Exercise-induced Muscle Injury Research Articles

ZnO/RuO2 nanocomposite modified glassy carbon electrode as sensor for determination of exercise-induced myoglobin biomarkers

A novel ZnO/RuO2 nanocomposite modified electrochemical sensor was developed for the rapid and ultrasensitive quantification of Mb biomarkers related to exercise-induced muscle injury. The sensor demonstrated a wide linear range from 0.1 to 100 nM along with an ultra-low detection limit down to 30 pM Mb under optimal conditions. A rapid response time below 10 s was achieved. The sensor surface showed excellent electrocatalytic activities towards Mb oxidation, attributing to the synergistic properties of the mixed transition metal oxide interface. Systematic investigations revealed reversible electrochemical behavior and diffusion controlled electron transfer kinetics governing the oxidation process. Negligible interferences were observed against potentially co-existing species. Spike-recovery experiments using real human serum samples yielded excellent recovery rates between 97.3% and 103.1%. Significantly enhanced post-exercise Mb levels up to 8.2 nM were successfully detected in clinical specimens, confirming the sensor's ability to sensitively monitor muscular trauma via minimally invasive blood tests. The sensor provided tangible analytical advantages over previous Mb detectors and immunoassays in terms of detection limit, sensitivity, simplicity and cost-effectiveness. Findings validate the feasible adoption of the sensor technology to facilitate prompt diagnosis of exercise-induced myoglobinemia in sports medicine clinics.

The role of ZBP1 in eccentric exercise-induced skeletal muscle necroptosis.

This study aimed to explore the occurrence of necroptosis in skeletal muscle after eccentric exercise and investigate the role and possible mechanisms of ZBP1 and its related pathway proteins in the process, providing a theoretical basis for the study of exercise-induced skeletal muscle injury and recovery. Forty-eight male adult Sprague-Dawley rats were randomly divided into a control group (C, n = 8) and an exercise group (E, n = 40). The exercise group was further divided into 0h (E0), 12h (E12), 24h (E24), 48h (E48), and 72h (E72) after exercise, with 8 rats in each subgroup. At each time point, gastrocnemius muscle was collected under general anesthesia. The expression levels of ZBP1 and its related pathway proteins were assessed using Western blot analysis. The colocalization of pathway proteins was examined using immunofluorescence staining. After 48h of eccentric exercise, the expression of necroptosis marker protein MLKL reached its peak (P < 0.01), and the protein levels of ZBP1, RIPK3, and HMGB1 also peaked (P < 0.01). At 48h post high-load eccentric exercise, there was a significant increase in colocalization of ZBP1/RIPK3 pathway proteins, reaching a peak (P < 0.01). (1) Eccentric exercise induced necroptosis in skeletal muscle, with MLKL, p-MLKLS358, and HMGB1 significantly elevated, especially at 48h after exercise. (2) After eccentric exercise, the ZBP1/RIPK3-related pathway proteins ZBP1, RIPK3, and p-RIPK3S232 were significantly elevated, particularly at 48h after exercise. (3) Following high-load eccentric exercise, there was a significant increase in the colocalization of ZBP1/RIPK3 pathway proteins, with a particularly pronounced elevation observed at 48h post-exercise.

Effects of branched-chain amino acid supplementation on skeletal muscle proteolytic pathways after exercise-induced muscle injury in rats

To explore the role of branched-chain amino acid(BCAA) supplementation on muscle damage and the regulation of Krüppel-like factor 15(KLF15) and nuclear factor kappa B(NF-κB) mediated proteolytic pathways after an acute eccentric exercise. Male SD rats were divided into placebo group(PLA) and BCAA group(BCAA) randomly, 32 rats per group. Both group were then placed into subgroups: placebo and pre-exercise group(PC), placebo and immediately after exercise group(PE), placebo and 6 h after exercise group(PE6), placebo and 12 h after exercise group(PE12), BCAA and pre-exercise group(BC), BCAA and immediately after exercise group(BE), BCAA and 6 h after exercise group(BE6), BCAA and 12 h after exercise group(BE12), 8 rats per group. Rats in BCAA groups were supplied with BCAA(1 g/(kg·d·BW), 3 days) before the exercise day and placebo groups with equal volume of distilled water. The exercised groups performed a 2 h eccentric exercise on treadmill(16 m/min, -16° slope). Blood and gastrocnemius were collected according to the time points. RT-qPCR was used to measure the mRNA expression of KLF15, NF-κB, FoxO1, Atrogin-1 and MuRF1 in gastrocnemius. (1) No damage was found in myocytes of BC and PC group. The process of morphological damage in BCAA group was relatively faster. (2) The mRNA expression levels of KLF15, FoXO1, Atrogin-1 and MuRF1 in PE were higher than those in PC(P&lt;0.05, P&lt;0.01), NF-κB and Atrogin-1 in PE12 were higher than those in PC(P&lt;0.05). The mRNA expression levels of FoXO1 in BE were higher than those in BC(P&lt;0.05). Compared with PE, the mRNA expression levels of KLF15, Atrogin-1 and MuRF1 in BE were lower(P&lt;0.05, P&lt;0.01), NF-κB and Atrogin-1 in BE12 were lower than those in PE12(P&lt;0.05). The level of serum 3-MH in PE12 group was higher than that in PC group(P&lt;0.05). The proteolysis of skeletal muscle after high-intensity eccentric exercise is mediated by two different pathways: KLF15 and NF-κB, whose activation is time-dependent. BCAA may reduce skeletal muscle proteolysis by lowering the level of gene transcription in the KLF15 and NF-κB related protein degradation pathway, which occurs immediately after exercise.

Circulating Inflammatory Biomarkers Predict Pain Change Following Exercise-Induced Shoulder Injury: Findings From the Biopsychosocial Influence on Shoulder Pain Preclinical Trial

Shoulder pain is a highly prevalent musculoskeletal condition that frequently leads to suboptimal clinical outcomes. This study tested the extent to which circulating inflammatory biomarkers are associated with reports of shoulder pain and upper-extremity disability for a high-risk genetic by psychological subgroup (catechol-O-methyltransferase [COMT] variation by pain catastrophizing [PCS]). Pain-free adults meeting high-risk COMT × PCS subgroup criteria completed an exercise-induced muscle injury protocol. Thirteen biomarkers were collected and analyzed from plasma 48 hours after muscle injury. Shoulder pain intensity and disability (Quick-DASH) were reported at 48 and 96 hours to calculate change scores. Using an extreme sampling technique, 88 participants were included in this analysis. After controlling for age, sex, and BMI, there were moderate positive associations between higher c-reactive protein (CRP; βˆ = .62; 95% confidence interval [CI] = −.03, 1.26), interleukin-6 (IL-6; βˆ = 3.13; CI = −.11, 6.38), and interleukin-10 (IL-10; βˆ = 2.51; CI = −.30, 5.32); and greater pain reduction from 48 to 96 hours post exercise muscle injury. Using an exploratory multivariable model to predict pain changes from 48 to 96 hours, we found participants with higher IL-10 were less likely to experience a high increase in pain (βˆ = −10.77; CI = −21.25, −2.69). Study findings suggest CRP, IL-6, and IL-10 are related to shoulder pain change for a preclinical high-risk COMT × PCS subgroup. Future studies will translate to clinical shoulder pain and decipher the complex and seemingly pleiotropic interplay between inflammatory biomarkers and shoulder pain change. PerspectiveIn a preclinical high-risk COMT × PCS subgroup, 3 circulating inflammatory biomarkers (CRP, IL-6, and IL-10) were moderately associated with pain improvement following exercise-induced muscle injury.

MSM Supplementation Is Associated with Reduced Inflammation and Improved Innate Immune Response following In Vitro LPS-Stimulation in Humans after a Bout of Downhill Running

Exercise-induced muscle injury and the subsequent release of Damage-Associated Molecular Patterns (DAMP) result in soreness and inflammation. Dietary supplements may accelerate the rate of recovery by supporting resolution of inflammation. The purpose of this study was to determine if methylsulfonylmethane (MSM) supplementation (30 d prior to exercise and during recovery) altered mRNA expression in LPS-exposed blood leukocytes after a bout of downhill running. Exercise consisted of 60 min of downhill running (−15% grade). Blood (baseline, pre-exercise, 4, 24, 48, and 72 h post-exercise) was diluted (1:10) and combined with LPS (20 µg/mL) for 24 h. Total RNA was isolated from leukocytes and analyzed for 574 immune-associated mRNA (Nanostring nCounter; ROSALIND.BIO). Data were expressed as log2 fold change from baseline for each condition (MSM and placebo). Compared to placebo, MSM supplementation was associated with an improved inflammation response (15 mRNA) and viral immune response (2 mRNA). The largest number of changes were found at 4 and 24 h post-exercise. The key finding in the present study is that MSM supplementation can improve inflammation management and the innate immune response after exercise.

Prolonged Moderate-Intensity Exercise Does Not Increase Muscle Injury Markers in Symptomatic or Asymptomatic Statin Users

BackgroundStatin use may exacerbate exercise-induced skeletal muscle injury caused by reduced coenzyme Q10 (CoQ10) levels, which are postulated to produce mitochondrial dysfunction. ObjectivesWe determined the effect of prolonged moderate-intensity exercise on markers of muscle injury in statin users with and without statin-associated muscle symptoms. We also examined the association between leukocyte CoQ10 levels and muscle markers, muscle performance, and reported muscle symptoms. MethodsSymptomatic (n = 35; age 62 ± 7 years) and asymptomatic statin users (n = 34; age 66 ± 7 years) and control subjects (n = 31; age 66 ± 5 years) walked 30, 40, or 50 km/d for 4 consecutive days. Muscle injury markers (lactate dehydrogenase, creatine kinase, myoglobin, cardiac troponin I, and N-terminal pro-brain natriuretic peptide), muscle performance, and reported muscle symptoms were assessed at baseline and after exercise. Leukocyte CoQ10 was measured at baseline. ResultsAll muscle injury markers were comparable at baseline (P > 0.05) and increased following exercise (P < 0.001), with no differences in the magnitude of exercise-induced elevations among groups (P > 0.05). Muscle pain scores were higher at baseline in symptomatic statin users (P < 0.001) and increased similarly in all groups following exercise (P < 0.001). Muscle relaxation time increased more in symptomatic statin users than in control subjects following exercise (P = 0.035). CoQ10 levels did not differ among symptomatic (2.3 nmol/U; IQR: 1.8-2.9 nmol/U), asymptomatic statin users (2.1 nmol/U; IQR: 1.8-2.5 nmol/U), and control subjects (2.1 nmol/U; IQR: 1.8-2.3 nmol/U; P = 0.20), and did not relate to muscle injury markers, fatigue resistance, or reported muscle symptoms. ConclusionsStatin use and the presence of statin-associated muscle symptoms does not exacerbate exercise-induced muscle injury after moderate exercise. Muscle injury markers were not related to leukocyte CoQ10 levels. (Exercise-induced Muscle Damage in Statin Users; NCT05011643)

Pain and Disability Following Exercise-Induced Injury in Prognostic and Intervention Studies: The Why May Be More Important Than the How.

In preclinical prognostic studies, the description of expected outcomes during an informed consent process indicates that the extent of pain and disability experienced and recovery time is unknown. In intervention studies, the consent process suggests that pain and disability will definitely occur and a treatment provided. Our objective was to determine whether study design (prognosis or intervention) was associated with the severity of pain intensity and disability reports from a preclinical model. We pooled pain and disability outcomes from prognostic and intervention studies using an exercise-induced muscle injury model of pain. Pain intensity, disability, and fear of pain were collected by validated self-report measures. Pain and disability data were z-transformed for pooled analyses and compared across the study design. Data from 310 people were included. The primary findings were that self-reported pain intensity and disability were: (1) higher in prognostic studies than in the intervention studies and (2) associated with fear of pain. A secondary finding was that fear of pain was lower in the intervention compared with the prognostic studies. Although there are other possible explanations, we speculate that these results could be related to the uncertainty inherent to providing informed consent for a prognostic study. In light of these findings, we recommend that informed consent language be more carefully considered when pain is induced in a controlled manner. Incorporating informed consent language commonly used in prognostic studies could result in higher pain intensity and disability ratings in studies that use preclinical models to test the efficacy of pain interventions.

FUNÇÃO DA PROTEÍNA DE SORO DE LEITE NA RECUPERAÇÃO PÓS-TREINO

ABSTRACT Introduction: Evidence indicates that whey protein supplementation may accelerate tissue repair and be useful for exercise-induced muscle injury (EIMD) by accelerating recovery and elevating protein synthesis and blood amino acids. However, the potential role of whey protein after EIMD in humans is inconsistent. Objective: Find the effective role of whey protein in post-exercise recovery from EIMD. Methods: Scopus, Medline, and Google scholar, were systematically searched until March 2022. To assess the risk of bias, the Cochrane collaboration tool was applied. Weighted mean differences (WMD), 95% confidence intervals (CI), and random effect models to calculate the total effect. Results: The result of the review indicated that the decreasing impact of whey protein intake is significant on creatine kinase (CK) [WMD = −19.11 IU.L-1, CI: −36.200, −2.036; P = 0.028]. The effect of whey protein supplementation on lactate dehydrogenase (LDH) concentration indicated that the impact of whey protein on changing LDH levels is significant. In addition, subgroup analysis showed significant decreases in CK and LDH based on post-exercise follow-up times, whey protein dosage, test duration, supplementation time, exercise types, and training status. Conclusion: The results showed the efficacy of whey protein in decreasing CK and LDH levels among adults in general and in subgroup analysis. Therefore, whey protein could have an effective role in the post-exercise recovery of EIMD. Level of evidence II; Therapeutic studies – review of results.

Etiology, risk factors and complications of exercise induced muscle injury

Healthy lifestyle includes physical activity as the basic component however, exercises with eccentricity have been associated to a higher risk of muscle injury and slower recovery. The development of exercise-induced muscle injury is a phenomenon that results from atypical or unaccustomed activity; the intensity of the pain and the extent of the damage steadily deteriorate over time, and when the exercise session contains an eccentric component, they may last for several days. Increasing levels of muscle-specific circulating protein are present, along with increased levels of muscular pain and decreased muscle strength. The extent of severity of the symptoms following eccentric exercise varies greatly. Exercise-induced muscle injury is influenced by a number of factors including intensity, duration, mode, muscle group, age, gender, genetics, and dietary state. Numerous scientific studies illustrate the circumstances under which exercise causes muscle injury. It is widely acknowledged that exercise that is unfamiliar, particularly exercise that involves eccentric contractions, causes damage. exercise-induced muscle injury is accompanied by an inflammatory response involving numerous mediators, including the production of muscle-specific creatine kinase and interleukins and interleukins receptor antagonist and acute phase proteins. Complications of exercise-induced muscle injury include temporary muscle inflammation, loss of strength, muscle discomfort, restricted range of motion, elevated passive tension, discomfort, and a momentary decline in insulin sensitivity and can also lead to rhabdomyolysis. The purpose of this research is to review the available information about an etiology, risk factors and complications of exercise-induced muscle injury.

FP.06 Use of an exercise challenge system to define a universal proteomic signature of muscle injury in a diverse set of adults with inherited myopathy

Several inherited myopathies are defined by an enhanced injury response to exercise. However, current understanding of muscle injury depending on the underlying genetic lesion is poorly understood. We used an established exercise intervention along with the SOMAscan 7K platform to characterize serum proteomic signatures of exercise-induced muscle injury in a diverse set of adults with myopathy. Participants included healthy volunteers, Becker muscular dystrophy (BMD), Limb-girdle muscular dystrophies R9 (LGMDR9) and R12 (LGMDR12), and McArdle disease (McA). Muscle injury was induced by an exercise challenge consisting of high-intensity interval cycling exercise followed by a leg strength test, which has been shown to cause injury in BMD and McA. Blood samples were collected before exercise and at intervals of up to 24 hours post-exercise. We identified an indication-independent novel cluster of 27 plasma-based biomarkers that distinguished pre-exercise myopathy individuals from healthy controls. The exercise response of this distinguishing cluster revealed two subsets of proteins, those that further changed after exercise and those that were exercise-independent. Exercise-dependent biomarkers demonstrated a clear time-dependency, with >90% increasing to maximal levels at 2-4 hours post-injury. When comparing indication-specific injury responses, BMD, LGMDR9, and McA revealed a surprising degree of overlap (33 proteins), including 15 proteins that were not increased at baseline in any indication. In comparison, LGMDR12 individuals demonstrated elevated baseline signature markers but no significant injury response. The controls showed no significant biomarker response to the exercise challenge. These data not only provide several new biomarker candidates for distinguishing muscle injury but highlight significant common features between indications, suggesting a common mechanism of muscle injury and breakdown, independent of the underlying pathophysiology.

The role of clock gene BMAL1 in exercise-induced skeletal muscle injury recovery

Objective: To investigate the role of clock gene BMAL1 in exercise-induced skeletal muscle injury recovery. Methods: Two hundred and eight 8-week-old SD rats were randomly divided into the control group (Group C, n=104) and the exercise group (Group E, n=104). Group E performed a 90-minute downhill run on the treadmill. After exercise, the gastrocnemius muscle of 8 rats in Group C and Group E were collected at 0 h, 6 h, 12 h, 18 h, 24 h, 30 h, 36 h, 42 h, 48 h, 54 h, 60 h, 66 h and 72 h. The expression of skeletal muscle core clock gene, BMAL1 was measured by real-time fluorescence quantitative PCR. The parameters of fitting cosine curve were obtained by cosine analysis software circacompare (R package), and the change trend of rhythmic oscillation was analyzed. The ultrastructure of skeletal muscle fibers was observed by transmission electron microscope. The expressions of skeletal muscle BMAL1 and DESMIN were detected by Western blot; Immunofluorescence was used to observe the localization and contents of BMAL1 and DESMIN. Results: In Group C, three complete circadian rhythm cycles of mRNA BMAL1 were observed within 72 hours; in Group E, the circadian rhythm of BMAL1 mRNA disappeared at 0 h～24 h. Compared with Group C, the expression level of BMAL1 mRNA was significantly increased at 0 h, 6 h, 12 h, and 18 h after exercise in Group E (P＜0.05), and the expression of BMAL1 protein was significantly increased at 0 h and 12 h after exercise(P＜0.05), and recovered to the level of that in Group C from 24 h to 72 h(P＞0.05). The expression of DESMIN protein was decreased at 0 h and 12 h after exercise(P＜0.05), gradually increased at 24 h, increased significantly at 48 h(P＜0.01), and recovered to the control level at 72 h (P＞0.05). In Group E, BMAL1 and DESMIN were co-localized at 0 h, 12 h, and 24 h after exercise; the colocalization at 0 h～24 h showed a trend of first decreasing and then increasing, and the fluorescence intensity at 24 h reached the highest value. Conclusion: The post-exercise clock gene BMAL1 may be involved in the enhanced synergy of regulating the cytoskeletal protein DESMIN, it is thus related to the promotion of muscle fiber structure recovery.

Acupuncture Activates Ca2+Signaling And Mitochondrial Network Homeostasis Through TRP Channels In Eccentric Exercise-induced Skeletal Muscle Injury

PURPOSE: Explore how acupuncture activates Ca2+ signaling and mitochondrial network homeostasis through TRP channels in eccentric exercise-induced skeletal muscle injury. The aim is reveal the mechanism of acupuncture which reduces scar production in injured skeletal muscles and promotes repair of skeletal muscle injuries. METHODS: 72 8-week-old C57BL6 mice were randomly divided into control group (C), electrical stimulation group (E), electrical stimulation and acupuncture group (EA), electrical stimulation and acupuncture group, electrical stimulation and acupuncture TRP, NCX (sodium-calcium exchanger) Ryanodine receptors (RYRs) inhibitor group (EAT), (EAN) and (EAR), transfect TA muscle with cDNAs encoding for either 2mtYC2 or pMitoTimer using electroporation, and mouse TA muscle injury model was established after 10 days of recovery, using stainless steel acupuncture needle for EA, EAT and EAN group. Imaging was performed on a Zeiss microscope Average YFP/CFP ratio values were determined and analyzed with ImageJ. Data analysis was made using two-way ANOVA with repeated measures. RESULTS: There were no statistical differences in the indicators of each group before the experiment (P > 0.05). The Ca2+ YFP/CFP ratio of group E was not significantly different from that of groups EAT, EAN, and EAR (P > 0.05), but it is significantly higher than the groups C, EA (1.50 + 0.20vs 0.80 + 0.20vs 1.00 + 0.20, P < 0.05). The area of mitochondrial damage in group E was not significantly different from that in groups EAT, EAN and EAR (P > 0.05), but it is larger than groups C, EA (2643.41 + 150.00 vs 0.00 + 10 vs 1452.26 + 150.00um2, P < 0.05); Outside the injury area, group E mitophagy area diameter is longer than group EA (164.56 + 30.92 vs 5.86 + 3.10 um + 0.20 P < 0.05) CONCLUSION: Acupuncture triggered TRP channel activating RyRs and NCX, prevented Ca2+ concentration from overloading, regulated intracellular mitochondrial Ca2+ uptake to maintain eccentric injury skeletal muscle mitochondrial network homeostasis.

Platelet Activation Favours NOX2-Mediated Muscle Damage in Elite Athletes: The Role of Cocoa-Derived Polyphenols.

Mechanisms of exercise-induced muscle injury with etiopathogenesis and its consequences have been described; however, the impact of different intensities of exercise on the mechanisms of muscular injury development is not well understood. The aim of this study was to exploit the relationship between platelet activation, oxidative stress and muscular injuries induced by physical exercise in elite football players compared to amateur athletes. Oxidant/antioxidant status, platelet activation and markers of muscle damage were evaluated in 23 elite football players and 23 amateur athletes. Compared to amateurs, elite football players showed lower antioxidant capacity and higher oxidative stress paralleled by increased platelet activation and muscle damage markers. Simple linear regression analysis showed that sNOX2-dp and H2O2, sCD40L and PDGF-bb were associated with a significant increase in muscle damage biomarkers. In vitro studies also showed that plasma obtained from elite athletes increased oxidative stress and muscle damage in human skeletal muscle myoblasts cell line compared to amateurs’ plasma, an effect blunted by the NOX2 inhibitor or by the cell treatment with cocoa-derived polyphenols. These results indicate that platelet activation increased muscular injuries induced by oxidative stress. Moreover, NOX2 inhibition and polyphenol extracts treatment positively modulates redox status and reduce exercise-induced muscular injury.

Preconditioning with whole-body or regional hyperthermia attenuates exercise-induced muscle damage in rodents.

Our aim was to investigate whether hyperthermia before exercise protects against exercise-induced skeletal muscle damage. Two hyperthermia protocols were evaluated. In the first, male ICR mice were exposed to 30 min of whole-body heat in an environmental chamber at an ambient temperature of 42 °C. Heat-exposed and non-heat-exposed mice subsequently completed 60 min of downhill running on a treadmill, 24 h after exposure. Heat exposure significantly increased HSP70 and HSP25 content in the soleus muscle compared to controls. Plasma creatine kinase, muscle beta-glucuronidase, and histochemical (hematoxylin and eosin stain) analysis demonstrated that muscle damage was lower in the heat-exposed mice than in the non-heat-exposed mice. In the second, the effect of regional heating of the legs, by microwave diathermy, on the prevention of exercise-induced muscle damage was evaluated in male Wistar rats. Microwave-treated and non-microwave-treated rats again completed the running protocol 24 h after exposure. Microwave diathermy increased the muscle temperature to 40 °C, significantly increased HSP70 and HSP25 content in the soleus muscle, and significantly attenuated exercise-induced muscle damage. Therefore, hyperthermia before exercise increases skeletal muscle HSPs and attenuates the risk of exercise-induced muscle injury.

Passive-Stretch Induced Skeletal Muscle Injury Platform for Duchenne Muscular Dystrophy Modeling

<h3>Research Objectives</h3> Inactivity following skeletal muscle dysfunction in DMD usually causes compromised soft tissue and decreased joint range of motion. Passive stretch techniques in combination with an exercise program are used as interventions to prevent musculoskeletal complications in children with DMD. However, the exact role of stretch-based rehabilitation methods is not well established in children with DMD. In fact, the underlying molecular and cellular mechanisms of how stretch-based rehabilitation methods in dystrophin-deficient muscle fibers might worsen the disease phenotype have not been fully explained. Therefore, the purpose was to establish an in vitro stretch-induced injury model in normal and dystrophic rat skeletal muscle fibers. <h3>Design</h3> Randomized experimental. <h3>Setting</h3> Laboratory Setting. <h3>Participants</h3> Normal and dystrophic primary rat myoblasts (N=8) were platted on two (control and experimental) nanopatterned plates. The experimental setting was replicated three times. <h3>Interventions</h3> Myofibers were subjected to passive stretch on day three differentiation using the Cytostretcher device for 10 hours. <h3>Main Outcome Measures</h3> A electrochemiluminescence assay was used to quantify concentrations of skeletal muscle-specific injury biomarkers, FABP3, Myl3, and STnI. Two-way analysis of variance (ANOVA) with repeated measure test was used. <h3>Results</h3> STnI concentration was significantly higher on day four post differentiation compared to day three in the DMD-stretched group; whereas STnI concentration in all three groups did not show significant changes between the two-time points. FABP3 concentrations showed a significant increase on day four of differentiation compared to pre-stretch in both the DMD-stretched and the WT-stretched groups. However, MyL3 concentration decreased across all groups on day four of differentiation compared to day three. <h3>Conclusions</h3> The initial findings of this study supported the hypothesis that the passive-stretch protocol caused a greater magnitude of injury in dystrophic myofibers compared to normal. However, the preliminary findings did not support the hypothesis that dystrophin deficiency could worsen the response to passive-stretch-induced injury. These findings will guide the development of future in vitro studies for disease modeling, and to better understand the molecular mechanism(s) responsible for adaptation to exercise-induced muscle injury. <h3>Author(s) Disclosures</h3> The authors declare no conflict of interest.

Metric-Based Muscle Synergy Consistency for Upper Limb Motor Functions

The hypothesis of muscle synergy has been dominantly accepted in research due to the evidence of being well investigated its existence in multiple disciplines, such as health science. Motor function assessment using muscle synergy provides a quantitative approach from the physiological features of muscles. Given the synergy coordinating multiple muscles in a natural motion, this article proposes a surface electromyography (sEMG)-driven metric to measure the consistency of the muscle synergy patterns of upper limb motor functions. The metric-based consistency algorithm primarily comprises three stages: 1) to construct nonnegative matrix factorization (NNMF)-based sEMG muscle synergy patterns; 2) to validate synergy similarities via cosine similarity; and 3) to conduct the patterns consistency between motion cycles checking via the Mahalanobis distance (MD). The proposed measure is employed to validate synergy consistency in upper limb motor function of isokinetic movement protocols involving ten subjects. The muscle synergy similarity has achieved averages of 88&#x0025; and 97&#x0025; for intersubject and intrasubject, respectively. The synergy consistency via MD is significantly positively correlated with the maximum joint torque fluctuation between motion cycles to indicate its efficiency. This quantitative measurement confirms that muscle synergy can be used to measure muscle motor function, paving the way for motion protocol assessment, such as stroke rehabilitation and exercise-induced muscle injury avoidance through monitoring the consistency of the linear combination of muscle activations during movement.

Response: Does Obesity Affect the Severity of Exercise-Induced Muscle Injury? (J Obes Metab Syndr 2021;30:132-40).

Response: Does Obesity Affect the Severity of Exercise-Induced Muscle Injury? (J Obes Metab Syndr 2021;30:132-40).

Does Obesity Affect the Severity of Exercise-Induced Muscle Injury?

This literature review investigates the effects of obesity on exercise-induced muscle injury and reexamines the potential mechanisms of exercise-induced muscle injury related to obesity. Several studies reported that high body mass index and percent body fat can significantly affect the markers of muscle injury after exercise, including maximal strength, delayed onset muscle soreness, creatinine kinase level, and myoglobin level. The potential mechanisms resulting in these outcomes include structural changes in the cell membrane induced by high fat levels, increased inflammatory responses due to adipose tissues, reduced muscle satellite cell activation and myogenesis due to lipid overload, differences in muscle fiber distributions, and sedentary behaviors. These mechanisms, however, must be verified through more research. As obesity is a potential risk factor increasing the severity of exercise-induced muscle injuries, the exercise intensity and duration for obese patients must be carefully selected, and a preconditioning intervention (e.g., low-intensity eccentric training) may be considered before or during the early stages of the exercise program.

Mechanism of the effect of traditional Chinese medicine fumigation on blood lactic acid in exercise body

The production of blood lactic acid in exercise can make the body feel tired and affect the normal movement of the body. Therefore, from the aspects of energy metabolism, mechanical injury, inflammation, free radicals and lipid peroxidation, and growth factors regulating the repair of skeletal muscle injury, the mechanism of Chinese herbal compound on skeletal muscle exercise induced injury is systematically analyzed and discussed. In order to provide theoretical basis for sports training, public health and labor hygiene, one or two of the seven Chinese herbal prescriptions which have good effects on exercise-induced muscle injury are selected. The paper delivers guidelines for avoiding and decreasing exercise caused lactate accumulation and lactic acid. The results show that Chinese herbal fumigation lotion can effectively remove blood lactic acid, accelerate the recovery of muscle strength, and obviously eliminate exercise-induced muscle fatigue.

Basement membrane recovery process in rat soleus muscle after exercise-induced muscle injury

ABSTRACT Purpose: Collagen IV is a component of the basement membrane (BM) that provides mechanical support for muscle fibers. In addition, transcription factor 4 (TCF4) is highly expressed in muscle connective tissue fibroblasts and regulates muscle regeneration. However, the expression of collagen IV and TCF4 (+) cells in response to exercise-induced muscle injury is not well known. Here, we investigated the expression and localization of collagen IV and TCF4 (+) cells during the recovery process after muscle injury induced by different exercise loads. Materials and Methods: Muscle injury was observed in the soleus muscle of young Wistar rats after 12 or 18 sets—downhill running (DR) on a treadmill. After running, the rats were permitted to recover for a period of 0.5 days, 2 days, or 7 days. Results: Ectopic localization of collagen IV in injured muscle fibers was observed after DR, and the number increased at 0.5 days after 18 sets DR and at 2 days after 12 or 18 sets DR as compared to the number observed at baseline. BM disruption was observed after DR. TCF4 (+) cells appeared in the inside and around injured muscle fibers at 0.5 day of recovery. After 18 sets DR, TCF4 (+) cells were more abundant for a longer period than that observed after 12 sets DR. Conclusions: DR induces BM disruption accompanied by muscle fiber damage. It is possible that BM destruction may be accompanied by muscle damage and that TCF4 (+) cells contribute to muscle fiber and BM recovery.