THE POTASSIUM UPTAKE AND RATE OF OXYGEN CONSUMPTION OF ISOLATED FROG SKELETAL MUSCLE IN THE PRESENCE OF INSULIN AND LACTATE

1956 ◽  
Vol 34 (1) ◽  
pp. 893-902 ◽  
Author(s):  
J. F. Manery ◽  
D. R. H. Gourley ◽  
Kenneth C. Fisher
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Concentration Gradient ◽  
Skeletal Muscles ◽  
Potassium Uptake ◽  
Frog Skeletal Muscle ◽  
High Concentration ◽  
Ringer’S Solution ◽  
Rate Of Oxygen Consumption

Insulin (5.0 × 10−2 units per ml.) and lactate (5.0 × 10−3 M) caused an uptake of potassium by intact frog skeletal muscles in vitro, and a concomitant loss of potassium from the medium surrounding the muscles; this fluid was Ringer's solution containing 2.1 meq. of potassium per liter. Thus a movement of potassium against a high concentration gradient has been demonstrated. In general, the conditions under which potassium uptake occurred stimulated the oxygen consumption of the muscles. Monoiodoacetic acid (2.5 × 10−4 M) abolished the effect of insulin on the potassium uptake and greatly reduced its effect on the oxygen consumption.

THE POTASSIUM UPTAKE AND RATE OF OXYGEN CONSUMPTION OF ISOLATED FROG SKELETAL MUSCLE IN THE PRESENCE OF INSULIN AND LACTATE

1956 ◽  
Vol 34 (5) ◽  
pp. 893-902 ◽  
Author(s):  
J. F. Manery ◽  
D. R. H. Gourley ◽  
Kenneth C. Fisher
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Concentration Gradient ◽  
Skeletal Muscles ◽  
Potassium Uptake ◽  
Frog Skeletal Muscle ◽  
High Concentration ◽  
Ringer’S Solution ◽  
Rate Of Oxygen Consumption

Insulin (5.0 × 10−2 units per ml.) and lactate (5.0 × 10−3 M) caused an uptake of potassium by intact frog skeletal muscles in vitro, and a concomitant loss of potassium from the medium surrounding the muscles; this fluid was Ringer's solution containing 2.1 meq. of potassium per liter. Thus a movement of potassium against a high concentration gradient has been demonstrated. In general, the conditions under which potassium uptake occurred stimulated the oxygen consumption of the muscles. Monoiodoacetic acid (2.5 × 10−4 M) abolished the effect of insulin on the potassium uptake and greatly reduced its effect on the oxygen consumption.

Combination of Insulin With Frog Skeletal Muscle

1957 ◽  
Vol 189 (3) ◽  
pp. 489-494 ◽  
Author(s):  
D. R. H. Gourley
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Muscle Cell ◽  
Skeletal Muscles ◽  
Sufficient Conditions ◽  
Potassium Uptake ◽  
Frog Skeletal Muscle ◽  
Reactive Site ◽  
Cell Surfaces ◽  
Insulin Solution

Isolated intact frog skeletal muscles, equilibrated for a brief period of time in a solution of insulin and then rinsed thoroughly, showed an increased consumption of oxygen and an increased potassium uptake compared to controls when incubated for 6 hours without insulin. This has been interpreted as a firm binding of insulin to special reactive sites at the muscle cell surfaces. An equilibration period of 1 minute and an insulin concentration of 0.5 U/ml were sufficient conditions for saturating all of the sites concerned with oxygen consumption but not for all of those concerned with potassium transfer. In addition an aged insulin solution lost its ability to stimulate potassium uptake before the effect on oxygen consumption was altered. It is therefore concluded that there is one type of reactive site concerned with oxygen consumption with which insulin combines rapidly and another type of reactive site concerned with potassium transfer with which insulin combines relatively more slowly.

scholarly journals Bioengineered in vitro skeletal muscles as new tools for muscular dystrophies preclinical studies

2021 ◽  
Vol 12 ◽  
pp. 204173142098133
Author(s):  
Juan M. Fernández-Costa ◽  
Xiomara Fernández-Garibay ◽  
Ferran Velasco-Mallorquí ◽  
Javier Ramón-Azcón
Keyword(s):  
Skeletal Muscle ◽  
Tissue Engineering ◽  
Electrical Stimulation ◽  
Skeletal Muscles ◽  
Screening Tools ◽  
Muscular Dystrophies ◽  
Preclinical Studies ◽  
Technological Advances ◽  
Topographical Cues

Muscular dystrophies are a group of highly disabling disorders that share degenerative muscle weakness and wasting as common symptoms. To date, there is not an effective cure for these diseases. In the last years, bioengineered tissues have emerged as powerful tools for preclinical studies. In this review, we summarize the recent technological advances in skeletal muscle tissue engineering. We identify several ground-breaking techniques to fabricate in vitro bioartificial muscles. Accumulating evidence shows that scaffold-based tissue engineering provides topographical cues that enhance the viability and maturation of skeletal muscle. Functional bioartificial muscles have been developed using human myoblasts. These tissues accurately responded to electrical and biological stimulation. Moreover, advanced drug screening tools can be fabricated integrating these tissues in electrical stimulation platforms. However, more work introducing patient-derived cells and integrating these tissues in microdevices is needed to promote the clinical translation of bioengineered skeletal muscle as preclinical tools for muscular dystrophies.

scholarly journals Oxygen consumption in mouse skeletal muscles stimulated Na-permeability in vitro

1989 ◽  
Vol 49 ◽  
pp. 169
Author(s):  
Hideto Awano ◽  
Tetsuya Hasegawa ◽  
Masakazu Nishimura ◽  
Osamu Yagasaki ◽  
Katsuaki Ito
Keyword(s):  
Oxygen Consumption ◽  
Skeletal Muscles ◽  
Na Permeability

Proximal tubule dysfunction in cystine-loaded tubules: effect of phosphate and metabolic substrates

1996 ◽  
Vol 271 (3) ◽  
pp. F717-F722
Author(s):  
G. Bajaj ◽  
M. Baum
Keyword(s):  
Oxygen Consumption ◽  
Proximal Tubule ◽  
Tricarboxylic Acid Cycle ◽  
Dimethyl Ester ◽  
Proximal Tubules ◽  
Intracellular Atp ◽  
Metabolic Substrates ◽  
Rate Of Oxygen Consumption ◽  
Intracellular Phosphate

Intracellular cystine loading by use of cystine dimethyl ester (CDME) results in a generalized inhibition in proximal tubule transport due, in part, to a decrease in intracellular ATP. The present study examined the importance of phosphate and metabolic substrates in the proximal tubule dysfunction produced by cystine loading. Proximal tubule intracellular phosphorus was 1.8 +/- 0.1 in control tubules and 1.1 +/- 0.1 nmol/mg protein in proximal tubules incubated in vitro with CDME P < 0.001). Infusion of sodium phosphate in rabbits and subsequent incubation of proximal tubules with a high-phosphate medium attenuated the decrease in proximal tubule respiration and prevented the decrease in intracellular ATP with cystine loading. Tricarboxylic acid cycle intermediates have been shown to preserve oxidative metabolism in phosphate-depleted proximal tubules. In proximal tubules incubated with either 1 mM valerate or butyrate, there was a 42 and 34% reduction (both P < 0.05) in the rate of oxygen consumption with cystine loading. However, tubules incubated with 1 mM succinate or citrate had only a 13 and 14% P = NS) reduction in the rate of oxygen consumption, respectively. These data are consistent with a limitation of intracellular phosphate in the pathogenesis of the proximal tubule dysfunction with cystine loading.

scholarly journals Tenogenic Contribution to Skeletal Muscle Regeneration: The Secretome of Scleraxis Overexpressing Mesenchymal Stem Cells Enhances Myogenic Differentiation In Vitro

2020 ◽  
Vol 21 (6) ◽  
pp. 1965
Author(s):  
Maximilian Strenzke ◽  
Paolo Alberton ◽  
Attila Aszodi ◽  
Denitsa Docheva ◽  
Elisabeth Haas ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Skeletal Muscles ◽  
Myogenic Differentiation ◽  
Muscular Contraction ◽  
Myoblast Fusion ◽  
Skeletal Muscle Regeneration ◽  
Potential Candidate ◽  
Musculoskeletal Tissue

Integrity of the musculoskeletal system is essential for the transfer of muscular contraction force to the associated bones. Tendons and skeletal muscles intertwine, but on a cellular level, the myotendinous junctions (MTJs) display a sharp transition zone with a highly specific molecular adaption. The function of MTJs could go beyond a mere structural role and might include homeostasis of this musculoskeletal tissue compound, thus also being involved in skeletal muscle regeneration. Repair processes recapitulate several developmental mechanisms, and as myotendinous interaction does occur already during development, MTJs could likewise contribute to muscle regeneration. Recent studies identified tendon-related, scleraxis-expressing cells that reside in close proximity to the MTJs and the muscle belly. As the muscle-specific function of these scleraxis positive cells is unknown, we compared the influence of two immortalized mesenchymal stem cell (MSC) lines—differing only by the overexpression of scleraxis—on myoblasts morphology, metabolism, migration, fusion, and alignment. Our results revealed a significant increase in myoblast fusion and metabolic activity when exposed to the secretome derived from scleraxis-overexpressing MSCs. However, we found no significant changes in myoblast migration and myofiber alignment. Further analysis of differentially expressed genes between native MSCs and scleraxis-overexpressing MSCs by RNA sequencing unraveled potential candidate genes, i.e., extracellular matrix (ECM) proteins, transmembrane receptors, or proteases that might enhance myoblast fusion. Our results suggest that musculotendinous interaction is essential for the development and healing of skeletal muscles.

scholarly journals Simultaneous measurement of Ca2+ in muscle with Ca electrodes and aequorin. Diffusible cytoplasmic constituent reduces Ca(2+)-independent luminescence of aequorin.

1991 ◽  
Vol 98 (6) ◽  
pp. 1141-1160 ◽  
Author(s):  
L A Blatter ◽  
J R Blinks
Keyword(s):  
Skeletal Muscle ◽  
Simultaneous Measurement ◽  
Light Emission ◽  
Ringer Solution ◽  
Light Signal ◽  
Frog Skeletal Muscle ◽  
Stable Level ◽  
Total Absence ◽  
Normal Ringer

Estimates of cytoplasmic Ca2+ concentration ([Ca2+]i) were made essentially simultaneously in the same intact frog skeletal muscle fibers with aequorin and with Ca-selective microelectrodes. In healthy fibers under truly resting conditions [Ca2+]i was too low to be measured reliably with either technique. The calibration curves for both indicators were essentially flat in this range of [Ca2+], and the aequorin light signal was uniformly below the level to be expected in the total absence of Ca2+. When [Ca2+]i had been raised to a stable level below the threshold for contracture by increasing [K+]o to 12.5 mM, [Ca2+]i was 38 nM according to aequorin and 59 nM according to the Ca-selective microelectrodes. These values are not significantly different. Our estimates of [Ca2+]i are lower than most others obtained with microelectrodes, probably because the presence of aequorin in the cells allowed us to detect damaging microelectrode impalements that otherwise we would have had no reason to reject. The observation that the light emission from aequorin-injected fibers in normal Ringer solution was below the level expected from the Ca(2+)-independent luminescence of aequorin in vitro was investigated further, with the conclusion that the myoplasm contains a diffusible macromolecule (between 10 and 30 kD) that interacts with aequorin to reduce light emission in the absence of Ca2+.

Structural and functional remodeling of skeletal muscle microvasculature is induced by simulated microgravity

2000 ◽  
Vol 278 (6) ◽  
pp. H1866-H1873 ◽  
Author(s):  
Michael D. Delp ◽  
Patrick N. Colleran ◽  
M. Keith Wilkerson ◽  
Matthew R. McCurdy ◽  
Judy Muller-Delp
Keyword(s):  
Skeletal Muscle ◽  
Soleus Muscle ◽  
Skeletal Muscles ◽  
Gastrocnemius Muscle ◽  
Fluid Pressure ◽  
Hindlimb Unloading ◽  
Cross Sectional ◽  
Luminal Diameter ◽  
Structural Remodeling

Hindlimb unloading of rats results in a diminished ability of skeletal muscle arterioles to constrict in vitro and elevate vascular resistance in vivo. The purpose of the present study was to determine whether alterations in the mechanical environment (i.e., reduced fluid pressure and blood flow) of the vasculature in hindlimb skeletal muscles from 2-wk hindlimb-unloaded (HU) rats induces a structural remodeling of arterial microvessels that may account for these observations. Transverse cross sections were used to determine media cross-sectional area (CSA), wall thickness, outer perimeter, number of media nuclei, and vessel luminal diameter of feed arteries and first-order (1A) arterioles from soleus and the superficial portion of gastrocnemius muscles. Endothelium-dependent dilation (ACh) was also determined. Media CSA of resistance arteries was diminished by hindlimb unloading as a result of decreased media thickness (gastrocnemius muscle) or reduced vessel diameter (soleus muscle). ACh-induced dilation was diminished by 2 wk of hindlimb unloading in soleus 1A arterioles, but not in gastrocnemius 1A arterioles. These results indicate that structural remodeling and functional adaptations of the arterial microvasculature occur in skeletal muscles of the HU rat; the data suggest that these alterations may be induced by reductions in transmural pressure (gastrocnemius muscle) and wall shear stress (soleus muscle).

Reversal of enhanced muscle glucose transport after exercise: roles of insulin and glucose

1990 ◽  
Vol 259 (5) ◽  
pp. E685-E691 ◽  
Author(s):  
E. A. Gulve ◽  
G. D. Cartee ◽  
J. R. Zierath ◽  
V. M. Corpus ◽  
J. O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Transport Process ◽  
Sugar Transport ◽  
Transport Activity ◽  
High Concentration ◽  
Exercise Induced ◽  
Muscle Glucose Transport

Exercise stimulates insulin-independent glucose transport in skeletal muscle and also increases the sensitivity of the glucose transport process in muscle to insulin. A previous study [D. A. Young, H. Wallberg-Henriksson, M. D. Sleeper, and J. O. Holloszy. Am. J. Physiol. 253 (Endocrinol. Metab. 16): E331–E335, 1987] showed that the exercise-induced increase in glucose transport activity disappears rapidly when rat epitrochlearis muscles are incubated for 3 h in vitro in the absence of insulin and that 7.5 microU/ml insulin in the incubation medium apparently slowed the loss of enhanced sugar transport. We examined whether addition of insulin several hours after exercise increases glucose transport to the same extent as continuous insulin exposure. Addition of 7.5 microU/ml insulin 2.5 h after exercise (when glucose transport has returned to basal levels) increased sugar transport to the same level as that which resulted from continuous insulin exposure. This finding provides evidence for an increase in insulin sensitivity rather than a slowing of reversal of the exercise-induced increase in insulin-independent glucose transport activity. Glucose transport was enhanced only at submaximal, not at maximal, insulin concentrations. Exposure to a high concentration of glucose and a low insulin concentration reduced the exercise-induced increase in insulin-sensitive glucose transport. Incubation with a high concentration of 2-deoxy-D-glucose (2-DG) did not alter the increase in insulin sensitivity, even though a large amount of 2-DG entered the muscle and was phosphorylated.(ABSTRACT TRUNCATED AT 250 WORDS)

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