Effects of Six Weeks of Modified and Standard Nordic Hamstring Exercises on Electromyography of Hamstring, Hip And Trunk Muscles and Sprint Performance in Young Male Football Players

Background and Aims hamstring injury is the most common injury in football. Nordic hamstring exercise (NHE) is one of the best hamstring injury prevention strategies. This study was aims to compare the effect of six weeks of standard NHE and modified NHE on electromyography of hamstring, hip and trunk muscles and sprint performance in young male football playersMethods In this study, participants were 26 male football players in Kerman, Iran who were selected using purposeful and convenience sampling methods and randomly divided into two groups of NHE (Age: 16.31±0.51 years, Height: 173.08±5.15 cm, weight: 59.85±5.71 kg) and modified NHE (Age: 16.41±0.54 years, Height: 173±6.84 cm, weigh: 64.20±8.76 kg). Sprint performance was measured by the 20-meter sprint test, and muscles activity was measured by electromyography. Repeated-measure analysis of variance was used for data analysis.Results In the modified NHE group, there was a significant difference between the pretest and posttest phases in the electrical activity of biceps femoris (P=0.001), semitendinosus (P=0.001), gluteus maximus (P=0.016) and erector spinae muscles (P=0.001). In the NHE group, although the activity of muscles increased by 13% in the biceps femoris, 11% in the Semitendinosus, 9% in the gluteus maximus and 4% in erector spinae muscles, the difference was significant only in the biceps femoris (P=0.001) and Semitendinosus (P=0.024). The results also showed a significant difference between the two groups in electrical activity of biceps femoris (P=0.021), semitendinosus (P=0.046) and erector spinae muscles (P=0.039). Conclusion Both standard and modified NHE are effective in preventing hamstring injury by increasing the electrical activity of the Biceps femoris and Semitendinosus, but the modified NHE is more effective in prevention of injury by changing the parameters of NHE and increasing the training load

Cardiac dysfunction in cancer survivors unmasked during exercise

Introduction: The cardiac dysfunction associated with anthracycline-based chemotherapy cancer treatment can exist sub-clinically for decades before overt presentation. Stress echocardiography, the measurement of left ventricular (LV) deformation and arterial haemodynamic evaluation have separately been used to identify sub-clinical cardiovascular (CV) dysfunction in several patient groups including those with hypertension and diabetes. The purpose of the present cross-sectional study was to determine whether the combination of these techniques could be used to improve the characterisation of sub-clinical CV dysfunction in long-term cancer survivors previously treated with anthracyclines. Materials and methods: Thirteen long-term cancer survivors (36±10 years) with prior anthracycline exposure (11±8 years post-treatment) and 13 age-matched controls were recruited. Left ventricular structure, function and deformation were assessed using echocardiography. Augmentation index was used to quantify arterial haemodynamic load and was measured using applanation tonometry. Measurements were taken at rest and during two stages of low-intensity incremental cycling.Results: At rest, both groups had comparable global LV systolic, diastolic and arterial function (all P>0.05), however longitudinal deformation was significantly lower in cancer survivors (-18±2 v -20±2, P<0.05). During exercise this difference between groups persisted and further differences were uncovered with significantly lower apical circumferential deformation in the cancer survivors (-24±5 v -29±5, -29±5 v 35±8 for first and second stage of exercise respectively, both P<0.05). Conclusion: In contrast to resting echocardiography the measurement of LV deformation at rest and during exercise provides a more comprehensive characterisation of sub-clinical LV dysfunction. Larger studies are required to determine the clinical relevance of these preliminary findings

Results of the ontology alignment evaluation initiative 2020

The Ontology Alignment Evaluation Initiative (OAEI) aims at comparing ontology matching systems on precisely defined test cases. These test cases can be based on ontologies of different levels of complexity and use different evaluation modalities (e.g., blind evaluation, open evaluation, or consensus). The OAEI 2020 campaign offered 12 tracks with 36 test cases, and was attended by 19 participants. This paper is an overall presentation of that campaign

Results of the Ontology Alignment Evaluation Initiative 2021

The Ontology Alignment Evaluation Initiative (OAEI) aims at comparing ontology matching systems on precisely defined test cases. These test cases can be based on ontologies of different levels of complexity and use different evaluation modalities (e.g., blind evaluation, open evaluation, or consensus). The OAEI 2021 campaign offered 13 tracks and was attended by 21 participants. This paper is an overall presentation of that campaig

Exercise-induced Oxidative Shift of Lactate Dehydrogenase Isoforms in Cerebrospinal Fluid of Male Wistar Rats

Abstract Background: The aim of the present study was to investigate the effect of endurance training on the content of lactate dehydrogenase isoforms (LDHA and LDHB) and isozymes in cerebrospinal fluid of male wistar rats. Materials and Methods: Seventeen animals (5 weeks old) were randomly divided into two groups according their body weight: control (C; n = 9) and trained (T; n = 8). The animals from the T group were underwent a training program for 12 weeks (started at 20 m/min for 30 min and finished at 26 m/min for 60 min at the last week). Cerebrospinal fluid (CSF) samples were collected from cisterna Magna 72 hours after the last exercise session. LDH Isoforms and isozymes were measured by ELISA and Electrophoresis techniques, and the comparisons between groups were evaluated by student t-test. Results: Both LDHA and LDHB isoforms were found in the CSF of the C group; LDH1 and LDH5 had the highest and lowest content, respectively. Following the twelve-week training protocol, LDHB (p<0.01), LDH1 (p<0.01), and LDH2 concentrations (p<0.01) were significantly increased in the T group compared with those from the C group and LDH3 concentrations (p<0.01) and LDHA/LDHB ratio (p<0.01) were significantly decreased. Endurance training had no effect on LDHA and LDH4. Conclusion: Endurance training is associated with oxidative shift of lactate dehydrogenase isoforms and isozymes in cerebrospinal fluid which could be considered as a prelude to aerobic metabolism of lactate in the brain

Lactate Transporters Expression in Tumor of Balb/c Mice Bearing Breast Cancer after Endurance Training

Background & aim: Changes in the metabolism of cancer cells plays a major role in the survival and their expansion. The aim of this study was to determine expression of lactate transmitters in Balb/c mice with breast cancer after endurance training. Methods: In this experimental study twenty-five Balb C mice were randomly divided into two groups of breast cancer control (N=13) and breast cancer training (N=12). Breast cancer was induced in mammary fat pad by injection of cancer cells (MC4L2) in mice and endurance training protocol was applied for 7 weeks in the experimental group. Tumor volume and MCT1, MCT4, and CD147 expression were measured by micro digital caliper and western blotting technique respectively. Data were analyzed statistically using Student t and Pearson. Results: Significant decreases was found in weight and CD147 expression of tumor after 7 weeks of endurance training in the exercise group compared to the control group. No significant differences were seen in MCT4 expression and tumor volume between the groups (05 / 0p>0.05). Significant correlation was found between tumor MCT1 and CD147 expression (P < 0.05), while the relationship between MCT4 and CD147 expression in tumors was not statistically significant. Conclusion: Endurance training can reduce lactate metabolism in cancer cells through suppression of lactate transporters expression and provides a useful tool in breast cancer treatment or prevention

Exercise-induced lactate accumulation regulates intramuscular triglyceride metabolism via transforming growth factor-β1 mediated pathways

The mechanism regulating the utilization of intramuscular triacylglycerol (IMTG) during high-intensity interval training (HIIT) and post-exercise recovery period remains elusive. In this study, the acute and long-term effects of HIIT on transforming growth factor beta 1 (TGF-β1) abundance in rat skeletal muscle and role of lactate and TGF-β1 in IMTG lipolysis during post-exercise recovery period were examined. TGF-β1 and Adipose triacylglycerol lipase (ATGL) abundance as well as total lipase activity in the gastrocnemius muscle significantly increased to a maximum value 10 h after acute bout of HIIT. Inhibition of TGF-β1 signaling by intramuscular injection of SB431542 30 min prior to the acute exercise attenuated ATGL abundance and total lipase activity in the gastrocnemius muscle in response to acute exercise. Intramuscular acute injection of lactate increased TGF-β1 and ATGL abundance in the gastrocnemius muscle and there were a significant increase in Muscle TGF-β1 and ATGL abundance after 5 weeks of HIIT/lactate treatment. These results indicate that exercise-induced lactate accumulation regulates intramuscular triglyceride metabolism via transforming growth factor-β1 mediated pathways during post-exercise recovery from strenuous exercise

Lactate regulates autophagy through ROS-mediated activation of ERK1/2/m-TOR/p-70S6K pathway in skeletal muscle

The role of autophagy and lysosomal degradation pathway in the regulation of skeletal muscle metabolism was previously studied. However, underlying molecular mechanisms are poorly understood. L-lactate which is utilized as an energetic substrate by skeletal muscle can also augment genes expression related to metabolism and up-regulate those being responsive to reactive oxygen species (ROS). Since ROS is the most important regulator of autophagy in skeletal muscle, we tested if there is a link between cellular lactate metabolism and autophagy in differentiated C2C12 myotubes and the gastrocnemius muscle of male wistar rats. C2C12 mouse skeletal muscle was exposed to 2, 6, 10, and 20 mM lactate and evaluated for lactate autophagic effects. Lactate dose-dependently increased autophagy and augmented ROS generation in differentiated C2C12 myotubes. The autophagic effect of lactate deterred in N-acetylcysteine presence (NAC, a ROS scavenger) indicated lactate regulates autophagy with ROS participation. Lactate-induced up-regulation of extracellular signal-regulated kinase 1/2 (ERK1/2) through ROS was required to regulate the autophagy by lactate. Further analysis about ERK1/2 up- and downstream indicated that lactate regulates autophagy through ROS-mediated the activation of ERK1/2/mTOR/p70S6K pathway in skeletal muscle. The in vitro effects of lactate on autophagy also occurred in the gastrocnemius muscle of male Wistar rats. In conclusion, we provided the lactate-associated regulation evidence of autophagy in skeletal muscle by activating ROS-mediated ERK1/2/mTOR/p70S6K pathway. Since the increase in cellular lactate concentration is a hallmark of energy deficiency, the results provide insight into a skeletal muscle mechanism to fulfill its enhanced energy requirement. © 2021, The International CCN Society

Endurance training and MitoQ supplementation increase PERM1 and SMYD1 gene expression and improve hemodynamic function in cardiac muscle of male Wistar rats

Background:The histone methyltransferase (SMYD1) and the muscle-specific protein (PERM1) play an important role in maintaining cardiac energetics and function. The present study aimed to examine the effect of two types of endurance training (running and swimming) plus MitoQ supplementation on gene expression of PERM1 and SMYD1 plus hemodynamic function in the cardiac muscle of male Wistar rats.Methods: The animals underwent MitoQ supplementation or endurance training or endurance training + MitoQ supplementation for eight weeks. Gene expression of PERM1 and SMYD1, measured by Real Time-PCR and quantified by 2-∆∆CT method, and hemodynamic function were compared between groups using two-way multivariate analysis of variance. Results: Cardiac gene expression of PERM1 and SMYD1 increased significantly through running (PERM1, P < 0.05; SMYD1, P < 0.01), swimming (PERM1, P < 0.05; SMYD1, P < 0.05). and MitoQ supplementation (PERM1, P < 0.001). The effects of MitoQ supplementation were additive to both running and swimming effects on cardiac gene expression of (PERM1, P < 0.001; SMYD1, P < 0.05). Swimming-induced enhancement in cardiac expression of PERM1 and SMYD1 was associated with a significant increase in ±dP/dt max (P < 0.05)). Conclusion: Expression of genes involved in cardiac metabolism can be affected by endurance training and this effect could be improved through MitoQ supplementatio

Resistance training-induced muscle hypertrophy is mediated by TGF-β1-Smad signaling pathway in male Wistar rats

The TGF-β1-Smad pathway is a well-known negative regulator of muscle growth; however, its potential role in resistance training-induced muscle hypertrophy is not clear. The present study proposed to determine whether and how this pathway may be involved in resistance training-induced muscle hypertrophy. Skeletal muscle samples were collected from the control, trained (RT), control + SB431542 (CITGF), and trained + SB431542 (RTITGF) animals following 3, 5, and 8 weeks of resistance training. Inhibition of the TGF-β1-Smad pathway by SB431542 augmented muscle satellite cells activation, upregulated Akt/mTOR/S6K1 pathway, and attenuated FOXO1 and FOXO3a expression in the CITGF group (all p &lt;.01), thereby causing significant muscle hypertrophy in animals from the CITGF. Resistance training significantly decreased muscle TGF-β1 expression and Smad3 (P-Smad3S423/425) phosphorylation at COOH-terminal residues, augmented Smad2 (P-Smad2-LS245/250/255) and Smad3 (P-Smad3-LSer208) phosphorylation levels at linker sites (all p &lt;.01), and led to a muscle hypertrophy which was unaffected by SB431542, suggesting that the TGF-β1-Smad signaling pathway is involved in resistance training-induced muscle hypertrophy. The effects of inhibiting the TGF-β1-Smad signaling pathway were not additive to the resistance training effects on FOXO1 and FOXO3a expression, muscle satellite cells activation, and the Akt/mTOR/S6K1 pathway. Resistance training effect of satellite cell differentiation was independent of the TGF-β1-Smad signaling pathway. These results suggested that the effect of the TGF-β1-Smad signaling pathway on resistance training-induced muscle hypertrophy can be attributed mainly to its diminished inhibitory effects on satellite cell activation and protein synthesis. Suppressed P-Smad3S423/425 and enhanced P-Smad2-LS245/250/255 and P-Smad3-LSer208 are the molecular mechanisms that link the TGF-β1-Smad signaling pathway to resistance training-induced muscle hypertrophy. © 2020 Wiley Periodicals, Inc