Exercise-induced Muscle Injury Research Articles

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.

Plasma Concentrations of Select Inflammatory Cytokines Predicts Pain Intensity 48 Hours Post-Shoulder Muscle Injury.

The relationship between elevated inflammatory cytokine levels and peak pain intensity following acute musculoskeletal injury has not been fully elucidated in high risk subgroups. Identifying the role that these cytokines have on pain responses may help with developing tailored therapeutic approaches. Data were collected from 54 participants who were vulnerable to a robust pain response and delayed recovery following musculoskeletal injury. Participants completed baseline active and resting pain measurements and a blood draw before an exercised induced shoulder muscle injury. Participants returned at 24 and 48 hours postinjury for follow-up pain measurements and blood draws. Blood plasma was analyzed for interleukin (IL)-1β, IL-6, IL-8, IL-10, and tumor necrosis factor α. Pearson bivariate correlations were performed between cytokines and pain measurements to identify candidate variables for stepwise multiple linear regression predicting pain intensity reports. Pearson bivariate correlation identified 13/45 correlations between inflammatory cytokines and resting pain intensity and 9/45 between inflammatory cytokines and active pain (P<0.05, r≥0.3 or r≤-0.3). This led to 5 stepwise multiple linear regression models, of which 4 met the statistical criterion (P<0.0167); including IL-10 baseline plasma concentrations predicting active pain (r=0.19) and resting pain (r=0.15) intensity 48 hours postinjury. IL-6 and IL-10 plasma concentrations at 48 hours were respectively associated with active and resting pain at 48 hours. These findings suggest that elevated concentrations of inflammatory cytokines, specifically IL-10 (at baseline and 48 h) and IL-6 (at 48 h), may play a role in heightened pain responses following exercise-induced muscle injury.

Effects Of Exercise-induced Muscle Injury On Quadriceps Muscle EMG During Locomotion

Effects Of Exercise-induced Muscle Injury On Quadriceps Muscle EMG During Locomotion

To Elucidate the Inhibition of Excessive Autophagy of Rhodiola crenulata on Exhaustive Exercise-Induced Skeletal Muscle Injury by Combined Network Pharmacology and Molecular Docking.

Autophagy can remodel skeletal muscle in response to exercise. However, excessive autophagy can have adverse effects on skeletal muscle. Although Rhodiola crenulata (R. crenulata) is thought to regulate autophagy, its active ingredients and mechanisms of action remain unclear. In this study, molecular docking and network pharmacology were used to screen for autophagy-related targets of R. crenulata. Subsequently, protein-protein interaction (PPI) analysis was used to find the relationships between the inverse docking targets and autophagy-related targets and therefore highlight the key targets. And then the Database for Annotation, Visualization, and Integrated Discovery (DAVID) database was recruited to explain the functions and enrichment pathways of the target proteins. Finally, the potential targets were validated by immunohistochemistry of a mouse model of exhaustive exercise-induced skeletal muscle injury. We found a network of 15 major constituents of R. crenulata with 30 autophagy-related and 105 inverse-docking targets by molecular docking and network pharmacology. The results of PPI analysis indicated that 16 inverse-docking targets interacted 8 autophagy-related proteins. Further pathway analysis showed that R. crenulata could regulate exercise-induced skeletal muscle autophagy through mammalian target of rapamycin (mTOR), AMP activated protein kinase (AMPK) and Forkhead box protein O (FoxO). The results of our animal experiments indicated that R. crenulata could suppress the expression of Ubiquitin-like protein ATG12 (ATG12), Beclin-1 (BECN1), and Serine/threonine-protein kinase ULK1 (ULK1), while increasing the expression of MTOR, NAD-dependent protein deacetylase sirtuin-1 (SIRT1), and Microtubule-associated protein tau (MAPT). In conclusion, this study demonstrated that R. crenulata may protect skeletal muscle injury induced by exhaustive exercise via regulating the mTOR, AMPK, and FoxO singling pathway.

Plasma MMP-9, TIMP-1, and TGF-β1 Responses to Exercise-Induced Muscle Injury.

The purpose of this study was to analyze changes in the levels of matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), and transforming growth factor-β1 (TGF-β1) in response to strength recovery after eccentric exercise in humans. In this study, 16 healthy males participated and were divided into a faster recovery (FR) group (n = 8, >80% of baseline) and a slower recovery (SR) group (n = 8, <40% of baseline) on the basis of their recovery of maximal isometric strength (MIS) 96 h after eccentric exercise. For both groups, measurements were taken of muscle soreness, creatine kinase (CK) activity, and MMP-9, TIMP-1, and TGF-β1 levels during the 24- to 96-h period after eccentric muscle contraction of their non-dominant elbow flexor. Muscle soreness (p < 0.001), CK activity (p < 0.01), and TGF-β1 level (p < 0.01) were significantly lower in the FR group compared with SR group, whereas no significant differences in MMP-9 and TIMP-1 levels were found between the two groups (p > 0.05). These results suggest that scar tissue formation caused by the pro-fibrotic activity of growth factors such as TGF-β1 is a potential cause of delay in strength recovery after exercise-induced muscle injury.

Eccentric exercise results in a prolonged increase in interleukin-6 and tumor necrosis factor-α levels in rat skeletal muscle.

Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) are well-known cytokines with pro-inflammatory capabilities, and have been shown to be involved in adaptation to exercise as multifaceted myokines. However, the precise role of IL-6 and TNF-α during exercise-induced skeletal muscle injury and subsequent repair processes is not fully understood. In this study, IL-6 and TNF-α were examined in soleus muscles at the gene and protein levels using in situ hybridization and immunohistochemical staining, respectively, and serum levels of IL-6 and TNF-α were determined before and after a 90-min downhill running session in rats. There were no changes in serum levels of IL-6 and TNF-α after exercise, but IL-6 and TNF-α mRNA increased and maintained high expression in muscles for 1-2weeks after exercise. IL-6 and TNF-a mRNAs were identified in both the cytoplasm and the nuclei of myocytes, as well as in invading inflammatory cells. IL-6 and TNF-α protein mainly distributed in cytoplasm unevenly and had a prolonged expression until 2weeks after eccentric exercise. Our results demonstrate that there is increased IL-6 and TNF-α expression in skeletal muscle that is induced by eccentric exercise and that the high expression of IL-6 and TNF-α in the long-term phase after eccentric exercise may be more involved in the subsequent recovery of damaged muscle.

MRI Quantitative Analysis of Eccentric Exercise-induced Skeletal Muscle Injury in Rats

The aim of this study was to investigate the value of magnetic resonance (MR) quantitative analysis (MR-T2 mapping technique) for the evaluation of eccentric exercise-induced skeletal muscle injury. We established an animal model of eccentric exercise-induced damage of Sprague Dawley rat skeletal muscle and evaluated the animals by MR imaging, determined the serum levels of fast skeletal troponin (fsTnI), and examined muscle histopathology, at 0, 1, 2, 4, and 7 days after eccentric exercise. The associations between MR imaging findings, and histopathological and laboratory results were evaluated. T2-weighted images (WIs) of quadriceps femoris muscles showed obvious high signal intensities after exercise, and the T2 values and serum fsTnI levels continued to increase, peaking at day 2 after exercise, p< 0.05. The histopathological findings in muscle specimens, which included swollen and ruptured cells, enlarged extracellular spaces, inflammation, and regeneration of muscle fibers, showed similar trends. After day 2, muscle specimens began to show evidence of self-repair, the T2WI signals decreased in intensity, and the T2 values and serum fsTnI levels decreased; however, at day 7 post injury, the values remained slightly higher than those in the control animals, p< 0.05. The T2 value was significantly correlated with the serum fsTnI level (r = 0.896, p< 0.01). T2 mapping technology accurately reflects the histopathological and fsTnI abnormalities and the degree of skeletal muscle damage associated with eccentric exercise followed by recovery. Because T2 mapping technology is noninvasive and can be quantitatively analyzed, it might become the preferred method for performing the diagnosis of eccentric exercise-induced skeletal muscle injury.

Low-Dose Rapamycin Facilitates Recovery from Exercise-Induced Muscle Injury

Rapamycin has been shown to have a dose-dependent effect on multiple signaling proteins in skeletal muscle cells that influence protein synthesis and calcium handling. However, it has yet to be determined if a low-dose of rapamycin impacts skeletal muscle during recovery from an exercise-induced injury. PURPOSE: To determine if low-dose rapamycin affects the rate of isometric strength recovery, muscle ubiquitination levels and markers of autophagy compared to saline control 14 days after exercise induced injury. METHODS: Mice were injected with either saline (SAL; 0.9%) or low-dose rapamycin (RAP; 10 μg/kg body weight) every other day for 2 weeks before and after a single bout of 150 eccentric contractions of the left anterior crural muscles. The recovery of strength of the anterior crural muscles was measured in vivo immediately, 7 days, and 14 days after injury induction. The magnitude of expression of beclin-1, ubiquitin, and ubiquitinated protein in injured and contralateral control TA muscles (i.e., primary anterior crural muscle) were analyzed via Western blot at 14 days after injury. RESULTS: Isometric twitch torque values did not differ between groups at any time point. No group differences in peak isometric tetanic torque were observed pre-injury, post-injury or 7 days following injury. However at 14 days, RAP mice recovered to pre-injury peak isometric torque values (Pre= 2.30 ± .07 Nmm; 14d= 2.25 ± 0.08 Nmm) while SAL group was significantly lower than pre-injury. At 14 days, RAP mice generated 15.4% higher maximal torque than SAL group (p = 0.04). Beclin-1 and free ubiquitin expression in TA muscles were significantly increased in both SAL (1.4-fold and 2.3-fold, respectively) and RAP (2.2-fold and 8.0-fold, respectively) mice at 14 days after injury compared to the uninjured muscle. The increase in the free ubiquitin in the injured muscle was 3.3-fold greater in the RAP treatment compared to SAL (p = 0.001). There were no significant changes in the ubiquitination of proteins among the groups at 14 days post-injury. CONCLUSION: Chronic low-dose rapamycin treatment in mice enhances recovery of skeletal muscle from eccentric contraction-induced injury at the 14th day and accentuates the upregulation of free ubiquitin.

Effects of Supplementation and Training on Ameliorating Lipid Profiles and Protection against Coronary Artery Disease; an Experimental Study.

The use of antioxidants may reduce the harmful effects of radicals during exercise and extreme sports. The Current study aimed to investigate the effect of this supplement on the lipid profiles in exercise-induced muscle injury. In this experimental study, 64 Wistar rats were randomly divided into four groups of control, exercise, exercise + Resveratrol (REV) and REV. After a week of adaptation, endurance and acute exercises were conducted in a motor driven treadmill, followed by using a training protocol in which running speed was gradually elevated until 19 weeks of age. Finally, the levels of cholesterol (CHO), triglycerides (TG), low-density lipoproteins (LDL), high-density lipoproteins (HDL), and very low-density lipoproteins (VLDL) were compared between the groups. There was no statistically significant difference in CHO plasma level between the studied groups after acute and endurance exercises. There was a significant increase in the level of TG in the exercise group (p = 0.001) and the exercise + REV (p = 0.004) group after acute and endurance exercises. After the implementation of the endurance and acute exercises none of the studied groups had statistically significant changes in HDL plasma level. There was a significant decrease in LDL plasma levels in the exercise (p = 0.007) and the exercise + REV (p = 0.01) groups. After performing endurance protocol, VLDL plasma levels increased significantly in the exercise (p = 0.001) and the exercise+ REV (p = 0.005) groups in comparison with control group. Based on the findings, there was no difference in the level of CHO and HDL between the training groups, REV and control groups. However, both endurance exercise and acute exercise trainings resulted in an increase in TG and VLDL levels and decrease in LDL level, compared with the control group.

Does vibration benefit delayed-onset muscle soreness?: a meta-analysis and systematic review.

ObjectiveDelayed-onset muscle soreness (DOMS) is a symptom of exercise-induced muscle injury that is commonly encountered in athletes and fitness enthusiasts. Vibration is being increasingly used to prevent or treat DOMS. We therefore carried out a meta-analysis to evaluate the effectiveness of vibration in patients with DOMS.MethodWe searched nine databases for randomized controlled trials of vibration in DOMS, from the earliest date available to 30 May 2018. Visual analogue scale (VAS) and creatine kinase (CK) levels were set as outcome measures.ResultsThe review included 10 identified studies with 258 participants. The meta-analysis indicated that vibration significantly improved the VAS at 24, 48, and 72 hours after exercise, and significantly improved CK levels at 24 and 48 hours, but not at 72 hours.ConclusionVibration is a beneficial and useful form of physiotherapy for alleviating DOMS. However, further studies are needed to clarify the role and mechanism of vibration in DOMS.

Evaluating the Effects of Systemic, Exercise-Induced Skeletal Muscle Injury using Whole Transcriptome Sequencing

Abstract Recent advances in next generation sequencing have dramatically reduced the cost of whole transcriptome sequencing to measure differential gene expression. Extreme physical performances represent a unique model for investigating the combined effects of oxidative stress and eccentric muscle contraction on systemic skeletal muscle injury outcomes. Studying changes in whole transcriptome RNA expression may allow identification of specific potential treatment targets for a variety of disease states associated with chronic inflammation and oxidative stress. The purpose of this study was to investigate changes in whole transcriptome RNA expression in response to prolonged endurance running. The protocols were approved by the University IRB committee (in accordance with the latest Declaration of Helsinki) and subjects gave written informed consent to participate. Blood samples were collected in PAXgene RNA tubes at baseline, 4-h, and 24-h after performing a half-marathon race. After collection, tubes were frozen and total RNA was extracted and verified using accepted methods. RNAseq analysis was conducted using an Illumina NextSeq 500 sequencing platform. RNAseq analysis revealed distinct changes in injury, inflammation, anti-oxidant defense, and stress-associated RNA expression with responses appearing more pronounced at 24-h compared to 4-h post-race. These results confirm the systemic changes that occur following whole-body exercise-induced muscle injury in a human model. The next step in this research is to test potential therapeutic strategies to determine their effectiveness on altering the changes in the transcriptome.

ALDH2 Restores Exhaustive Exercise-induced Mitochondrial Dysfunction in Skeletal Muscle

Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is highly expressed in heart and skeletal muscles, and is the major enzyme that metabolizes acetaldehyde and toxic aldehydes. The cardioprotective effects of ALDH2 during cardiac ischemia/reperfusion injury have been recognized. However, less is known about the function of ALDH2 in skeletal muscle. PURPOSE: This study was designed to evaluate the effect of ALDH2 on exhaustive exercise-induced skeletal muscle injury. METHODS: We created transgenic mice expressing ALDH2 in skeletal muscles. Male wild-type C57/BL6 (WT) and ALDH2 transgenic mice (ALDH2-Tg), 8-weeks old, were challenged with exhaustive exercise for 1 week to induce skeletal muscle injury. Animals were sacrificed 24 h post-exercise and muscle tissue was excised. RESULTS: ALDH2-Tg mice displayed significantly increased treadmill exercise capacity compared to WT mice. Exhaustive exercise caused an increase in mRNA levels of the muscle atrophy markers, Atrogin-1 and MuRF1, and reduced mitochondrial biogenesis and fusion in WT skeletal muscles; these effects were attenuated in ALDH2-Tg mice. Exhaustive exercise also enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of Beclin1 and Bnip3; the effects of which were mitigated by ALDH2 overexpression. In addition, ALDH2-Tg reversed the increase of an oxidative stress biomarker (4-hydroxynonenal) and decreased levels of mitochondrial antioxidant proteins, including manganese superoxide dismutase and NAD(P)H:quinone oxidoreductase 1, in skeletal muscle induced by exhaustive exercise. CONCLUSIONS: ALDH2 may reverse skeletal muscle mitochondrial dysfunction due to exhaustive exercise by regulating mitochondria dynamic remodeling and enhancing the quality of mitochondria.

Response of macrophages in rat skeletal muscle after eccentric exercise

PurposeMacrophages are known to be important for healing numerous injured tissues depending on their functional phenotypes in response to different stimuli. The objective of this study was to reveal macrophage phenotypic changes involved in exercise-induced skeletal muscle injury and regeneration. MethodsAdult male Sprague-Dawley rats experienced one session of downhill running (16° decline, 16 m/min) for 90 min. After exercise the blood and soleus muscles were collected at 0 h, 6 h, 12 h, 1 d, 2 d, 3 d, 1 w and 2 w after exercise, separately. ResultsIt was showed that CD68+ M1 macrophages mainly infiltrated into muscle necrotic sites at 1–3 d, while CD163+ M2 macrophages were present in muscles from 0 h to 2 weeks after exercise. Using transmission electron microscopy, we observed activated satellite cells 1 d after exercise. Th1-associated transcripts of iNOS and Ccl2 were inhibited post exercise, while COX-2 mRNA was dramatically increased 12 h after running (p < 0.01). M2 phenotype marker Arg-1 increased 12 h and 3 d (p < 0.05, p < 0.01) after exercise, and Clec10a and Mrc2 were up-regulated in muscles 12 h following exercise (p < 0.05, p < 0.05). ConclusionThe data demonstrate the dynamic patterns of macrophage phenotype in skeletal muscle upon eccentric exercise stimuli, and M1 and M2 phenotypes perform different functions during exercise-induced skeletal muscle injury and recovery.

Is Branched-Chain Amino Acids Supplementation an Efficient Nutritional Strategy to Alleviate Skeletal Muscle Damage? A Systematic Review.

Amino acids and more precisely, branched-chain amino acids (BCAAs), are usually consumed as nutritional supplements by many athletes and people involved in regular and moderate physical activities regardless of their practice level. BCAAs have been initially shown to increase muscle mass and have also been implicated in the limitation of structural and metabolic alterations associated with exercise damage. This systematic review provides a comprehensive analysis of the literature regarding the beneficial effects of BCAAs supplementation within the context of exercise-induced muscle damage or muscle injury. The potential benefit of a BCAAs supplementation was also analyzed according to the supplementation strategy—amount of BCAAs, frequency and duration of the supplementation—and the extent of muscle damage. The review protocol was registered prospectively with Prospective Register for Systematic Reviews (registration number CRD42017073006) and followed Preferred Reporting Items for Systematic reviews and Meta-Analyses guidelines. Literature search was performed from the date of commencement until August 2017 using four online databases (Medline, Cochrane library, Web of science and ScienceDirect). Original research articles: (i) written in English; (ii) describing experiments performed in Humans who received at least one oral BCAAs supplementation composed of leucine, isoleucine and valine mixture only as a nutritional strategy and (iii) reporting a follow-up of at least one day after exercise-induced muscle damage, were included in the systematic review analysis. Quality assessment was undertaken independently using the Quality Criteria Checklist for Primary Research. Changes in indirect markers of muscle damage were considered as primary outcome measures. Secondary outcome measures were the extent of change in indirect markers of muscle damage. In total, 11 studies were included in the analysis. A high heterogeneity was found regarding the different outcomes of these studies. The risk of bias was moderate considering the quality ratings were positive for six and neutral for three. Although a small number of studies were included, BCAAs supplementation can be efficacious on outcomes of exercise-induced muscle damage, as long as the extent of muscle damage was low-to-moderate, the supplementation strategy combined a high daily BCAAs intake (>200 mg kg−1 day−1) for a long period of time (>10 days); it was especially effective if taken prior to the damaging exercise.

Biopsychosocial influence on shoulder pain: Rationale and protocol for a pre-clinical trial

BackgroundChronic musculoskeletal pain conditions are a prevalent and disabling problem. Preventing chronic musculoskeletal pain requires multifactorial treatment approaches that address its complex etiology. Prior cohort studies identified a high risk subgroup comprised of variation in COMT genotype and pain catastrophizing. This subgroup had increased chance of heightened pain responses (in a pre-clinical model) and higher 12month post-operatives pain intensity ratings (in a clinical model). This pre-clinical trial will test mechanisms and efficacy of personalized pain interventions matched to the genetic and psychological characteristics of the high-risk subgroup. MethodsPotential participants will be screened for high risk subgroup membership, appropriateness for exercise-induced muscle injury protocol, and appropriateness for propranolol administration. Eligible participants that consent to the study will then be randomized into one of four treatment groups; 1) personalized pharmaceutical and psychological education; 2) personalized pharmaceutical and general education; 3) placebo pharmaceutical and psychological education; 4) placebo pharmaceutical and psychological education. Over the 5-day study period participants will complete an exercise-induced muscle injury protocol and receive study interventions. Pain and disability assessments will be completed daily, with primary outcomes being duration of shoulder pain (number of days until recovery), peak shoulder pain intensity, and peak shoulder disability. Secondary outcomes include inflammatory markers, psychological mediators, and measures of pain sensitivity regulation. ConclusionThis pre-clinical trial builds on prior cohort studies and its completion will provide foundational data supporting efficacy and mechanisms of personalized interventions for individuals that may be at increased risk for developing chronic shoulder pain. Trial registrationClinicalTrials.gov registry, NCT02620579 (Registered on November 13, 2015).

ALDH2 restores exhaustive exercise-induced mitochondrial dysfunction in skeletal muscle

BackgroundMitochondrial aldehyde dehydrogenase 2 (ALDH2) is highly expressed in heart and skeletal muscles, and is the major enzyme that metabolizes acetaldehyde and toxic aldehydes. The cardioprotective effects of ALDH2 during cardiac ischemia/reperfusion injury have been recognized. However, less is known about the function of ALDH2 in skeletal muscle. This study was designed to evaluate the effect of ALDH2 on exhaustive exercise-induced skeletal muscle injury. MethodsWe created transgenic mice expressing ALDH2 in skeletal muscles. Male wild-type C57/BL6 (WT) and ALDH2 transgenic mice (ALDH2-Tg), 8-weeks old, were challenged with exhaustive exercise for 1 week to induce skeletal muscle injury. Animals were sacrificed 24 h post-exercise and muscle tissue was excised. ResultsALDH2-Tg mice displayed significantly increased treadmill exercise capacity compared to WT mice. Exhaustive exercise caused an increase in mRNA levels of the muscle atrophy markers, Atrogin-1 and MuRF1, and reduced mitochondrial biogenesis and fusion in WT skeletal muscles; these effects were attenuated in ALDH2-Tg mice. Exhaustive exercise also enhanced mitochondrial autophagy pathway activity, including increased conversion of LC3-I to LC3-II and greater expression of Beclin1 and Bnip3; the effects of which were mitigated by ALDH2 overexpression. In addition, ALDH2-Tg reversed the increase of an oxidative stress biomarker (4-hydroxynonenal) and decreased levels of mitochondrial antioxidant proteins, including manganese superoxide dismutase and NAD(P)H:quinone oxidoreductase 1, in skeletal muscle induced by exhaustive exercise. ConclusionALDH2 may reverse skeletal muscle mitochondrial dysfunction due to exhaustive exercise by regulating mitochondria dynamic remodeling and enhancing the quality of mitochondria.

Plasma Actin, Gelsolin and Orosomucoid Levels after Eccentric Exercise.

The present study investigated the acute effect of eccentric exercise on blood plasma actin, gelsolin (GSN) and orosomucoid (AGP) levels in untrained and moderately trained individuals, and their correlation with exercise induced muscle damage (EIMD) markers (CK, intensity of muscle soreness and maximal voluntary contraction torque deficit). Healthy physical education students (6 untrained, 12 moderately trained) participated in this research. Actin, GSN, AGP and CK levels were measured in blood plasma at baseline, immediately, 1 h, 6 h and 24 h post-exercise comprising 90 eccentric quadriceps contractions performed on a dynamometer. There was significant time main effect for GSN, AGP, CK and significant difference was found between baseline and the lowest value of post-exercise GSN (p < 0.05), as well as baseline and the highest value of post-exercise AGP (p < 0.05). Relationships were found between GSN levels and other indirect EIMD markers (between all GSN levels at post-exercise and CK activity at 6 h, p < 0.05; GSNMIN and muscle soreness at post-exercise, p < 0.04), GSN and AGP; however, actin did not correlate at any time points with GSN. Actin, GSN, AGP and CK responses after eccentric exercise do not seem sensitive to training status. The plasma actin level is used as an indicator of injury, however, our results suggest that it is not an accurate marker of EIMD, while plasma GSN concentrations show a better relationship with EIMD and the post-exercise inflammatory process. The elevated plasma AGP and the correlation between GSN and AGP seem to be promising for assessment of exercise-induced muscle injury.

Changes in expression of specific miRNAs and their target genes in repair of exercise-induced muscle injury in rats.

The effects of muscle-specific miRNAs in the repair of exercise-induced muscle injury were investigated by examining the changes in their expression and that of the target genes in rat skeletal muscle. Two-month-old agile male rats were randomly divided into exercise and static control groups, the former subdivided into 0-h, 6-h, 12-h, 1-day, 2-day, 3-day, 1-week, and 2-week groups based on time after exercise. Left gastrocnemii of rats were hematoxylin-eosin stained whereas the right gastrocnemii were used for expression analysis of muscle-specific miRNAs (miR-1 and miR-206) and their target genes, Cx43 and HDAC. Cellular swelling and increased cell volume and intercellular spaces were observed histologically in the 0-h group. Unlike the control group, cells continued to swell whereas intercellular spaces decreased slightly, in the 6-h, 12-h, 1-day, and 2-day groups. Cell swelling was most serious in the 3-day group. In the 1-week group, inflammatory cell infiltration decreased and in the 2-week group, repair was almost complete. The differences in miR-1 expression between the groups were neither obvious nor significant. miR-206 expression increased; however, it differed significantly from that in group C only in the 1-week group. Cx43 and HDAC4 mRNA expression first decreased and then increased compared to that in the control group; differences in HDAC4 mRNA expression were significant in the 1-week group. Compared to the control group, the differences in Cx43 protein levels were significant in the 0-h and 3-day groups. Thus, miR-206 and Cx43 are involved in the repair of exercise-induced muscle injury.

Effect of pre-exercise massage on exercise-induced muscle injury in sled dogs

Previous necropsy studies have shown that up to 60% of sled dogs competing in endurance sled dog races have areas of muscle damage. Human athletes and trainers have maintained a strong belief, based mostly on personal experiences, that massage can be effective for pre-race preparation and expedited recovery between consecutive events. We proposed that massage could lessen the degree of creatine phosphokinase (CPK) release when utilised prior to endurance activities. A randomised crossover study was performed using minimally conditioned sled dogs from a sled dog racing kennel. Each dog in the treatment group received a 14 min massage immediately prior to controlled endurance exercise. The pre-exercise CPK activity was 64±11 IU/l (mean ± standard deviation). The difference between pre-exercise CPK and post-exercise CPK for both groups was expressed as delta CPK. The delta CPK for the massage group was 62±22 IU/l and 74±55 IU/l for the control group. There was no significant change in concentration of CPK between pre- and post-exercise in the treatment and control group (P=0.2282). The lack of a significant difference between the control and massage group suggests that pre-exercise massage may not reduce the severity of exercise-induced muscle damage.