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PubMed1999

Muscle LIM protein: expressed in slow muscle and induced in fast muscle by enhanced contractile activity.

To identify early changes in gene expression during the fast-to-slow transition induced by chronic low-frequency stimulation, total RNA was extracted from 12-h-stimulated tibialis anterior (TA) muscles of rats and amplified by differential display RT-PCR. Among the signals of differentially expressed mRNAs, a cDNA approximately 300 bp in length, which was almost undetectable in control TA muscles but prominent in stimulated TA and normal soleus muscles, was identified. This cDNA was cloned and identified as corresponding to the mRNA of the muscle LIM protein (MLP). Its differential expression in control, stimulated TA, and soleus muscles was verified by Northern blotting. Antibodies against MLP were used to identify by immunoblot analysis a protein of 22 kDa, the predicted molecular mass of MLP. Immunohistochemistry revealed strong reactivity for MLP in all fibers of normal soleus muscle and faint staining of some type IIA and type I fibers in control TA muscle. These fibers increased in number and staining intensity in 4-day-stimulated TA muscle. MLP thus seems to play an essential role during the rearrangement of cytoskeletal and/or myofibrillar structures in transforming adult muscle fibers.

Amino Acid Sequence↗
PubMed2002

Degeneration of skeletal muscle fibers in the rat administrated carbon tetrachloride: similar histological findings of the muscle in a 64-year-old patient of LC with muscle cramp.

It is well known that painful muscle cramps occur frequently in patients with advanced liver cirrhosis (LC). Although many studies discuss the pathophysiological causes of these muscle cramps in various conditions, the results are not clear as far as the cause associated to LC is concerned. In order to investigate the cause of muscle cramps in LC, we examined the histological findings of skeletal muscle fibers in LC rat model and in a patient with LC. LC (n=9) was induced in rats by chronic carbon tetrachloride administration. The histological findings of skeletal muscle tissues from the lower leg in LC rats and those of the upper arm in a patient with LC were compared. The degenerated muscle fibers and centronucleus in LC rats were similar to the opaque fibers frequently observed in myotonic dystrophy with severe muscle rigidity in patients with LC. In conclusion, results of this study suggest that one of the causes for muscle cramps in patients with LC is due to skeletal muscle fiber degeneration. Therefore, histological observation of skeletal muscle fibers should be considered in the treatment of painful muscle cramps.

Journal Article↗
PubMed1996

Regenerated rat fast muscle transplanted to the slow muscle bed and innervated by the slow nerve, exhibits an identical myosin heavy chain repertoire to that of the slow muscle.

The hypothesis that the limited adaptive range observed in fast rat muscles in regard to expression of the slow myosin is due to intrinsic properties of their myogenic stem cells was tested by examining myosin heavy chain (MHC) expression in regenerated rat extensor digitorum longus (EDL) and soleus (SOL) muscles. The muscles were injured by bupivacaine, transplanted to the SOL muscle bed and innervated by the SOL nerve. Three months later, muscle fibre types were determined. MHC expression in muscle fibres was demonstrated immunohistochemically and analysed by SDS-glycerol gel electrophoresis. Regenerated EDL transplants became very similar to the control SOL muscles and indistinguishable from the SOL transplants. Slow type 1 fibres predominated and the slow MHC-1 isoform was present in more than 90% of all muscle fibres. It contributed more than 80% of total MHC content in the EDL transplants. About 7% of fibres exhibited MHC-2a and about 7% of fibres coexpressed MHC-1 and MHC-2a. MHC-2x/d contributed about 5-10% of the whole MHCs in regenerated EDL and SOL transplants. The restricted adaptive range of adult rat EDL muscle in regard to the synthesis of MHC-1 is not rooted in muscle progenitor cells; it is probably due to an irreversible maturation-related change switching off the gene for the slow MHC isoform.

Adenosine Triphosphatases↗
PubMed1981

Relationship between muscle length, muscle activity, and torque of the hamstring muscles.

The relationship between muscle length, integrated electromyographic activity, and torque of the biceps femoris muscle was investigated while the line of action of the muscle at the knee was held constant. Muscle length was changed by varying the hip joint angle. Sixteen subjects produced 1) maximal isometric contractions, 2) contractions with constant submaximal torque, and 3) contractions with constant submaximal muscle activity at four different hip positions (0, 45, 90, and 135 degrees of flexion). Simultaneous readings of hip angle, muscle torque, and raw and integrated electromyographic activity revealed that changes in muscle length influence production of integrated muscle activity and development of torque differently. During maximal isometric contraction, an increase in integrated electromyographic activity and a decrease in torque occurred as the muscle was shortened; the opposite occurred when the muscle was at lengthened positions. A greater difference in this relationship was noted when the respective electromyographic activity and torque were held constant. Some clinical questions were raised.

Adult↗
PubMed1999

Effects of muscle contraction on skeletal muscle blood flow: when is there a muscle pump?

PURPOSE: The purpose of this study was to determine the effects of rhythmic muscle contraction on the dynamics of venous outflow in rat skeletal muscle. METHODS: The effects of frequency and duration of tetanic contraction on venous blood flow (BF) were examined with transonic flow probes placed on the femoral artery and vein. RESULTS: Results reveal that instrumentation of the venous system with cannulas or flow probes alters vascular mechanics so that the muscle pump effect is masked. Measurements conducted without instrumentation of the venous vasculature in situ, as well as experiments with conscious exercising animals, indicate that the muscle pump enhances BF during exercise. Also, recent in vivo studies of humans indicate an important role for the muscle pump. In contrast, results reported herein and recent results from in situ experiments, which allow control of more parameters, indicate that there is no measurable muscle pump effect on BF during rhythmic muscle contraction. Review of the literature indicates that many in vitro/in situ experiments used instrumented veins that may have altered venous vascular mechanics and the interactions of muscle contraction and venous vascular mechanics, thus minimizing or abolishing the muscle pump effect. CONCLUSIONS: The muscle pump contributes to the initial increase in BF at exercise onset and to maintenance of BF during exercise.

Animals↗
PubMedDate not supplied

Fine structure of muscle in human disuse atrophy: significance of proximal muscle involvement in muscle disorders.

The universal occurrence of weakness of skeletal musculature on disuse, however produced, and the paucity of published reports on the fine structural changes in human disuse atrophy, prompted the present investigation. The quadriceps muscle of a leg immobilized in plaster cast (for fracture) and of the opposite non-immobilized limb was biopsied in four adult males, after periods of immobilization from 50 to 75 days. These 8 muscle specimens were examined for histopathological changes, and muscle fibre diameters were measured by micrometry from paraffin sections. The histograms revealed a larger proportion of small fibres (less than 20 micron) and a smaller proportion of large fibres (greater than 40 micron) in the immobilized limb compared to the opposite. Thus, light microscopy showed only atrophic changes. This was confirmed by electronmicroscopy, where atrophy of few to several muscle fibres was seen in the form of loss of myofibrils, collapse and folding of the basement membrane and prominence of glycogen or muscle nuclei. The atrophic change was more severe in the immobilized limbs, but it was also noticeable in all the non-immobilized limbs. Degenerative changes, especially disorganization and breakdown of myofibrils, and fragmentation of plasma membrane, were also seen in occasional atrophied muscle fibres, again more frequently in the immobilized limb. Lipofuscin was often found accumulated in muscle fibres and occasionally in endothelial cells of intramuscular blood vessels; the latter showed prominent pinocytotic vesicles or thickened basement membrane. It is concluded that both atrophy and degeneration of fibres of proximal muscles can occur as non-specific consequences of disuse of the limb in man, that degeneration is a latter and more severe change, that muscles even of the non-immobilized leg are subjected to disuse atrophy during bed-rest, and that the proximal muscles in man seem to have a natural susceptibility to atrophy and degeneration in any muscular disorders.

Adult↗
PubMed2001

Muscle length affects the architecture and pattern of innervation differently in leg muscles of mouse, guinea pig, and rabbit compared to those of human and monkey muscles.

The innervation pattern and fascicular anatomy of muscles of different lengths in mouse, guinea pig, rabbit, macaque monkey and human legs were analyzed. Neuromuscular junctions, muscle tendon junctions and ends of intrafascicularly terminating fibers were stained for acetylcholinesterase, and fascicle lengths measured. A high correlation between increasing fascicle length and increasing number of neuromuscular junctions was found, with non-primate (mouse, guinea pig, rabbit) and primate (macaque monkey, human) muscles forming two discrete groups. In non-primates, muscles with a single endplate band, fascicles were always shorter than 35 mm, fixing the limit of fiber length served by one neuromuscular junction. Muscles with fascicles longer than this had multiple discrete bands of motor endplates crossing their width at regular intervals. An increase in muscle length across or within species corresponded to an equivalent, standard increase of 10-12 mm fascicle length per motor endplate band. All human and monkey leg muscles, with the exception of gracilis and sartorius, were singly innervated and all muscle fibers ran the full distance from tendon to tendon. Singly innervated primate muscle fibers were up to 140 mm long whereas the mean distance between endplate bands in the two multiply innervated muscles was also considerably greater than in non-primates. These data indicate that allometric effects of increasing fascicle length, are distinct in common laboratory animals and two primates, when architecture and pattern of innervation are compared.

Acetylcholinesterase↗
PubMed2001

Skeletal muscle characteristics, muscle strength and thigh muscle area in patients before and after cardiac transplantation.

BACKGROUND: Patients with chronic heart failure demonstrate several skeletal muscle abnormalities. The underlying mechanisms are unclear. After cardiac transplantation, cardiac function is restored, but exercise capacity is still impaired. AIM: To evaluate the influence of cardiac transplantation on skeletal muscle fibre composition, fibre area and capillarization as well as muscle enzymes, lactate, thigh muscle area and strength. METHODS: Ten patients were longitudinally investigated before, 1-3 and 6-9 months after transplantation. Ten healthy individuals served as controls. A biopsy from the lateral vastus muscle was obtained and the thigh muscle area was measured with computed tomography. Muscle strength in the knee extensors and exercise capacity were also evaluated. RESULTS: Muscle lactate was elevated in patients vs. controls (3.6+/-3.0 vs. 1.5+/-0.7 mmol/kg wet wt., P=0.037), and decreased to normal (1.4+/-0.3 mmol/kg wet wt., P=0.038) after transplantation. Citrate synthase activity was decreased in patients (5.6+/-1.5 micromol/g wet wt./min) vs. controls (8.1+/-1.6 micromol/g wet wt./min, P=0.0018), and did not change post transplantation. Patients had decreased number of capillaries in contact with each fibre vs. controls (2.6+/-0.5 vs. 3.5+/-1.0, P=0.039) which persisted post transplantation. Exercise capacity increased after transplantation (74+/-22 vs. 118+/-26 W, P=0.0002), whereas muscle strength did not improve significantly. CONCLUSION: The persisting intrinsic abnormalities in skeletal muscle after cardiac transplantation may contribute to the impaired exercise capacity observed in cardiac transplant recipients.

Case-Control Studies↗
PubMed2002

Stable expression of calpain 3 from a muscle transgene in vivo: immature muscle in transgenic mice suggests a role for calpain 3 in muscle maturation.

Limb-girdle muscular dystrophy, type 2A (LGMD 2A), is an autosomal recessive disorder that causes late-onset muscle-wasting, and is due to mutations in the muscle-specific protease calpain 3 (C3). Although LGMD 2A would be a feasible candidate for gene therapy, the reported instability of C3 in vitro raised questions about the potential of obtaining a stable, high-level expression of C3 from a transgene in vivo. We have generated transgenic (Tg) mice with muscle-specific overexpression of full-length C3 or C3 isoforms, which arise from alternative splicing, to test whether stable expression of C3 transgenes could occur in vivo. Unexpectedly, we found that full-length C3 can be overexpressed at high levels in vivo, without toxicity. In addition, we found that Tg expressing C3 lacking exon 6, an isoform expressed embryonically, have muscles that resemble regenerating or developing muscle. Tg expressing C3 lacking exon 15 shared this morphology in the soleus, but not other muscles. Assays of inflammation or muscle membrane damage indicated that the Tg muscles were not degenerative, suggesting that the immature muscle resulted from a developmental block rather than degeneration and regeneration. These studies show that C3 can be expressed stably in vivo from a transgene, and indicate that alternatively spliced C3 isoforms should not be used in gene-therapy applications because they impair proper muscle development.

Animals↗
PubMed2002

Thermosensitivity of muscle: high-intensity thermal stimulation of muscle tissue induces muscle pain in humans.

Small-calibre afferent units responding to thermal stimuli have previously been reported to exist in muscle. The question as to whether these receptors in humans mediate subjective thermal sensations from muscle remains unresolved. The aims of the present study were to determine in humans whether intramuscular injection of warm and cold isotonic saline elicits temperature sensations, muscle pain or any other sensations. In 15 subjects, no thermal sensations assessed on a temperature visual analogue scale (VAS) could be detected with intramuscular injections of isotonic saline (1.5 ml) into the anterior tibial muscle at temperatures ranging from 8 to 48 degrees C. The same subjects recorded strongly increasing scores on a temperature VAS when thermal stimuli in the same intensity range were applied to the skin overlying the muscle by a contact thermode. However, I.M. isotonic saline of 48 degrees C induced muscle pain with peak scores of 3.2 +/- 0.8 cm on a VAS scale ranging from 0 to 10 cm. Using the the McGill pain questionnaire a subgroup, of subjects qualitatively described the pain using the 'thermal hot' and 'dullness' word groups. Temperature measurements within the muscle during the stimulating injections showed that the time course of the pain sensation elicited by saline at 48 degrees C paralleled that of the intramuscular temperature and far outlasted the injection time. The present data show that high-intensity thermal stimulation of muscle is associated with muscle pain. High-threshold warm-sensitive receptors may mediate the pain following activation by temperatures of 48 degrees C or more. Taken together, the data indicate that thermosensation from a given volume of muscle is less potent than nociception.

Adult↗
PubMed2004

A morphological study on the human obturator externus muscle with reference to anomalous muscle and anomalous fasciculus originating from the obturator externus muscle.

To elucidate the essential nature of the human obturator externus muscle (OE), the gross anatomy of the anomalous muscle and anomalous fasciculus originating from this muscle as well as the posterior division of the obturator nerve (P) were examined in 73 thighs of 45 Japanese adult cadavers. The investigation of anomalous muscle and anomalous fasciculus was effected by observation of the supernumerary muscular branch and supernumerary muscular twig from the P. The anomalous muscle occurring between the adductor brevis muscle (AB) and adductor minimus muscle (AMi) (37/73 thighs; 50.7%) and the anomalous fasciculus fused to the posterior surface of the AMi (18/73 thighs; 24.7%) were detected. It was demonstrated by the course of the P and the suppling nerve, that the OE was divided into its superior fasciculus (or fasciculi) (SF) and main belly by the P, moreover the anomalous muscle originated from the former and the anomalous fasciculus from the latter. Presumably, in the process of ontogeny, the SF of the original OE retained its original morphology (23/73 thighs; 31.5%), a part of the SF was converted to anomalous muscle (27/73 thighs; 37.0%), the entire SF was converted to anomalous muscle (10/73 thighs; 13.7%), and the entire SF underwent retrogression and disappeared (13/73 thighs; 17.8%). The presence (50/73 thighs; 68.5%) or absence (23/73 thighs; 31.5%) of piercing of the OE by the P seemed to depend upon the circumstances surrounding the morphological change in the SF. The original OE was considered to occur as an OE pierced by the P not possessing any supernumerary muscular branch or twig. Actually, the original OE was confirmed to occur with a low frequency (15/73 thighs; 20.5%). It was inferred that the original OE readily underwent variation in the process of ontogeny due to the influence of the obturator nerve. The segmental composition of the obturator nerve was considered not to be involved in the morphological change in the OE.

Adult↗
PubMed2026

Skeletal Muscles Do Not Compete for Growth: Activating Additional Muscle Mass Does Not Compromise Changes in Muscle Size.

Kataoka, R, Yamada, Y, Hammert, WB, Sallberg, RW, Kang, A, Song, JS, Kassiano, W, Metcalf, EE, and Loenneke, JP. Skeletal muscles do not compete for growth: Activating additional muscle mass does not compromise changes in muscle size. J Strength Cond Res 40(9): 1043-1049, 2026-This study investigated whether the magnitude of muscle size and strength differed based on the amount of muscle recruited during training sessions. One hundred five untrained individuals were randomly assigned to 1 of 3 groups: low-load unilateral elbow flexion exercise (a) to failure (LL-Failure, n = 36), (b) to failure and low-load knee extension exercise to failure (LL-Failure + Legs, n = 33), or (c) a time-matched nonexercise control (CON, n = 36). Training groups completed 18 supervised sessions over 6 weeks (2 sets at 30% 1 repetition maximum [1RM] to failure). LL-Failure + Legs group performed 4 additional sets of knee extension exercise in each leg (20-30 RM). Muscle thickness on the anterior upper arm (60 and 70% sites) and elbow flexor 1RM strength of the trained arm were measured at pretesting and posttesting. Changes were compared using the ANCOVA function of Bayes Factors for Informative Hypotheses (prevalues as the covariate). Specific hypotheses were evaluated by comparing Bayes factors and the posterior probabilities between models. Six weeks of training led to increases in muscle size and strength. However, performing additional leg exercise did not attenuate the muscle growth in the anterior upper arm (0.19 cm) compared with performing only arm exercise to failure (0.18 cm). Changes in 1RM strength also did not differ between training groups (0.32 and 0.25 kg for LL-Failure and LL-Failure + Legs, respectively). Overall, there was no evidence for competition of adaptations in muscle size and strength under uncontrolled nutritional conditions. Whether greater training volume or limited nutrient intake induces a competition for resources warrants further investigation.

Humans↗
PubMedDate not supplied

Turnover rates of muscle proteins in cardiac, skeletal, and smooth muscle: turnover rate related to muscle function.

The turnover rate of muscle proteins was related to the physiological function of the muscle in dogs, fowl, rats, and mice. The turnover rates of mixed muscle proteins were most rapid in cardiac muscle, intermediate in red tonic and mixed fiber-type muscles, and slowest in white twitch skeletal muscle. This same progression in turnover rates also was shown in the subcellular fractions of muscle-sarcoplasmic and myofibrillar proteins-as well as in purified proteins, myosin, and tropomyosin. The RNA concentration of muscle was highly correlated with the protein turnover rate, and the RNA activity, i.e., the translational efficiency of the RNA, was similar in the different muscle types.

Animals↗
PubMed1989

Increased muscle tension and reduced elasticity of affected muscles in recent-onset Graves' disease caused primarily by active muscle contraction.

In 3 patients with Graves' disease of recent onset, length-tension diagrams were made during surgery for squint under eyedrop anesthesia. The affected muscles were found to be very stiff when the other eye looked straight ahead. It was expected that these stiff muscles would be able to shorten to some extent but would be unable to lengthen, due to fibrosis of the muscle. We found that the affected muscles did not shorten very much when the other eye looked into the field of action of the muscle. Unexpectedly however, they lengthened considerably when the other eye looked out of the field of action of the muscle. This finding implies that the raised muscle tension and reduced elasticity of affected muscles in these cases of Graves' disease of recent onset were primarily caused by active muscle contraction, not by fibrosis.

Diplopia↗
PubMed2003

Spatial relationships between masticatory muscles and their innervating nerves in man with special reference to the medial pterygoid muscle and its accessory muscle bundle.

The relationships between the positional arrangement of the surrounding and innervating nerves of the muscles supplied by the mandibular nerve, in particular those medial to the main trunk of the nerve, were examined in 24 head halves from 12 Japanese cadavers by dissection from the inside after removal of the bony elements except for the mandible. In ten sides of five heads, the lingual nerve pierced the medial pterygoid muscle, and the bundle lateral to the nerve was found to be separated as an accessory muscle bundle. The accessory bundle was frequently attached to the mylohyoid muscle. In addition, the inferior alveolar nerve and the lingual nerve frequently communicated, and in four specimens a branch from the lingual nerve entered the mylohyoid to communicate with the proper nerve. The innervation pattern indicated that the medial pterygoid muscle consists of the anteromedial and the posterolateral main parts, and sometimes has an accessory bundle. Based on the present findings and the previous studies of the positional relationships between the muscles and nerves by our research group, we propose that the muscles innervated by the mandibular nerve could be classified as an inner group (the lateral pterygoid) and an outer group (the other muscles). A possible scheme of the positional relationships between the muscles and nerves is presented.

Aged↗
PubMed2006

Expansion of revertant fibers in dystrophic mdx muscles reflects activity of muscle precursor cells and serves as an index of muscle regeneration.

Duchenne muscular dystrophy and the mdx mouse myopathies reflect a lack of dystrophin in muscles. However, both contain sporadic clusters of revertant fibers (RFs) that express dystrophin. RF clusters expand in size with age in mdx mice. To test the hypothesis that the expansion of clusters is achieved through the process of muscle degeneration and regeneration, we analyzed muscles of mdx mice in which degeneration and regeneration were inhibited by the expression of micro-dystrophins or utrophin transgenes. Postnatal RF expansion was diminished in direct correlation to the protective effect of the transgene expression. Similarly, expansion of RFs was inhibited when muscle regeneration was blocked by irradiation. However, in irradiated muscles, irradiation-tolerant quiescent muscle precursor cells reactivated by notexin effectively restored RF expansion. Our observations demonstrate that revertant events occur initially within a subset of muscle precursor cells. The proliferation of these cells, as part of the regeneration process, leads to the expansion of RF clusters within degenerating muscles. This expansion of revertant clusters depicts the cumulative history of regeneration, thus providing a useful index for functional evaluation of therapies that counteract muscle degeneration.

Animals↗