Slow-twitch Muscle Research Articles

Nicotinamide Phosphoribosyltransferase-elevated NAD+ biosynthesis prevents muscle disuse atrophy by reversing mitochondrial dysfunction.

It is well known that muscle disuse atrophy is associated with mitochondrial dysfunction, which is implicated in reduced nicotinamide adenine dinucleotide (NAD+ ) levels. Nicotinamide phosphoribosyltransferase (NAMPT), a rate-limiting enzyme in NAD+ biosynthesis, may serve as a novel strategy to treat muscle disuse atrophy by reversing mitochondrial dysfunction. To investigate the effects of NAMPT on the prevention of disuse atrophy of skeletal muscles predominantly composed of slow-twitch (type I) or fast-twitch (type II) fibres, rabbit models of rotator cuff tear-induced supraspinatus muscle atrophy and anterior cruciate ligament (ACL) transection-induced extensor digitorum longus (EDL) atrophy were established and then administered NAMPT therapy. Muscle mass, fibre cross-sectional area (CSA), fibre type, fatty infiltration, western blot, and mitochondrial function were assayed to analyse the effects and molecular mechanisms of NAMPT in preventing muscle disuse atrophy. Acute disuse of the supraspinatus muscle exhibited significant loss of mass (8.86±0.25 to 5.10±0.79g; P<0.001) and decreased fibre CSA (3939.6±136.1 to 2773.4±217.6μm2 , P<0.001), which were reversed by NAMPT (muscle mass 6.17±0.54g, P=0.0033; fibre CSA, 3219.8±289.4μm2 , P=0.0018). Disuse-induced impairment of mitochondrial function were significantly improved by NAMPT, including citrate synthase activity (40.8±6.3 to 50.5±5.6nmol/min/mg, P=0.0043), and NAD+ biosynthesis (279.9±48.7 to 392.2±43.2pmol/mg, P=0.0023). Western blot revealed that NAMPT increases NAD+ levels by activating NAMPT-dependent NAD+ salvage synthesis pathway. In supraspinatus muscle atrophy due to chronic disuse, a combination of NAMPT injection and repair surgery was more effective than repair in reversing muscle atrophy. Although the predominant composition of EDL muscle is fast-twitch (type II) fibre type that differ from supraspinatus muscle, its mitochondrial function and NAD+ levels are also susceptible to disuse. Similar to the supraspinatus muscle, NAMPT-elevated NAD+ biosynthesis was also efficient in preventing EDL disuse atrophy by reversing mitochondrial dysfunction. NAMPT-elevated NAD+ biosynthesis can prevent disuse atrophy of skeletal muscles that predominantly composed with either slow-twitch (type I) or fast-twitch (type II) fibres by reversing mitochondrial dysfunction.

Diversity and Differential Expression of MicroRNAs in the Human Skeletal Muscle with Distinct Fiber Type Composition.

The ratio of fast- and slow-twitch fibers in human skeletal muscle is variable and largely determined by genetic factors. In this study, we investigated the contribution of microRNA (miRNA) in skeletal muscle fiber type composition. The study involved biopsy samples of the vastus lateralis muscle from 24 male participants with distinct fiber type ratios. The miRNA study included samples from five endurance athletes and five power athletes with the predominance of slow-twitch (61.6-72.8%) and fast-twitch (69.3-80.7%) fibers, respectively. Total and small RNA were extracted from tissue samples. Total RNA sequencing (N = 24) revealed 352 differentially expressed genes between the groups with the predominance of fast- and slow-twitch muscle fibers. Small RNA sequencing showed upregulation of miR-206, miR-501-3p and miR-185-5p, and downregulation of miR-499a-5p and miR-208-5p in the group of power athletes with fast-twitch fiber predominance. Two miRtronic miRNAs, miR-208b-3p and miR-499a-5p, had strong correlations in expression with their host genes (MYH7 and MYH7B, respectively). Correlations between the expression of miRNAs and their experimentally validated messenger RNA (mRNA) targets were calculated, and 11 miRNA-mRNA interactions with strong negative correlations were identified. Two of them belonged to miR-208b-3p and miR-499a-5p, indicating their regulatory links with the expression of CDKN1A and FOXO4, respectively.

Sarcoplasmic Reticulum Ca2+ Buffer Proteins: A Focus on the Yet-To-Be-Explored Role of Sarcalumenin in Skeletal Muscle Health and Disease.

Sarcalumenin (SAR) is a luminal Ca2+ buffer protein with high capacity but low affinity for calcium binding found predominantly in the longitudinal sarcoplasmic reticulum (SR) of fast- and slow-twitch skeletal muscles and the heart. Together with other luminal Ca2+ buffer proteins, SAR plays a critical role in modulation of Ca2+ uptake and Ca2+ release during excitation-contraction coupling in muscle fibers. SAR appears to be important in a wide range of other physiological functions, such as Sarco-Endoplasmic Reticulum Calcium ATPase (SERCA) stabilization, Store-Operated-Calcium-Entry (SOCE) mechanisms, muscle fatigue resistance and muscle development. The function and structural features of SAR are very similar to those of calsequestrin (CSQ), the most abundant and well-characterized Ca2+ buffer protein of junctional SR. Despite the structural and functional similarity, very few targeted studies are available in the literature. The present review provides an overview of the role of SAR in skeletal muscle physiology, as well as of its possible involvement and dysfunction in muscle wasting disorders, in order to summarize the current knowledge on SAR and drive attention to this important but still underinvestigated/neglected protein.

Impacts of thermal acclimatization on fish skeletal muscle

Thermal acclimation allows ectotherms to maintain physiological homeostasis while occupying habitats with constantly changing temperatures. This process is especially important in skeletal muscle which powers most movements necessary for life. We aimed to understand how fish skeletal muscle is impacted by acclimatization in the laboratory. To accomplish this, we compared muscle contraction kinetics of four-week lab acclimatized fish (at 20 °C) to fish taken directly from the field when sea surface temperatures were similar to lab treatment temperature (ocean temperature ranged from 17.7 to 19.9 °C in the four weeks prior to collection at 20 °C). To examine these effects, we chose to study tautog (Tautoga onitis) and cunner (Tautogolabrus adspersus) from Long Island Sound. We found that timing of contraction kinetics in cunner and tautog did not differ from the lab acclimatized and field acclimatized groups. However, lab acclimatized cunner produced greater contraction force than fish taken directly from the field. This increased force production allowed lab acclimatized cunner to produce greater power when compared to cunner from the field treatment. Furthermore, laboratory acclimatized cunner did not express any slow myosin heavy chain, suggesting that their muscle had transitioned to mostly fast twitch fibers after being held at a constant temperature in the lab. None of these effects were seen in tautog. In this work we highlight the importance of considering the impacts laboratory conditions have on experimental conditions.

Differences in protein expression, at the basal state and at 2h of insulin infusion, in muscle biopsies from healthy Arab men with high or low insulin sensitivity measured by hyperinsulinemic euglycemic clamp.

Skeletal muscle is the main site for insulin-dependent glucose disposal. The hyperinsulinemic euglycemic clamp (HIEC) is the gold standard for the assessment of insulin sensitivity (IS). We have previously shown that insulin sensitivity, measured by HIEC, varied widely among a group of 60 young healthy men with normoglycemia. The aim of this study was to correlate the proteomic profile of skeletal muscles to insulin sensitivity. Muscle biopsies from 16 subjects having the highest (M ≥ 13; n = 8, HIS) and lowest (M ¾ 6, n = 8, LIS) IS were obtained at baseline and during insulin infusion after stabilization of the blood glucose level and glucose infusion rate at the end of the HIEC. The samples were processed using a quantitative proteomic analysis approach. At baseline, 924 proteins were identified in the HIS and LIS groups. Among the 924 proteins detected in both groups, three were suppressed and three were increased significantly in the LIS subjects compared with the HIS subjects. Following insulin infusion, 835 proteins were detected in both groups. Among the 835 proteins, two showed differential responsiveness to insulin; ATP5F1 protein was decreased, and MYLK2 was higher in the LIS group compared with that in the HIS group. Our data suggest that alteration in mitochondrial proteins and an increased number of proteins involved in fast-twitch fiber correlate to insulin sensitivity in healthy young Arab men. These results suggest a change in a small number of differentially expressed proteins. A possible reason for this small change could be our study cohorts representing a homogeneous and healthy population. Additionally, we show differences in protein levels from skeletal muscle in low and high insulin sensitivity groups. Therefore, these differences may represent early events for the development of insulin resistance, pre-diabetes, and type 2 diabetes.

Muscle length alters activation kinetics in fast-twitch edl muscle and relaxation kinetics in slow-twitch soleus muscle.

Mammalian skeletal muscles typically comprise mixtures of slow and fast-twitch fiber types. By studying muscles that homogenously express fast-twitch (EDL) and slow-twitch soleus (SOL) fibers, we can compare the activation and relaxation kinetics in fast and slow muscle fibers in intact and permeabilized muscle preparations at different sarcomere lengths (SL). Intact EDL muscle at optimal length (L0) had significantly longer times (p<0.05) to 50% (½ time) activation at 38.02 ± 2.26 ms (t1/2ACT), compared to 95% L0 and 90% L0 (33.65±1.86 and 31.31±1.61 respectfully). There were, however, no significant differences in activation ½ times of intact SOL muscle as muscle length increases. The relaxation ½ times are indistinguishable for intact EDL muscle at different muscle lengths, while the relaxation ½ times for intact SOL muscle increased as the muscle lengthen increased. To deconvolute the contribution of calcium transients and intrinsic myofilament kinetics to the length dependent activation and relaxation kinetics seen in intact muscle, we next investigate the kinetics of skinned myofibrils at different sarcomere lengths. Rate constant values for initial myofibril activation for EDL preparations showed significant (p<0.05) length dependence, decreasing from 7.25±0.47 s−1 to 5.97±0.44 s−1, 4.99±0.477 s−1, and 3.98±0.41 s−1 at 2.2, 2.5, 2.75, and 2.90 µm respectively). In contrast, SOL myofibrils had minimal length dependence, with no significant changes in activation rate constants. Fast relaxation rates for soleus muscle increased from 11.51±0.91 s−1 to 13.26±0.86 s−1, 15.13±0.99 s−1, and 16.34±1.02 s−1 (at 2.2, 2.5, 2.75, and 2.90 μm respectively) while EDL preparations showed no change. The results suggest that activation kinetics in EDL muscle and relaxation kinetics in SOL are length dependent and are intrinsic properties of the myofilaments.

Thin filament regulation of striated muscle power output: implications for targets to improve failing human hearts.

The heart's pumping capacity is determined by myofilament power generation. Power is work done per unit time and measured as the product of force and velocity. At a sarcomere level, these contractile properties are linked to the number of attached cross-bridges and their cycling rate; and many signaling pathways modulate one or both of these factors. We previously showed that rodent permeabilized cardiac myocyte power is increased following PKA-mediated phosphorylation of myofibrillar proteins (Herron, Korte, McDonald, Circ. Res. 2001). This increase in power demonstrates a capacity for improved myofilament function and this therapeutic potential adds significance for identification of the molecular specificity underlying enhanced power output. To address molecular specificity at the thin filament level, myofilament mechanical properties were measured before and after exchange of endogenous troponin with recombinant human Tn complex, which contained cardiac (c)TnT, cTnC and either WT cTnI or pseudo-phosphorylated cTnI at sites Ser23/24Asp, Y26E, or the combinatorial Ser23/24Asp and Y26E in single permeabilized rat slow-twitch skeletal muscle fibers. We found that cTnI Ser23/24Asp, Y26E, and combinatorial Ser23/24Asp and Y26E were sufficient for a ∼20% increase in power. We then tested the power reserve capacity in myofilaments from failing human hearts. We found that PKA increased power by ∼35% in permeabilized cardiac myocyte preparations from human failing hearts. Next, we determined if pseudo-phosphorylated cTnI at Ser23/24 was sufficient to increase power in cardiac myocytes from human failing hearts. Following cTn exchange that included cTnI Ser23/24Asp, power output increased ∼20% in permeabilized cardiac myocyte preparations from the left ventricle of human failing hearts. These results implicate cTnI N-terminal phosphorylation is a molecular regulator of myocyte power and could serve as a target to augment myocyte power reserve capacity in failing human hearts.

High-intensity interval training using electrical stimulation improves mitochondrial dysfunction and muscle endurance in rats with chronic kidney disease.

Mitochondrial dysfunction in skeletal muscle has recently been highlighted as a major pathophysiological factor of chronic kidney disease (CKD)-associated muscle fatigue. However, effective therapeutic interventions to improve mitochondrial function have not been established. Here we examined the effects of high-intensity interval training (HIIT) using electrical stimulation (ES) intervention on skeletal muscle in CKD rats. CKD was induced by 5/6 nephrectomy (Nx) in male Wistar rats, and sham-operated rats served as controls (Sham). We defined the left leg of Nx rat trained with HIIT as the Nx-HIIT leg and the untrained right leg as the Nx-CNT leg. HIIT was enforced by electrically stimulating plantar flexor muscles every other day for 4 weeks. In vivo muscle endurance analysis using repeated fatiguing stimulation measured 24 h after the last training session showed a significantly greater force depression in the Nx-CNT leg compared to that in the Sham leg, which was significantly improved in the Nx-HIIT leg. Pyruvate/malate-driven ADP- and uncoupler-stimulated mitochondrial respiration in isolated muscle mitochondria from the Nx-CNT leg assessed by Seahorse XFe96 analyzer were significantly decreased compared with those from the Sham leg, which were also significantly recovered in those of the Nx-HIIT leg. Consistent with improved mitochondrial function, myosin heavy chain (MyHC) electrophoresis showed a significant increase in the proportion of fast-twitch MyHC IIB fibers in the Nx-CNT leg compared to that in the Sham and the Nx-HIIT leg. HIIT with ES improved muscle fatigue and mitochondrial function in a rat model of CKD-associated cachexia. HIIT with ES may lead to an innovative therapeutic intervention that can be utilized for patients with CKD-associated cachexia who have difficulty with full-body exercise.

Garcinol Promotes the Formation of Slow-Twitch Muscle Fibers by Inhibiting p300-Dependent Acetylation of PGC-1α.

The conversion of skeletal muscle fiber from fast-twitch to slow-twitch is crucial for sustained contractile and stretchable events, energy homeostasis, and anti-fatigue ability. The purpose of our study was to explore the mechanism and effects of garcinol on the regulation of skeletal muscle fiber type transformation. Forty 21-day-old male C57/BL6J mice (n = 10/diet) were fed a control diet or a control diet plus garcinol at 100 mg/kg (Low Gar), 300 mg/kg (Mid Gar), or 500 mg/kg (High Gar) for 12 weeks. The tibialis anterior (TA) and soleus muscles were collected for protein and immunoprecipitation analyses. Dietary garcinol significantly downregulated (p < 0.05) fast myosin heavy chain (MyHC) expression and upregulated (p < 0.05) slow MyHC expression in the TA and soleus muscles. Garcinol significantly increased (p < 0.05) the activity of peroxisome proliferator-activated receptor gamma co-activator 1α (PGC-1α) and markedly decreased (p < 0.05) the acetylation of PGC-1α. In vitro and in vivo experiments showed that garcinol decreased (p < 0.05) lactate dehydrogenase activity and increased (p < 0.05) the activities of malate dehydrogenase and succinic dehydrogenase. In addition, the results of C2C12 myotubes showed that garcinol treatment increased (p < 0.05) the transformation of glycolytic muscle fiber to oxidative muscle fiber by 45.9%. Garcinol treatment and p300 interference reduced (p < 0.05) the expression of fast MyHC but increased (p < 0.05) the expression of slow MyHC in vitro. Moreover, the acetylation of PGC-1α was significantly decreased (p < 0.05). Garcinol promotes the transformation of skeletal muscle fibers from the fast-glycolytic type to the slow-oxidative type through the p300/PGC-1α signaling pathway in C2C12 myotubes.

Effects of Resistance Exercise on Slow-Twitch Soleus Muscle of Infarcted Rats.

Three months after MI induction, male Wistar rats were assigned to Sham (n = 14), MI (n = 9), and resistance exercised MI (R-MI, n = 13) groups. The rats trained three times a week for 12 weeks on a climbing ladder. An echocardiogram was performed before and after training. Protein expression of the insulin-like growth factor (IGF)-1/protein kinase B (Akt)/rapamycin target complex (mTOR) pathway was analyzed by Western blot. Mortality rate was higher in MI than Sham; in the R-MI group, mortality rate was between that in MI and Sham and did not differ significantly from either group. Exercise increased maximal load capacity without changing cardiac structure and left ventricular function in infarcted rats. Infarction size did not differ between infarcted groups. Catalase activity was lower in MI than Sham and glutathione peroxidase lower in MI than Sham and R-MI. Protein expression of p70S6K was lower in MI than Sham and p-FoxO3 was lower in MI than Sham and R-MI. Energy metabolism did not differ between groups, except for higher phosphofrutokinase activity in R-MI than MI. Resistance exercise is safe and increases muscle strength regardless structural and functional cardiac changes in myocardial-infarcted rats. This exercise modality attenuates soleus glycolytic metabolism changes and improves the expression of proteins required for protein turnover and antioxidant response.

LSD1 defines the fiber type-selective responsiveness to environmental stress in skeletal muscle.

Skeletal muscle exhibits remarkable plasticity in response to environmental cues, with stress-dependent effects on the fast-twitch and slow-twitch fibers. Although stress-induced gene expression underlies environmental adaptation, it is unclear how transcriptional and epigenetic factors regulate fiber type-specific responses in the muscle. Here, we show that flavin-dependent lysine-specific demethylase-1 (LSD1) differentially controls responses to glucocorticoid and exercise in postnatal skeletal muscle. Using skeletal muscle-specific LSD1-knockout mice and in vitro approaches, we found that LSD1 loss exacerbated glucocorticoid-induced atrophy in the fast fiber-dominant muscles, with reduced nuclear retention of Foxk1, an anti-autophagic transcription factor. Furthermore, LSD1 depletion enhanced endurance exercise-induced hypertrophy in the slow fiber-dominant muscles, by induced expression of ERRγ, a transcription factor that promotes oxidative metabolism genes. Thus, LSD1 serves as an 'epigenetic barrier' that optimizes fiber type-specific responses and muscle mass under the stress conditions. Our results uncover that LSD1 modulators provide emerging therapeutic and preventive strategies against stress-induced myopathies such as sarcopenia, cachexia, and disuse atrophy.

Sarcopenia phenotype and impaired muscle function in male mice with fast-twitch muscle-specific knockout of the androgen receptor

Sarcopenia is distinct from normal muscle atrophy in that it is closely related to a shift in the muscle fiber type. Deficiency of the anabolic action of androgen on skeletal muscles is associated with sarcopenia; however, the function of the androgen receptor (AR) pathway in sarcopenia remains poorly understood. We generated a mouse model (fast-twitch muscle-specific AR knockout [fmARKO] mice) in which the AR was selectively deleted in the fast-twitch muscle fibers. In young male mice, the deletion caused no change in muscle mass, but it reduced muscle strength and fatigue resistance and induced a shift in the soleus muscles from fast-twitch fibers to slow-twitch fibers (14% increase, P = 0.02). After middle age, with the control mice, the male fmARKO mice showed much less muscle function, accompanied by lower hindlimb muscle mass; this phenotype was similar to the progression of sarcopenia. The bone mineral density of the femur was significantly reduced in the fmARKO mice, indicating possible osteosarcopenia. Microarray and gene ontology analyses revealed that in male fmARKO mice, there was downregulation of polyamine biosynthesis-related geneswhich was confirmed by liquid chromatography-tandem mass spectrometry assay and the primary cultured myofibers. None of the AR deletion-related phenotypes were observed in female fmARKO mice. Our findings showed that the AR pathway had essential muscle type- and sex-specific roles in the differentiation toward fast-twitch fibers and in the maintenance of muscle composition and function. The AR in fast-twitch muscles was the dominant regulator of muscle fiber-type composition and muscle function, including the muscle-bone relationship.

Parvalbumin: A Major Fish Allergen and a Forensically Relevant Marker.

Parvalbumins (PVALBs) are low molecular weight calcium-binding proteins. In addition to their role in many biological processes, PVALBs play an important role in regulating Ca2+ switching in muscles with fast-twitch fibres in addition to their role in many biological processes. The PVALB gene family is divided into two gene types, alpha (α) and beta (β), with the β gene further divided into two gene types, beta1 (β1) and beta2 (β2), carrying traces of whole genome duplication. A large variety of commonly consumed fish species contain PVALB proteins which are known to cause fish allergies. More than 95% of all fish-induced food allergies are caused by PVALB proteins. The authentication of fish species has become increasingly important as the seafood industry continues to grow and the growth brings with it many cases of food fraud. Since the PVALB gene plays an important role in the initiation of allergic reactions, it has been used for decades to develop alternate assays for fish identification. A brief review of the significance of the fish PVALB genes is presented in this article, which covers evolutionary diversity, allergic properties, and potential use as a forensic marker.

LncRNA-TBP mediates TATA-binding protein recruitment to regulate myogenesis and induce slow-twitch myofibers

BackgroundSkeletal muscle is comprised of heterogeneous myofibers that differ in their physiological and metabolic parameters. Of these, slow-twitch (type I; oxidative) myofibers have more myoglobin, more mitochondria, and higher activity of oxidative metabolic enzymes compared to fast-twitch (type II; glycolytic) myofibers.MethodsIn our previous study, we found a novel LncRNA-TBP (for “LncRNA directly binds TBP transcription factor”) is specifically enriched in the soleus (which has a higher proportion of slow myofibers). The primary myoblast cells and animal model were used to assess the biological function of the LncRNA-TBP in vitro or in vivo. Meanwhile, we performed a RNA immunoprecipitation (RIP) and pull-down analysis to validate this interaction between LncRNA-TBP and TBP.ResultsFunctional studies demonstrated that LncRNA-TBP inhibits myoblast proliferation but promotes myogenic differentiation in vitro. In vivo, LncRNA-TBP reduces fat deposition, activating slow-twitch muscle phenotype and inducing muscle hypertrophy. Mechanistically, LncRNA-TBP acts as a regulatory RNA that directly interacts with TBP protein to regulate the transcriptional activity of TBP-target genes (such as KLF4, GPI, TNNI2, and CDKN1A).ConclusionOur findings present a novel model about the regulation of LncRNA-TBP, which can regulate the transcriptional activity of TBP-target genes by recruiting TBP protein, thus modulating myogenesis progression and inducing slow-twitch fibers.-DFPHBQnDUMKtGyF_FPyKxVideo

Endurance training changes the expression of miR-1 and miR-133 and predicted genes in slow and fast twitch muscles

Purpose of the researchEndurance training can modify signaling and gene expression pathways that play a pivotal role in determining the phenotype of the fibers. The present study aimed to investigate the effects of endurance training on the expression of some myomiRs and related genes in slow and fast twitch muscles. MethodsTwenty healthy male adult Wistar rats (281 ± 14 g) were randomized to either control (n = 10) or treated (n = 10). The treated group performed an endurance program for eight weeks (running on a treadmill for eight weeks, 50 min, 23 m/min). After the end of the training protocol, the slow (soleus) and fast (EDL) twitch muscles were removed to assess the miR-1, miR-133 expression, and hdac4, mef2c genes, and protein by real-time PCR and western blot, respectively. ResultsThe soleus muscle miR-1 expression and mef2c gene in the treated group were significantly lower compared control (p = 0.0001). In contrast, miR-133 and hdac4 gene expression of the soleus muscle of the treated group increased significantly (p = 0001), and the EDL miR-133 and mef2c expression of the treated group increased in the compared control group (p = 0.0001). The EDL MEF2c protein expression in the treated group significantly decreased compared to the control group, although the expression of EDL HDAC4 protein significantly increased (p = 0.0001). ConclusionsEndurance training changes the expression of the miR-1, miR-133, and their predicted genes in slow and fast twitch muscles. Also, the rate of HDAC4 and MEF2c protein synthesis, which are upstream and downstream of these myomiRs, was affected by endurance training.

Tissue Distribution of mtDNA Copy Number And Expression Pattern of An mtDNA-Related Gene in Three Teleost Fish Species.

Teleosts are the most speciose vertebrates and have diverse swimming performance. Based on swimming duration and speed, teleosts are broadly divided into sustained, prolonged, and burst swimming fish. Teleosts with different swimming performance have different energy requirements. In addition, energy requirement also varies among different tissues. As mitochondrial DNA (mtDNA) copy number is correlated with ATP production, we speculated that mtDNA copy number varies among fish with different swimming performance, as well as among different tissues. In other species, mtDNA copy number is regulated by tfam (mitochondrial transcription factor A) through mtDNA compaction and mito-genome replication initiation. In order to clarify the tissue distribution of mtDNA copy number and expression pattern of tfam in teleosts with disparate swimming performance, we selected representative fish with sustained swimming (Pseudocaranx dentex), prolonged swimming (Takifugu rubripes), and burst swimming (Paralichthys olivaceus). We measured mtDNA copy number and tfam gene expression in 10 tissues of these three fish. The results showed the mtDNA content pattern of various tissues was broadly consistent among three fish, and high-energy demanding tissues contain higher mtDNA copy number. Slow-twitch muscles with higher oxidative metabolism possess a greater content of mtDNA than fast-twitch muscles. In addition, relatively higher mtDNA content in fast-twitch muscle of P. olivaceus compared to the other two fish could be an adaptation to their frequent burst swimming demands. And the higher mtDNA copy number in heart of P. dentex could meet their oxygen transport demands of long-distance swimming. However, tfam expression was not significantly correlated with mtDNA copy number in these teleosts, suggesting tfam may be not the only factor regulating mtDNA content among various tissues. This study can lay a foundation for studying the role of mtDNA in the adaptive evolution of various swimming ability in teleost fish.

Muscle architecture a new dimension of talent identification: A mini review

Talent Identification in the field of exercise science is growing exponentially, where muscle is considered as most reliable method for determining muscle fiber type and selecting sports activity accordingly. Muscle architecture a new fiber type determination technique is now in trend, which refers to the macroscopic arrangement of muscle fibres that influences a muscle's mechanical function. Previous research has shown a relationship between muscle architecture (such as fascicle length, muscle thickness, and pennation angle) and muscle fibre types (e.g. slow twitch fibres and fast twitch fibers). This small review attempts to briefly discuss how muscle architecture has been investigated in the realm of sport/exercise performance, as well as how various muscle fibre types have varied muscle architecture characteristics.

A comparative study of vertical jump parameters in men's college basketball and volleyball players

This study aimed to compare lower limb strength disparities between male college volleyball and basketball players in four distinct vertical jump types. We recruited 100 second-level (above the national standard) male college athletes (50 basketball and 50 volleyball players) from Capital University of Physical Education and Sports who volunteered to participate. We assessed the performance of each athlete with regards to the squat jump (SJ), countermovement jump (CMJ), continuous jump with straight legs (CJs), and continuous jump with bent legs (CJb). Data analysis was performed by independent samples t-tests in SPSS version 25.0. software. In the CMJ test, volleyball players had a significantly higher vertical jump displacement (VJD; p = 0.047, t = −2.018), squat displacement (SD; p = 0.005, t = −2.883), peak force (p = 0.023, t = −1.964), and peak velocity (p = 0.011, t = −1.687) than basketball players. In the SJ test, volleyball players had a significantly higher VJD (p = 0.041, t = −1.21) and SD (p = 0.008, t = −1.46) than basketball players. In the CJs test, volleyball players had a significantly higher average vertical jump displacement (AVJD; p = 0.042, t = −2.067) than basketball players. In the CJb test, volleyball players had a significantly higher AVJD (p = 0.001, t = −3.448), average squat displacement (p = 0.017, t = −2.44), and average contact time (p = 0.045, t = −2.038) than basketball players. The overall vertical jump ability of college volleyball players was better than that of college basketball players. CMJ, SJ, CJs and CJb training should be included in daily training sessions and considered in the selection of basketball and volleyball players. In addition, coaches can use fast twitch Fibers, the effect of pre-stretch and k as the main evaluation indicators to assess daily training progress.

Possibility of uncoupling protein 1 expression in bovine fast-twitch muscle fibers.

Uncoupling protein 1 (UCP1) is responsible for non-shivering thermogenesis in brown/beige adipocytes in humans and rodents. Previously, we showed unexpected expression of UCP1 in bovine skeletal muscles. Here we evaluated Ucp1 mRNA levels in the muscle tissue of Japanese Black steers. Expression of Ucp1 was higher in 30-month-old cattle than in 26-month-old cattle. Levels of myosin heavy chain (Myh)1, an MYH predominantly expressed in fast-twitch muscles, were also significantly higher in cattle aged 30 months. A similar tendency was observed in the expression of other Myhs that are highly expressed in fast-twitch muscles, Myh2 and Myh4. Ucp1 expression was positively correlated with expression of Myh1, Myh2, and Myh4. Our results indicate the possibility of Ucp1 expression in fast-twitch muscle fibers.

Influence of Different Obstetric Factors on Early Postpartum Pelvic Floor Function in Primiparas After Vaginal Delivery.

This study sought to explore the obstetric factors affecting early postpartum pelvic floor function of primiparas after vaginal delivery. We included 3362 primiparas who underwent postpartum re-examination in International Peace Maternity and Child Health Hospital at 42-60 days after delivery. The Glazer Protocol was used to evaluate their pelvic floor function, and univariate and multivariate logistic regression analyses were performed to identify obstetric factors that might affect it. Forceps-assisted delivery significantly increased the risk of the decline in fast- and slow-twitch muscle strength in the early postpartum period when compared with natural vaginal delivery (P < 0.05). Women with a pre-pregnancy body mass index (BMI) of ≥18.5 kg/m2 had a decreased risk of decline in fast-twitch muscle strength than those with a pre-pregnancy BMI of <18.5 kg/m2 (P < 0.05). Women who had a pre-pregnancy BMI of 24.0 to <28.0 kg/m2 bore a decreased risk of decline in slow-twitch muscle strength than those with a pre-pregnancy BMI of <18.5 kg/m2 (P < 0.05). The risk of decline in fast-twitch muscle strength and slow-twitch muscle in women with anemia during pregnancy was significantly increased (P < 0.05); women with second-stage labors of >2 h had an increased risk of fast-twitch and slow-twitch muscle strength decline than those with <2 h (P < 0.05). Both pre-pregnancy underweight and obesity may cause impairment of early postpartum pelvic floor function. Forceps delivery, anemia during pregnancy, and the length of second stage of labor are independent factors leading to pelvic floor function impairment.