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Nutrition, Metabolism, and... Dec 2013Changes in muscle mass may result from changes in protein turnover, reflecting the balance between protein synthesis and protein degradation, and changes in cell... (Review)
Review
Changes in muscle mass may result from changes in protein turnover, reflecting the balance between protein synthesis and protein degradation, and changes in cell turnover, reflecting the balance between myonuclear accretion and myonuclear loss. Myonuclear accretion, i.e. increase in the number of myonuclei within the muscle fibers, takes place via proliferation and fusion of satellite cells, myogenic stem cells associated to skeletal muscle fibers and involved in muscle regeneration. In developing muscle, satellite cells undergo extensive proliferation and most of them fuse with myofibers, thus contributing to the increase in myonuclei during early postnatal stages. A similar process is induced in adult skeletal muscle by functional overload and exercise. In contrast, satellite cells and myonuclei may undergo apoptosis during muscle atrophy, although it is debated whether myonuclear loss occurs in atrophying muscle. An increase in myofiber size can also occur by changes in protein turnover without satellite cell activation, e.g. in late phases of postnatal development or in some models of muscle hypertrophy. The relative role of protein turnover and cell turnover in muscle adaptation and in the establishment of functional muscle hypertrophy remains to be established. The identification of the signaling pathways mediating satellite cell activation may provide therapeutic targets for combating muscle wasting in a variety of pathological conditions, including cancer cachexia, renal and cardiac failure, neuromuscular diseases, as well as aging sarcopenia.
Topics: Animals; Humans; Hypertrophy; Muscle, Skeletal; Muscular Atrophy; Sarcopenia; Satellite Cells, Skeletal Muscle; Signal Transduction
PubMed: 22621743
DOI: 10.1016/j.numecd.2012.02.002 -
Skinmed 2006A 41-year-old woman presented with a 3-year history of purpuric lesions followed by superficial, painful ulcers and development of lesions on the lower legs and on the... (Review)
Review
A 41-year-old woman presented with a 3-year history of purpuric lesions followed by superficial, painful ulcers and development of lesions on the lower legs and on the dorsa of the feet, particularly in the summer. The patient was asymptomatic during the winter months. On physical examination she had irregular, scleroatrophic, white-ivory, coalescent lesions on a livedoid basis, with purpuric and, in some lesions, pigmented borders with numerous telangiectatic capillaries. These lesions were localized on the medial sides of the lower legs and on the dorsa of the feet (Figure 1). Laboratory investigations were normal or negative, including complete blood cell count, platelets, coagulation indexes, erythrocyte sedimentation rate, serum immunoglobulins, antinuclear antibodies, anti-double-stranded DNA, anticardiolipin, antiphospholipids, antineutrophilic cytoplasmic antibodies, circulating immunocomplexes, complement fractions (C3, C4), cryoglobulins, rheumatoid factor, and Rose-Waaler reaction. The only laboratory abnormality was an elevated fibrinogen level (472 mg/dL). Doppler velocimetry excluded a chronic venous insufficiency. Thoracic x-ray and abdominal ultrasound were normal. A digital photoplethysmograph revealed functional Raynaud's phenomenon. A biopsy specimen taken from a purpuric lesion showed an atrophic epidermis with parakeratosis and focal spongiosis. An increased number of small-sized vessels were observed within a sclerotic dermis. Most of the vessels in the upper dermis were dilated and showed endothelial swelling; some were occluded due to amorphous hyaline microthrombi (Figure 2). There were fibrinoid deposits around the vessels with thickening of the vessel walls. Extravasated erythrocytes were found throughout the upper and mid-dermis. There was a sparse perivascular lymphocytic infiltrate but no vasculitis. Direct immunofluorescence showed a perivascular microgranular deposit of IgM (+), C3 (++), and fibrinogen/fibrin (+++). On the basis of clinical, serologic, histopathologic, and immunopathologic findings, a diagnosis of idiopathic atrophie blanche was made. The patient was treated with dapsone (50 mg p.o. q.d.) and pentoxifylline (400 mg p.o. t.i.d.) with pain relief and complete resolution of the ulcerations after 6 weeks of therapy.
Topics: Administration, Oral; Adult; Anti-Inflammatory Agents; Atrophy; Dapsone; Diagnosis, Differential; Drug Therapy, Combination; Female; Humans; Leg Ulcer; Pentoxifylline; Skin; Skin Diseases, Vesiculobullous
PubMed: 16687988
DOI: 10.1111/j.1540-9740.2006.04541.x -
The Medical Journal of Australia Aug 1980
Topics: Humans; Muscular Atrophy
PubMed: 7421676
DOI: 10.5694/j.1326-5377.1980.tb76938.x -
Acta Medica Scandinavica 1946
Topics: Humans; Muscular Atrophy; Neuromuscular Diseases; Spinal Muscular Atrophies of Childhood
PubMed: 21026460
DOI: 10.1111/j.0954-6820.1946.tb06167.x -
The International Journal of... Oct 2016Studies of skeletal muscle disuse, either in patients on bed rest or experimentally in animals (immobilization), have demonstrated that decreased protein synthesis is...
Studies of skeletal muscle disuse, either in patients on bed rest or experimentally in animals (immobilization), have demonstrated that decreased protein synthesis is common, with transient parallel increases in protein degradation. Muscle disuse atrophy involves a process of transition from slow to fast myosin fiber types. A shift toward glycolysis, decreased capacity for fat oxidation, and substrate accumulation in atrophied muscles have been reported, as has accommodation of the liver with an increased gluconeogenic capacity. Recent studies have modeled skeletal muscle disuse by using cyclic stretch of differentiated myotubes (C2C12), which mimics the loading pattern of mature skeletal muscle, followed by cessation of stretch. We utilized this model to determine the metabolic changes using non-targeted metabolomics analysis of the media. We identified increases in amino acids resulting from muscle atrophy-induced protein degradation (largely sarcomere) that occurs with muscle atrophy that are involved in feeding the Kreb's cycle through anaplerosis. Specifically, we identified increased alanine/proline metabolism (significantly elevated proline, alanine, glutamine, and asparagine) and increased α-ketoglutaric acid, the proposed Kreb's cycle intermediate being fed by the alanine/proline metabolic anaplerotic mechanism. Additionally, several unique pathways not clearly delineated in previous studies of muscle unloading were seen, including: (1) elevated keto-acids derived from branched chain amino acids (i.e. 2-ketoleucine and 2-keovaline), which feed into a metabolic pathway supplying acetyl-CoA and 2-hydroxybutyrate (also significantly increased); and (2) elevated guanine, an intermediate of purine metabolism, was seen at 12h unloading. Given the interest in targeting different aspects of the ubiquitin proteasome system to inhibit protein degradation, this C2C12 system may allow the identification of direct and indirect alterations in metabolism due to anaplerosis or through other yet to be identified mechanisms using a non-targeted metabolomics approach.
Topics: Animals; Biomechanical Phenomena; Cell Line; Mechanical Phenomena; Metabolomics; Mice; Muscular Atrophy
PubMed: 27515590
DOI: 10.1016/j.biocel.2016.08.012 -
Maandschrift Voor Kindergeneeskunde Jul 1951
Topics: Arthritis; Atrophy; Bone Marrow; Deafness; Leukemia; Polychondritis, Relapsing
PubMed: 14862311
DOI: No ID Found -
Paris Medical Feb 1946
Topics: Disease; Humans; Knee; Muscle, Skeletal; Muscles; Muscular Atrophy; Thigh
PubMed: 21019418
DOI: No ID Found -
Journal of Medical Genetics Aug 1976Chronic spinal muscular atrophy of FSH type affecting a mother and her son and daughter is reported. The relevant literature is reviewed and the relation between this...
Chronic spinal muscular atrophy of FSH type affecting a mother and her son and daughter is reported. The relevant literature is reviewed and the relation between this conditon and Kugelberg-Welander (K-W) disease is discussed. Chronic spinal muscular atrophy of FSH type is considered to be a different entity from the eponymous K-W disease. Each type of muscular dystrophy, e.g. limb-girdle, FSH, distal, ocular, or oculopharyngeal type, has its counterpart of nuclear origin. A classification of the chronic spinal muscular atrophies is suggested following the classification of muscular dystrophy.
Topics: Action Potentials; Adolescent; Adult; Chronic Disease; Female; Genes, Dominant; Humans; Male; Middle Aged; Muscles; Muscular Atrophy; Pedigree
PubMed: 957378
DOI: 10.1136/jmg.13.4.285 -
Neuropediatrics Oct 1992An infant presented at birth with symmetrical flaccid paraparesis limited to lower legs and feet, and involving the proximal and distal muscle group. Limitation of the...
An infant presented at birth with symmetrical flaccid paraparesis limited to lower legs and feet, and involving the proximal and distal muscle group. Limitation of the ankle joints was noticed. There were no sensory deficits to painful stimuli and no evidence of loss of sphincter control. Muscle CT revealed severe muscle atrophy in the pelvis and lower limbs, and electromyographic study of the bilateral hamstrings showed polyphasic giant potentials. Motor and sensory nerve conduction velocities were within normal limits, and the spinal MRI showed no structural abnormalities in the cord and the lower spine. These features suggest a congenital segmental abnormality at the anterior horn cell level in the lumbosacral spinal cord, which we propose to call "congenital caudal spinal atrophy".
Topics: Arthrogryposis; Atrophy; Female; Humans; Infant; Infant, Newborn; Magnetic Resonance Imaging; Spinal Cord; Spinal Muscular Atrophies of Childhood; Tomography, X-Ray Computed
PubMed: 1454146
DOI: 10.1055/s-2008-1071354 -
Sports Medicine (Auckland, N.Z.) Mar 1988Strength training is commonly used in the rehabilitation of muscles atrophied as a result of injury and/or disuse. Studies on the effects of conventional leg extension... (Review)
Review
Strength training is commonly used in the rehabilitation of muscles atrophied as a result of injury and/or disuse. Studies on the effects of conventional leg extension training in healthy subjects have shown the changes to be very task-specific to the training manoeuvre itself. After conventional leg extension training for the quadriceps muscle the major improvement was in weightlifting ability with only small increases in isometric strength. The maximum dynamic force and power output during sprint cycling showed no improvement. These results suggest that the major benefit of this type of training is learning to coordinate the different muscle groups involved in the training movement rather than intrinsic increases in strength of the muscle group being trained. Other studies have shown changes in strength to be specific to the length and speed at which the muscle has been trained. The implication for rehabilitation is that strength training for isolated muscle groups may not be the most effective way of increasing functional ability. As the major changes are task-specific it may be better to incorporate the training into task-related practice. This would have the advantage of strengthening the muscle groups affected whilst increasing performance in those activities which are required in daily life.
Topics: Humans; Muscular Atrophy; Physical Therapy Modalities; Wounds and Injuries
PubMed: 3285437
DOI: 10.2165/00007256-198805030-00006