Fast Muscle Fibers Research Articles

Passive static stretching alters the characteristics of the force-velocity curvature differently for fast and slow muscle groups-A practical application of Hill's equation.

Studies showed fast muscle fibers have a greater constant b value of Hill's equation than that of slow muscle fibers, and the changing ratio of b/Vmax indicates the altered characteristics of muscles under certain conditions such as static stretching. This study was to investigate the effect of acute passive static stretching on the curvature of force-velocity curve in people with different muscle fiber types. A two-step work was conducted in current study through using Hill's equation: 1) calculated b values for each subject at different conditions (non-stretched and stretched) to determine muscle groups, and 2) examined the effect of static stretching on different muscle groups. Sixty-five college students performed isokinetic leg extensions at 5 speeds to test peak torque, following either a non-stretching or two passive static quadriceps stretching exercises. The peak torque and corresponding velocity were used to calculate the b constant. Data reduction consisted of calculating a Z score for each non-stretched and stretched b values. Individuals, whose non-stretched b constant was above or below one standard deviation of the Z score, were designated as the less curved (fast) and more curved (slow) groups, respectively. A paired t-test was used to analyze the pre and post intervention effect on b values for each group (p<0.05). This study found passive static stretching significantly altered the b constant of the fast group, but no effect on slow group. Therefore, we suggest static stretching should be avoided immediately before fast or explosive activities in individuals using predominantly fast muscle fibers.

Prolonged caloric restriction ameliorates age-related atrophy in slow and fast muscle fibers of rat soleus muscle.

Aging causes loss of skeletal muscle mass and function, which is called sarcopenia. While sarcopenia impairs the quality of life of older adults and is a major factor in long-term hospitalization, its detailed pathogenic mechanism and preventive measures remain to be identified. Caloric restriction (CR) suppresses age-related physiological and pathological changes in many species and prolongs the average and healthy life expectancy. It has recently been reported that CR suppresses the onset of sarcopenia; however, few studies have analyzed the effects of long-term CR on age-related skeletal muscle atrophy. Thus, we investigated the aging and CR effects on soleus (SOL) muscles of 9-, 24-, and 29-month-old ad libitum-fed rats (9AL, 24AL, and 29AL, respectively) and of 29-month-old CR (29CR) rats. The total muscle cross sectional area (mCSA) of the entire SOL muscle significantly decreased in the 29AL rats, but not in the 24AL rats, compared with the 9AL rats. SOL muscle of the 29AL rats exhibited marked muscle fiber atrophy and increases in the number of muscle fibers with a central nucleus, in fibrosis, and in adipocyte infiltration. Additionally, although the decrease in the single muscle fiber cross-sectional area (fCSA) and the muscle fibers' number occurred in both slow-type and fast-type muscle fibers, the degree of atrophy was more remarkable in the fast-type fibers. However, CR suppressed the muscle fiber atrophy observed in the 29AL rats' SOL muscle by preserving the mCSA and the number of muscle fibers that declined with aging, and by decreasing the number of muscle fibers with a central nucleus, fibrosis and denervated muscle fibers. Overall, these results revealed that advanced aging separately reduces the number and fCSA of each muscle fiber type, but long-term CR can ameliorate this age-related sarcopenic muscle atrophy.

What's all the hype with fibre type? Selective single fibre adaptations with lifelong endurance exercise.

What's all the hype with fibre type? Selective single fibre adaptations with lifelong endurance exercise.

Pim1 knockout alleviates sarcopenia in aging mice via reducing adipogenic differentiation of PDGFRα+ mesenchymal progenitors.

BackgroundSarcopenia widely exists in elderly people and triggers numerous age‐related events. The essential pathologic change lies in the increased intramuscular adipose tissue after aging with no exception to non‐obese objects. Pim1 appears to be associated with adipogenic differentiation in recent studies, inspiring us to explore whether it regulates adipogenesis in aging muscles and affects sarcopenia.MethodsWild‐type and Pim1 knockout C57/BL6J mice were randomized into young and old groups. Histo‐pathological and molecular biological methods were applied to assess the intramuscular adipose tissue content, the atrophy and regeneration, and the expressions of Pim1 and adipogenic transcription factors. PDGFRα+ mesenchymal progenitors were separated and their replicative aging model were established. Different time of adipogenic induction and different amounts of Pim1 inhibitor were applied, after which the adipogenic potency were evaluated. The expressions of Pim1 and adipogenic transcription factors were measured through western blotting.ResultsThe aging mice demonstrated decreased forelimb grip strength (P = 0.0003), hanging impulse (P < 0.0001), exhaustive running time (P < 0.0001), tetanic force (P = 0.0298), lean mass (P = 0.0008), and percentage of gastrocnemius weight in body weight (P < 0.0001), which were improved by Pim1 knockout (P = 0.0015, P = 0.0222, P < 0.0001, P = 0.0444, P = 0.0004, and P = 0.0003, respectively). To elucidate the mechanisms, analyses showed that Pim1 knockout decreased the fat mass (P = 0.0005) and reduced the intramuscular adipose tissue content (P = 0.0008) by inhibiting the C/EBPδ pathway (P = 0.0067) in aging mice, resulting in increased cross‐sectional area of all and fast muscle fibres (P = 0.0017 and 0.0024 respectively), decreased levels of MuRF 1 and atrogin 1 (P = 0.0001 and 0.0329 respectively), and decreased content of Pax7 at the basal state (P = 0.0055). In vitro, senescent PDGFRα+ mesenchymal progenitors showed significantly increased the intracellular adipose tissue content (OD510) compared with young cells after 6 days of adipogenic induction (P < 0.0001). The Pim1 expression was elevated during adipogenic differentiation, and Pim1 inhibition significantly reduced the OD510 in senescent cells (P = 0.0040) by inhibiting the C/EBPδ pathway (P = 0.0047).ConclusionsPim1 knockout exerted protective effects in sarcopenia by inhibiting the adipogenic differentiation of PDGFRα+ mesenchymal progenitors induced by C/EBPδ activation and thus reducing the intramuscular adipose tissue content in aging mice. These results provide a potential target for the treatment of sarcopenia.

Comparison of Shear Wave Elastography and Dynamometer Test in Muscle Tissue Characterization for Potential Medical and Sport Application.

Skeletal muscle status and its dynamic follow up are of particular importance in the management of several diseases where weight and muscle mass loss and, consequently, immobilization occurs, as in cancer and its treatment, as well as in neurodegenerative disorders. But immobilization is not the direct result of body and muscle mass loss, but rather the loss of the maximal tension capabilities of the skeletal muscle. Therefore, the development of a non-invasive and real-time method which can measure muscle tension capabilities in immobile patients is highly anticipated. Our aim was to introduce and evaluate a special ultrasound measurement technique to estimate a maximal muscle tension characteristic which can be used in medicine and also in sports diagnostics. Therefore, we determined the relationship between the results of shear wave elastography measurements and the dynamometric data of individuals. The measurements were concluded on the m. vastus lateralis. Twelve healthy elite athletes took part in our preliminary proof of principle study—five endurance (S) and seven strength (F) athletes showing unambiguously different muscle composition features, nine healthy subjects (H) without prior sports background, and four cancer patients in treatment for a stage 3 brain tumor (T). Results showed a high correlation between the maximal dynamometric isometric torque (Mmax) and mean elasticity value (E) for the non-athletes [(H + T), (r = 0.795)] and for the athletes [(S + F), (r = 0.79)]. For the athletes (S + F), the rate of tension development at contraction (RTDk) and E correlation was also determined (r = 0.84, p < 0.05). Our measurements showed significantly greater E values for the strength athletes with fast muscle fiber dominance than endurance athletes with slow muscle fiber dominance (p < 0.05). Our findings suggest that shear wave ultrasound elastography is a promising method for estimating maximal muscle tension and, also, the human skeletal muscle fiber ratio. These results warrant further investigations with a larger number of individuals, both in medicine and in sports science.

Single muscle fibre contractile characteristics with lifelong endurance exercise.

A hallmark trait of ageing skeletal muscle health is a reduction in size and function, which is most pronounced in the fast muscle fibres. We studied older men (74±4years) with a history of lifelong (>50years) endurance exercise to examine potential benefits for slow and fast muscle fibre size and contractile function. Lifelong endurance exercisers had slow muscle fibres that were larger, stronger, faster and more powerful than young exercisers (25±1years) and age-matched non-exercisers (75±2years). Limited benefits with lifelong endurance exercise were noted in the fast muscle fibres. These findings suggest that additional exercise modalities (e.g. resistance exercise) or other therapeutic interventions are needed to target fast muscle fibres with age. We investigated single muscle fibre size and contractile function among three groups of men: lifelong exercisers (LLE) (n=21, 74±4years), old healthy non-exercisers (OH) (n=10, 75±2years) and young exercisers (YE) (n=10, 25±1years). On average, LLE had exercised ∼5 daysweek-1 for ∼7 hweek-1 over the past 53±6years. LLE were subdivided based on lifelong exercise intensity into performance (LLE-P) (n=14) and fitness (LLE-F) (n=7). Muscle biopsies (vastus lateralis) were examined for myosin heavy chain (MHC) slow (MHC I) and fast (MHC IIa) fibre size and function (strength, speed, power). LLE MHC I size (7624±2765μm2 ) was 25-40% larger (P<0.001) than YE (6106±1710μm2 ) and OH (5476±2467μm2 ). LLE MHC I fibres were ∼20% stronger, ∼10% faster and ∼30% more powerful than YE and OH (P<0.05). By contrast, LLE MHC IIa size (6466±2659μm2 ) was similar to OH (6237±2525μm2 ; P=0.854), with both groups ∼20% smaller (P<0.001) than YE (7860±1930μm2 ). MHC IIa contractile function was variable across groups, with a hierarchical pattern (OH > LLE > YE; P<0.05) in normalized power among OH (16.7±6.4WL-1 ), LLE (13.9±4.5WL-1 ) and YE (12.4±3.5WL-1 ). The LLE-P and LLE-F had similar single fibre profiles with MHC I power driven by speed (LLE-P) or force (LLE-F), suggesting exercise intensity impacted slow muscle fibre mechanics. These data suggest that lifelong endurance exercise benefited slow muscle fibre size and function. Comparable fast fibre characteristics between LLE and OH, regardless of training intensity, suggest other exercise modes (e.g. resistance training) or myotherapeutics may be necessary to preserve fast muscle fibre size and performance with age.

Skeletal muscle and fiber type-specific intramyocellular lipid accumulation in obese mice.

ABSTRACTIn obesity, accumulation of lipid droplets in skeletal muscle fibers and a shift towards fast muscle fiber types can both contribute to insulin resistance. However, it is not yet clear how intramyocellular lipid accumulation and fiber type changes are associated. Therefore, we investigated to what extent the lipids accumulated in a fiber type-specific manner in the functionally similar fast-, intermediate- and slow-twitch gastrocnemius, plantaris, and soleus muscles, respectively, in high-fat diet-induced obese 54-week-old female C57BL/6JOlaHsd mice (n = 9) compared to control standard-diet-treated lean mice (n = 9). A high-fat diet was administered for 26 weeks. Fiber-type specific intramyocellular lipid content analysis and muscle fiber typing were performed using histochemical analysis of lipids with Sudan Black and immunohistochemical analysis of myosin heavy chains on serial sections of skeletal muscles. Compared to the lean mice, the lipid accumulation was most prominent in types 2a and 2x/d fibers (p < 0.05) of fast-twitch gastrocnemius and intermediate plantaris muscles in the obese mice, while in slow-twitch soleus muscle, there was no significant lipid accumulation in the obese animals. Furthermore, the slow-twitch soleus muscle of the obese mice with no significant change in muscle fiber diameters exhibited the most pronounced shift towards fast-type myosin heavy chain isoform expression (p < 0.05). In contrast, the fast-twitch and intermediate-twitch gastrocnemius and plantaris muscles, respectively, in which the muscle fiber diameters increased (p < 0.05), were more resistant toward myosin heavy chain expression changes. In conclusion, we demonstrated both muscle- and fiber-type specificity in intramyocellular lipid accumulation in obese mice, suggesting that in obesity, similar muscle fiber types in different muscles accumulate lipids differentially.

Angiotensin 1-7 protects against ventilator-induced diaphragm dysfunction.

Mechanical ventilation (MV) is a life‐saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery. Unfortunately, an unintended consequence of prolonged MV is the development of inspiratory weakness due to both diaphragmatic atrophy and contractile dysfunction; this syndrome is labeled ventilator‐induced diaphragm dysfunction (VIDD). VIDD is clinically important because diaphragmatic weakness is an important contributor to problems in weaning patients from MV. Investigations into the pathogenesis of VIDD reveal that oxidative stress is essential for the rapid development of VIDD as redox disturbances in diaphragm fibers promote accelerated proteolysis. Currently, no standard treatment exists to prevent VIDD and, therefore, developing a strategy to avert VIDD is vital. Guided by evidence indicating that activation of the classical axis of the renin‐angiotensin system (RAS) in diaphragm fibers promotes oxidative stress and VIDD, we hypothesized that activation of the nonclassical RAS signaling pathway via angiotensin 1‐7 (Ang1‐7) will protect against VIDD. Using an established animal model of prolonged MV, our results disclose that infusion of Ang1‐7 protects the diaphragm against MV‐induced contractile dysfunction and fiber atrophy in both fast and slow muscle fibers. Further, Ang1‐7 shielded diaphragm fibers against MV‐induced mitochondrial damage, oxidative stress, and protease activation. Collectively, these results reveal that treatment with Ang1‐7 protects against VIDD, in part, due to diminishing oxidative stress and protease activation. These important findings provide robust evidence that Ang1‐7 has the therapeutic potential to protect against VIDD by preventing MV‐induced contractile dysfunction and atrophy of both slow and fast muscle fibers.

Robust Regeneration of Adult Electric Pulse Fish and the Formation of Its Electric Organ from Fast Muscle Fibers

In most weakly electric fish species, the cells that make up the electric organ (EO) are called electrocytes (EC) and these derive from a subpopulation of striated muscle fibers that undergo an extreme phenotypic conversion to replace their contractile function for an electrogenic one that fish use to navigate, communicate, mate, and detect prey/predators. Our previous findings using the knifefish Sternopygus macrurus revealed that ECs form from the fusion of fast muscle fiber types during adult tail regeneration. Whether or not this EC formation process is conserved in other highly regenerative electric fish species is the focus of this study. Specifically, we used immunolabeling to begin characterizing the morphology and muscle-protein expression of mature electrocytes in the species Brachyhypopomus pinnicaudatus and the muscle fiber type composition in the distal-most tail surrounding ECs prior to tail amputation. Regeneration of skeletal muscle and EO tissues was studied at different time points post tail cut – 1, 2, 3, 4, and 6 weeks. Our analyses to date show a distinct sexual dimorphism in EC length and cross-sectional area (CSA), with a mean (±SE) CSA of 4718µm2±543 in males (n= 3; triplicates per fish) and 1763µm2±181 in females (n=3; triplicates per fish) and a mean EC length of 19µm±2 in males (n= 3; triplicates per fish) and 13µm±1 in females (n= 3; triplicates per fish). Our immunolabeling studies detected the presence of the “muscle” protein desmin in all adult ECs. In addition, some but not all, ECs contained alpha-actinin, tropomyosin, titin, and sarcomeric myosin heavy chain (MHC) IIb. In B. pinnicaudatus, cell differentiation progressed from proximal to distal and peripheral to central, with muscle fibers being detected prior to ECs at each stage of regeneration studied. Myogenesis was evident by Day 7 with presence of fibers positively labeled with mouse antibody (MF20) against all MHC isoforms (n= 2). In addition, by Day 7, regenerating ECs were also evident in 1-week blastemas (n=2) fish based on the clustering of myofibers stained by cresyl violet and these early ECs were immunolabeled with MF20, cell shape transformation, and medial location relative to the muscle fibers. These data suggest that there are sexual dimorphic differences in the CSAs and lengths of ECs in the EOs of male and female B. pinnicaudatus. In addition, similar to S. macrurus, developing ECs in B. pinnicaudatus are given rise to by their type II fast muscle fiber precursors.

Tideglusib inhibition of GSK3 promotes the oxidative muscle phenotype and reduces serum creatine kinase in D2 mdx mice

Introduction Duchenne muscular dystrophy (DMD) is an X-linked disorder caused by an absence of dystrophin that compromises membrane integrity, ultimately resulting in muscle weakness, wasting, and premature death. The fast glycolytic muscle fibres are known to be most susceptible to dystrophic pathology, while slow oxidative fibres are less affected. Thus, promoting the slow oxidative phenotype has become a viable therapeutic strategy. Recent work from our lab has shown that inhibiting the enzyme glycogen synthase kinase 3 (GSK3) can promote the slow oxidative phenotype leading to enhancements in fatigue resistance. Furthermore, we have shown that inhibiting GSK3 augments muscle specific force production and myoblast fusion. Therefore, inhibiting GSK3 may aid in alleviating dystrophic pathology. Tideglusib is a potent GSK3 inhibitor currently undergoing clinical trials for myotonic dystrophy, another form of muscular dystrophy. Here, we tested whether treating the DMD preclinical mdx mouse with tideglusib would alter muscle oxidative phenotype, improve muscle function, and reduce serum creatine kinase (CK) levels, a marker of cellular damage. Methods Male DBA/2J wild type (WT) and mdx mice were ordered from Jackson Laboratories at 5-6 weeks of age. Three groups were included in this study; 1) WT healthy control, 2) mdx tideglusib (10 mg/kg/day, via oral gavage), and 3) mdx vehicle (26% peg400, 15% Chremaphor EL and water). The mdx-tideglusib and vehicle mice underwent their respective treatments for 2 weeks with ad libitum access to food and water. Subsequently, all mice were subjected to a hangwire test to assess muscle function. Mice were then euthanized and their serum extracted for CK activity analyses using a commercially available kit that was fitted onto a 96-well plate. Extensor digitorum longus (EDL) muscles were collected and homogenized for Western blotting to investigate phosphorylated (serine 9) and total GSK3b content along with myosin heavy chain (MHC) I and IIa levels. Results The hangwire test results showed that mdx mice treated with tideglusib were able to sustain hanging on the wire for a significantly longer period of time compared with the mdx vehicle group (p = 0.03). Serum CK analyses revealed that while the mdx vehicle group had significantly higher levels of activity compared with WT (p = 0.009), there was a 30% reduction in the mdx tideglusib mice that was no longer significantly different from WT. Western blotting revealed that though phosphorylated GSK3b levels were unaltered, tideglusib treatment led to a significant reduction in GSK3b content compared with vehicle (p = 0.04). Additionally, there was a significant increase in the oxidative MHC isoforms (I and IIa, p = 0.02) in the mdx tideglusib group compared with vehicle. Conclusions Our results demonstrate the potential use of tideglusib for DMD. We show that tideglusib treatment inhibited GSK3 in mdx mice through a reduction in total GSK3 content. In turn, we also found a significant increase in oxidative MHC isoforms (I and IIa), which was associated with enhanced muscle performance and reduced muscle damage.

LncRNA-FKBP1C regulates muscle fiber type switching by affecting the stability of MYH1B

Long non-coding RNAs (lncRNAs) are well-known to participate in a variety of important regulatory processes in myogenesis. In our previous RNA-seq study (accession number GSE58755), we found that lncRNA-FKBP1C was differentially expressed between White Recessive Rock (WRR) and Xinghua (XH) chicken. Here, we have further demonstrated that lncRNA-FKBP1C interacted directly with MYH1B by biotinylated RNA pull-down assay and RNA immunoprecipitation (RIP). Protein stability and degradation experiments identified that lncRNA-FKBP1C enhanced the protein stability of MYH1B. Overexpression of lncRNA-FKBP1C inhibited myoblasts proliferation, promoted myoblasts differentiation, and participated in the formation of skeletal muscle fibers. LncRNA-FKBP1C could downregulate the fast muscle genes and upregulate slow muscle genes. Conversely, its interference promoted cell proliferation, repressed cell differentiation, and drove the transformation of slow-twitch muscle fibers to fast-twitch muscle fibers. Similar results were observed after knockdown of the MYH1B gene, but the difference was that the MYH1B gene had no effects on fast muscle fibers. In short, these data demonstrate that lncRNA-FKBP1C could bound with MYH1B and enhance its protein stability, thus affecting proliferation, differentiation of myoblasts and conversion of skeletal muscle fiber types.

How do exercise training variables stimulate processes related to mitochondrial biogenesis in slow and fast trout muscle fibres?

What is the central question of this study? Exercise is known to promote mitochondrial biogenesis in skeletal muscle, but what are the most relevant training protocols to stimulate it? What is the main finding and its importance? As in mammals, training in rainbow trout affects slow and fast muscle fibres differently. Exercise intensity, relative to volume, duration and frequency, is the most relevant training variable to stimulate the processes related to mitochondrial biogenesis in both red and white muscles. This study offers new insights into muscle fibre type-specific transcription and expression of genes involved in mitochondrial adaptations following training. Exercise is known to be a powerful way to improve health through the stimulation of mitochondrial biogenesis in skeletal muscle, which undergoes cellular and molecular adaptations. One of the current challenges in human is to define the optimal training stimulus to improve muscle performance. Fish are relevant models for exercise training physiology studies mainly because of their distinct slow and fast muscle fibres. Using rainbow trout, we investigated the effects of six different training protocols defined by manipulating specific training variables (such as exercise intensity, volume, duration and frequency), on mRNAs and some proteins related to four subsystems (AMP-activated protein kinase-peroxisome proliferator-activated receptor γ coactivator-1α signalling pathway, mitochondrial function, antioxidant defences and lactate dehydrogenase (LDH) metabolism) in both red and white muscles (RM and WM, respectively). In both muscles, high-intensity exercise stimulated more mRNA types and enzymatic activities related to mitochondrial biogenesis than moderate-intensity exercise. For volume, duration and frequency variables, we demonstrated fibre type-specific responses. Indeed, for high-intensity interval training, RM transcript levels are increased by a low training volume, but WM transcript responses are stimulated by a high training volume. Moreover, transcripts and enzymatic activities related to mitochondria and LDH show that WM tends to develop aerobic metabolism with a high training volume. For transcript stimulation, WM requires a greater duration and frequency of exercise than RM, whereas protein adaptations are efficient with a long training duration and a high frequency in both muscles.

Chronic fatigue syndrome: Abnormally fast muscle fiber conduction in the membranes of motor units at low static force load

ObjectiveChronic fatigue syndrome (CFS) and fibromyalgia (FM) are disorders of unknown etiology and unclear pathophysiology, with overlapping symptoms of – especially muscular –fatigue and pain. Studies have shown increased muscle fiber conduction velocity (CV) in the non-painful muscles of FM patients. We investigated whether CFS patients also show CV abnormalities. MethodsFemales with CFS (n = 25), with FM (n = 22), and healthy controls (n = 21) underwent surface electromyography of the biceps brachii, loaded up to 20% of maximum strength, during short static contractions. The mean CV and motor unit potential (MUP) velocities with their statistical distribution were measured. ResultsThe CV changes with force differed between CFS-group and both FM-group and controls (P = 0.01). The CV of the CFS-group increased excessively with force (P < 0.001), whereas that of the controls increased only slightly and non-significantly, and that of the FM-group did not increase at all. In the CFS-group, the number of MUPs conveying very high conduction velocities increased abundantly with force and the MUPs narrowed. ConclusionOur results suggest disturbed muscle membrane function in CFS patients, in their motor units involved in low force generation. Central neural deregulation may contribute to this disturbance. SignificanceThese findings help to detangle the underlying mechanisms of CFS.

MicroRNA-494-3p inhibits formation of fast oxidative muscle fibres by targeting E1A-binding protein p300 in human-induced pluripotent stem cells

MYOD-induced microRNA-494-3p expression inhibits fast oxidative myotube formation by downregulating myosin heavy chain 2 (MYH2) in human induced pluripotent stem cells (hiPSCs) during skeletal myogenesis. However, the molecular mechanisms regulating MYH2 expression via miR-494-3p remain unknown. Here, using bioinformatic analyses, we show that miR-494-3p potentially targets the transcript of the E1A-binding protein p300 at its 3′-untranslated region (UTR). Myogenesis in hiPSCs with the Tet/ON-myogenic differentiation 1 (MYOD1) gene (MyoD-hiPSCs) was induced by culturing them in doxycycline-supplemented differentiation medium for 7 days. p300 protein expression decreased after transient induction of miR-494-3p during myogenesis. miR-494-3p mimics decreased the levels of p300 and its downstream targets MYOD and MYH2 and myotube formation efficiency. p300 knockdown decreased myotube formation efficiency, MYH2 expression, and basal oxygen consumption rate. The binding of miR-494-3p to the wild type p300 3′-UTR, but not the mutated site, was confirmed using luciferase assay. Overexpression of p300 rescued the miR-494-3p mimic-induced phenotype in MyoD-hiPSCs. Moreover, miR-494-3p mimic reduced the levels of p300, MYOD, and MYH2 in skeletal muscles in mice. Thus, miR-494-3p might modulate MYH2 expression and fast oxidative myotube formation by directly regulating p300 levels during skeletal myogenesis in MyoD-hiPSCs and murine skeletal muscle tissues.

Is there hope that transpinal direct current stimulation corrects motoneuron excitability and provides neuroprotection in amyotrophic lateral sclerosis?

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of largely unknown pathophysiology, characterized by the progressive loss of motoneurons (MNs). We review data showing that in presymptomatic ALS mice, MNs display reduced intrinsic excitability and impaired level of excitatory inputs. The loss of repetitive firing specifically affects the large MNs innervating fast contracting muscle fibers, which are the most vulnerable MNs in ALS. Interventions that aimed at restoring either the intrinsic excitability or the synaptic excitation result in a decrease of disease markers in MNs and delayed neuromuscular junction denervation. We then focus on trans‐spinal direct current stimulation (tsDCS), a noninvasive tool, since it modulates the activity of spinal neurons and networks. Effects of tsDCS depend on the polarity of applied current. Recent work shows that anodal tsDCS induces long‐lasting enhancement of MN excitability and synaptic excitation of spinal MNs. Moreover, we show preliminary results indicating that anodal tsDCS enhances the excitatory synaptic inputs to MNs in ALS mice. In conclusion, we suggest that chronic application of anodal tsDCS might be useful as a complementary method in the management of ALS patients.

Assessments of muscle fibre distribution by non-invasive methods

The objective of the present study was to assess muscle fibre composition by non-invasive methods for various sports events. 53 males of marathon (n=5), football (n=22), baseball (n=14), basketball (n=8) and tennis (n=4) athletes volunteered to participate in this study. The following 7 tests (overhead medicine ball throw, pull up, standing broad jump, sit up, shuttle run 10 x5, push up, vertical jump) are relatively easy to perform and to gather information about fibre composition through fitness levels. It can be used to assess the performance of strength using standard tables and to receive an indication of the degree of their share of fast (type II) and slow (type I) muscle fibres. For the study, a data analysis program in Microsoft Excel was used to view the mean and standard deviation of muscle fibre types. As a result, it was possible to speculate that the ratio of muscle fibre types differed according to the type of exercise. The results were obtained after sport motor tests of the mean value of muscle fibre composition by different sports events. Fibre type distribution remained with about 74.8% type 1 and 25.2% type 2 by marathoners, 43.8% type 1 and 53.2% type 2 by football athletes, 36.3% type 1 and 63.8% type 2 by baseball athletes, 46.6% type 1 and 53.5% type 2 by basketball athletes, and 40.0% type 1 and 60.0% type 2 by tennis athletes. Through these tests, the direction of the athletes’ muscle development can be considered, and it is possible to check the muscle fibre composition of elite athletes for the improvement of performance for each sport event. Moreover, it assumes that if this test is used for children, adolescents and young athletes, it will help to design scientific and effective training programs, thereby improving athletes’ ability to perform.

Estimation model of muscle fatigue based on muscle fiber type using electromyography

AbstractIn muscle rehabilitation and training, it is important to evaluate a patient's muscle state. In general, training is based on physical therapy, but there has not been quantitative assessment of the actual effects on muscles. The authors previously tried to quantify muscle fatigue and defined “Muscle‐fatigue time (MFT)” as the quantitative evaluation index of muscle fatigue based on electromyography and the use ratio of the muscle fiber type. MFT is the time when the use ratio of the slow muscle fiber (Type I) and the fast muscle fiber (Type IIb) intersects. Furthermore, the authors also proposed a method to estimate MFT by modeling the relationship between each muscle load and MFT. This paper examines the appropriate evaluation method for MFT containing variation, and generalization performance of the constructed model.

223 The effects of supplemental zinc and ractopamine hydrochloride on the Longissimus dorsi proteome of finishing beef steers

Abstract The objective of this study was to determine how steer growth rate and Zn nutrition affects the muscle proteome. Forty-eight, high percentage Angus steers (494 ± 18.2 kg) were blocked by BW and GeneMax gain score (GeneMax Focus, Zoetis, Parsippany, NJ) to treatments arranged in a 2×2 factorial. On d 0, steers were assigned to control (CON; 36 mg Zn/kg dry matter [DM]) or supranutritional Zn (SUPZN; CON + 60 mg Zn/kg DM as ZnSO4+ 60 mg Zn/kg DM as Zn-amino acid complex) dietary treatment (ZNTRT), and housed in pens (n = 6 or 8 steers/pen) with Growsafe bunks. On d 62, within ZNTRT steers were assigned to ractopamine hydrochloride treatments (RACTRT) of 0 (NO) or 300 mg·steer-1·d-1(RAC) for 28 d. Longissimus dorsi biopsies (between 12thand 13thrib) were collected on d 77. Sarcoplasmic fractions were extracted and submitted for proteomics analysis using mass spectrometry (LC-MS/MS). Data were log transformed and comparisons made using t-tests with adjusted P-value cutoffs of 0.1. Differences were noted in abundance of proteins involved in glycolytic, retinol and fatty acid metabolism. A shift from slow to fast muscle fiber type was suggested by decreased abundance of myoglobin and slow skeletal troponin 1 in steers fed RAC compared to steers not fed RAC within CON (P ≤ 0.04), while these proteins also tended to be lesser due to SUPZN within steers not fed RAC (P ≤0.09). The intermediate filament associated protein, vimentin, tended to be less abundant in RAC steers (P ≤ 0.09), suggesting RAC affects cellular remodeling. Proteins involved in immune function were also affected; for instance, the acute phase protein alpha-1-acid glycoprotein was more abundant in CON-RAC compared to either SUPZN-RAC (P = 0.001) or CON-NO (P = 0.02). Ractopamine hydrochloride and supranutritional Zn, independently and collectively, affect proteins involved in muscle metabolism, cellular remodeling and immune function in beef steers.

Computational Assessment of Transport Distances in Living Skeletal Muscle Fibers Studied In Situ

Transport distances in skeletal muscle fibers are mitigated by these cells having multiple nuclei. We have studied mouse living slow (soleus) and fast (extensor digitorum longus) muscle fibers in situ and determined cellular dimensions and the positions of all the nuclei within fiber segments. We modeled the effect of placing nuclei optimally and randomly using the nuclei as the origin of a transportation network. It appeared that an equidistant positioning of nuclei minimizes transport distances along the surface for both muscles. In the soleus muscle, however, which were richer in nuclei, positioning of nuclei to reduce transport distances to the cytoplasm were of less importance, and these fibers exhibit a pattern not statistically different from a random positioning of nuclei. We also simulated transport times for myoglobin and found that they were remarkably similar between the two muscles despite differences in nuclear patterning and distances. Together, these results highlight the importance of spatially distributed nuclei to minimize transport distances to the surface when nuclear density is low, whereas it appears that the distribution are of less importance at higher nuclear densities.

Effects of electroacupuncture combined with passive stretch exercise on disused muscle atrophy and expression of skeletal troponin in mice

To observe the efficacy of electroacupuncture (EA) plus passive stretch exercise in the treatment of disused atrophy of gastrocnemius and soleus muscles in mice. Fifty C57BL/6 mice were randomly and equally divided into 5 groups: blank control, model, passive stretch exercise (exercise), EA and EA+exercise groups. The muscular atrophy model was established by fixing the gastrocnemius and soleus muscles with plaster immobilization (by putting the right leg into a plastic vial and then twining the vial with medical plaster bandage from the ankle upwards to the thigh and groin to maintain the knee-joint flexion and ankle joint plantar flexion for 7 days). EA (2 Hz/100 Hz, 1 mA)was applied to bilateral "Zusanli"(ST36) for 10 min, once a day for 4 weeks. For mice with the passive exercise, the plastic vial was removed first, followed by pulling out the hindleg to seize the toes to stretch them until the right hindleg is fully extended, then, pushed the leg towards the body. The procedures were repeated once again and again for 10 min. The exercise was conducted once daily, for 4 weeks. The cross-sectional area of fast and slow muscle fibers of the soleus and gastrocnemius was measured under electronic microscope after ATPase histochemical stain and the expression of slow skeletal muscle troponin (TNNI1) and fast skeletal muscle troponin (TNNI2) in the soleus and gastrocnemius was detected by Western blot. Compared with the blank control group, the cross-sectional areas of the fast and slow muscle fibers of the soleus and gastrocnemius muscles were significantly decreased in the model group (P<0.05, P<0.01). Following the interventions, the cross-sectional areas of the fast and slow muscle fibers of soleus muscle in the EA+exercise group, and those of the fast and slow muscle fibers of the gastrocnemius muscle in the EA and EA+exercise groups, and the expression levels of TNNI1 and TNNI2 proteins in the gastrocnemius muscle of the EA+exercise group were significantly increased in comparison with the model group (P<0.05, P<0.01). EA combined with passive stretch exercise can promote the recovery of the soleus and gastrocnemius muscles in disused muscle atrophy mice, which may be related to its effect in up-regulating the expression of TNNI1 and TNNI2 proteins.