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PubMed1995

Regeneration pattern of cardiac and skeletal muscle after transplantation into a skeletal muscle bed in rats.

BACKGROUND: The ability of skeletal muscle to regenerate after injury is well established. In contrast, cardiac muscle is incapable of regeneration and recovery after injury. The aim of the present study was to evaluate and compare the regeneration pattern of cardiac and skeletal muscle after transplantation into a skeletal muscle bed in rats. METHODS: The following group of transplants were performed at the site prepared by removing the host extensor digitorum longus (EDL) muscle. The first group consisted of cardiac muscle transplanted as one piece or after mincing into 1-mm pieces. The second group included cotransplants of cardiac and skeletal muscle minces that were intermixed. Entire EDL muscle or minced EDL muscle were also transplanted for comparison. Rats were sacrificed 3-30 days after transplantation for morphological analysis. RESULTS: The results demonstrated that skeletal muscle transplants underwent rapid regeneration, and by 30 days the entire muscle was filled with regenerated myofibers. In transplants of cardiac muscle significant inflammation, myocardial degeneration and necrosis were observed. In spite of the necrosis and fibrosis, the presence of a few regenerated myotubes in the outer region was observed. In cardiac and skeletal muscle cotransplants, the inflammation was restricted to cardiac tissue; however, by 30 days the entire cotransplant was filled with regenerated myotubes and myofibers. CONCLUSIONS: These results show that skeletal muscle is capable of growth, regeneration, and integration with the cardiac muscle after cotransplantation. Combination of skeletal and cardiac muscle may prove useful in defining the cellular processes necessary for enhancing cardiac repair after injury.

Animals↗
PubMed2000

The formation of the chick ileal muscle layers as revealed by alpha-smooth muscle actin immunohistochemistry.

The genesis of intestinal smooth muscle layers was immunohistochemically investigated by use of an antibody to alpha-smooth muscle actin (alpha-SMA) in the developing chick ileum. Myoblast cells positive for alpha-SMA were already found in the presumptive circular muscle layer on E 8.5. On E 11.5 radially oriented muscle fibers were protruded from the outermost layer of the developing circular musculature and then formed a tuft-like aggregates. These radial muscle bundles were bent into an L-shape. The long distal extension of muscle bundles run parallel to the long axis of the ileal loop and developed into the longitudinal muscle layer. The obliquely oriented muscle fibers, locating at the intermuscular space of the muscularis propria, probably are to be considered a remnant of the short extension of radial muscle bundles. The muscularis mucosae was formed by the processes equivalent to the genesis of longitudinal muscle layer. On E 14.5 centripetally oriented muscle fibers emerged from the innermost layer of circular musculature. The long distal extension of centripetal fibers lay along the inner surface of developing circular musculature. On E 19.5 the longitudinal muscle layer of the muscularis mucosae was newly formed by separating from the circular musculature. The villous myoblast cells initially developed from the innermost layer of the muscularis mucosae on E 18.5, and were widely distributed in the lamina propria mucosae on E 20.5. Temporal and chronological pattern in expression of alpha-SMA was observed during the development of the chick intestinal smooth muscle. By E 14.5 the entire layer of the muscularis propria was intensely immunostained for alpha-SMA, but from E 15.5 onward the staining intensity gradually began to decrease from the outer half of the circular musculature. Finally, the immunoreactivity was localized in the inner layer of circular muscle and the longitudinal muscle layer. A possible functional role of this inner layer of circular muscle is discussed.

Actins↗
PubMed2004

Muscle tension dynamics of isolated frog muscle with application of perpendicular distortion.

The purpose of the present study was to confirm the relationship between isolated frog muscle tension and muscle hardness by conducting physiological evaluation in vivo. Two different mounting forms of the muscle were adopted. One form placed the gastrocnemius muscle (GA) on a base plate; this dented the muscle as a "mass". The other form tightened the sartorius muscle (SA) between holders in Ringer's solution; this bent the muscle as a "string". The first experimental method allowed testing of muscle hardness during stretching up to 140% (experiment 1) and the other method allowed testing of hardness during tetanic muscle contraction (experiment 2). The response force to vertical distortion, measured as muscle hardness, increased linearly with resting tension increase and this relationship was not influenced by the hysteresis (experiment 1). The response force increments at each level of tetanic muscle tension were proportional to the contracting tension (experiment 2). Although the muscle mounting forms were different, the response force increment to muscle tension in GA and SA showed quite similar relationships in both tests. It seems likely that muscle hardness evaluated by the response force must depend on the amplitude of the tension at the instant of the hardness measurement, regardless of the mounting form or the stretching phase (ascending or descending). In conclusion, muscle hardness measured by perpendicular distortion has physiological significance related to the changes in passive and active muscle tension.

Animals↗
PubMed1994

Distribution of muscle degeneration in Welander distal myopathy--a magnetic resonance imaging and muscle biopsy study.

Seven patients with Welander distal myopathy were subjected to magnetic resonance imaging (MRI) of the lower extremity, and muscle biopsies of the tibialis anterior, soleus and vastus lateralis muscles. MRI revealed abnormalities in both the anterior and posterior compartments of the lower leg in three of the patients, and in only the posterior compartment in the rest of the patients. No MRI abnormalities were found in either the proximal muscles of the leg or in the peroneal or posterior tibial muscle groups. Affected muscles had T1- and T2-values indicating a replacement of muscle fibres with fat tissue. Muscle biopsies showed pathological changes varying from slight to severe in tibialis anterior and soleus muscles in all patients. No muscle fibre abnormalities were seen in the vastus lateralis muscle in any of the patients. In accordance with earlier reports from patients with Welander distal myopathy, there was muscle degeneration of tibialis anterior muscles corresponding to the weakness of dorsal extension of the feet, but also degeneration in the muscles of the posterior compartment. The patients did not, however, show any clinical signs of weakness related to posterior muscle groups. There is no evidence of involvement of proximal muscles of the leg clinically, with MRI or in muscle biopsies.

Adult↗
PubMed2004

Evaluation of the influence of muscle deactivation on other muscles and joints during gait motion.

When any muscle in the human musculoskeletal system is damaged, other muscles and ligaments tend to compensate for the role of the damaged muscle by exerting extra effort. It is beneficial to clarify how the roles of the damaged muscles are compensated by other parts of the musculoskeletal system from the following points of view: From a clinical point of view, it will be possible to know how the abnormal muscle and joint forces caused by the acute compensations lead to further physical damage to the musculoskeletal system. From the viewpoint of rehabilitation, it will be possible to know how the role of the damaged muscle can be compensated by extra training of the other muscles. A method to evaluate the influence of muscle deactivation on other muscles and joints is proposed in this report. Methodology based on inverse dynamics and static optimization, which is applicable to arbitrary motion was used in this study. The evaluation method was applied to gait motion to obtain matrices representing (1) the dependence of muscle force compensation and (2) the change to bone-on-bone contact forces. These matrices make it possible to evaluate the effects of deactivation of one of the muscles of the musculoskeletal system on the forces exerted by other muscles as well as the change to the bone-on-bone forces when the musculoskeletal system is performing the same motion. Through observation of this matrix, it was found that deactivation of a muscle often results in increment/decrement of force developed by muscles with completely different primary functions and bone-on-bone contact force in different parts of the body. For example, deactivation of the iliopsoas leads to a large reduction in force by the soleus. The results suggest that acute deactivation of a muscle can result in damage to another part of the body. The results also suggest that the whole musculoskeletal system must go through extra retraining in the case of damage to certain muscles.

Adaptation, Physiological↗
PubMed2004

A predictive model of moment-angle characteristics in human skeletal muscle: application and validation in muscles across the ankle joint.

In the present work, a generic model for the prediction of moment-angle characteristics in individual human skeletal muscles is presented. The model's prediction is based on the equation M = V x Lo(-1)sigma c cos phi x d, where M, V, and Lo are the moment-generating potential of the muscle, the muscle volume and the optimal muscle fibre length, respectively, and sigma, phi and d are the stress-generating potential of the muscle fibres, their pennation angle and the tendon moment arm length, respectively, at any given joint angle. The input parameters V, Lo, sigma, phi and d can be measured or derived mechanistically. This eliminates the common problem of the necessity to estimate one or more of the input parameters in the model by fitting its outcome to experimental results often inappropriate for the function modelled. The model's output was validated by comparisons with the moment-angle characteristics of the gastrocnemius (GS) and tibialis anterior (TA) muscles in six men, determined experimentally using voluntary contractions at several combinations of ankle and knee joint angles for the GS muscle and electrical stimulation for the TA muscle. Although the model predicted realistically the pattern of moment-angle relationship in both muscles, it consistently overestimated the GS muscle M and consistently underestimated the TA muscle M, with the difference gradually increasing from dorsiflexion to plantarflexion in both cases. The average difference between predicted and measured M was 14% for the GS muscle and 10% for the TA muscle. Approximating the muscle fibres as a single sarcomere in both muscles and failing to achieve complete TA muscle activation by electrical stimulation may largely explain the differences between theory and experiment.

Analysis of Variance↗
PubMed1997

Characterization of troponin-C interactions in skinned barnacle muscle: comparison with troponin-C from rabbit striated muscle.

Previously it was shown that when troponin-C (TnC) is extracted from barnacle myofibrillar bundles they lose their Ca2+ sensitivity, which can be restored by adding back barnacle TnC (either isoform, BTnC1 or BTnC2). Thus barnacle muscle shows thin filament regulation, as does rabbit psoas skeletal muscle. In this paper we compare the interactions of barnacle and rabbit fast muscle TnC in their respective muscles. We demonstrate that muscle fibres from the giant barnacle, Balanus nubilus, contain about 186 microM kg-1 muscle tissue of BTnC1 plus BTnC2 compared to about 91 microM kg-1 of TnC in rabbit psoas muscle fibres. Extraction of BTnC is achieved using similar low ionic strength, low divalent ion Ca(2+)-low Mg2+ conditions which are required for TnC extraction in rabbit psoas skinned muscle fibres; extraction was prevented by 1 mM Mg2+. Full reconstitution of Ca(2+)-sensitivity was achieved by adding back BTnC (1 + 2, or 2). Reconstitution of barnacle muscle with rabbit fast skeletal TnC (RTnC) was more complex, with partial recovery of Ca(2+)-sensitivity with reconstitution in the presence of 3 mM Mg2+ and more fully with reconstitution in the presence of activating Ca2+ (pCa 4.0). This suggests that the barnacle TnC-TnI (troponin I) recognition sites may be more complex than in rabbit because the barnacle sites appear to have at least two different conformations or types, in which one recognizes RTnC in the presence of Mg2+ and the other only in the presence of Ca2+ and Mg2+. This is consistent with the presence of several TnI isoforms in barnacle striated myofibrils. RTnC has two C-terminal Ca(2+)-Mg2+ binding sites that are thought to be involved in the Mg(2+)-sensitive binding of RTnC in rabbit muscle, yet it has been suggested that this site in barnacle muscle does not bind Mg2+, even though Mg2+ stabilizes BTnC binding in barnacle muscle. Consistent with this stabilizing action of Mg2+, using fluorescent probes IAANS or IAE on isolated BTnC2 we demonstrate that BTnC2 binds both Ca2+ and Mg2+, but the data do not suggest direct competition. Consistent with the C-terminal sites on BTnC being Ca(2+)-specific, BTnC1 + 2 could only reconstitute low levels of force (about 1/3) in TnC-extracted rabbit skinned muscle fibers in the presence of pCa 4.0 (not just Mg2+) and only at low ionic strengths (0.09 M). Ca(2+)-activation of contraction was further examined using fluorescently labelled BTnC2 (labelled with IANBD) incorporated into skinned barnacle myofibrillar bundles. Maximal Ca2+ binding produced structural changes in BTnC which resulted in a 45% decrease in the fluorescence compared to the value at pCa 9.2. The magnitude of the fluorescence decrease paralleled the increase in force with increasing Ca2+. The Hill fits to the data gave pCa1/2 and n of 5.61 +/- 0.02 and 2.06 +/- 0.12 for force, and 5.52 +/- 0.02 and 1.88 +/- 0.10 for fluorescence. Removing MgATP to induce rigor in the fibre decreased BTnC2-NBD fluorescence only about 11%, but the addition of Ca2+ in rigor further decreased the fluorescence to a slightly larger extent than under maximal Ca2+ activating conditions. These fluorescence changes are qualitatively similar to the fluorescence enhancement seen with Ca(2+)-activation and rigor with RTnCDanz exchanged into rabbit psoas skinned muscle fibres. The data support a similar model for Ca(2+)-activation of force in barnacle muscle and in rabbit psoas skeletal muscle fibres.

Animals↗