Showing papers on "Skeletal muscle published in 1972"
1,302 citations
TL;DR: Succinate dehydrogenase and phosphofructokinase activities and the histochemical identification of fiber types and localization of oxidative activity were determined on biopsy samples from the vastus lateralis and deltoid muscles of 74 untrained and trained men.
Abstract: GOLLNICK, P. D., R. B. ARMSTRONG, C. W. SAUBERT IV, K. PIEHL, AND B. SALTIN. Enzyme activity and Jiber composition in skeletal muscle of untrained and trained men. J. Appl. Physiol. 33(3): 3 12-3 19, 1972.-Succinate dehydrogenase (SDH) and phosphofructokinase (PFK) activities and the histochemical identification of fiber types and localization of oxidative activity were determined on biopsy samples from the vastus lateralis and deltoid muscles of 74 untrained and trained men. SDH activities were highest in the muscles of the groups participating in endurance training. Highest activities existed in the muscles that were extensively engaged in the endurance work. Only minor differences existed for PFK activities. Only slow twitch (ST) and fast twitch (FT) fibers were identified in the muscle samples. ST fibers predominated in the muscles of the endurance athletes. A wide variety of fiber populations existed in all groups. The percent distribution of a fiber was found to be indicative of the relative area that the fiber occupied in the muscle. Oxidative capacity of both fiber types was greater in the endurance athletes than in the other groups. Muscle glycogen was highest in the trained subjects. No consistent pattern for glycogen storage in the two fiber types existed.
905 citations
TL;DR: When actin molecules form “rigor complexes” with nucleotide-free myosin, tropomn binds calcium with greater affinity and in a cooperative response the remaining actin molecule not cornplexed with myOSin are “turned on” even though calcium is absent.
Abstract: When actin molecules form “rigor complexes” with nucleotide-free myosin, tropomn binds calcium with greater affinity and in a cooperative response the remaining actin molecules not cornplexed with myosin are “turned on” even though calcium is absent.
673 citations
TL;DR: This is the first report of a protein endogenous to muscle that is able to catalyze degradation of the myofibril, and the very low level of unbound Ca2+ in muscle cells in vivo may regulate activity of this protein fraction, or alternatively, thisprotein fraction may be localized in lysosomes.
Abstract: Removal of rabbit psoas strips immediately after death and incubation in a saline solution containing 1 mM Ca2+ and 5 nM Mg2+ for 9 hr at 37°C and pH 7.1 causes complete Z-line removal but has no ultrastructurally detectable effect on other parts of the myofibril. Z lines remain ultrastructurally intact if 1 mM 1,2-bis-(2-dicarboxymethylaminoethoxy)-ethane (EGTA) is substituted for 1 mM Ca2+ and the other conditions remain unchanged. Z lines are broadened and amorphous but are still present after incubation for 9 hr at 37°C if 1 mM ethylenediaminetetraacetate (EDTA) is substituted for 1 mM Ca2+ and 5 mM Mg2+ in the saline solution. A protein fraction that causes Z-line removal from myofibrils in the presence of Ca2+ at pH 7.0 can be isolated by extraction of ground muscle with 4 mM EDTA at pH 7.0–7.6 followed by isoelectric precipitation and fractionation between 0 and 40% ammonium sulfate saturation. Z-line removal by this protein fraction requires Ca2+ levels higher than 0.1 mM, but Z lines are removed without causing any other ultrastructurally detectable degradation of the myofibril. This is the first report of a protein endogenous to muscle that is able to catalyze degradation of the myofibril. The very low level of unbound Ca2+ in muscle cells in vivo may regulate activity of this protein fraction, or alternatively, this protein fraction may be localized in lysosomes.
344 citations
TL;DR: It is tentatively concluded that, in the regulation of chicken skeletal muscle myogenesis, cell fusion potential and the potential for myosin synthesis are developed not simultaneously, but sequentially.
302 citations
TL;DR: The threshold for caffeine contractures in the frog sartorius and rectus muscles is raised from 2.0 to 4.0 mM in the presence of dantrolene sodium in rat diaphragm-phrenic nerve preparations as mentioned in this paper.
Abstract: In rat diaphragm-phrenic nerve preparations, dantrolene sodium has been shown to have no effect on neuromuscular transmission. KCl and acetylcholine contractures in the frog rectus muscle are depressed in the presence of dantrolene sodium. The threshold for caffeine contractures in the frog sartorius and rectus muscles is raised from 2.0 to 4.0 mM. In isolated frog sartorius muscles, the tetanic fusion frequency is increased by 29%, and the twitch response is depressed more than the tetanic.
261 citations
TL;DR: Results are consistent with the interpretation that α-bungarotoxin binds specifically to the acetylcholine receptor of mammalian skeletal muscle.
Abstract: Experiments were performed to determine the specificity of [125I]α-bungarotoxin binding to skeletal muscle. In adult rat diaphragm, [125I]α-bungarotoxin was found to bind almost exclusively to those regions of the muscle that contain endplates and are known to be sensitive to acetylcholine. In contrast, chronically denervated adult muscle and muscle from neonatal rats, both of which are sensitive along their entire lengths, bound substantial amounts of toxin in all regions. Toxin binding to all muscles was inhibited by d-tubocurarine and by carbamylcholine, but not by atropine. The bound [125I]toxin was solubilized by homogenization of the tissue in 1% Triton X-100 and was recovered as a single band, distinct from free toxin, after zone sedimentation. Treatment of the solubilized, toxin-bound complex with 2-mercaptoethanol and sodium dodecyl sulfate resulted in the recovery of free toxin. A toxin-bound complex was also obtained when toxin was incubated directly with extracts of muscle endplate regions prepared by homogenization in Triton X-100. No such complex was observed with extracts prepared from muscle lacking endplates. These results are consistent with the interpretation that α-bungarotoxin binds specifically to the acetylcholine receptor of mammalian skeletal muscle.
256 citations
TL;DR: In the isolated rat diaphragm, 14C02 production from L-leucine-1 -14C occurred at 86 y0 of the rate of its incorporation into protein, which indicates muscle is probably the major site of leucine catabolism in the animal.
Abstract: ODESSEY, RICHARD, AND ALFRED L. GOLDBERG. Oxidation of leucine by rat skeletal muscle. Am. J. Physiol. 223(6) : 1376-1383. 1972.-In the isolated rat diaphragm, 14C02 production from L-leucine-1 -14C occurred at 86 y0 of the rate of its incorporation into protein. Experiments with L-leucine-U-14C indicate complete oxidation of leucine under these conditions. 14C02 production from leucine-1-14C was inhibited slightly by glucose (15 %) but not by acetate, pyruvate, P-hydroxbutyrate, or palmitate. Amino acids at plasma concentrations inhibited 14C02 production (3O40 (r,) without affecting protein synthesis. Cycloheximide blocked incorporation into protein but stimulated 14C02 production, whereas cyanide and iodoacetate inhibited both processes. Addition of ouabain or the removal of Na+ from the incubation medium inhibited incorporation into protein but not oxidation. Appreciable oxidation of leucine also occurred in the dark soleus and the pale extensor digitorum longus muscles. The diaphragm catabolized leucine at rates similar to liver slices but severalfold less actively than epidydimal fat pad or kidney and brain slices. Since skeletal muscle accounts for over 400/, of the body mass, muscle is probably the major site of leucine catabolism in the animal.
241 citations
TL;DR: In cats anesthetized with chloralose the lengths and diameters of the different vascular segments in the tenuissimus muscle were measured in the vital microscope and the flow characteristics, including red cell velocity, were registered.
Abstract: In cats anesthetized with chloralose the lengths and diameters of the different vascular segments in the tenuissimus muscle were measured in the vital microscope. The flow characteristics, including red cell velocity, were registered. Fixed and stained muscle specimens were analyzed histologically as well as Indian ink-perfused muscles treated according to the method of Spalteholz. The average muscle fibre diameter was 44 μm. 62% of the muscle fibres were red (48% B-fibres, diameter 41 μm and 14% C-fibres, diameter 26 μm) and the remaining 38% were white (A-fibres, diameter 55 μm). The average muscle fibre was surrounded by 3.6 capillaries. The capillaries were 1015 ± 16.3 (S.E.) μm long and 5.3 ± 0.0(3) (S.E.) μm in internal diameter. The calculated capillary surface area was 0.9 m2/100 cm3 of muscle tissue. Average red cell velocity in the capillaries was found to be 0.5 mm/s, but there was a wide variation with time and between different capillaries. Neither “spontaneous” changes in internal diameters of the microvessels nor a distinct precapillary sphincter activity could be observed. Arterio-venous anastomoses within the muscle tissue were rare exceptions.
204 citations
TL;DR: Clinical features consistent with the presence of magnesium deficiency were found in all five magnesium-deficient patients and these features were, with few exceptions, corrected by magnesium replacement.
Abstract: Magnesium levels in serum, erythrocytes, skeletal muscle, and bone were measured in 10 patients with valvular heart disease who had received diuretic therapy for heart failure for an average of 3.3 years. Five patients were found to have diminished values for skeletal muscle, indicating significant magnesium deficit. Values for erythrocytes were low in only two of the five patients, and none had low values for serum ultrafiltrate and bone: Magnesium replacement therapy restored skeletal muscle values to normal. Clinical features consistent with the presence of magnesium deficiency were found in all five magnesium-deficient patients. These features were, with few exceptions, corrected by magnesium replacement. The latter also corrected low skeletal muscle potassium values present in all five patients with low skeletal muscle magnesium, four of whom showed clinical features of digoxin poisoning before magnesium therapy was given. Concomitant secondary aldosteronism, inadequate dietary intake, and digoxin therapy had probably augmented the magnesium loss due to diuretic therapy.
168 citations
TL;DR: Repeated administration of ethanol for 28 days increased serum creatine phosphokinase activity and produced ultrastructural changes in skeletal muscle of human volunteers, suggesting that alcoholic myopathy results from ethanol toxicity, rather than from nutritional or other factors.
Abstract: Repeated administration of ethanol (42 percent of total calories) for 28 days increased serum creatine phosphokinase activity and produced ultrastructural changes in skeletal muscle of human volunteers. The data suggest that alcoholic myopathy results from ethanol toxicity, rather than from nutritional or other factors.
TL;DR: The effects of inhibitors of protein synthesis on the in vivo development of extrajunctional cholinergic receptors, tetrodotoxin‐resistant action potentials, slowing of the time course of the action potential, and on the fall in the resting membrane potential in denervated mouse skeletal muscle are studied.
Abstract: 1. A study was made of the effects of inhibitors of protein synthesis (actinomycin D, chloramphenicol and cycloheximide) on the in vivo development of extrajunctional cholinergic receptors, tetrodotoxin-resistant action potentials, slowing of the time course of the action potential, and on the fall in the resting membrane potential in denervated mouse skeletal muscle.
2. Actinomycin D (0·5 mg/kg, I.P.) reduced the incorporation of uridine into skeletal muscle by 50–60% for 4-5 days. There was no simultaneous reduction in L-leucine incorporation.
3. Actinomycin D (0·5 mg/kg I.P., 1 day after denervation) inhibited the development of extrajunctional cholinergic receptors, tetrodotoxin-resistant action potentials and the fall in resting membrane potential for approximately 4 days.
4. The post-denervation fall in the maximum rate of rise and in the amplitude of the overshoot of the muscle fibre action potential was unaffected by actinomycin D treatment.
5. Actinomycin D failed to inhibit the appearance of the membrane changes if given later than 2 days after denervation.
6. Chloramphenicol (6 g/kg in divided doses) and cycloheximide (40 g/kg every 12 hr) were also able to inhibit the appearance of the membrane changes.
7. It is concluded that some denervation induced changes in the muscle fibre membrane depend on the synthesis of new proteins. The results imply that the motor nerve cell normally exerts a regulatory influence on the genome of the muscle cell.
TL;DR: The regulation of adenylate cyclase in skeletal muscle may be classified as a "V" allosteric system since metal ions, F-, and epinephrine all result in increased maximal velocity of the enzyme reaction.
TL;DR: It is concluded that dantrolene sodium has no effect on the electrical excitability of the muscle and uncouples excitation-contraction mechanisms.
Abstract: Dantrolene sodium, a skeletal muscle relaxant, inhibits the twitch response by direct action on the muscle. The action potentials from dantrolene sodium depressed muscles have been examined by taking their first derivative, and membrane capacitance has been measured with cable analysis techniques. It is concluded that dantrolene sodium has no effect on the electrical excitability of the muscle and uncouples excitation-contraction mechanisms.
TL;DR: Electrical stimulation was applied continuously to the denervated rat diaphragm in vivo to mimic the normal activity pattern, and found that muscle activity may account for "neurotrophic" regulation of the acetylcholine sensitivity.
Abstract: Denervation of skeletal muscle results in a spread of acetylcholine sensitivity over the entire surface membrane. Electrical stimulation, programmed to mimic the normal activity pattern, was applied continuously to the denervated rat diaphragm in vivo. After 4 days, the acetylcholine sensitivity was far less in the stimulated diaphragms than in denervated controls. Muscle activity may account for "neurotrophic" regulation of the acetylcholine sensitivity.
TL;DR: In the older muscles some spindles showed changes consistent with denervation and these changes were always associated with moderately severe grouped denervation atrophy in these muscles, which form a basis for studies of changes in muscle spindle morphology in neuromuscular disease.
TL;DR: Muscle degeneration induced by immobilization in a plaster cast and the regeneration that takes place after immobilization is discontinued, provide ideal models for the histochemical and microenzymatic studies that will be required to elucidate the mechanisms that initiate and control muscle degeneration and regeneration.
Abstract: In a physiological and morphological study of the muscles of the hind limb of cats, we demonstrated that immobilization initiates muscle-cell disintegration which is reflected by a decrease in weight to 30 per cent of normal after twenty-two weeks. During this interval, contraction time and relaxation time increase, but they return to normal one week after release from immobility. In immobilized muscle these times increase much less than they do in denervated muscle. Finally in immobilized muscle the tension during both total twitch and tetanus decreases more than muscle weight.
Most of the classic pathological changes in muscle which are visible by light microscopy and have been described in many experiments and in association with disease can be produced by immobility. Immobilized muscle fibers undergo a more or less well defined sequence of degenerative changes in which many fibers remain simply as sarcotubes which are enclosed by basement membrane and contain only fluid, precipitated protein, and fragments of the sarcolemma. If these changes extend throughout an entire fiber, they indicate irreversible damage. Comparison of the changes induced by immobilization with those produced by other means reveals that despite the complex structure of muscle, its responses to injury are relatively limited.
Immobilized skeletal muscle with an intact blood and nerve supply and intact sarcotubes has great regenerative potential after release from immobilization. Restoration of damaged muscle fibers begins three to five days after release. As the result of endomysial proliferation, tubes are formed which guide the regenerating contractile elements during a well defined sequence of regenerative changes.
Muscle degeneration induced by immobilization in a plaster cast and the regeneration that takes place after immobilization is discontinued, provide ideal models for the histochemical and microenzymatic studies that will be required to elucidate the mechanisms that initiate and control muscle degeneration and regeneration. We agree with the too long-neglected admonition of Eisenhauer and Key who, in 1945, remarked that they were not able to extend their investigations on muscle atrophy, but warned, "It is important that this work be carried to its ultimate conclusion because this will place much of the treatment of injured extremities on a sound experimental basis instead of on the basis of accumulated clinical impressions."17
Journal Article•
TL;DR: Red cell velocity profiles in individual capillaries were studied in the sartorius muscle of the cat during reactive hyperemia using a dual-slit photometric system and it is concluded that augmentation of Aow in previously open capillary is the primary source of reactiveyperemia.
Abstract: BURTON, K.. S., AND P. C. JOHNSON. Reactive hyperemia in individual capillaries of skeletal muscle. Am. J. Physiol. 223 (3) : 517-524. 1972.-Red cell velocity profiles in individual capillaries were studied in the sartorius muscle of the cat during reactive hyperemia using a dual-slit photometric system. The velocity profiles varied considerably from each other and from the simultaneously measured volume flow. The profiles were divided into four groups on the basis of the duration of reactive hyperemia following a 60-set occlusion and the time required to attain peak velocity. One group showed almost no response. A second group had a long period of increased flow (60 & 8 set) and reached a peak value in 35 & 16 sec. The duration of reactive hyperemia for the third group (22 ~fr 3 set) was comparable to that of the gross flow (28 of= 6 set) and reached its peak value after 10 rt 4 sec. The peak response in the fourth group occurred after 5 =t 3 set as compared with 6 =t 1 set in the gross flow and was followed by an interval of zero flow (7 =I= 3 set) before returning to normal. The distributions of the 57 capillaries studied were 28, 14, 2 1, and 37 %, respectively. The question of whether reactive hyperemia was due to the opening of new capillaries or to increased flow in previously open capillaries was investigated. Comparing the ratio of peak velocity to control for the average of all flowing capillaries (1.5 : 1) with that of the gross flow (1.8:1), we conclude that augmentation of Aow in previously open capillaries is the primary source of reactive hyperemia.
TL;DR: The presence of binding sites between the membranes of the sarcoplasmic vesicles and a glycogen-enzyme complex suggests that this association plays a role in the glycogenolysis during muscle contraction.
Abstract: Sarcoplasmic vesicles and s-glycogen particles 30–40 mµ in diameter were isolated from perfused rabbit skeletal muscle by the differential precipitation-centrifugation method. This microsomal fraction was subjected to zonal centrifugation on buffered sucrose gradients, in a B XIV Anderson type rotor, for 15 hr at 45,000 rpm in order to separate the two cytoplasmic organelles. Zonal profiles of absorbance at 280 mµ, proteins, glycogen, and enzymatic activities (phosphorylase b kinase, phosphorylase b, and glycogen synthetase) were performed. Whereas the entire synthetase activity was found combined with the glycogen particles, 39% of phosphorylase and 53% of phosphorylase b kinase activities, present in the microsomal fraction, were recovered in the purified vesicular fraction (d = 1.175). This latter fraction consists of vesicles, derived from the sarcoplasmic reticulum, and of small particles 10–20 mµ in diameter attached to the outer surface of the membranes. These particles disappear after α-amylase treatment. Incubation of the sarcovesicular fraction with 14C-labeled glucose-1-phosphate confirms the localization of a polysaccharide synthesis at the level of the membranes. "Flash activation" of phosphorylase b, i.e. Ca "activation" of phosphorylase kinase followed by a conversion of phosphorylase b into a, was demonstrated in the purified sarcovesicular fraction. Moreover, the active enzymatic sites were detected on the membranes by electron microscopy. The presence of binding sites between the membranes of the sarcoplasmic vesicles and a glycogen-enzyme complex suggests that this association plays a role in the glycogenolysis during muscle contraction.
TL;DR: It is proposed that the purine nucleotide cycle accounts for the production of ammonia during muscular work through the conversion of aspartate to ammonia and fumarate plus malate in rat skeletal muscle.
TL;DR: A microsomal cell fraction derived from the intimal-medial layer of rabbit aorta takes up calcium in the presence of magnesium and adenosine triphosphate, which is slower than that observed in skeletal muscle microsomes.
Abstract: A microsomal cell fraction derived from the intimal-medial layer of rabbit aorta takes up calcium in the presence of magnesium and adenosine triphosphate. The rate of uptake of calcium is slower than that observed in skeletal muscle microsomes. Uptake of calcium by mitochondria from the aorta is even more limited and, unlike microsomal uptake, is inhibited by azide.
TL;DR: These experiments provide evidence that creatine, an end product of contraction unique to muscle, is involved in the control of muscle-protein synthesis and seems to be selective for cell-specific proteins(s).
Abstract: These experiments provide evidence that creatine, an end product of contraction unique to muscle, is involved in the control of muscle-protein synthesis. Skeletal muscle cells formed both in vitro and in vivo synthesize myosin heavy chain faster when supplied creatine in vitro. The response is apparent within four hours after addition of creatine to the culture medium, and is dependent on concentration over a range of 10-100 μM creatine. The effect seems to be selective for cell-specific proteins(s), since the rate of total protein synthesis is unaffected.
TL;DR: Results indicated that rates of protein synthesis in heart, but not in skeletal, muscle would be maintained during fasting or in diabetic animals by increased plasma concentration of fatty acid.
Abstract: A method for perfusion in vitro of a preparation of rat hemicorpus was developed for study of the metabolism of skeletal muscle. The preparation was stable during perfusion, as indicated by maintenance of ATP concentration, perfusion pressure, and oxygen consumption for up to 90 min. The perfused hemicorpus provided the following advantages for study of protein synthesis in skeletal muscle: (a) hormones and substrates reached the muscle cells through an intact capillary bed, and (b) the preparation included the psoas muscle, which was sufficiently large to allow measurements of intermediates in the pathway of protein synthesis and was readily homogenized for preparation of ribosomes and ribosomal subunits. Perfusion of psoas muscle from fasted rats with buffer containing glucose and insulin reduced the concentration of ribosomal subunits and increased phenylalanine incorporation as compared to perfusion with buffer containing glucose alone. In addition, the hormone increased glucose uptake from the perfusate and inhibited release of free fatty acids from the preparation. When the muscle was perfused with buffer that contained glucose and palmitate, the concentration of ribosomal subunits and phenylalanine incorporation were unchanged. Since fatty acid is known to stimulate protein synthesis in heart muscle, these results indicated that rates of protein synthesis in heart, but not in skeletal, muscle would be maintained during fasting or in diabetic animals by increased plasma concentration of fatty acid.
TL;DR: In liver, cyclic AMP increased prenatally and for the first 10 postnatal days; protein kinase levels were high prenatals and declined during the first10 postnatal Days; both phosphorylase and phosphoryLase kinase in liver increased rapidly prenatALLY and more slowly postnatally.
TL;DR: It is concluded that, despite a quantitative deficiency in the mass of regenerating muscle, those fibers which are present rapidly approach the normal condition in functional as well as morphological characteristics.
TL;DR: The gangliosides in muscles are components of the muscle cell membranes and are not derived from the nerve fibers, and it is suggested that these two lipids found in muscle are derived from nerve fibers.
TL;DR: Compensatory hypertrophy of rat skeletal muscles induced by incapacitation of synergistic muscles is accompanied by increased incorporation of3H-thymidine in interstitial cells and muscle satellite cells and the number of satellite cells is correspondingly increased during early stages of compensatoryhypertrophy.
Abstract: Compensatory hypertrophy of rat skeletal muscles induced by incapacitation of synergistic muscles is accompanied by increased incorporation of3H-thymidine in interstitial cells and muscle satellite cells. The number of satellite cells is correspondingly increased during early stages of compensatory hypertrophy.
TL;DR: Sequence studies show that 21-day-old rabbit skeletal muscle myosin is a mixture of foetal non-methylated and adult, methylated protein, which also vary at several other positions.
Abstract: Sequence studies show that 21-day-old rabbit skeletal muscle myosin is a mixture of foetal non-methylated and adult, methylated protein, which also vary at several other positions. Comparison with cardiac myosin indicates the presence of at least three myosin genes.
TL;DR: No simple relationship exists between plasma levels of digoxin and its concentration in the heart muscle, but total myocardial concentration may not accurately reflect therapeutic activity.
Abstract: The digoxin content was measured in samples of left ventricular papillary muscle, skeletal muscle, and plasma obtained during mitral valve replacement from eight patients on maintenance treatment with the drug. The content in papillary muscle ranged from 15·5 to 132 ng/g (mean 77·7) and in skeletal muscle from 7·5 to 23 ng/g (mean 11·3). The ratio of myocardial digoxin concentration to plasma concentration varied between patients from 39:1 to 155:1. No simple relationship exists between plasma levels of digoxin and its concentration in the heart muscle, but total myocardial concentration may not accurately reflect therapeutic activity.