spearman correlation.ResultsCompared to controls, patients with RA had 75% greater muscle concentrations of IL-6 protein (p = 0.006). In patients with RA, muscle concentrations of inflammatory markers were positively associated (p < 0.05 for all) with disease activity (IL-1β, IL-8), disability (IL-1β, IL-6), pain (IL-1β, TNF-α, toll-like receptor (TLR)-4), and physical inactivity (IL-1β, IL-6). Muscle cytokines were not related to corresponding systemic cytokines. Prominent among the gene sets differentially expressed in muscles in RA versus controls were those involved in skeletal muscle repair processes and glycolytic metabolism. Metabolic profiling revealed 46% higher concentrations of pyruvate in muscle in RA (p < 0.05), and strong positive correlation between levels of amino acids involved in fibrosis (arginine, ornithine, proline, and glycine) and disability (p < 0.05).ConclusionRA is accompanied by broad-ranging molecular alterations in skeletal muscle. Analysis of inflammatory markers, gene expression, and metabolic intermediates linked disease-related disruptions in muscle inflammatory signaling, remodeling, and metabolic programming to physical inactivity and disability. Thus, skeletal muscle dysfunction might contribute to a viscous cycle of RA disease activity, physical inactivity, and disability.

Muscle Stem Cells: A Model System for Adult Stem Cell Biology.

Skeletal muscle stem cells, originally termed satellite cells for their position adjacent to differentiated muscle fibers, are absolutely required for the process of skeletal muscle repair and regeneration. In the last decade, satellite cells have become one of the most studied adult stem cell systems and have emerged as a standard model not only in the field of stem cell-driven tissue regeneration but also in stem cell dysfunction and aging. Here, we provide background in the field and discuss recent advances in our understanding of muscle stem cell function and dysfunction, particularly in the case of aging, and the potential involvement of muscle stem cells in genetic diseases such as the muscular dystrophies.

Utility of 17-(allylamino)-17-demethoxygeldanamycin treatment for skeletal muscle injury.

Repeated eccentric contractions can injure skeletal muscle and result in functional deficits that take several weeks to fully recover. The 70-kDa heat shock protein (Hsp70) is a stress-inducible molecular chaperone that maintains protein quality and plays an integral role in the muscle's repair processes following injury. Here, we attempted to hasten this recovery by pharmacologically inducing Hsp70 expression in mouse skeletal muscle with 17-(allylamino)-17-demethoxygeldanamycin (17-AAG) (40mg/kg) both prior to and throughout the first 7days after an injurious bout of 150 maximal eccentric contractions. Hsp70 content in the injured skeletal muscle was strongly induced following the eccentric contractions and remained elevated over the next 7days as the muscle underwent repair. Treatment with 17-AAG increased Hsp70 content ∼fivefold; however, this was significantly less than that induced by the injury. Moreover, 17-AAG treatment did not recover the decrements to in vivo isometric torque production following the bout of eccentric contractions. Together, these findings demonstrate that although Hsp70 content was induced in the uninjured skeletal muscle, treatment of 17-AAG (40mg/kg) was not a preventive measure to either reduce the severity of skeletal muscle damage or enhance functional recovery following a bout of maximal eccentric contractions.

Investigation of the Comparative Effects of Red and Infrared Laser Therapy on Skeletal Muscle Repair in Diabetic Rats.

The aim of this study was to evaluate the in vivo response of 2 different laser wavelengths (red and infrared) on skeletal muscle repair process in diabetic rats. Forty Wistar rats were randomly divided into 4 experimental groups: basal control-nondiabetic and muscle-injured animals without treatment (BC); diabetic muscle-injured without treatment (DC); diabetic muscle-injured, treated with red laser (DCR) and infrared laser (DCIR). The injured region was irradiated daily for 7 consecutive days, starting immediately after the injury using a red (660 nm) and an infrared (808 nm) laser. The histological results demonstrated in both treated groups (red and infrared wavelengths) a modulation of the inflammatory process and a better tissue organization located in the site of the injury. However, only infrared light significantly reduced the injured area and increased MyoD and myogenin protein expression. Moreover, both red and infrared light increased the expression of the proangiogenic vascular endothelial growth factor and reduced the cyclooxygenase 2 protein expression. These results suggest that low-level laser therapy was efficient in promoting skeletal muscle repair in diabetic rats. However, the effect of infrared wavelength was more pronounced by reducing the area of the injury and modulating the expression proteins related to the repair.

Monoclonal antibodies against muscle actin isoforms: epitope identification and analysis of isoform expression by immunoblot and immunostaining in normal and regenerating skeletal muscle.

Higher vertebrates (mammals and birds) express six different highly conserved actin isoforms that can be classified in three subgroups: 1) sarcomeric actins, α-skeletal (α-SKA) and α-cardiac (α-CAA), 2) smooth muscle actins (SMAs), α-SMA and γ-SMA, and 3) cytoplasmic actins (CYAs), β-CYA and γ-CYA. The variations among isoactins, in each subgroup, are due to 3-4 amino acid differences located in their acetylated N-decapeptide sequence. The first monoclonal antibody (mAb) against an actin isoform (α-SMA) was produced and characterized in our laboratory in 1986 (Skalli et al., 1986). We have further obtained mAbs against the 5 other isoforms. In this report, we focus on the mAbs anti-α-SKA and anti-α-CAA obtained after immunization of mice with the respective acetylated N-terminal decapeptides using the Repetitive Immunizations at Multiple Sites Strategy (RIMMS). In addition to the identification of their epitope by immunoblotting, we describe the expression of the 2 sarcomeric actins in mature skeletal muscle and during muscle repair after micro-lesions. In particular, we analyze the expression of α-CAA, α-SKA and α-SMA by co-immunostaining in a time course frame during the muscle repair process. Our results indicate that a restricted myocyte population expresses α-CAA and suggest a high capacity of self-regeneration in muscle cells. These antibodies may represent a helpful tool for the follow-up of muscle regeneration and pathological changes.

Monoclonal antibodies against muscle actin isoforms: epitope identification and analysis of isoform expression by immunoblot and immunostaining in normal and regenerating skeletal muscle

Higher vertebrates (mammals and birds) express six different highly conserved actin isoforms that can be classified in three subgroups: 1) sarcomeric actins, α-skeletal (α-SKA) and α-cardiac (α-CAA), 2) smooth muscle actins (SMAs), α-SMA and γ-SMA, and 3) cytoplasmic actins (CYAs), β-CYA and γ-CYA. The variations among isoactins, in each subgroup, are due to 3-4 amino acid differences located in their acetylated N-decapeptide sequence. The first monoclonal antibody (mAb) against an actin isoform (α-SMA) was produced and characterized in our laboratory in 1986 (Skalli et al., 1986) . We have further obtained mAbs against the 5 other isoforms. In this report, we focus on the mAbs anti-α-SKA and anti-α-CAA obtained after immunization of mice with the respective acetylated N-terminal decapeptides using the Repetitive Immunizations at Multiple Sites Strategy (RIMMS). In addition to the identification of their epitope by immunoblotting, we describe the expression of the 2 sarcomeric actins in mature skeletal muscle and during muscle repair after micro-lesions. In particular, we analyze the expression of α-CAA, α-SKA and α-SMA by co-immunostaining in a time course frame during the muscle repair process. Our results indicate that a restricted myocyte population expresses α-CAA and suggest a high capacity of self-regeneration in muscle cells. These antibodies may represent a helpful tool for the follow-up of muscle regeneration and pathological changes.

Red and Infrared Low-Level Laser Therapy Prior to Injury with or without Administration after Injury Modulate Oxidative Stress during the Muscle Repair Process.

IntroductionMuscle injury is common among athletes and amateur practitioners of sports. Following an injury, the production of reactive oxygen species (ROS) occurs, which can harm healthy muscle fibers (secondary damage) and delay the repair process. Low-level laser therapy (LLLT) administered prior to or following an injury has demonstrated positive and protective effects on muscle repair, but the combination of both administration times together has not been clarified.AimTo evaluate the effect of LLLT (660 nm and 780 nm, 10 J/cm², 40 mW, 3.2 J) prior to injury with or without the administration after injury on oxidative stress during the muscle repair process.MethodsWistar rats were divided into following groups: control; muscle injury alone; LLLT 660 nm + injury; LLLT 780 nm + injury; LLLT 660 nm before and after injury; and LLLT 780 nm before and after injury. The rats were euthanized on days 1, 3 and 7 following cryoinjury of the tibialis anterior (TA) muscle, which was then removed for analysis.ResultsLipid peroxidation decreased in the 660+injury group after one day. Moreover, red and infrared LLLT employed at both administration times induced a decrease in lipid peroxidation after seven days. CAT activity was altered by LLLT in all periods evaluated, with a decrease after one day in the 780+injury+780 group and after seven days in the 780+injury group as well as an increase in the 780+injury and 780+injury+780 groups after three days. Furthermore, increases in GPx and SOD activity were found after seven days in the 780+injury+780 group.ConclusionThe administration of red and infrared laser therapy at different times positively modulates the activity of antioxidant enzymes and reduces stress markers during the muscle repair process.

Monoclonal antibodies against muscle actin isoforms: epitope identification and analysis of isoform expression by immunoblot and immunostaining in normal and regenerating skeletal muscle

Higher vertebrates express six different highly conserved actin isoforms that can be classified in three subgroups: 1) sarcomeric actins, α-skeletal (α-SKA) and α-cardiac (α-CAA), 2) smooth muscle actins (SMAs), α-SMA and γ-SMA, and 3) cytoplasmic actins (CYAs), β-CYA and γ-CYA. The variations among isoactins, in each subgroup, are due to 3-4 amino acid differences located in their acetylated N-decapeptide sequence. The first monoclonal antibody (mAb) against an actin isoform (α-SMA) was produced and characterized in our laboratory in 1986 (Skalli et al., 1986). We have further obtained mAbs against the 5 other isoforms. In this report, we focus on the mAb anti-α-SKA and anti-α-CAA obtained after immunization of mice with the respective acetylated N-terminal decapeptides using the Repetitive Immunizations at Multiple Sites Strategy (RIMMS). In addition to the identification of their epitope by immunoblotting, we describe the expression of the 2 sarcomeric actins in mature skeletal muscle and during muscle repair after micro-lesions. In particular, we analyze the expression of α-CAA, α-SKA and α-SMA by co-immunostaining in a time course frame during the muscle repair process. Our results indicate that a restricted myocyte population expresses α-CAA and suggest a high capacity of self-renewal in muscle cells. These antibodies may represent a helpful tool for the follow-up of muscle regeneration and pathological changes.

Light-emitting diode therapy increases collagen deposition during the repair process of skeletal muscle.

This study analyzed the effects of light-emitting diode (LED) therapy on the morphology of muscle tissue as well as collagen remodeling and matrix metalloproteinase 2 (MMP-2) activity in the skeletal muscle of rats following acute injury. Wistar rats were divided into four groups: (1) control, (2) sham, (3) untreated cryoinjury, and (4) cryoinjury treated with LED. Cryoinjury was induced by two applications of a metal probe cooled in liquid nitrogen directly onto the belly of the tibialis anterior muscle. For treatment, the LED equipment (wavelength 850 nm, output power 30 mW, and total energy 3.2 J) was used daily. The study periods were 1, 3, and 7 days after cryoinjury. Morphological aspects were evaluated through hematoxylin-eosin staining. The amount of collagen fibers was evaluated using Picro Sirius Red staining under polarized light. The gelatinase activity of MMP-2 was evaluated using zymography. The results showed significant reductions in inflammatory infiltrate after 3 days and an increased number of immature muscle fibers after 7 days. Furthermore, treatment induced a reduction in the gelatinolytic activity of MMP-2 after 1, 3, and 7 days in comparison to the untreated injury groups and increased the collagen deposition after 3 and 7 days in the treated groups. LED therapy at 850 nm induced a significant reduction in inflammation, decreased MMP-2 activity, and increased the amount of immature muscle and collagen fibers during the muscle repair process following acute injury.

Wnt and β-Catenin Signaling and Skeletal Muscle Myogenesis in Response to Muscle Damage and Resistance Exercise and Training

The factors that regulate skeletal muscle hypertrophy in human adults in response to resistance training (RT) has largely focused on endogenous endocrine responses. However, the endocrine response to RT as having an obligatory role in muscle hypertrophy has come under scrutiny, as other mechanisms and pathways seem to also be involved in up-regulating muscle protein synthesis (MPS). Skeletal muscle myogenesis is a multifactorial process of tissue growth and repair in response to resistance training is regulated by many factors. As a result, satellite cell-fused myogenesis is a possible factor in skeletal muscle regeneration and hypertrophy in response to RT. The Wnt family ligands interact with various receptors and activate different downstream signaling pathways and have been classified as either canonical (β-catenin dependent) or non-canonical (β-catenin independent). Wnt is secreted from numerous tissues in a paracrine fashion. The Wnt/β-catenin signaling pathway is a highly-regulated and intricate pathway that is essential to skeletal muscle myogenesis. The canonical Wnt/β-catenin pathway may influence satellite cells to myogenic commitment, differentiation, and fusion into muscle fibers in response to injury or trauma, self-renewal, and normal basal turnover. The current literature has shown that, in response mechanical overload from acute resistance exercise and chronic resistance training, that the Wnt/β-catenin signaling pathway is stimulated which may actuate the process of muscle repair and hypertrophy in response to exercise-induced muscle damage. The purpose of this review is to elaborate on the Wnt/β-catenin signaling pathway, the current literature investigating the relationship of the Wnt/β-catenin pathway and its effects on myogenesis is response to muscle damage and resistance exercise and training. Keywords: skeletal muscle, hypertrophy, myogenesis, cell signaling, protein synthesis, resistance training

Interaction between HSP 70 and iNOS in skeletal muscle injury and repair.

Muscle injuries are frequently occurred in various sports. The biological process and mechanism of muscle repair after injury are well known through the many studies. This study aimed at presenting heat shock protein and nitric oxide synthase are to respond to muscle damage and repair. This section discusses the results obtained through many articles. Heat shock proteins (HSPs) are considered to play an essential role in protecting cells from damage, preparing them to survive on new environmental challenges. In addition, exercise-induced changes such as heat shock, oxidative, metabolic, muscular, and cytokine stress seem to be responsible for the HSP response to exercise. Also, inducible nitric oxide synthase (iNOS) generates nitric oxide (NO) for prolonged period and causes pathophysiological effects. Furthermore, iNOS is involved in processes such as cell injury, wound repair, embryogenesis, tissue differentiation, and suppression of tumorigenesis. In conclusion, the inhibition of HSP 70 on caspase-3 and apoptosis is associated with its inhibition on iNOS that leads to less NO production.

Modeled Osteopathic Manipulative Treatments: A Review of Their in Vitro Effects on Fibroblast Tissue Preparations.

A key osteopathic tenet involves the body's ability to self-heal. Osteopathic manipulative treatment (OMT) has been evolved to improve this healing capacity. The authors' in vitro work has focused on modeling 2 common OMT modalities: myofascial release (MFR) and counterstrain. Their studies have evaluated the effects of these modalities on wound healing, cytokine secretion, and muscle repair. The key components of the host response to mechanical forces are fibroblasts, which are the main fascial cells that respond to different types of strain by secreting anti-inflammatory chemicals and growth factors, thus improving wound healing and muscle repair processes. The purpose of this review is to discuss the cellular and molecular mechanisms by which MFR and other OMT modalities work, in particular, the role of strained fibroblasts in inflammation, wound healing, and muscle repair and regeneration. Changing MFR parameters, such as magnitude, duration, direction, and frequency of strain, might uniquely affect the physiologic response of fibroblasts, muscle contraction, and wound healing. If such results are clinically translatable, the mechanisms underlying the clinical outcomes of OMT modalities will be better understood, and these treatments will be more widely accepted as evidence-based, first-line therapies.

Recovery of skeletal muscle function following injury is not augmented by acute resveratrol supplementation

Background and Aim: Skeletal muscle function is significantly reduced following traumatic muscle injury and complete recovery can take several weeks. Pharmacological agents like nonsteroidal anti-inflammatory drugs have been used to minimize pain and inflammation associated with muscle injury. However, their safety and efficacy to improve muscle repair have been challenged. To that end, safer and more effective treatment options remain to be identified. Accordingly, resveratrol use has numerous health benefits in clinical population. Further, resveratrol has been shown to promote myoblast differentiation in 0 vitro , which suggests it could be used to improve skeletal muscle regeneration in vivo. Methods: Experimental mice received resveratrol supplementation (0.05% wt/wt) 4 weeks prior to injury, which persisted throughout recovery. Muscle injury was induced by injecting a diluted barium chloride solution into the tibialis anterior (TA). Isometric tetanic and twitch torque of the anterior crural muscles were measured prior to the injury and 7, 14, or 21 days postinjury. Results: Resveratrol supplementation had no effect on preinjury isometric tetanic and twitch torque of the anterior crural muscles. Seven days after injury, tetanic torque production was reduced by 80% compared to preinjury values. Functional and structural recovery steadily improved at 14 days and was completed 21 days after injury. However, resveratrol treatment had no beneficial effects on isometric torque or regenerated fiber area. Conclusion: Acute, low-dose resveratrol supplementation did not improve functional or structural recovery of regenerating mouse TA after injury. Further research is likely required that explores alternate resveratrol dosing strategies and their effects on skeletal muscle repair processes.

Effects of low-level laser therapy on skeletal muscle repair: a systematic review.

A review of the literature was performed to demonstrate the most current applicability of low-level laser therapy (LLLT) for the treatment of skeletal muscle injuries, addressing different lasers, irradiation parameters, and treatment results in animal models. Searches were performed in the PubMed/MEDLINE, SCOPUS, and SPIE Digital Library databases for studies published from January 2006 to August 2013 on the use of LLLT for the repair of skeletal muscle in any animal model. All selected articles were critically appraised by two independent raters. Seventeen of the 36 original articles on LLLT and muscle injuries met the inclusion criteria and were critically evaluated. The main effects of LLLT were a reduction in the inflammatory process, the modulation of growth factors and myogenic regulatory factors, and increased angiogenesis. The studies analyzed demonstrate the positive effects of LLLT on the muscle repair process, which are dependent on irradiation and treatment parameters. The findings suggest that LLLT is an excellent therapeutic resource for the treatment of skeletal muscle injuries in the short-term.

Changes in CEBPB expression in circulating leukocytes following eccentric elbow-flexion exercise.

In mouse models, CCAAT enhancer-binding protein beta (CEBPB) is necessary for M2 macrophage-mediated regeneration after muscle injury. In humans, CEBPB expression in blood was strongly associated with muscle strength. In this study we aimed to test whether CEBPB expression in blood in people is increased 2 days after exercise designed to induce muscle damage and subsequent repair. Sixteen healthy male volunteers undertook elbow flexor exercises designed to induce acute muscle micro-damage. Peripheral blood samples were collected at baseline and days 1, 2, 4 and 7 following exercise. Expression of CEBPB and related genes were analysed by qRT-PCR. Extent of muscle damage was determined by decline in maximal voluntary isometric torque and by plasma creatine kinase activity. Nine subjects had peak (day 4) creatine kinase activity exceeding 10,000 U/l. In this subgroup, CEBPB expression was elevated from baseline to 2 days post exercise (paired-samples t (1,8) = 3.72, p = 0.006). Related expression and selected cytokine changes after exercise did not reach significance. Muscle-damaging exercise in humans can be followed by induction of CEBPB transcript expression in peripheral blood. Associations between CEBPB expression in blood and muscle strength may be consistent with the CEBPB-dependent muscle repair process.Electronic supplementary materialThe online version of this article (doi:10.1007/s12576-014-0350-7) contains supplementary material, which is available to authorized users.