Fiber Type Proportions Research Articles

Critical power is positively related to skeletal muscle capillarity and type I muscle fibers in endurance-trained individuals.

The asymptote [critical power (CP)] and curvature constant ( W') of the hyperbolic power-duration relationship can predict performance within the severe-intensity exercise domain. However, the extent to which these parameters relate to skeletal muscle morphology is less clear, particularly in endurance-trained individuals, who, relative to their lesser-trained counterparts, possess skeletal muscles that can support high levels of oxygen transport and oxidative capacity, i.e., elevated type I fiber proportion and cross-sectional area (CSA) and capillarity. Fourteen endurance-trained men performed a maximal incremental test to determine peak oxygen uptake (V̇o2peak; 63.2 ± 4.1 ml·min-1·kg-1, mean ± SD) and maximal aerobic power (406 ± 63 W) and three to five constant-load tests to task failure for the determination of CP (303 ± 52 W) and W' (17.0 ± 3.0 kJ). Skeletal muscle biopsies were obtained from the vastus lateralis and analyzed for percent proportion of fiber types, CSA, and indexes of capillarity. CP was positively correlated with the percent proportion ( r = 0.79; P = 0.001) and CSA ( r = 0.73; P = 0.003) of type I fibers, capillary-to-fiber ratio ( r = 0.88; P < 0.001), and capillary contacts around type I fibers ( r = 0.94; P < 0.001) and type II fibers ( r = 0.68; P = 0.008). W' was not correlated with any morphological variables. These data reveal a strong positive association between CP and skeletal muscle capillarity. Our findings support the assertion that CP is an important parameter of aerobic function and offer novel insights into the physiological bases of CP. NEW & NOTEWORTHY This investigation demonstrated very strong positive correlations between critical power and skeletal muscle capillarity, particularly around type I fibers, and type I fiber composition. These correlations were demonstrated in endurance-trained individuals expected to possess well-adapted skeletal muscles, such as high levels of oxygen transport structures and high oxidative capacities, supporting the view that critical power is an important parameter of aerobic function. In contrast, the curvature constant W' was not associated with fiber type composition or capillarity.

Protective role of Parkin in skeletal muscle contractile and mitochondrial function

Parkin, an E3 ubiquitin ligase encoded by the Park2 gene, has been implicated in the regulation of mitophagy, a quality control process in which defective mitochondria are degraded. The exact physiological significance of Parkin in regulating mitochondrial function and contractility in skeletal muscle remains largely unexplored. Using Park2-/- mice, we show that Parkin ablation causes a decrease in muscle specific force, a severe decrease in mitochondrial respiration, mitochondrial uncoupling and an increased susceptibility to opening of the permeability transition pore. These results demonstrate that Parkin plays a protective role in the maintenance of normal mitochondrial and contractile functions in skeletal muscles. Parkin is an E3 ubiquitin ligase encoded by the Park2 gene. Parkin has been implicated in the regulation of mitophagy, a quality control process in which defective mitochondria are sequestered in autophagosomes and delivered to lysosomes for degradation. Although Parkin has been mainly studied for its implication in neuronal degeneration in Parkinson disease, its role in other tissues remains largely unknown. In the present study, we investigated the skeletal muscles of Park2 knockout (Park2-/- ) mice to test the hypothesis that Parkin plays a physiological role in mitochondrial quality control in normal skeletal muscle, a tissue highly reliant on mitochondrial content and function. We first show that the tibialis anterior (TA) of Park2-/- mice display a slight but significant decrease in its specific force. Park2-/- muscles also show a trend for type IIB fibre hypertrophy without alteration in muscle fibre type proportion. Compared to Park2+/+ muscles, the mitochondrial function of Park2-/- skeletal muscles was significantly impaired, as indicated by the significant decrease in ADP-stimulated mitochondrial respiratory rates, uncoupling, reduced activities of respiratory chain complexes containing mitochondrial DNA (mtDNA)-encoded subunits and increased susceptibility to opening of the permeability transition pore. Muscles of Park2-/- mice also displayed a decrease in the content of the mitochondrial pro-fusion protein Mfn2 and an increase in the pro-fission protein Drp1 suggesting an increase in mitochondrial fragmentation. Finally, Park2 ablation resulted in an increase in basal autophagic flux in skeletal muscles. Overall, the results of the present study demonstrate that Parkin plays a protective role in the maintenance of normal mitochondrial and contractile functions in normal skeletal muscles.

Muscle Fiber Type Adaptations To Exercise Differ In Obese And Non-obese Volunteers

Human skeletal muscle is composed of slow fibers (type I), fast fibers (IIa and IIx), and a continuum of hybrid fibers co-expressing different myosin heavy chains. Cellular responses to exercise involve changes in fiber type proportions and cross sectional area (CSA). To our knowledge, the impact of obesity on these responses is not yet known. PURPOSE: To determine if obesity impacts changes in fiber type proportions and CSA in response to endurance exercise in a sedentary population. METHODS: Twenty-two obese sedentary healthy men and women (O, BMI>30kg/m2) and 15 non-obese (Lean, L, BMI<26kg/m2) volunteers participated in a 4 months supervised endurance exercise intervention. 18 endurance trained volunteers matched by gender and age (60-79) served as controls (C). Vastus lateralis muscle biopsies were analyzed using immunohistochemistry to determine fiber type distribution and CSA. Baseline group comparisons were made using 1-way ANOVA. Pre/post-intervention changes were assessed by paired t tests. RESULTS: At baseline, both L and O had less type I fibers than C. No difference was found in proportions of type IIa, IIx or hybrid I-IIa fibers. The proportion of hybrid type IIa-IIx was higher in O than C. Type I CSA was larger in O than L. No difference in CSA was found for type IIa, IIx or hybrid fibers. With intervention, proportions of type I, IIa, IIx and hybrid type IIa-IIx were not modified. An increase in proportion of hybrid type I-IIa was seen in L but not in O. Type I CSA increased in O and L, while IIa CSA increased only in L. CONCLUSION: Different adaptations in proportion of fiber types and CSA were observed in O and L previously sedentary volunteers. The increased proportion of hybrid I-IIa fibers with intervention observed in L could be interpreted as a shift of fibers towards a more oxidative muscle such as the profile of C. This transition was not observed in O. As exercise dose was similar in both groups, this unequal shift may be time-dependent, thus not yet apparent here in O. Although fiber CSA was on average 1.5x larger in O than L at baseline, similar CSA increments were observed with endurance exercise in both groups. In previously sedentary seniors, increments of CSA with exercise, even if concurrent to a significant weight loss in the obese subjects, are crucial to prevent age related muscle atrophy.

Determination of the Proportions of Muscle Fibre Types from Selected Muscles of the Forelimb: A Comparative Study of Cattle (Bos taurus indicus) and One-humped Camel (Camelus dromedaries)

A total number of fifty forelimbs comprising Twenty-five forelimbs male dromedary camels (camelus dromedaries) and those of male cattle, Zebu type, (Bos taurus indicus) within the ages of 6 months, 1 year, 3 years, 5 years and 7 years, were purchased from Sokoto Municipal Modern abattoir. Selected muscles sampled (1 cm2) from the forelimbs of both cattle and camel were taken from the middle part of the muscle bellies (from the biceps brachii, triceps brachii and deltoideus), fixed inBouin’s solution and prepared forhistochemical analyses. The photomicrographs obtained from the biceps brachii, deltoideus and triceps brachii among both cattle and camel demonstrated the morphology of the different fibre types (type I, type IIA and type IIB). Muscle fibre types showed different proportions. Even though the overall mean proportion of muscle fibre type I, type IIA and type IIB could not present any significant (p>0.05) differences between the camel and the cattle looking at it holistically. As revealed in this work, the effects of the interactions of species versus age, species versus muscle and muscle versus age on the proportion of muscle fibre type I revealed that the deltoideus muscle of 1 year old camel had significantly (p<0.05) higher proportion. Type IIA muscle fibre obtained from the deltoideus muscle of 5-year-old camel showed a significantly highest value, while muscle fibre type IIB showed significantly higher value from the triceps brachii of cattle aged 1 year. The importance of the knowledge of microscopic characteristics in the determination of myofibre types could be of help in advancing the knowledge on muscle morphology (anatomy) and as well be of help in meat science industry.

Skeletal myofiber VEGF‐A‐targeted gene deletion induces mitochondrial, structural and contractile alterations in mouse diaphragm

Respiratory muscle weakness is a hallmark of COPD, heart failure, and critical illness. Vascular endothelial growth factor (VEGF) may be an important therapeutic target in chronic cardiopulmonary disease as it is essential for neovascularization and vessel repair following trauma. We hypothesized that respiratory muscle, which is required to persistently function, would exhibit impaired mitochondrial, structural, and contractile function in skeletal myofiber VEGF gene deleted mice.We measured diaphragm biochemistry, structure, and contractile function in adult mice with conditional deletion of the VEGF‐A gene in skeletal myofibers (SkmVEGF−/−). Male SkmVEGF−/− mice (n=12) were compared to wild type (WT) controls (n=13) – both on a C57BL/6J background. Fiber bundles were isolated and electrically stimulated in vitro to evaluate force‐frequency and fatigue profiles. Mitochondrial O2 consumption and H2O2 flux (index of mitochondrial ROS) were simultaneously measured in saponin‐permeabilized fiber bundles (Oroboros, Innsbruck, AT). Fiber structure and biochemistry were measured using standard techniques (IHC, Western, ELISA).Diaphragm VEGF protein was lower in SkmVEGF−/− than WT mice (1.5±0.2 vs. 3.0±0.4 pg/total protein, p&lt;0.05). Compared to WT mice, the force‐frequency relationship was depressed in SkmVEGF−/− (F[7,161]=15.0, p&lt;0.05), with maximal specific force reduced by ~10 % (24±1 vs. 21±1 N/cm2; p&lt;0.05). However, fatigue resistance tended to be greater following SkmVEGF−/− (F[2,115]=3.3, p=0.06). Fiber type proportions were unchanged, but type I fiber cross‐sectional area was reduced in SkmVEGF−/− (653±45 vs 493±53 μm2; p&lt;0.05). Compared to WT, sarcomeric actin protein expression was reduced by ~30% in SkmVEGF−/− (p&lt;0.05) while myosin heavy chain, MAFbx, MuRF1, PGC1α, and HIF1α protein remained unchanged (p&gt;0.05). Mitochondrial respiration was not different between SkmVEGF−/− and WT (F[1,80]=0.9, p&gt;0.05) in each of the respiratory states. However, H2O2 flux was reduced in SkmVEGF−/− (F[1,75]=14.6, p&lt;0.05).Skeletal myofiber‐specific VEGF deletion contributed to diaphragm weakness, but tended to improve fatigue resistance in this highly oxidative muscle. Reductions in oxidative fiber size, sarcomeric actin protein content, and ROS generation following VEGF gene deletion may contribute to protecting mitochondrial respiratory function in the diaphragm. The adaptations may be part of compensatory mechanisms mitigating larger deficits in force generation and fatigue resistance.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Determination of the Proportions of Muscle Fibre Types from Selected Muscles of the Forelimb: A Comparative Study of Cattle (Bos taurus indicus) and One-humped Camel (Camelus dromedaries)

Determination of the Proportions of Muscle Fibre Types from Selected Muscles of the Forelimb: A Comparative Study of Cattle (Bos taurus indicus) and One-humped Camel (Camelus dromedaries)

Skeletal muscle mitochondrial bioenergetics and associations with myostatin genotypes in the Thoroughbred horse.

Variation in the myostatin (MSTN) gene has been reported to be associated with race distance, body composition and skeletal muscle fibre composition in the horse. The aim of the present study was to test the hypothesis that MSTN variation influences mitochondrial phenotypes in equine skeletal muscle. Mitochondrial abundance and skeletal muscle fibre types were measured in whole muscle biopsies from the gluteus medius of n = 82 untrained (21 ± 3 months) Thoroughbred horses. Skeletal muscle fibre type proportions were significantly (p < 0.01) different among the three MSTN genotypes and mitochondrial content was significantly (p < 0.01) lower in the combined presence of the C-allele of SNP g.66493737C>T (C) and the SINE insertion 227 bp polymorphism (I). Evaluation of mitochondrial complex activities indicated higher combined mitochondrial complex I+III and II+III activities in the presence of the C-allele / I allele (p ≤ 0.05). The restoration of complex I+III and complex II+III activities following addition of exogenous coenzyme Q1 (ubiquinone1) (CoQ1) in vitro in the TT/NN (homozygous T allele/homozygous no insertion) cohort indicated decreased coenzyme Q in these animals. In addition, decreased gene expression in two coenzyme Q (CoQ) biosynthesis pathway genes (COQ4, p ≤ 0.05; ADCK3, p ≤ 0.01) in the TT/NN horses was observed. This study has identified several mitochondrial phenotypes associated with MSTN genotype in untrained Thoroughbred horses and in addition, our findings suggest that nutritional supplementation with CoQ may aid to restore coenzyme Q activity in TT/NN horses.

Tumor necrosis factor-like weak inducer of apoptosis regulates quadriceps muscle atrophy and fiber-type alteration in a rat model of chronic obstructive pulmonary disease

BackgroundIn chronic obstructive pulmonary disease (COPD), weakness and muscle mass loss of the quadriceps muscle has been demonstrated to predict survival and mortality rates of patients. Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK), as a member of the TNF superfamily, has recently been identified as a key regulator of skeletal muscle wasting and metabolic dysfunction. So our aim was to study the role of TWEAK during quadriceps muscle atrophy and fiber-type transformation in COPD model rats and its possible pathway.MethodsForty-four healthy male adult Wistar rats were randomly divided into two groups: A normal control group (n = 16) and a COPD model group (n = 28). The COPD group was exposed to cigarette smoke for 90 d and injected with porcine pancreatic elastase on day 15, whereas the control group was injected with saline alone. Following treatment, weights of the quadriceps muscles were measured and hematoxylin and eosin staining was performed to identify structural changes in lung and quadriceps muscle tissue. Immunohistochemical staining was also conducted to determine the localization of TWEAK, nuclear factor (NF)-κB, muscle ring finger (MuRF)-1 and proliferator-activated coactivator (PGC)-1a proteins in the quadriceps muscle, and western blotting was used to assess the level of protein expression.ResultsCompared with controls, COPD model rats exhibited significantly lower quadriceps muscle weight (P < 0.05) accompanied by fiber atrophy and disordered fiber arrangement, a wide gap between adjacent muscle fibers, a significant reduction in nuclear number (P < 0.05) and an uneven size distribution. The proportion of fiber types was also significantly altered (P < 0.05). In addition, TWEAK expression in the quadriceps muscle of COPD model rats was significantly higher than that in control rats (P < 0.05), and was significantly associated with quadriceps atrophy and fiber-type alteration (P < 0.05). Levels of NF-κB, MuRF1 and PGC-1α expression also significantly differed between the two groups (P < 0.05).ConclusionsCollectively these data suggest that increased levels of TWEAK may lead to skeletal muscle atrophy and fiber-type alteration, which in turn may be associated with activation of the ubiquitin-proteasome pathway, involving NF-κB, MuRF1 and PGC-1α as potential regulatory factors. These preliminary results in rats suggest that TWEAK may be a therapeutic target for the treatment of muscle atrophy in COPD.

Effect of carcinogen 1,2-dimethylhydrazine treatment on fiber types in skeletal muscles of male Wistar rats.

The cancerogen 1,2-dimethylhydrazine (DMH), widely used in the experimental animal model of carcinogenesis, affects various organs, but its effect on muscle fibers is unknown. To evaluate the effect of 15-week DMH treatment on the fiber size and myosin heavy chain (MyHC) isoforms, which substantially determine fiber types and their contractile characteristics, pure and hybrid fiber types were immunohistochemically determined according to the MyHC isoform expression in soleus, extensor digitorum longus, gastrocnemius medialis and lateralis muscles of DMH-treated and control male Wistar rats. Whereas the size of fibers was mostly unaffected, the MyHC isoform expression was partially affected in both gastrocnemius samples, but not in the soleus and extensor digitorum longus of DMH-treated rats. The lower proportions of hybrid fiber types and especially that of type 1/2x in most gastrocnemius samples of DMH-treated rats resulted in a shift towards a single MyHC isoform expression, but the extent and pattern of the MyHC isoform shift varied across the different gastrocnemius samples. Such variable response to DMH treatment across muscles indicates that each muscle possesses its own adaptive range. These findings are essential for an accurate evaluation of skeletal muscle characteristics in DMH animal model.

Muscular and neuromotor control and learning in the athletic horse

Athletic performance or the kinematics of locomotion is ultimately the result of the actions of muscles. Muscular actions differ depending on the muscle group involved with anatomical and functional properties depending on the primary roles of the muscle; from stabilisation to powering locomotion. The functional (contractile and metabolic) properties of a muscle are determined by its fibre type or relative fibre type proportions in the muscle. The actions of muscle require the coordination of the nervous system with muscle contraction to produce movement or resist movement to avoid unwanted motion and tissue damage. The coordination of muscular action with the nervous system is termed neuromotor control and it requires precise proprioceptive input from the periphery, processing and input from the central nervous system (including learned or trained movements) and involves timing of muscle recruitment as well as muscle contraction. Training of muscles involves training for strength (or force generation) and stamina with measureable physiological changes with training including increased fibre size, alterations in fibre type, alterations in glycogen concentrations and lactate transport and alterations in mitochondrial and capillary density. As well as standard athletic training, skills training can make the difference in athletic performance and injury prevention in the equine athlete. This involves training of neuromotor control; training motor skills by motor relearning and conditional learning. Practical specific training techniques can be used in injury prevention, rehabilitation post injury and maintenance of the athlete. In this review we will focus on the thoracolumbar and hindlimb areas of the horse and review the importance of muscular control of locomotion, neuromotor control, the physiological effects of training and practical ways to maximise performance potential by specific physiotherapy skills training.

Zilpaterol Hydrochloride affects Cellular Muscle Metabolism and Lipid Components of 10 Different Muscles in Feedlot Heifers

This study determined if zilpaterol hydrochloride (ZH) altered muscle metabolism and lipid components of 10 muscles. Crossbred heifers were either supplemented with ZH (n = 9) or not (Control; n = 10). Muscle tissue was collected (adductor femoris, biceps femoris, gluteus medius, infraspinatus, latissimus dorsi, longissimus dorsi, pectoralis profundi, semitendinosus, subscapularis, trapezius) immediately following carcass splitting. The mRNA abundance of AMPkɑ, IGF-I, MHC-I, IIA and IIX, β1-adrenergic receptor (βAR) and β2AR was determined, as well as, cross-sectional area and proportion of myosin isoforms, β1AR, β2AR, β3AR, nuclei, and satellite cell density. Furthermore, neutral (NL) and polar lipid (PL) fatty acids (FA) were quantified (mg/g). Zilpaterol hydrochloride decreased MHC-IIA mRNA (P = 0.007). In addition, ZH decreased total nuclei and β1AR and increased MHC-IIX cross-sectional area (P ≤ 0.021). Quantity of NL FA were not affected by ZH (P ≥ 0.173). However, among PL FA the ratio of PUFA:SFA was greater with ZH (P = 0.048). Muscle type impacted mRNA concentration of AMPkɑ, IGF-I, MHC-I, IIA, IIX, and β1AR mRNA concentration (P ≤ 0.037). Furthermore, the fiber type proportion, fiber cross-sectional area, and the densities of nuclei, β1AR, β2AR, β3AR, and satellite cells were influenced by muscle type (P ≤ 0.030). Total NL FA were affected by muscle (P ≤ 0.046). Meanwhile, total PL FA did not differ due to muscle (P = 0.242). However, prominent PL FA,18:0, 18:1 trans, and 18:2 n-6 were each greater (P &lt; 0.05) among the oxidative subscapularis compared with glycolytic semitendinosus and adductor femoris. Overall, these data reveal that ZH impacts muscle metabolism and myogenic activity that establishes protein deposition. Meanwhile, ZH did not alter triglyceride content (NL), but cell membrane saturation (PL) was influenced, in accordance with alterations to muscle fiber type. Muscle also influenced muscle fiber type and lipid components. Therefore, muscle biology is greatly influenced by muscle but also through dietary inclusion of ZH.

Skeletal muscle contractile properties in a novel murine model for limb girdle muscular dystrophy 2i.

Limb-girdle muscular dystrophy (LGMD) 2i results from mutations in fukutin-related protein and aberrant α-dystroglycan glycosylation. Although this significantly compromises muscle function and ambulation, the comprehensive characteristics of contractile dysfunction are unknown. Therefore, we quantified the in situ contractile properties of the medial gastrocnemius in young adult P448L mice, an affected muscle of a novel model of LGMD2i. Normalized maximal twitch force, tetanic force, and power were significantly smaller in P448L mice, compared with sex-matched, wild-type mice. These differences were consistent with the replacement of contractile fibers by passive tissue. The shape of the active force-length relationships were similar in both groups, regardless of sex, consistent with an intact sarcomeric structure in P448L mice. Passive force-length curves normalized to maximal isometric force were steeper in P448L mice, and passive elements contribute disproportionately more to total contractile force in P448L mice. Sex differences were mostly noted in the force-velocity curves, as normalized values for maximal and optimal velocities were significantly slower in P448L males, compared with wild-type, but not in P448L females. This suggests that the dystrophic phenotype, which may include possible changes in cross-bridge kinetics and fiber-type proportions, progresses more quickly in P448L males. These results together indicate that active force and power generation are compromised in both sexes of P448L mice, while passive forces increase. More importantly, the results identified several functional markers of disease pathophysiology that could aid in developing and assessment of novel therapeutics for LGMD2i and possibly other dystroglycanopathies as well. NEW & NOTEWORTHY Comprehensive assessments of muscle contractile function have, until now, never been performed in an animal model for any dystroglycanopathy. This study suggests that skeletal muscle contractile properties are significantly compromised in a recently developed model for limb-girdle muscular dystrophy 2i, the P448L mouse. It further identifies novel pathological markers of muscle function that are suitable for developing therapeutics and for better understanding of disease pathogenesis.

Muscle fiber type proportions are not altered in independently ambulatory children with cerebral palsy

Muscle fiber type proportions are not altered in independently ambulatory children with cerebral palsy

Fine-mapping of genes determining extrafusal fiber properties in murine soleus muscle.

Muscle fiber cross-sectional area (CSA) and proportion of different fiber types are important determinants of muscle function and overall metabolism. Genetic variation plays a substantial role in phenotypic variation of these traits; however, the underlying genes remain poorly understood. This study aimed to map quantitative trait loci (QTL) affecting differences in soleus muscle fiber traits between the LG/J and SM/J mouse strains. Fiber number, CSA, and proportion of oxidative type I fibers were assessed in the soleus of 334 genotyped female and male mice of the F34 generation of advanced intercross lines (AIL) derived from the LG/J and SM/J strains. To increase the QTL detection power, these data were combined with 94 soleus samples from the F2 intercross of the same strains. Transcriptome of the soleus muscle of LG/J and SM/J females was analyzed by microarray. Genome-wide association analysis mapped four QTL (genome-wide P < 0.05) affecting the properties of muscle fibers to chromosome 2, 3, 4, and 11. A 1.5-LOD QTL support interval ranged between 2.36 and 4.67 Mb. On the basis of the genomic sequence information and functional and transcriptome data, we identified candidate genes for each of these QTL. The combination of analyses in F2 and F34 AIL populations with transcriptome and genomic sequence data in the parental strains is an effective strategy for refining QTL and nomination of the candidate genes.

Transcriptomic gene profiling of porcine muscle tissue depending on histological properties.

In pig, the histological profile of muscle tissue, especially the proportion of individual fiber types, is one of the main factors affecting meat quality properties. In the present research, RNA sequencing (RNA-seq) by using next generation sequencing method was applied to estimate the whole gene expression profile of Longissimus lumborum muscle of pigs (Large White breed) differing in the percentage of two fiber types (slow-twitch (type I) fibers and fast-twitch glycolytic (type IIB) fibers). The RNA-seq approach allowed us to identify 355 differentially expressed genes (DEGs) indicated as significant (false discovery rate-adjusted P<0.05) using three types of software: DESeq2, edgeR and baySeq. Detected genes and pathways deregulated in muscle depending on tissue microstructure were associated with: metabolic processes - 158 genes; cellular processes - 122; biological regulation - 62; localization - 51; and 35 genes with developmental processes. The DEGs were included in: PI3K-Akt; FoxO and MAPK signaling pathways, regulation of actin cytoskeleton, lysine degradation and insulin signaling pathway as well as mTOR and Hippo signaling pathways. These results highlight the mainly metabolic pathways related to glucose metabolism and contraction processes of muscle cells. Detection of genes involved in variation of fiber-type distribution will be useful in understanding of the genetic factors affecting muscle structure, metabolic process and indirectly, meat quality traits.

Muscle fiber type proportion and size is not altered in mcardle disease.

McArdle disease is a metabolic myopathy that presents with exercise intolerance and episodic rhabdomyolysis. Excessive muscle recruitment has also been shown to be present during strenuous exercise, suggesting decreased power output. These findings could potentially be explained by either impaired contractility, decreased fiber size, or altered fiber type proportion. However, there is a paucity of data on the morphological features seen on muscle histology. We examined muscle biopsies of patients with McArdle disease from a Spanish cohort and compared the findings with healthy controls. We found no significant difference in the fiber type proportion or mean fiber size between McArdle patients and controls in the biceps brachii or vastus lateralis muscles. No alterations in muscle fiber type proportion or size were found on muscle histology of patients with McArdle disease. Future research should focus on assessment of muscle fiber contractility to investigate the functional impairment. Muscle Nerve 55: 916-918, 2017.

Properties of the motor unit action potential shape in proximal and distal muscles of the upper limb in healthy and post-stroke individuals.

Spectral analysis of surface electromyograms (sEMG) is often used to estimate central and peripheral characteristics of a motor unit (MU) population, such as average conduction velocity, proportion of muscle fiber types, and pattern of MU recruitment. This estimation is based on the assumption that the sEMG adequately reflects the frequency characteristics of the underlying MU action potentials (MUAP). However, sEMG has limitations in this respect, based on physiological and non-physiological factors that influence its frequency content. We present a method to examine characteristics of a MU population more reliably by assessing the distributions of frequency content and amplitude for a collection of individual MUAPs, identified using high-density sEMG decomposition. We demonstrate the use of this approach to examine how MU characteristics differ across muscles and in the post-stroke state by presenting preliminary data from deltoid (DELT), biceps (BIC), and finger flexor (FF) MU populations from 12 post-stroke individuals and 8 able-bodied controls. The results show differences in the magnitude and range of MUAP median frequencies across muscles in both groups. The group median values were higher in the stroke group for the DELT and FF and lower in the stroke group for the BIC. The range of frequencies was larger in the stroke group for all muscles. The distribution of MUAP RMS amplitude in both stroke and control groups had a substantially larger range in FF than in DELT and BIC. The group median values for the FF were twice as large in the stroke group. In addition, there were differences in the frequency and amplitude results between MUAP and global sEMG analyses. The implications of these findings and possible applications of the approach are discussed.

Intrauterine growth-restricted sheep fetuses exhibit smaller hindlimb muscle fibers and lower proportions of insulin-sensitive Type I fibers near term.

Intrauterine growth restriction (IUGR) reduces muscle mass and insulin sensitivity in offspring. Insulin sensitivity varies among muscle fiber types, with Type I fibers being most sensitive. Differences in fiber-type ratios are associated with insulin resistance in adults, and thus we hypothesized that near-term IUGR sheep fetuses exhibit reduced size and proportions of Type I fibers. Placental insufficiency-induced IUGR fetuses were ∼54% smaller (P < 0.05) than controls and exhibited hypoxemia and hypoglycemia, which contributed to 6.9-fold greater (P < 0.05) plasma norepinephrine and ∼53% lower (P < 0.05) plasma insulin concentrations. IUGR semitendinosus muscles contained less (P < 0.05) myosin heavy chain-I protein (MyHC-I) and proportionally fewer (P < 0.05) Type I and Type I/IIa fibers than controls, but MyHC-II protein concentrations, Type II fibers, and Type IIx fibers were not different. IUGR biceps femoris muscles exhibited similar albeit less dramatic differences in fiber type proportions. Type I and IIa fibers are more responsive to adrenergic and insulin regulation than Type IIx and may be more profoundly impaired by the high catecholamines and low insulin in our IUGR fetuses, leading to their proportional reduction. In both muscles, fibers of each type were uniformly smaller (P < 0.05) in IUGR fetuses than controls, which indicates that fiber hypertrophy is not dependent on type but rather on other factors such as myoblast differentiation or protein synthesis. Together, our findings show that IUGR fetal muscles develop smaller fibers and have proportionally fewer Type I fibers, which is indicative of developmental adaptations that may help explain the link between IUGR and adulthood insulin resistance.

Exercise Training Prevents Skeletal Muscle Atrophy And Dysfunction In Hypertension Involving A Set Of MicroRNAs

PURPOSE: Aerobic exercise training (ET) has been used as an important non-pharmacological treatment of hypertension. MicroRNAs (miRNAs) are a new class of gene regulators in which inhibit protein expression by base-pairing with the 3’ UTRs of mRNA targets. We evaluated the skeletal muscle miRNAs profile and their target genes involved in hypertension-associated muscle disorders and checked the therapeutic role of ET on these parameters. METHODS AND RESULTS: Spontaneously hypertensive rats (SHR) aged 6 months and their controls Wistar Kyoto (WKY) were assigned to 4 groups: SHR, trained SHR (SHR-T), WKY and trained WKY (WKY-T). Swimming ET consisted of 60 min of duration, 1x/day/10 weeks, with 4% body weight workload. SHR showed an increased in systolic blood pressure (207 ± 5.5 mmHg) compared to WKY (133 ± 3.9 mmHg) analyzed by tail-cuff system, with no changes in baseline heart rate. We observed a reduction in VO2 peak (WKY: 62 ± 1.5; SHR: 53 ± 2.5 mL.kg-1.min-1) accompanied by soleus muscle atrophy (cross-sectional area: fiber type I - WKY: 4039 ± 195; SHR: 2658 ± 53; type IIa - WKY: 2903 ± 182, SHR: 2050 ± 68; Intermediate - WKY: 2663 ± 136, SHR: 1967 ± 95 μm2), change in fiber type profile (type I - WKY: 92.7 ± 1.5; SHR: 77.5 ± 1.8; type IIa - WKY: 4.8 ± 1.5; SHR: 18.5 ± 1.4; Intermediate - WKY: 1.1 ± 0.2; SHR: 3.9 ± 0.4 %) and dysfunction (specific force evaluated in the organ bath- tetanus 80Hz: WKY: 10.9 ± 0.3; SHR: 7.8 ± 0.2 g/mm2) in SHR. In contrast, ET promoted reduction in blood pressure and resting bradycardia in trained animals. ET corrected the VO2 peak reduction, change in proportion of muscle fiber types, soleus atrophy and dysfunction in SHR-T toward control levels. Interestingly, the muscle miRNA microarray analyzed by LC Science revealed a miRNAs profile involved in muscle remodeling (miRNAs-96, -205, -182, -140, -328a, -665, -1, -499, -208b and -99b) making it possible to identify target genes modified by hypertension and ET. Thus, targets involved in changing the fiber profile and protein synthesis by the IGF-I/ Akt /mTOR pathway were impaired in hypertension and corrected by ET. CONCLUSION: The results support the hypothesis that the structural and functional changes arising from the progression of hypertension may be regulated by a set of miRNAs and target genes; and ET participates in restoring the muscle mass and function.

Skeletal muscle fiber characteristics and oxidative capacity in hemiparetic stroke survivors.

Skeletal muscle is changed after stroke, but conflicting data exist concerning muscle morphology and oxidative enzyme capacity. In 36 chronic stroke patients bilateral rectus femoris muscle biopsies were analyzed, and fiber type proportions and cross-sectional areas were determined by ATPase histochemistry. Enzymatic concentrations of citrate synthase (CS) and 3-Hydroxyacyl-coenzymeA-dehydrogenase (HAD) were determined using freeze-dried muscle tissue. Findings were correlated with clinical outcomes. In the paretic muscles the mean fiber area was smaller (P = 0.0004), and a lower proportion of type 1 fibers (P = 0.0016) and a higher proportion of type 2X fibers (P = 0.0002) were observed. The paretic muscle had lower CS (P = 0.013) and HAD concentrations (P = 0.037). Mean fiber area correlated with muscle strength (r = 0.43; P = 0.041), and CS concentration correlated with aerobic capacity (r = 0.47; P = 0.01). In stroke survivors there is a phenotypic shift toward more fatigable muscle fibers with reduced oxidative enzymatic capacity that relates to clinical outcomes.