Effect of stimulation frequency on contraction-induced glucose transport in rat skeletal muscle

2000 ◽  
Vol 279 (4) ◽  
pp. E862-E867 ◽  
Author(s):  
Jacob Ihlemann ◽  
Thorkil Ploug ◽  
Ylva Hellsten ◽  
Henrik Galbo
Keyword(s):  
Metabolic Rate ◽  
Glucose Transport ◽  
Stimulation Frequency ◽  
Total Force ◽  
Glycogen Depletion ◽  
Force Development ◽  
The Face ◽  
Flexor Digitorum Brevis ◽  
Ampk Activity ◽  
Flexor Digitorum

Previous studies have indicated that frequency of stimulation is a major determinant of glucose transport in contracting muscle. We have now studied whether this is so also when total force development or metabolic rate is kept constant. Incubated soleus muscles were electrically stimulated to perform repeated tetanic contractions at four different frequencies (0.25, 0.5, 1, and 2 Hz) for 10 min. Resting length was adjusted to achieve identical total force development or metabolic rate (glycogen depletion and lactate accumulation). Overall, at constant total force development, glucose transport (2-deoxyglucose uptake) increased with stimulation frequency ( P < 0.05; basal: 25 ± 2, 0.25 Hz: 50 ± 4, 0.5 Hz: 50 ± 3, 1 Hz: 81 ± 5, 2 Hz: 79 ± 3 nmol · g−1 · 5 min−1). However, glucose transport was identical ( P > 0.05) at the two lower (0.25 and 0.5 Hz) as well as at the two higher (1 and 2 Hz) frequencies. Glycogen decreased ( P < 0.05; basal: 19 ± 1, 0.25 Hz: 13 ± 1, 0.5 Hz: 12 ± 2, 1 Hz: 7 ± 1, 2 Hz: 7 ± 1 mmol/kg) and 5′-AMP-activated protein kinase (AMPK) activity increased ( P < 0.05; basal: 1.7 ± 0.4, 0.25 Hz: 32.4 ± 7.0, 0.5 Hz: 36.5 ± 2.1, 1 Hz: 63.4 ± 8.0, 2 Hz: 67.0 ± 13.4 pmol · mg−1 · min−1) when glucose transport increased. Experiments with constant metabolic rate were carried out in soleus, flexor digitorum brevis, and epitrochlearis muscles. In all muscles, glucose transport was identical at 0.5 and 2 Hz ( P > 0.05); also, AMPK activity did not increase with stimulation frequency. In conclusion, muscle glucose transport increases with stimulation frequency but only in the face of energy depletion and increase in AMPK activity. This indicates that contraction-induced glucose transport is elicited by metabolic demands rather than by events occurring early during the excitation-contraction coupling.

scholarly journals Effect of tension on contraction-induced glucose transport in rat skeletal muscle

1999 ◽  
Vol 277 (2) ◽  
pp. E208-E214 ◽  
Author(s):  
Jacob Ihlemann ◽  
Thorkil Ploug ◽  
Ylva Hellsten ◽  
Henrik Galbo
Keyword(s):  
Glucose Transport ◽  
Stimulation Frequency ◽  
Maximum Force ◽  
General View ◽  
Force Development ◽  
Ampk Activity ◽  
Per Se ◽  
Muscle Glucose Transport ◽  
Amp Activated Protein Kinase ◽  
Passive Stretch

We questioned the general view that contraction-induced muscle glucose transport only depends on stimulation frequency and not on workload. Incubated soleus muscles were electrically stimulated at a given pattern for 5 min. Resting length was adjusted to achieve either no force (0% P), maximum force (100% P), or 50% of maximum force (50% P). Glucose transport (2-deoxy-d-glucose uptake) increased directly with force development ( P < 0.05) [27 ± 2 (basal), 45 ± 2 (0% P), 68 ± 3 (50% P), and 94 ± 3 (100% P) nmol ⋅ g−1 ⋅ 5 min−1]. Glycogen decreased at 0% P but did not change further with force development ( P > 0.05). Lactate, AMP, and IMP concentrations were higher ( P < 0.05) and ATP concentrations lower ( P < 0.05) when force was produced than when it was not. 5′-AMP-activated protein kinase (AMPK) activity increased directly with force [20 ± 2 (basal), 60 ± 11 (0% P), 91 ± 12 (50% P), and 109 ± 12 (100% P) pmol ⋅ mg−1 ⋅ min−1]. Passive stretch (∼86% P) doubled glucose transport without altering metabolism. In conclusion, contraction-induced muscle glucose transport varies directly with force development and is not solely determined by stimulation frequency. AMPK activity is probably an essential determinant of contraction-induced glucose transport. In contrast, glycogen concentrations per se do not play a major role. Finally, passive stretch per se increases glucose transport in muscle.

Effect of fiber type and nutritional state on AICAR- and contraction-stimulated glucose transport in rat muscle

2002 ◽  
Vol 282 (6) ◽  
pp. E1291-E1300 ◽  
Author(s):  
Hua Ai ◽  
Jacob Ihlemann ◽  
Ylva Hellsten ◽  
Hans P. M. M. Lauritzen ◽  
D. Grahame Hardie ◽  
...  
Keyword(s):  
Glucose Transport ◽  
Fiber Type ◽  
Nutritional State ◽  
Fiber Types ◽  
Type Composition ◽  
Flexor Digitorum Brevis ◽  
Ampk Activity ◽  
Flexor Digitorum ◽  
Amp Activated Protein Kinase ◽  
Fasted Rats

AMP-activated protein kinase (AMPK) may mediate the stimulatory effect of contraction and 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) on glucose transport in skeletal muscle. In muscles with different fiber type composition from fasted rats, AICAR increased 2-deoxyglucose transport and total AMPK activity approximately twofold in epitrochlearis (EPI), less in flexor digitorum brevis, and not at all in soleus muscles. Contraction increased both transport and AMPK activity more than AICAR did. In EPI muscles, the effects of AICAR and contractions on glucose transport were partially additive despite a lower AMPK activity with AICAR compared with contraction alone. In EPI from fed rats, glucose transport responses were smaller than what was seen in fasted rats, and AICAR did not increase transport despite an increase in AMPK activity. AICAR and contraction activated both α1- and α2-isoforms of AMPK. Expression of both isoforms varied with fiber types, and α2 was highly expressed in nuclei. In conclusion, AICAR-stimulated glucose transport varies with muscle fiber type and nutritional state. AMPK is unlikely to be the sole mediator of contraction-stimulated glucose transport.

Glucose transporters and glucose transport in skeletal muscles of 1- to 25-mo-old rats

1993 ◽  
Vol 264 (3) ◽  
pp. E319-E327 ◽  
Author(s):  
E. A. Gulve ◽  
E. J. Henriksen ◽  
K. J. Rodnick ◽  
J. H. Youn ◽  
J. O. Holloszy
Keyword(s):  
Glucose Transport ◽  
Skeletal Muscles ◽  
Glucose Transporter ◽  
Contractile Activity ◽  
Transport Activity ◽  
Glut 4 ◽  
Flexor Digitorum Brevis ◽  
Old Rats ◽  
Growth And Aging ◽  
Flexor Digitorum

It is widely thought that aging results in development of insulin resistance in skeletal muscle. In this study, we examined the effects of growth and aging on the concentration of the GLUT-4 glucose transporter and on glucose transport activity in skeletal muscles of female Long-Evans rats. Relative amounts of immunoreactive GLUT-4 protein were measured in muscle homogenates of 1-, 10-, and 25-mo-old rats by immunoblotting with a polyclonal antibody directed against GLUT-4. In the epitrochlearis, plantaris, and the red and white regions of the quadriceps muscles, GLUT-4 immunoreactivity decreased by 14-33% between 1 and 10 mo of age and thereafter remained constant. In flexor digitorum brevis (FDB) and soleus muscles, GLUT-4 concentration was similar at all three ages studied. Glucose transport activity was assessed in epitrochlearis and FDB muscles by incubation with 2-deoxyglucose under the following conditions: basal, submaximal insulin, and either maximal insulin or maximal insulin combined with contractile activity. Glucose transport in the epitrochlearis muscle decreased by approximately 60% between 1 and 4 mo of age and then did not decline further between 4 and 25 mo of age. Transport activity in the FDB assessed with a maximally effective insulin concentration decreased only slightly (< 20%) between 1 and 7 mo of age. Aging, i.e., the transition from young adulthood to old age, was not associated with a decrease in glucose transport activity in either the epitrochlearis or the FDB.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose transport with brief dietary restriction: heterogenous responses in muscles

1994 ◽  
Vol 266 (6) ◽  
pp. E946-E952 ◽  
Author(s):  
G. D. Cartee ◽  
D. J. Dean
Keyword(s):  
Glucose Transport ◽  
Dietary Restriction ◽  
Time Course ◽  
Abdominal Fat ◽  
Transport Activity ◽  
Fischer 344 ◽  
Flexor Digitorum Brevis ◽  
Ad Libitum ◽  
Ad Libitum Intake ◽  
Flexor Digitorum

The time course (1, 5, or 20 days) for the effect of dietary restriction (DR; approximately 25% reduction below ad libitum intake) on epitrochlearis and flexor digitorum brevis (FDB) muscle glucose transport activity was studied in female Fischer 344 rats (8 mo old). Epitrochlearis glucose transport activity with 100 microU/ml insulin was increased by 38% after 5 days of DR (P < 0.05) despite no change in glucose transport activity with 0 or 20,000 microU/ml insulin. The increase with 100 microU/ml insulin was not further enhanced by 20 days of DR. DR did not result in a significant increase in the glucose transport activity of the FDB with 0, 100, or 20,000 microU/ml insulin. Abdominal fat content was significantly (P < 0.01) reduced below ad libitum levels only after 20 days of DR. These results demonstrate that DR-induced improvement in epitrochlearis glucose transport activity with a physiological insulin concentration can occur very rapidly, preceding detectable changes in basal or maximal insulin-stimulated glucose transport activity or abdominal fat pad mass, and the enhancement of insulin action does not occur simultaneously in all muscles.

Disruption of microtubules in rat skeletal muscle does not inhibit insulin- or contraction-stimulated glucose transport

2003 ◽  
Vol 285 (4) ◽  
pp. E836-E844 ◽  
Author(s):  
Hua Ai ◽  
Evelyn Ralston ◽  
Hans P. M. M. Lauritzen ◽  
Henrik Galbo ◽  
Thorkil Ploug
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Immunofluorescence Microscopy ◽  
Fiber Type ◽  
Force Production ◽  
Rat Skeletal Muscle ◽  
Microtubule Network ◽  
Type Composition ◽  
Flexor Digitorum Brevis ◽  
Flexor Digitorum

Insulin and muscle contractions stimulate glucose transport in skeletal muscle through a translocation of intracellular GLUT4 glucose transporters to the cell surface. Judged by immunofluorescence microscopy, part of the GLUT4 storage sites is associated with the extensive microtubule cytoskeleton found in all muscle fibers. Here, we test whether microtubules are required mediators of the effect of insulin and contractions. In three different incubated rat muscles with distinct fiber type composition, depolymerization of microtubules with colchicine for ≤8 h did not inhibit insulin- or contraction-stimulated 2-deoxyglucose transport or force production. On the contrary, colchicine at least partially prevented the ∼30% decrease in insulin-stimulated transport that specifically developed during 8 h of incubation in soleus muscle but not in flexor digitorum brevis or epitrochlearis muscles. In contrast, nocodazole, another microtubule-disrupting drug, rapidly and dose dependently blocked insulin- and contraction-stimulated glucose transport. A similar discrepancy between colchicine and nocodazole was also found in their ability to block glucose transport in muscle giant “ghost” vesicles. This suggests that the ability of insulin and contractions to stimulate glucose transport in muscle does not require an intact microtubule network and that nocodazole inhibits glucose transport independently of its microtubule-disrupting effect.

How muscle insulin sensitivity is regulated: testing of a hypothesis

2006 ◽  
Vol 291 (6) ◽  
pp. E1258-E1263 ◽  
Author(s):  
Paige C. Geiger ◽  
Dong Ho Han ◽  
David C. Wright ◽  
John O. Holloszy
Keyword(s):  
Insulin Sensitivity ◽  
Cell Surface ◽  
Glucose Transport ◽  
Acute Effect ◽  
Muscle Contractions ◽  
General Phenomenon ◽  
Flexor Digitorum Brevis ◽  
Acute Increase ◽  
Flexor Digitorum ◽  
Stimulation Of

Muscle contractions induce an increase in glucose transport. The acute effect of muscle contractions on glucose transport is independent of insulin and reverses rapidly after cessation of exercise. As the acute increase in glucose transport reverses, a marked increase in the sensitivity of muscle to insulin occurs. The mechanism for this phenomenon is unknown. We hypothesize that an increase in insulin sensitivity is a general phenomenon that occurs during reversal of an increase in cell surface GLUT4 induced by any stimulus, not just exercise. To test this hypothesis, epitrochlearis, rat soleus, and flexor digitorum brevis muscles were incubated for 30 min with a maximally effective insulin concentration (1.0 mU/ml). Muscles were allowed to recover for 3 h in the absence of insulin. Muscles were then exposed to 60 μU/ml insulin for 30 min followed by measurement of glucose transport. Preincubation with 1.0 mU/ml insulin resulted in an ∼2-fold greater increase in glucose transport 3.5 h later in response to 60 μU/ml insulin than that which occurred in control muscles treated with 60 μU/ml insulin. Pretreatment of muscles with combined maximal insulin and exercise stimuli greatly amplified the increase in insulin sensitivity. The increases in glucose transport were paralleled by increases in cell surface GLUT4. We conclude that stimulation of glucose transport by any agent is followed by an increase in sensitivity of glucose transport to activation that is mediated by translocation of more GLUT4 to the cell surface.

scholarly journals KATPchannel deficiency in mouse flexor digitorum brevis causes fibre damage and impairs Ca2+release and force development during fatiguein vitro

2007 ◽  
Vol 582 (2) ◽  
pp. 843-857 ◽  
Author(s):  
Carlo Cifelli ◽  
François Bourassa ◽  
Louise Gariépy ◽  
Krystyna Banas ◽  
Maria Benkhalti ◽  
...  
Keyword(s):  
Force Development ◽  
Flexor Digitorum Brevis ◽  
Flexor Digitorum

scholarly journals Percutaneous flexor digitorum brevis tenotomy: An anatomical study

2021 ◽  
Author(s):  
Paulo Carvalho ◽  
Miki Dalmau-Pastor ◽  
Caroline Lozi ◽  
Matheus Souza ◽  
Julien Lucas-Y-Hernandez ◽  
...  
Keyword(s):  
Anatomical Study ◽  
Flexor Digitorum Brevis ◽  
Flexor Digitorum

scholarly journals Consequences of SUR2[A478V] Mutation in Skeletal Muscle of Murine Model of Cantu Syndrome

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1791
Author(s):  
Rosa Scala ◽  
Fatima Maqoud ◽  
Nicola Zizzo ◽  
Giuseppe Passantino ◽  
Antonietta Mele ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Katp Channel ◽  
Ex Vivo ◽  
Channel Modulation ◽  
Flexor Digitorum Brevis ◽  
Inflammatory Edema ◽  
Flexor Digitorum ◽  
Channel Currents

(1) Background: Cantu syndrome (CS) arises from gain-of-function (GOF) mutations in the ABCC9 and KCNJ8 genes, which encode ATP-sensitive K+ (KATP) channel subunits SUR2 and Kir6.1, respectively. Most CS patients have mutations in SUR2, the major component of skeletal muscle KATP, but the consequences of SUR2 GOF in skeletal muscle are unknown. (2) Methods: We performed in vivo and ex vivo characterization of skeletal muscle in heterozygous SUR2[A478V] (SUR2wt/AV) and homozygous SUR2[A478V] (SUR2AV/AV) CS mice. (3) Results: In SUR2wt/AV and SUR2AV/AV mice, forelimb strength and diaphragm amplitude movement were reduced; muscle echodensity was enhanced. KATP channel currents recorded in Flexor digitorum brevis fibers showed reduced MgATP-sensitivity in SUR2wt/AV, dramatically so in SUR2AV/AV mice; IC50 for MgATP inhibition of KATP currents were 1.9 ± 0.5 × 10−5 M in SUR2wt/AV and 8.6 ± 0.4 × 10−6 M in WT mice and was not measurable in SUR2AV/AV. A slight rightward shift of sensitivity to inhibition by glibenclamide was detected in SUR2AV/AV mice. Histopathological and qPCR analysis revealed atrophy of soleus and tibialis anterior muscles and up-regulation of atrogin-1 and MuRF1 mRNA in CS mice. (4) Conclusions: SUR2[A478V] “knock-in” mutation in mice impairs KATP channel modulation by MgATP, markedly so in SUR2AV/AV, with atrophy and non-inflammatory edema in different skeletal muscle phenotypes.

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