ATP from glycolysis is required for normal sodium homeostasis in resting fast-twitch rodent skeletal muscle

2001 ◽  
Vol 281 (3) ◽  
pp. E479-E488 ◽  
Author(s):  
Ken Okamoto ◽  
Weiyang Wang ◽  
Jan Rounds ◽  
Elizabeth A. Chambers ◽  
Danny O. Jacobs
Keyword(s):  
Skeletal Muscles ◽  
Iodoacetic Acid ◽  
High Energy ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
High Energy Phosphates ◽  
Sodium Homeostasis ◽  
Carbonyl Cyanide ◽  
Fast Twitch

Myocellular sodium homeostasis is commonly disrupted during critical illness for unknown reasons. Recent data suggest that changes in intracellular sodium content and the amount of ATP provided by glycolysis are closely related. The role of glycolysis and oxidative phosphorylation in providing fuel to the Na+-K+ pump was investigated in resting rat extensor digitorum longus muscles incubated at 30°C for 1 h. Oxidative inhibition with carbonyl cyanide m-chlorophenylhydrazone, known as CCCP (0.2 μM), or by hypooxygenation did not alter myocellular sodium or potassium content ([Na+]i, [K+]i, respectively), whereas treatment with iodoacetic acid (0.3 mM), which effectively blocked glycolysis, dramatically increased [Na+]i and the [Na+]i/[K+]i ratio. Experiments using ouabain and measurements of myocellular high-energy phosphates indicate that Na+-K+-ATPase activity is only impaired when glycolysis is inhibited. The data suggest that normal glycolysis is required to regulate intracellular sodium in fast-twitch skeletal muscles, because it is the predominant source of the fuel for the Na+-K+-ATPase.

Cardioprotective Effects of Propofol and Sevoflurane in Ischemic and Reperfused Rat Hearts 

1999 ◽  
Vol 91 (5) ◽  
pp. 1349-1349 ◽  
Author(s):  
Sanjiv Mathur ◽  
Parviz Farhangkhgoee ◽  
Morris Karmazyn
Keyword(s):  
High Energy ◽  
Left Ventricular ◽  
High Energy Phosphates ◽  
Constant Flow Rate ◽  
Rat Hearts ◽  
Reperfusion Period ◽  
Coronary Syndromes ◽  
Cardioprotective Effects ◽  
Developed Pressure

Background Sodium ion-hydrogen ion (Na(+)-H(+)) exchange inhibitors are effective cardioprotective agents. The N(+)-H(+) exchange inhibitor HOE 642 (cariporide) has undergone clinical trials in acute coronary syndromes, including bypass surgery. Propofol and sevoflurane are also cardioprotective via unknown mechanisms. The authors investigated the interaction between propofol and HOE 642 in the ischemic reperfused rat heart and studied the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels in the myocardial protection associated with propofol and sevoflurane. Methods Isolated rat hearts were perfused by the Langendorff method at a constant flow rate, and left ventricular function and coronary pressures were assessed using standard methods. Energy metabolites were also determined. To assess the role of K(ATP) channels, hearts were pretreated with the K(ATP) blocker glyburide (10 microM). Hearts were then exposed to either control buffer or buffer containing HOE 642 (5 microM), propofol (35 microM), sevoflurane (2.15 vol%), the K(ATP) opener pinacidil (1 microM), or the combination of propofol and HOE 642. Each heart was then subjected to 1 h of global ischemia followed by 1 h of reperfusion. Results Hearts treated with propofol, sevoflurane, pinacidil, or HOE 642 showed significantly higher recovery of left ventricular developed pressure and reduced end-diastolic pressures compared with controls. The combination of propofol and HOE 642 provided superior protection toward the end of the reperfusion period. Propofol, sevoflurane, and HOE 642 also attenuated the onset and magnitude of ischemic contracture and preserved high-energy phosphates (HEPs) compared with controls. Glyburide attenuated the cardioprotective effects of sevoflurane and abolished the protection observed with pinacidil. In contrast, glyburide had no effect on the cardioprotection associated with propofol treatment. Conclusion HOE 642, propofol, and sevoflurane provide cardioprotection via different mechanisms. These distinct mechanisms may allow for the additive and superior protection observed with the combination of these anesthetics and HOE 642.

Muscle ATP turnover rate during isometric contraction in humans

1986 ◽  
Vol 60 (6) ◽  
pp. 1839-1842 ◽  
Author(s):  
A. Katz ◽  
K. Sahlin ◽  
J. Henriksson
Keyword(s):  
Isometric Contraction ◽  
Turnover Rate ◽  
Knee Extensor ◽  
High Energy ◽  
High Energy Phosphates ◽  
Atp Turnover ◽  
Contraction Duration ◽  
Extensor Muscles ◽  
Before And After ◽  
Fast Twitch

ATP turnover and glycolytic rates during isometric contraction in humans have been investigated. Subjects contracted the knee extensor muscles at two-thirds maximal voluntary force to fatigue (mean +/- SE, 53 +/- 4 s). Biopsies were obtained before and after exercise and analyzed for high-energy phosphates and glycogenolytic-glycolytic intermediates. Total ATP turnover was 190 +/- 7 mmol/kg dry muscle, whereas the average turnover rate was 3.7 +/- 0.2 mmol . kg dry muscle-1 . S-1. The average ATP turnover rate was positively correlated with the percentage of fast-twitch fibers in the postexercise biopsy (r = 0.71; P less than 0.05) and negatively correlated with contraction duration to fatigue (r = -0.88; P less than 0.05). At fatigue, phosphocreatine ranged from 1 to 11 mmol/kg dry muscle (86–99% depletion of value at rest), whereas lactate ranged from 59 to 101. The mean glycolytic rate was 0.83 +/- 0.05 mmol . kg dry muscle-1 . S-1 and was positively correlated with the rate of glucose 6-phosphate accumulation (r = 0.83; P less than 0.05). It is concluded that a major determinant of the ATP turnover rate is the muscle fiber composition, which is probably explained by a higher turnover rate in fast-twitch fibers; fatigue is more closely related to a low phosphocreatine content than to a high lactate content; and the increase in prephosphofructokinase intermediates is important for stimulating glycolysis during contraction.

scholarly journals Noninvasive Monitoring of Training Induced Muscle Adaptation with -MRS: Fibre Type Shifts Correlate with Metabolic Changes

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Eike Hoff ◽  
Lars Brechtel ◽  
Patrick Strube ◽  
Paul Konstanczak ◽  
Gisela Stoltenburg-Didinger ◽  
...  
Keyword(s):  
Fibre Type ◽  
Gastrocnemius Muscle ◽  
Noninvasive Monitoring ◽  
High Energy ◽  
Metabolic Changes ◽  
Resonance Spectroscopy ◽  
High Energy Phosphates ◽  
Type Ii ◽  
Fibre Type Composition ◽  
Fast Twitch

Purpose. To evaluate training induced metabolic changes noninvasively with magnetic resonance spectroscopy (-MRS) for measuring muscle fibre type adaptation.Methods. Eleven volunteers underwent a 24-week training, consisting of speed-strength, endurance, and detraining (each 8 weeks). Prior to and following each training period, needle biopsies and -MRS of the resting gastrocnemius muscle were performed. Fibre type distribution was analyzed histologically and tested for correlation with the ratios of high energy phosphates ([PCr]/[], [PCr]/[βATP] and [PCr + ]/[βATP]). The correlation between the changes of the -MRS parameters during training and the resulting changes in fibre composition were also analysed.Results. We observed an increased type-II-fibre proportion after speed-strength and detraining. After endurance training the percentage of fast-twitch fibres was reduced. The progression of the [PCr]/[]-ratio was similar to that of the fast-twitch fibres during the training. We found a correlation between the type-II-fibre proportion and [PCr]/[] (, ) or [PCr]/[βATP] (, ); the correlations between its changes (delta) and the fibre-shift were significant as well (delta[PCr]/[] , delta[PCr]/[βATP] , ).Conclusion. Shifts in fibre type composition and high energy phosphate metabolite content covary in human gastrocnemius muscle. Therefore -MRS might be a feasible method for noninvasive monitoring of exercise-induced fibre type transformation.

scholarly journals Role of cation gradients in hypercontracture of myocytes during simulated ischemia and reperfusion

1993 ◽  
Vol 264 (6) ◽  
pp. H1896-H1906 ◽  
Author(s):  
M. Nishida ◽  
S. Borzak ◽  
B. Kraemer ◽  
J. P. Navas ◽  
R. A. Kelly ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Extracellular Fluid ◽  
High Energy ◽  
Ischemia And Reperfusion ◽  
High Energy Phosphates ◽  
Twitch Contraction ◽  
Adult Rat ◽  
Simulated Ischemia ◽  
The Relationship

We examined the relationship between transsarcolemmal cation gradients and hypercontracture of cardiac myocytes in ischemia and reperfusion using adult rat ventricular myocytes superfused with buffer mimicking normal or ischemic extracellular fluid. Contractile performance of electrically stimulated cells was recorded by an optical video system simultaneously with measurements of intracellular Ca2+ concentration ([Ca2+]i) using fura-2 or intracellular pH (pHi) using 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. While cells were exposed to simulated ischemia buffer, the transsarcolemmal H+ gradient was abolished, [Ca2+]i transient stopped, and twitch contraction of myocytes ceased. Upon reperfusion with normal buffer, H+ gradient was quickly restored, Ca2+ transients restarted with transient increase in systolic Ca2+, and twitch contraction restarted with development of hypercontracture, which continued after [Ca2+]i returned to preischemic level even in the presence of near-normal concentrations of high-energy phosphates. When the transsarcolemmal proton, Na+, and Ca2+ gradients were altered so that Na+ entry via Na(+)-H+ exchange and Ca2+ entry via Ca(2+)-Na+ exchange were made less favorable, the transient systolic overshoot of Ca2+ at reperfusion and development of hypercontracture was largely avoided. These results suggest that Na+ and then Ca2+ entry via the Na(+)-H+ and Na(+)-Ca2+ exchangers, respectively, probably contribute to the increase in [Ca2+]i and hypercontracture of myocytes at time of reperfusion in this model.

Fast-twitch skeletal muscles of dystrophic mouse pups are resistant to injury from acute mechanical stress

2002 ◽  
Vol 283 (4) ◽  
pp. C1090-C1101 ◽  
Author(s):  
Robert W. Grange ◽  
Thomas G. Gainer ◽  
Krista M. Marschner ◽  
Robert J. Talmadge ◽  
James T. Stull
Keyword(s):  
Skeletal Muscles ◽  
Mechanical Injury ◽  
Membrane Injury ◽  
Glycoprotein Complex ◽  
Dystrophin Glycoprotein Complex ◽  
Duchenne's Muscular Dystrophy ◽  
Fast Twitch ◽  
Dystrophin Glycoprotein

Loss of the dystrophin-glycoprotein complex from muscle sarcolemma in Duchenne's muscular dystrophy (DMD) renders the membrane susceptible to mechanical injury, leaky to Ca2+, and disrupts signaling, but the precise mechanism(s) leading to the onset of DMD remain unclear. To assess the role of mechanical injury in the onset of DMD, extensor digitorum longus (EDL) muscles from C57 (control), mdx, and mdx-utrophin-deficient [ mdx:utrn(−/−); dystrophic] pups aged 9–12 days were subjected to an acute stretch-injury or no-stretch protocol in vitro. Before the stretches, isometric stress was attenuated for mdx:utrn(−/−) compared with control muscles at all stimulation frequencies ( P< 0.05). During the stretches, EDL muscles for each genotype demonstrated similar mean stiffness values. After the stretches, isometric stress during a tetanus was decreased significantly for both mdx and mdx:utrn(−/−) muscles compared with control muscles ( P < 0.05). Membrane injury assessed by uptake of procion orange dye was greater for dystrophic compared with control EDL ( P < 0.05), but, within each genotype, the percentage of total cells taking up dye was not different for the no-stretch vs. stretch condition. These data suggest that the sarcolemma of maturing dystrophic EDL muscles are resistant to acute mechanical injury.

ATP utilization and provision in fast-twitch skeletal muscle during tetanic contractions

1989 ◽  
Vol 257 (4) ◽  
pp. E595-E605 ◽  
Author(s):  
L. L. Spriet
Keyword(s):  
Average Energy ◽  
High Energy ◽  
Energy Costs ◽  
High Energy Phosphates ◽  
Phosphorylase Activity ◽  
Train Duration ◽  
Fast Twitch Muscle ◽  
Fast Twitch

Rat fast-twitch muscles were tetanically stimulated in situ with an occluded circulation to examine ATP utilization and provision during isometric tension production. Plantaris (PL) and gastrocnemius (G) muscles were stimulated for 60 s in four conditions: A) 1.0-Hz train rate, 200-ms train duration at 80 Hz, B) 1.0 Hz (100 ms, 80 Hz), C) 0.5 Hz (100 ms, 80 Hz), and D) 1.0 Hz (200 ms, 40 Hz). Muscles were sampled pre- and post-stimulation for pH, high-energy phosphates, and glycolytic intermediates. Contributions to total ATP utilization (all muscles and conditions) were 64-67% glycolysis, 24-28% phosphocreatine, and 8-9% endogenous ATP. Glycogenolysis and glycolysis were greatest in white G (WG), 40% lower in red G (RG), and intermediate in PL muscles. Average energy costs in conditions A and D were approximately 0.60 mumol ATP/(N.s). Decreasing the train duration to 100 ms in B and the number of tetani to 30 in C increased energy costs to 0.93 +/- 0.05 and 1.26 +/- 0.07 mumol ATP/(N.s). Despite a lower pH, WG glycogenolytic (phosphorylase) activity was constant during condition A, whereas RG activity decreased in the final 30 contractions. Larger accumulations of Pi and inosine monophosphate may account for the maintained phosphorylase activity. Glycolytic (phosphofructokinase, PFK) activity was highest in WG and associated with higher fructose 6-phosphate concentration, greater depletion of ATP and, in later contractions, a higher NH4+ concentration. During tetanic in situ stimulation of fast-twitch muscle, the H+ profiles of phosphorylase and PFK are extended beyond in vitro predictions via the accumulation of positive modulators. This permits significant anaerobic ATP production via the glycolytic pathway despite increasing [H+]. The findings also suggest that lengthening the duration of tetani, generating lower peak tensions, and prolonging relaxation time all contribute to lower energy costs in fast-twitch muscle.

Mechanism of impaired energy metabolism during acidosis: role of oxidative metabolism

1992 ◽  
Vol 262 (6) ◽  
pp. H1818-H1822 ◽  
Author(s):  
G. Suleymanlar ◽  
H. Z. Zhou ◽  
M. McCormack ◽  
N. Elkins ◽  
R. Kucera ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Energy Metabolism ◽  
Respiratory Control ◽  
High Energy ◽  
Metabolic Effects ◽  
High Energy Phosphates ◽  
Perfused Heart ◽  
Rat Hearts ◽  
Perfused Rat Hearts

Isolated perfused rat hearts were used to study the effects of metabolic acidosis on energy metabolism. Hearts perfused with different substrates (glucose, pyruvate, and succinate) were subjected to metabolic acidosis. With all substrates, there were comparable decrements in oxygen consumption (approximately 35%), cardiac function (decrease in first derivative of pressure of 65%), and similar changes in high-energy phosphates (approximately 150% increases in inorganic phosphate and 25% decreases in phosphocreatine concentrations) with metabolic acidosis. To further investigate the metabolic effects of acidosis, isolated cardiac mitochondria were exposed to different incubation media pH conditions and given simple metabolites (glutamate/malate, succinate, or pyruvate) or fatty acids (octanoate). Reduction of incubation media pH to 6.0 did not significantly affect either coupled respiration rate or the respiratory control ratio (RCR) with any substrate. These data suggest that metabolic acidosis induces decreases in energy production in the isolated perfused heart by inhibiting mitochondrial substrate utilization and not by impairing glycolysis. However, this impairment of mitochondrial function is not a direct effect of acidosis itself but appears to occur secondarily to some other effects of acidosis which are, as yet, incompletely understood.

scholarly journals Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 995 ◽  
Author(s):  
Kristina Lossow ◽  
Wolfgang Meyerhof ◽  
Maik Behrens
Keyword(s):  
Prolonged Exposure ◽  
Bitter Taste ◽  
Sodium Content ◽  
Dietary Sodium ◽  
Salt Appetite ◽  
Dietary Salt ◽  
Sodium Homeostasis ◽  
Salt Taste ◽  
Sodium Appetite

Renal excretion and sodium appetite provide the basis for sodium homeostasis. In both the kidney and tongue, the epithelial sodium channel (ENaC) is involved in sodium uptake and sensing. The diuretic drug amiloride is known to block ENaC, producing a mild natriuresis. However, amiloride is further reported to induce salt appetite in rodents after prolonged exposure as well as bitter taste impressions in humans. To examine how dietary sodium content and amiloride impact on sodium appetite, mice were subjected to dietary salt and amiloride intervention and subsequently analyzed for ENaC expression and taste reactivity. We observed substantial changes of ENaC expression in the colon and kidney confirming the role of these tissues for sodium homeostasis, whereas effects on lingual ENaC expression and taste preferences were negligible. In comparison, prolonged exposure to amiloride-containing drinking water affected β- and αENaC expression in fungiform and posterior taste papillae, respectively, next to changes in salt taste. However, amiloride did not only change salt taste sensation but also perception of sucrose, glutamate, and citric acid, which might be explained by the fact that amiloride itself activates bitter taste receptors in mice. Accordingly, exposure to amiloride generally affects taste impression and should be evaluated with care.

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