Effects of Exercise on Lactate Transport Into Mouse Skeletal Muscles

1994 ◽  
Vol 19 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Arend Bonen ◽  
Karl J. A. McCullagh
Keyword(s):  
Skeletal Muscle ◽  
Key Words ◽  
Muscle Glycogen ◽  
Skeletal Muscles ◽  
Treadmill Exercise ◽  
Lactate Transport ◽  
Muscle Lactate ◽  
Slow Twitch ◽  
Fast Twitch

Skeletal muscle lactate transport was investigated in vitro in isolated fast-twitch (EDL) and slow-twitch soleus (Sol) skeletal muscles from control and exercised mice. Exercise (23 m/min, 8% grade) reduced muscle glycogen by 37% in EDL (p < 0.05) and by 35% in Sol muscles (p < 0.05). Lactate transport measurements (45 sec) were performed after 60 min of exercise in intact EDL and Sol muscles in vitro, at differing pH (6.5 and 7.4) and differing lactate concentrations (4 and 30 mM). Lactate transport was observed to be greater in Sol than in EDL (p < 0.05). In the exercised muscles there was a small but significant increase in lactate transport (p < 0.05). Lactate transport was greater when exogenous lactate concentrations were greater (p < 0.05) and more rapid at the lower pH (p < 0.05). These studies demonstrated that lactate transport was increased with exercise. Key words: soleus, EDL, treadmill exercise

Effects of exercise and glycogen depletion on glyconeogenesis in muscle

1994 ◽  
Vol 76 (4) ◽  
pp. 1753-1758 ◽  
Author(s):  
A. Bonen ◽  
D. A. Homonko
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Extensor Digitorum Longus ◽  
Treadmill Exercise ◽  
Glycogen Depletion ◽  
Epinephrine Injection ◽  
Slow Twitch ◽  
Glycogen Repletion ◽  
Fast Twitch

In the present study, we investigated the hypotheses that 1) skeletal muscle glyconeogenesis will increase after exercise, 2) greater changes in glyconeogenesis will be observed after exercise in fast-twitch muscles than in slow-twitch muscles, and 3) glycogen repletion will reduce the rates of glyconeogenesis. Mouse soleus and extensor digitorum longus (EDL) glycogen depots were reduced to the same levels by treadmill exercise (60 min) or epinephrine injection (75 micrograms/100 g body wt ip). Untreated animals were used as controls. We were able to prevent glycogen repletion by incubating muscles in vitro with sorbitol (75 mM) and to increase glycogen concentrations in vitro by incubating muscles with glucose (75 mM). The experimental results showed that glyconeogenesis was increased by exercise (EDL, +51%; soleus, +82%) when glycogen levels were kept low. When glycogen depots were increased, the rate of glyconeogenesis was lowered in the exercised EDL (P < 0.05) but not in the soleus (P > 0.05). Reductions in muscle glycogen by epinephrine did not change the rate of glyconeogenesis in EDL, either when glycogen depots were kept low or were repleted (P > 0.05). In contrast, in the soleus, epinephrine-induced reductions in glycogen did stimulate glyconeogenesis (P < 0.05). Analyses in EDL showed that in nonexercised muscles glycogen concentrations were minimally effective in altering the rates of glyconeogenesis. A 30% decrement in glycogen increased glyconeogenesis by 5% in resting muscles, whereas the same decrement increased glyconeogenesis by 51% in exercised muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Lactate transport studied in sarcolemmal giant vesicles from rat skeletal muscles: effect of denervation

1995 ◽  
Vol 269 (4) ◽  
pp. E679-E682 ◽  
Author(s):  
H. Pilegaard ◽  
C. Juel
Keyword(s):  
Skeletal Muscles ◽  
Transport Capacity ◽  
Lactate Transport ◽  
Giant Vesicles ◽  
Muscle Lactate ◽  
Ldh Activity ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Sarcolemmal Vesicles ◽  
White Gastrocnemius

The effect of denervation on lactate transport capacity was studied in giant sarcolemmal vesicles obtained from rat muscle. The rate of lactate transport was determined in soleus and red (RG) and white gastrocnemius (WG) after 1, 3, and 21 days of denervation and in the corresponding contralateral muscles. In addition, muscle lactate dehydrogenase (LDH) and succinate dehydrogenase (SDH) activities were determined. After 1, 3, and 21 days of denervation the rate of lactate transport was lower (P < 0.05) in WG (9, 11, and 36%), RG (15, 21, and 41%), and soleus (12, 24, and 50%) compared with the contralateral muscles. After 21 days of denervation LDH activity was 26, 25, and 34% and SDH activity 33, 25, and 27% lower (P < 0.05) in WG, RG, and soleus, respectively, compared with the contralateral muscles. In the control muscles the lactate transport capacity was 20 and 32% lower (P < 0.05) in WG than in RG and soleus, respectively. The present findings provide support that the sarcolemmal lactate carrier is a plastic system; the transport capacity in soleus, RG, and WG already declines after 1 day of denervation and is further reduced after 21 days of denervation. In addition, the data suggest that the lactate transport capacity in fast-twitch glycolytic fibers < fast-twitch oxidative-glycolytic fibers < slow-twitch oxidative fibers.

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.

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.

scholarly journals Protein modification during biological aging: selective tyrosine nitration of the SERCA2a isoform of the sarcoplasmic reticulum Ca2+-ATPase in skeletal muscle

1999 ◽  
Vol 340 (3) ◽  
pp. 657-669 ◽  
Author(s):  
Rosa I. VINER ◽  
Deborah A. FERRINGTON ◽  
Todd D. WILLIAMS ◽  
Diana J. BIGELOW ◽  
Christian SCHÖNEICH
Keyword(s):  
Skeletal Muscle ◽  
Atpase Activity ◽  
Biological Aging ◽  
Tyrosine Nitration ◽  
Age Dependent ◽  
Slow Twitch Muscle ◽  
Slow Twitch ◽  
Fast Twitch

The accumulation of covalently modified proteins is an important hallmark of biological aging, but relatively few studies have addressed the detailed molecular-chemical changes and processes responsible for the modification of specific protein targets. Recently, Narayanan et al. [Narayanan, Jones, Xu and Yu (1996) Am. J. Physiol. 271, C1032-C1040] reported that the effects of aging on skeletal-muscle function are muscle-specific, with a significant age-dependent change in ATP-supported Ca2+-uptake activity for slow-twitch but not for fast-twitch muscle. Here we have characterized in detail the age-dependent functional and chemical modifications of the rat skeletal-muscle sarcoplasmic-reticulum (SR) Ca2+-ATPase isoforms SERCA1 and SERCA2a from fast-twitch and slow-twitch muscle respectively. We find a significant age-dependent loss in the Ca2+-ATPase activity (26% relative to Ca2+-ATPase content) and Ca2+-uptake rate specifically in SR isolated from predominantly slow-twitch, but not from fast-twitch, muscles. Western immunoblotting and amino acid analysis demonstrate that, selectively, the SERCA2a isoform progressively accumulates a significant amount of nitrotyrosine with age (≈ 3.5±0.7 mol/mol of SR Ca2+-ATPase). Both Ca2+-ATPase isoforms suffer an age-dependent loss of reduced cysteine which is, however, functionally insignificant. In vitro, the incubation of fast- and slow-twitch muscle SR with peroxynitrite (ONOO-) (but not NO/O2) results in the selective nitration only of the SERCA2a, suggesting that ONOO- may be the source of the nitrating agent in vivo. A correlation of the SR Ca2+-ATPase activity and covalent protein modifications in vitro and in vivo suggests that tyrosine nitration may affect the Ca2+-ATPase activity. By means of partial and complete proteolytic digestion of purified SERCA2a with trypsin or Staphylococcus aureus V8 protease, followed by Western-blot, amino acid and HPLC-electrospray-MS (ESI-MS) analysis, we localized a large part of the age-dependent tyrosine nitration to the sequence Tyr294-Tyr295 in the M4-M8 transmembrane domain of the SERCA2a, close to sites essential for Ca2+ translocation.

scholarly journals Immunoneutralization of TGFβ1 Improves Skeletal Muscle Regeneration: Effects on Myoblast Differentiation and Glycosaminoglycan Content

2009 ◽  
Vol 2009 ◽  
pp. 1-16 ◽  
Author(s):  
M. Zimowska ◽  
A. Duchesnay ◽  
P. Dragun ◽  
A. Oberbek ◽  
J. Moraczewski ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Regeneration ◽  
Skeletal Muscle Regeneration ◽  
Myoblast Differentiation ◽  
In Vitro Growth ◽  
Muscle Repair ◽  
Slow Twitch ◽  
Fast Twitch

When injured by crushing, the repair of the slow-twitch soleus rat muscle, unlike the fast-twitch EDL, is associated with fibrosis. As TGFβ1, whose activity can be controlled by glycosaminoglycans (GAG), plays a major role in fibrosis, we hypothesized that levels of TGFβ1 and GAG contents could account for this differential quality of regeneration. Here we show that the regeneration of the soleus was accompanied by elevated and more sustained TGFβ1 level than in the EDL. Neutralization of TGFβ1 effects by antibodies to TGFβ1 or its receptor TGFβ-R1 improved muscle repair, especially of the soleus muscle, increased in vitro growth of myoblasts, and accelerated their differentiation. These processes were accompanied by alterations of GAG contents. These results indicate that the control of TGFβ1 activity is important to improve regeneration of injured muscle and accelerate myoblast differentiation, in part through changes in GAG composition of muscle cell environment.

Phorbol esters affect skeletal muscle glucose transport in a fiber type-specific manner

2004 ◽  
Vol 287 (2) ◽  
pp. E305-E309 ◽  
Author(s):  
David C. Wright ◽  
Paige C. Geiger ◽  
Mark J. Rheinheimer ◽  
Dong Ho Han ◽  
John O. Holloszy
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Glucose Transport ◽  
Soleus Muscle ◽  
Insulin Signaling ◽  
Skeletal Muscles ◽  
Phorbol Esters ◽  
Serine Phosphorylation ◽  
Slow Twitch ◽  
Fast Twitch

Recent evidence has shown that activation of lipid-sensitive protein kinase C (PKC) isoforms leads to skeletal muscle insulin resistance. However, earlier studies demonstrated that phorbol esters increase glucose transport in skeletal muscle. The purpose of the present study was to try to resolve this discrepancy. Treatment with the phorbol ester 12-deoxyphorbol-13-phenylacetate 20-acetate (dPPA) led to an ∼3.5-fold increase in glucose transport in isolated fast-twitch epitrochlearis and flexor digitorum brevis muscles. Phorbol ester treatment was additive to a maximally effective concentration of insulin in fast-twitch skeletal muscles. Treatment with dPPA did not affect insulin signaling in the epitrochlearis. In contrast, phorbol esters had no effect on basal glucose transport and inhibited maximally insulin-stimulated glucose transport ∼50% in isolated slow-twitch soleus muscle. Furthermore, dPPA treatment inhibited the insulin-stimulated tyrosine phosphorylation of insulin receptor substrate (IRS)-1 and the threonine and serine phosphorylation of PKB by ∼50% in the soleus. dPPA treatment also caused serine phosphorylation of IRS-1 in the slow-twitch soleus muscle. In conclusion, our results show that phorbol esters stimulate glucose transport in fast-twitch skeletal muscles and inhibit insulin signaling in slow-twitch soleus muscle of rats. These findings suggest that mechanisms other than PKC activation mediate lipotoxicity-induced whole body insulin resistance.

scholarly journals Effects of epinephrine on glucose metabolism in contracting rat skeletal muscles

1998 ◽  
Vol 275 (3) ◽  
pp. E448-E456 ◽  
Author(s):  
Rune Aslesen ◽  
Jørgen Jensen
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transport ◽  
Skeletal Muscles ◽  
Contractile Activity ◽  
Phosphate Concentration ◽  
Insulin Stimulation ◽  
Glucose Phosphorylation ◽  
Slow Twitch ◽  
Fast Twitch

The effects of epinephrine on glucose metabolism during contractile activity and insulin stimulation were investigated in fast-twitch (epitrochlearis) and slow-twitch (soleus) muscles from Wistar rats. All muscles were mounted on contraction apparatuses, and some muscles were stimulated electrically for 30 min in vitro. Glucose uptake and glucose phosphorylation were measured with 2-[1,2-3H(N)]deoxy-d-glucose and glucose transport with 3- O-[ methyl-3H]methyl-d-glucose.d-[1-14C]mannitol was used to correct for extracellular space. In epitrochlearis, both contraction and insulin increased glucose transport by threefold, and combined they showed an additive effect. Epinephrine (10−6 M) did not influence glucose transport across the membrane during contractile activity or insulin stimulation. In the absence of epinephrine, similar glucose phosphorylation was obtained during contraction and during insulin stimulation in epitrochlearis (∼12 mmol ⋅ kg dry wt−1 ⋅ 30 min−1). In the presence of epinephrine, 9.5 ± 0.6 mmol ⋅ kg dry wt−1 ⋅ 30 min−1 glucose was phosphorylated during contraction, whereas only 2.0 ± 0.3 mmol ⋅ kg dry wt−1 ⋅ 30 min−1 was phosphorylated during insulin stimulation ( P < 0.01), despite a similar glucose 6-phosphate concentration. Comparable results were obtained in soleus. In conclusion, our data suggest that epinephrine inhibits glucose phosphorylation much less during contraction than during insulin stimulation.

Temporal responses of oxidative vs. glycolytic skeletal muscles to K+ deprivation: Na+ pumps and cell cations

1999 ◽  
Vol 276 (6) ◽  
pp. C1411-C1419 ◽  
Author(s):  
Curtis B. Thompson ◽  
Cheolsoo Choi ◽  
Jang H. Youn ◽  
Alicia A. McDonough
Keyword(s):  
Skeletal Muscle ◽  
Posttranscriptional Regulation ◽  
Skeletal Muscles ◽  
Extracellular Fluid ◽  
Protein Levels ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Low K ◽  
Muscle Specificity ◽  
White Gastrocnemius

When K+ output exceeds input, skeletal muscle releases intracellular fluid K+ to buffer the fall in extracellular fluid (ECF) K+. To investigate the mechanisms and muscle specificity of the K+ shift, rats were fed K+-deficient chow for 2–10 days, and two muscles at phenotypic extremes were studied: slow-twitch oxidative soleus and fast-twitch glycolytic white gastrocnemius (WG). After 2 days of low-K+ chow, plasma K+ concentration ([K+]) fell from 4.6 to 3.7 mM, and Na+-K+-ATPase α2 (not α1) protein levels in both muscles, measured by immunoblotting, decreased 36%. Cell [K+] decreased from 116 to 106 mM in soleus and insignificantly in WG, indicating that α2 can decrease before cell [K+]. After 5 days, there were further decreases in α2 (70%) and β2 (22%) in WG, not in soleus, whereas cell [K+] decreased and cell [Na+] increased by 10 mM in both muscles. By 10 days, plasma [K+] fell to 2.9 mM, with further decreases in WG α2 (94%) and β2 (70%); cell [K+] fell 19 mM in soleus and 24 mM in WG compared with the control, and cell [Na+] increased 9 mM in soleus and 15 mM in WG; total homogenate Na+-K+-ATPase activity decreased 19% in WG and insignificantly in soleus. Levels of α2, β1, and β2 mRNA were unchanged over 10 days. The ratios of α2 to α1 protein levels in both control muscles were found to be nearly 1 by using the relative changes in α-isoforms vs. β1- (soleus) or β2-isoforms (WG). We conclude that the patterns of regulation of Na+ pump isoforms in oxidative and glycolytic muscles during K+ deprivation mediated by posttranscriptional regulation of α2β1 and α2β2 are distinct and that decreases in α2-isoform pools can occur early enough in both muscles to account for the shift of K+ to the ECF.

Effect of catecholamines on glucose uptake and glycogenolysis in rat skeletal muscle

1985 ◽  
Vol 248 (5) ◽  
pp. C406-C409 ◽  
Author(s):  
D. A. Young ◽  
H. Wallberg-Henriksson ◽  
J. Cranshaw ◽  
M. Chen ◽  
J. O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Sugar Transport ◽  
Beta Agonist ◽  
Sugar Uptake ◽  
Rat Skeletal Muscle ◽  
Adrenergic Control ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Alpha Agonist

The effect of catecholamines on glycogenolysis and sugar transport was evaluated in rat epitrochlearis (fast-twitch) and soleus (slow-twitch) muscles in vitro. When muscles were incubated with 0.1 microM epinephrine (both an alpha- and beta-agonist), the proportion of phosphorylase in the a form increased from 6.2 +/- 0.7 to 37.4 +/- 5.7% in epitrochlearis muscle and from 9.1 +/- 0.7 to 21.6 +/- 1.3% in soleus muscle. Both the activation of phosphorylase and the resulting glycogenolysis could be prevented by preincubation with the beta-blocker, propranolol. The effect of catecholamines on the rate of sugar transport was also examined in epitrochlearis muscle. The beta-agonist, isoproterenol, significantly depressed the rate of 3-O-methylglucose uptake, while the alpha-agonist, phenylephrine, had no effect. Inclusion of 0.1% albumin in the incubation medium increased the resting rate of sugar transport twofold. When isoproterenol + albumin were present, rather than exerting a depressive effect the catecholamine further increased the rate of sugar uptake. This increase was prevented by preincubation with propranolol. It was concluded that glycogenolysis and sugar transport in rat skeletal muscle are solely under beta-adrenergic control.

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