Anaerobic Metabolism During Electrical Stimulation of Aged Rat Skeletal Muscle

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.

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The effect of repeated bouts of electrical stimulation‐induced muscle contractions on proteolytic signaling in rat skeletal muscle

Physiological Reports ◽

10.14814/phy2.14842 ◽

2021 ◽

Vol 9 (9) ◽

Author(s):

Takaya Kotani ◽

Junya Takegaki ◽

Yuki Tamura ◽

Karina Kouzaki ◽

Koichi Nakazato ◽

...

Keyword(s):

Skeletal Muscle ◽

Electrical Stimulation ◽

Muscle Contractions ◽

Rat Skeletal Muscle

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Insulin increases thermogenesis in rat skeletal muscle following exercise

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1985.248.1.e148 ◽

1985 ◽

Vol 248 (1) ◽

pp. E148-E151

Author(s):

T. W. Balon ◽

A. Zorzano ◽

M. N. Goodman ◽

N. B. Ruderman

Keyword(s):

Skeletal Muscle ◽

Insulin Secretion ◽

Glycogen Synthesis ◽

O2 Consumption ◽

Rat Skeletal Muscle ◽

Additional Energy ◽

Rat Muscle ◽

Prior Exercise ◽

Increase Insulin Secretion ◽

Stimulation Of

Insulin increased O2 consumption in isolated perfused rat muscle for upward of 2 h after a treadmill run. Insulin did not increase O2 consumption in nonexercised rats, nor did prior exercise increase O2 consumption in the absence of added insulin. The stimulation of glycogen synthesis by insulin was also enhanced in muscle of previously exercised rats. The additional energy required for this was not sufficient to account for the increase in O2 consumption, however. The results indicate that insulin increases thermogenesis in skeletal muscle after exercise. They also raise the possibility that in intact organisms the thermogenic effect of foods that increase insulin secretion could be increased by prior exercise.

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Effects of phenylarsine oxide on stimulation of glucose transport in rat skeletal muscle

AJP Cell Physiology ◽

10.1152/ajpcell.1990.258.4.c648 ◽

1990 ◽

Vol 258 (4) ◽

pp. C648-C653 ◽

Cited By ~ 32

Author(s):

E. J. Henriksen ◽

J. O. Holloszy

Keyword(s):

Skeletal Muscle ◽

Glucose Transport ◽

Cytochalasin B ◽

Contractile Activity ◽

Transport Activity ◽

Rat Skeletal Muscle ◽

Phenylarsine Oxide ◽

Muscle Glucose Transport ◽

Glucose Analogue ◽

Stimulation Of

The trivalent arsenical phenylarsine oxide (PAO) inhibits insulin-stimulated glucose transport in adipocytes and skeletal muscle through direct interactions with vicinal sulfhydryls. In muscle, glucose transport is also activated by contractile activity and hypoxia. It was therefore the purpose of the present study to investigate whether vicinal sulfhydryls are involved in the stimulation of glucose transport activity in the isolated rat epitrochlearis muscle by hypoxia or contractions. PAO (greater than 5 microM) caused a twofold increase in rate of transport of the nonmetabolizable glucose analogue 3-O-methylglucose (3-MG) that was completely prevented by cytochalasin B, the vicinal dithiol dimercaptopropanol, dantrolene, or 9-aminoacridine, both inhibitors of sarcoplasmic reticulum Ca2+ release, or omission of extracellular Ca2+. Although PAO treatment (greater than or equal to 20 microM) prevented approximately 80% of the increase in 3-MG transport caused by insulin, it resulted in only a approximately 50% inhibition of the stimulation of 3-MG transport by either hypoxia or contractile activity. PAO treatment (40 microM) of muscles already maximally stimulated by insulin, contractile activity, or hypoxia did not reverse the enhanced rate of 3-MG transport. These data suggest that vicinal sulfhydryls play a greater role in the activation of glucose transport by insulin than by muscle contractions or hypoxia. The finding that PAO inhibits the stimulation of glucose transport, but does not affect glucose transport after it has been stimulated, provides evidence that vicinal sulfhydryls are involved in the pathways for glucose transport activation in muscle, but not in the glucose transport mechanism itself.

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Ca2+ Uptake Coupled to Glycogen Phosphorolysis in the Glycogenolytic-Sarcoplasmic Reticulum Complex from Rat Skeletal Muscle

Zeitschrift für Naturforschung C ◽

10.1515/znc-1996-7-819 ◽

1996 ◽

Vol 51 (7-8) ◽

pp. 591-598 ◽

Cited By ~ 8

Author(s):

M. Nogues ◽

A. Cuenda ◽

F. Henao ◽

C. Gutiérrez-Merino

Keyword(s):

Skeletal Muscle ◽

Sarcoplasmic Reticulum ◽

Glycogen Phosphorylase ◽

Rat Skeletal Muscle ◽

Subcellular Structure ◽

Sequential Action ◽

Physiological Conditions ◽

Low Concentrations ◽

Ischemic Muscle ◽

Stimulation Of

Abstract The glycogenolytic-sarcoplasmic reticulum complex from rat skeletal muscle accumulates Ca2+ upon stimulation of glycogen phosphorolysis in the absence of added ATP. It is shown that an efficient Ca2+ uptake involves the sequential action of glycogen phosphorylase, phosphoglucomutase and hexokinase, which generate low concentrations of ATP (approximately 1 -2 μм) compartmentalized in the immediate vicinity of the sarcoplasmic reticulum Ca2+, Mg2+-ATPase (the Ca2+ pump). The Ca2+ uptake supported by glycogenolysis in this subcellular structure is strongly stimulated by micromolar concentrations of AMP, showing that the glycogen phosphorylase associated with this complex is in the dephosphorylated b form. The results point out that the flux through this compartmentalized metabolic pathway should be enhanced in physiological conditions leading to increased AMP concentrations in the sarcoplasm, such as long-lasting contractions and in ischemic muscle.

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Neurogenically derived nitrosyl factors mediate sympathetic vasodilation in the hindlimb of the rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1997.272.5.h2369 ◽

1997 ◽

Vol 272 (5) ◽

pp. H2369-H2376 ◽

Cited By ~ 14

Author(s):

R. L. Davisson ◽

O. S. Possas ◽

S. P. Murphy ◽

S. J. Lewis

Keyword(s):

Nitric Oxide ◽

Skeletal Muscle ◽

Electrical Stimulation ◽

Sympathetic Neurons ◽

Specific Inhibitor ◽

No Synthase ◽

Systemic Administration ◽

Sympathetic Chain ◽

Low Intensity ◽

Stimulation Of

Skeletal muscle vasculature of the hindlimb is innervated by a sympathetic noncholinergic vasodilator system. The aim of this study was to determine whether this vasodilator system may represent postganglionic lumbar sympathetic neurons that synthesize and release nitric oxide (NO) or related NO-containing factors. We examined whether NO synthase (NOS)-positive postganglionic lumbar nerves innervate the hindlimb vasculature of the rat and whether the hindlimb vasodilation produced by electrical stimulation of the lumbar sympathetic chain of anesthetized rats is reduced after the systemic administration of the specific inhibitor of neuronal NOS 7-nitroindazole (7-NI). Subpopulations of lumbar sympathetic cell bodies stained intensely for NOS. Postganglionic fibers and varicosities within the iliac and femoral arteries also stained for NOS. Double ligation of the lumbar chain demonstrated that NOS was transported from the cell bodies toward the peripheral terminals. Low-intensity electrical stimulation of the lumbar chain produced a pronounced hindlimb vasodilation that was markedly diminished by pretreatment with 7-NI (45 mg/kg i.v.). In contrast, the vasodilator potency of acetylcholine and S-nitrosocysteine were augmented by 7-NI. These results suggest that postganglionic lumbar sympathetic neurons may synthesize and release NO-containing factors.

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