Recovery of Plantaris Muscle from Impaired Physical Mobility

1999 ◽  
Vol 1 (1) ◽  
pp. 4-11 ◽  
Author(s):  
Christine E. Kasper
Keyword(s):  
Skeletal Muscle ◽  
Animal Model ◽  
Recovery Period ◽  
Hindlimb Suspension ◽  
Plantaris Muscle ◽  
Physical Mobility ◽  
Morphological Adaptations ◽  
Slow Twitch ◽  
Fast Twitch

The purpose of this investigation was to describe and compare various methods of recovering atrophied fast-twitch skeletal muscle following long-term impaired physical mobility. An animal model was used to study morphological adaptations of atrophied plantaris muscles to the effects of 28 days of hindlimb suspension (HS) followed by either sedentary recovery or run training during a 28-day recovery period. Significant atrophy, demonstrated by decreased mean fiber area (MFA,mm2), occurred during the 28-day period of HS. However, run training following long-term atrophy induced by HS did not result in the high levels of frank muscle damage and type IIC fibers previously reported in slow-twitch soleus muscle following longterm (28 days) atrophy.

Effects of diabetes on protein synthesis in fast- and slow-twitch rat skeletal muscle

1980 ◽  
Vol 239 (1) ◽  
pp. E88-E95 ◽  
Author(s):  
K. E. Flaim ◽  
M. E. Copenhaver ◽  
L. S. Jefferson
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Peptide Chain ◽  
Fiber Types ◽  
Chain Initiation ◽  
Rapid Reversal ◽  
Slow Twitch ◽  
Fast Twitch

The effects of acute (2-day) and long-term (7-day) diabetes on rates of protein synthesis, peptide-chain initiation, and levels of RNA were examined in rat skeletal muscles that are known to have differing proportions of the three fiber types: fast-twitch white, fast-twitch red, and slow-twitch red. Short-term diabetes resulted in a 15% reduction in the level of RNA in all the muscles studied and an impairment in peptide-chain initiation in muscles with mixed fast-twitch fibers. In contrast, the soleus, a skeletal muscle with high proportions of slow-twitch red fibers, showed little impairment in initiation. When the muscles were perfused as a part of the hemicorpus preparation, addition of insulin to the medium caused a rapid reversal of the block in initiation in mixed fast-twitch muscles but had no effect in the soleus. The possible role of fatty acids in accounting for these differences is discussed. Long-term diabetes caused no further reduction in RNA, but resulted in the development of an additional impairment to protein synthesis that also affected the soleus and that was not corrected by perfusion with insulin. The defect resulting from long-term diabetes may involve elongation or termination reactions.

β-Adrenoceptor signaling in regenerating skeletal muscle after β-agonist administration

2007 ◽  
Vol 293 (4) ◽  
pp. E932-E940 ◽  
Author(s):  
Felice Beitzel ◽  
Martin N. Sillence ◽  
Gordon S. Lynch
Keyword(s):  
Skeletal Muscle ◽  
Coupling Efficiency ◽  
Therapeutic Implications ◽  
Threefold Increase ◽  
Signaling Mechanisms ◽  
Slow Twitch ◽  
Ac Response ◽  
Early Regeneration ◽  
Fast Twitch

Stimulating the β-adrenoceptor (β-AR) signaling pathway can enhance the functional repair of skeletal muscle after injury, but long-term use of β-AR agonists causes β-AR downregulation, which may limit their therapeutic effectiveness. The aim was to examine β-AR signaling during early regeneration in rat fast-twitch [extensor digitorum longus (EDL)] and slow-twitch (soleus) muscles after bupivacaine injury and test the hypothesis that, during regeneration, β-agonist administration does not cause β-AR desensitization. Rats received either the β-AR agonist fenoterol (1.4 mg·kg−1·day−1 ip) or saline for 7 days postinjury. Fenoterol reduced β-AR density in regenerating soleus muscles by 42%. Regenerating EDL muscles showed a threefold increase in β-AR density, and, again, these values were 43% lower with fenoterol treatment. An amplified adenylate cyclase (AC) response to isoproterenol was observed in cell membrane fragments from EDL and soleus muscles 7 days postinjury. Fenoterol attenuated this increase in regenerating EDL muscles but not soleus muscles. β-AR signaling mechanisms were assessed using AC stimulants (NaF, forskolin, and Mn2+). Although β-agonist treatment reduces β-AR density in regenerating muscles, these muscles can produce large cAMP responses relative to healthy (uninjured) muscles. Desensitization of β-AR signaling in regenerating muscles is prevented by altered rates of β-AR synthesis and/or degradation, changes in G protein populations and coupling efficiency, and altered AC activity. These mechanisms have important therapeutic implications for modulating β-AR signaling to enhance muscle repair after injury.

ATP-sensitive potassium channels mediate hyperosmotic stimulation of NKCC in slow-twitch muscle

2004 ◽  
Vol 286 (3) ◽  
pp. C586-C595 ◽  
Author(s):  
Aidar R. Gosmanov ◽  
Zheng Fan ◽  
Xianqiang Mi ◽  
Edward G. Schneider ◽  
Donald B. Thomason
Keyword(s):  
Skeletal Muscle ◽  
Soleus Muscle ◽  
Potassium Current ◽  
Plantaris Muscle ◽  
Channel Inhibition ◽  
Slow Twitch Muscle ◽  
Inhibition Of Glycolysis ◽  
Slow Twitch ◽  
Mapk Inhibitors ◽  
Fast Twitch

In mildly hyperosmotic medium, activation of the Na+-K+-2Cl- cotransporter (NKCC) counteracts skeletal muscle cell water loss, and compounds that stimulate protein kinase A (PKA) activity inhibit the activation of the NKCC. The aim of this study was to determine the mechanism for PKA inhibition of NKCC activity in resting skeletal muscle. Incubation of rat slow-twitch soleus and fast-twitch plantaris muscles in isosmotic medium with the PKA inhibitors H-89 and KT-5720 caused activation of the NKCC only in the soleus muscle. NKCC activation caused by PKA inhibition was insensitive to MEK MAPK inhibitors and to insulin but was abolished by the PKA stimulators isoproterenol and forskolin. Furthermore, pinacidil [an ATP-sensitive potassium (KATP) channel opener] or inhibition of glycolysis increased NKCC activity in the soleus muscle but not in the plantaris muscle. Preincubation of the soleus muscle with glibenclamide (a KATP channel inhibitor) prevented the NKCC activation by hyperosmolarity, PKA inhibition, pinacidil, and glycolysis inhibitors. In contrast, glibenclamide stimulated NKCC activity in the plantaris muscle. In cells stably transfected with the Kir6.2 subunit of the of KATP channel, inhibition of glycolysis activated potassium current and NKCC activity. We conclude that activation of KATP channels in slow-twitch muscle is necessary for activation of the NKCC and cell volume restoration in hyperosmotic conditions.

Studies of the halothane-cooling contractures of skeletal muscle

1987 ◽  
Vol 65 (4) ◽  
pp. 697-703 ◽  
Author(s):  
Roberto T. Sudo ◽  
Gisele Zapata ◽  
Guilherme Suarez-Kurtz
Keyword(s):  
Skeletal Muscle ◽  
Synergistic Effects ◽  
Rabbit Muscle ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Dose Dependent ◽  
Muscle Biopsies ◽  
Ca Homeostasis ◽  
Potential Use

The characteristics of transient contractures elicited by rapid cooling of frog or mouse muscles perfused in vitro with solutions equilibrated with 0.5–2.0% halothane are reviewed. The data indicate that these halothane-cooling contractures are dose dependent and reproducible, and their amplitude is larger in muscles containing predominantly slow-twitch type fibers, such as the mouse soleus, than in muscles in which fast-twitch fibers predominate, such as the mouse extensor digitorum longus. The halothane-cooling contractures are potentiated in muscles exposed to succinylcholine. The effects of Ca2+-free solutions, of the local anesthetics procaine, procainamide, and lidocaine, and of the muscle relaxant dantrolene on the halothane-cooling contractures are consistent with the proposal that the halothane-cooling contractures result from synergistic effects of halothane and low temperature on Ca sequestration by the sarcoplasmic reticulum. Preliminary results from skinned rabbit muscle fibers support this proposal. The halothane concentrations required for the halothane-cooling contractures of isolated frog or mouse muscles are comparable with those observed in serum of patients during general anesthesia. Accordingly, fascicles dissected from muscle biopsies of patients under halothane anesthesia for programmed surgery develop large contractures when rapidly cooled. The amplitude of these halothane-cooling contractures declined with the time of perfusion of the muscle fascicles in vitro with halothane-free physiological solutions. It is suggested that the halothane-cooling contractures could be used as a simple experimental model for the investigation of the effects of halothane on Ca homeostasis and contractility in skeletal muscle and for study of drugs of potential use in the management of the contractures associated with the halothane-induced malignant hyperthermia syndrome. It is shown that salicylates, but not indomethacin or mefenamic acid, inhibit the halothane-cooling contractures.

scholarly journals The Functional Role of Calcineurin in Hypertrophy, Regeneration, and Disorders of Skeletal Muscle

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Kunihiro Sakuma ◽  
Akihiko Yamaguchi
Keyword(s):  
Skeletal Muscle ◽  
Functional Role ◽  
Muscular Hypertrophy ◽  
Growth And Remodeling ◽  
Muscular Disorders ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Calcineurin Activity ◽  
Muscle Remodeling

Skeletal muscle uses calcium as a second messenger to respond and adapt to environmental stimuli. Elevations in intracellular calcium levels activate calcineurin, a serine/threonine phosphatase, resulting in the expression of a set of genes involved in the maintenance, growth, and remodeling of skeletal muscle. In this review, we discuss the effects of calcineurin activity on hypertrophy, regeneration, and disorders of skeletal muscle. Calcineurin is a potent regulator of muscle remodeling, enhancing the differentiation through upregulation of myogenin or MEF2A and downregulation of the Id1 family and myostatin. Foxo may also be a downstream candidate for a calcineurin signaling molecule during muscle regeneration. The strategy of controlling the amount of calcineurin may be effective for the treatment of muscular disorders such as DMD, UCMD, and LGMD. Activation of calcineurin produces muscular hypertrophy of the slow-twitch soleus muscle but not fast-twitch muscles.

Glutamine synthetase induction by glucocorticoids is preserved in skeletal muscle of aged rats

1996 ◽  
Vol 271 (6) ◽  
pp. E1061-E1066 ◽  
Author(s):  
D. Meynial-Denis ◽  
M. Mignon ◽  
A. Miri ◽  
J. Imbert ◽  
E. Aurousseau ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glutamine Synthetase ◽  
Skeletal Muscles ◽  
Female Rats ◽  
Mrna Levels ◽  
Aged Rats ◽  
Adult Rats ◽  
Adult Age ◽  
Slow Twitch ◽  
Fast Twitch

Glutamine synthetase (GS) is a glucocorticoid-inducible enzyme that has a key role for glutamine synthesis in muscle. We hypothesized that the glucocorticoid induction of GS could be altered in aged rats, because alterations in the responsiveness of some genes to glucocorticoids were reported in aging. We compared the glucocorticoid-induced GS in fast-twitch and slow-twitch skeletal muscles (tibialis anterior and soleus, respectively) and heart from adult (age 6-8 mo) and aged (age 22 mo) female rats. All animals received dexamethasone (Dex) in their drinking water (0.77 +/- 0.10 and 0.80 +/- 0.08 mg/day per adult and aged rat, respectively) for 5 days. Dex caused an increase in both GS activity and GS mRNA in fast-twitch and slow-twitch skeletal muscles from adult and aged rats. In contrast, Dex increased GS activity in heart of adult rats, without any concomitant change in GS mRNA levels. Furthermore, Dex did not affect GS activity in aged heart. Thus the responsiveness of GS to an excess of glucocorticoids is preserved in skeletal muscle but not in heart from aged animals.

Na current density at and away from end plates on rat fast- and slow-twitch skeletal muscle fibers

1992 ◽  
Vol 262 (1) ◽  
pp. C229-C234 ◽  
Author(s):  
R. L. Ruff
Keyword(s):  
Skeletal Muscle ◽  
Current Density ◽  
Muscle Fibers ◽  
Postsynaptic Membrane ◽  
Na Current ◽  
End Plate ◽  
Skeletal Muscle Fibers ◽  
Slow Twitch ◽  
Slow Twitch Fibers ◽  
Fast Twitch

Na current density and membrane capacitance were studied with the loose patch voltage clamp technique on rat fast- and slow-twitch skeletal muscle fibers at three different regions on the fibers: 1) the end plate border, 2) greater than 200 microns from the end plate (extrajunctional), and 3) on the end plate postsynaptic membrane. Fibers were treated with collagenase to improve visualization of the end plate and to enzymatically remove the nerve terminal. The capacitance of membrane patches was similar on fast- and slow-twitch fibers and patches of membrane on the end plate had twice the capacitance of patches elsewhere. For fast- and slow-twitch fibers, the sizes of the Na current normalized to the area of the patch were as follows: end plate greater than end plate border greater than extrajunctional. For both types of fibers, the amplitudes of the Na current normalized to the capacitance of the membrane patch were as follows: end plate approximately end plate border greater than extrajunctional. At each of the three regions, the Na current densities were larger on fast-twitch fibers and fast-twitch fibers had a larger increase in Na current density at the end plate border compared with extrajunctional membrane.

Resistance exercise and growth hormone as countermeasures for skeletal muscle atrophy in hindlimb-suspended rats

1994 ◽  
Vol 267 (2) ◽  
pp. R365-R371 ◽  
Author(s):  
J. K. Linderman ◽  
K. L. Gosselink ◽  
F. W. Booth ◽  
V. R. Mukku ◽  
R. E. Grindeland
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Resistance Exercise ◽  
Protein Content ◽  
Muscle Atrophy ◽  
Myofibrillar Protein ◽  
Hindlimb Suspension ◽  
Skeletal Muscle Atrophy ◽  
Plantar Flexor ◽  
Fast Twitch

Unweighting of rat hindlimb muscles results in skeletal muscle atrophy, decreased protein synthesis, and reduced growth hormone (GH) secretion. Resistance exercise (ladder climbing) and GH treatment partially attenuate skeletal muscle atrophy in hypophysectomized hindlimb-suspended rats. It was hypothesized that a combination of multiple bouts of daily resistance exercise and GH (1 mg.kg-1.day-1) would prevent skeletal muscle atrophy in growing nonhypophysectomized hindlimb-suspended rats. Hindlimb suspension decreased the absolute (mg/pair) and relative (mg/100 g body wt) weights of the soleus, a slow-twitch plantar flexor, by 30 and 21%, respectively, and the absolute and relative weights of the gastrocnemius, a predominantly fast-twitch plantar flexor, by 20 and 11%, respectively (P < 0.05). Exercise did not increase soleus mass but attenuated loss of relative wet weight in the gastrocnemius muscles of hindlimb-suspended rats (P < 0.05). Hindlimb suspension decreased gastrocnemius myofibrillar protein content and synthesis (mg/day) by 26 and 64%, respectively (P < 0.05). The combination of exercise and GH attenuated loss of gastrocnemius myofibrillar protein content and synthesis by 70 and 23%, respectively (P < 0.05). Results of the present investigation indicate that a combination of GH and resistance exercise attenuates atrophy of unweighted fast-twitch skeletal muscles.

scholarly journals Fibre-type specific modification of the activity and regulation of skeletal muscle pyruvate dehydrogenase kinase (PDK) by prolonged starvation and refeeding is associated with targeted regulation of PDK isoenzyme 4 expression

2000 ◽  
Vol 346 (3) ◽  
pp. 651-657 ◽  
Author(s):  
Mary C. SUGDEN ◽  
Alexandra KRAUS ◽  
Robert A. HARRIS ◽  
Mark J. HOLNESS
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Pyruvate Dehydrogenase ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Pyruvate Dehydrogenase Kinase ◽  
Acid Cycle ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Anterior Tibialis

Using immunoblot analysis with antibodies raised against recombinant pyruvate dehydrogenase kinase (PDK) isoenzymes PDK2 and PDK4, we demonstrate selective changes in PDK isoenzyme expression in slow-twitch versus fast-twitch skeletal muscle types in response to prolonged (48 h) starvation and refeeding after starvation. Starvation increased PDK activity in both slow-twitch (soleus) and fast-twitch (anterior tibialis) skeletal muscle and was associated with loss of sensitivity of PDK to inhibition by pyruvate, with a greater effect in anterior tibialis. Starvation significantly increased PDK4 protein expression in both soleus and anterior tibialis, with a greater response in anterior tibialis. Starvation did not effect PDK2 protein expression in soleus, but modestly increased PDK2 expression in anterior tibialis. Refeeding for 4 h partially reversed the effect of 48-h starvation on PDK activity and PDK4 expression in both soleus and anterior tibialis, but the response was more marked in soleus than in anterior tibialis. Pyruvate sensitivity of PDK activity was also partially restored by refeeding, again with the greater response in soleus. It is concluded that targeted regulation of PDK4 isoenzyme expression in skeletal muscle in response to starvation and refeeding underlies the modulation of the regulatory characteristics of PDK in vivo. We propose that switching from a pyruvate-sensitive to a pyruvate-insensitive PDK isoenzyme in starvation (a) maintains a sufficiently high pyruvate concentration to ensure that the glucose → alanine → glucose cycle is not impaired, and (b) may ‘spare’ pyruvate for anaplerotic entry into the tricarboxylic acid cycle to support the entry of acetyl-CoA derived from fatty acid (FA) oxidation into the tricarboxylic acid cycle. We further speculate that FA oxidation by skeletal muscle is both forced and facilitated by upregulation of PDK4, which is perceived as an essential component of the operation of the glucose-FA cycle in starvation.

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