scholarly journals Transient increase in glucose 1,6-bisphosphate in human skeletal muscle during isometric contraction

1989 ◽  
Vol 258 (3) ◽  
pp. 915-918 ◽  
Author(s):  
A D Lee ◽  
A Katz
Keyword(s):  
Isometric Contraction ◽  
Human Skeletal Muscle ◽  
Adenine Nucleotide ◽  
Quadriceps Femoris Muscle ◽  
Muscle Ph ◽  
Before And After ◽  
Ph Decrease ◽  
Fructose 1,6 Bisphosphate ◽  
Adenine Nucleotide Pool ◽  
Femoris Muscle

Changes in glucose 1,6-bisphosphate and regulators of glucose-1,6-bisphosphate synthase and phosphatase during isometric contraction have been determined. Biopsies were obtained from the quadriceps femoris muscle before and after 20 s of contraction and at fatigue. Glucose 1,6-bisphosphate increased by 35% after 20 s of contraction (P less than 0.001) with no further change at fatigue (P greater than 0.05 versus 20 s). Pi, fructose 1,6-bisphosphate and glycerate 3-phosphate, all inhibitors of the synthase, increased significantly during the first 20 s (P less than 0.05-0.001), whereas muscle pH (decrease in which inhibits synthase) decreased continuously. The decrease in the total adenine nucleotide pool, which is stoichiometric with the increase in IMP (an activator of phosphatase), was not significant after 20 s, but was 15% at fatigue (P less than 0.001). The rapid increase in glucose 1,6-bisphosphate, despite increases in the inhibitors of synthase, suggests that the synthase was activated, possibly by the substrate glycerate 1,3-bisphosphate and/or a yet unknown activator(s). The lack of any further change in glucose 1,6-bisphosphate during the latter part of contraction may be due to concomitant activation of the synthase and phosphatase.

Fasting inhibits insulin-mediated glycolysis and anaplerosis in human skeletal muscle

1991 ◽  
Vol 261 (5) ◽  
pp. E598-E605 ◽  
Author(s):  
C. E. Castillo ◽  
A. Katz ◽  
M. K. Spencer ◽  
Z. Yan ◽  
B. L. Nyomba
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Glycogen Synthase ◽  
Fat Free Mass ◽  
Whole Body ◽  
Glucose Disposal ◽  
Glycolytic Flux ◽  
Quadriceps Femoris Muscle ◽  
Before And After ◽  
Femoris Muscle

uglycemic (approximately 5.5 mM) hyperinsulinemic (60 mU.m-2.min-1) clamps were performed for 2 h after a 10-h fast and after a prolonged (72-h) fast. Biopsies were obtained from the quadriceps femoris muscle before and after each clamp. The rate of whole body glucose disposal was approximately 50% lower during the clamp after the 72-h fast (P less than or equal to 0.001). The increase in carbohydrate (CHO) oxidation (which is proportional to glycolysis) during the clamp after the 10-h fast (to 13.8 +/- 1.5 mumol.kg fat free mass-1.min-1) was completely abolished during the clamp after the 72-h fast (1.7 +/- 0.6; P less than or equal to 0.001). During the clamp after the 10-h fast, postphosphofructokinase (PFK) intermediates and malate in muscle increased, whereas glutamate decreased (P less than or equal to 0.05-0.001 vs. basal) and citrate did not change. During the clamp after the 72-h fast, there were no significant changes in post-PFK intermediates or glutamate (P greater than 0.05 vs. basal), but there was a decrease in citrate (P less than or equal to 0.01 vs. basal). Euglycemic hyperinsulinemia increased glycogen synthase fractional activity in muscle under both conditions but to a greater extent after the 72-h fast (P less than or equal to 0.01). It is concluded that insulin (after 10-h fast) increases glycolytic flux and the content of malate in muscle, which is probably due to increased anaplerosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Epinephrine increases tricarboxylic acid cycle intermediates in human skeletal muscle

1991 ◽  
Vol 260 (3) ◽  
pp. E436-E439 ◽  
Author(s):  
M. K. Spencer ◽  
A. Katz ◽  
I. Raz
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Adenine Nucleotides ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acid Cycle ◽  
Quadriceps Femoris Muscle ◽  
Before And After ◽  
Tricarboxylic Acid Cycle Intermediates ◽  
Femoris Muscle

The effects of epinephrine (E) and insulin infusions on the contents of tricarboxylic acid cycle intermediates (TCAI), adenine nucleotides and their catabolites, and amino acids in skeletal muscle have been investigated. Eight men were studied on two separate occasions: 1) during 120 min of euglycemic hyperinsulinemia (UH, approximately 5 mM; 40 mU.m-2.min-1) and 2) during UH while E was infused (UHE, 0.05 microgram.kg-1.min-1). Biopsies were taken from the quadriceps femoris muscle before and after each clamp. The sum of citrate, malate, and fumarate in muscle did not change significantly during UH (P greater than 0.05) but doubled during UHE (P less than 0.001). There were no significant changes in any of the adenine nucleotides, their catabolites (including inosine monophosphate), or aspartate during UH and UHE (P greater than 0.05); nor were there any significant changes in pyruvate or alanine contents during UH (P greater than 0.05). On the other hand, there were significant increases in pyruvate and alanine contents during UHE (P less than 0.01 and 0.05, respectively), suggesting that there was increased production of 2-oxoglutarate (a TCAI) via the alanine aminotransferase (ALT) reaction. It is concluded that E infusion increases the contents of TCAI in human skeletal muscle, and it is likely that at least part of the increase is attributable to increased flux through the ALT reaction.

Effect of induced metabolic acidosis on intracellular pH, buffer capacity and contraction force of human skeletal muscle

1985 ◽  
Vol 69 (5) ◽  
pp. 505-510 ◽  
Author(s):  
E. Hultman ◽  
S. Del Canale ◽  
H. Sjöholm
Keyword(s):  
Buffer Capacity ◽  
Recovery Period ◽  
Mean Values ◽  
Muscle Ph ◽  
Before And After ◽  
Ph Buffer ◽  
Total Capacity ◽  
Ph Decrease ◽  
Muscle Biopsies

1. Five volunteers were studied before and after oral administration of NH4Cl (0.3 g/kg body wt.) given in order to create a moderate acidosis. 2. The quadriceps femoris muscles were stimulated electrically for 75 s and muscle biopsies for determination of pH and metabolite content were taken before, at the end of contraction and after 10 min in the recovery period. 3. Muscle pH at rest (mean 7.04) was not significantly decreased after acidification despite an extracellular pH decrease of 0.15 unit. 4. After contraction muscle pH was significantly lower after NH4Cl. Mean values before and after acidification were 6.70 and 6.54 respectively. 5. The buffer capacity calculated as the total capacity of the muscle to buffer H+ produced during the isometric contraction before and after NH4Cl ingestion was reduced from 68.6 sl to 54.5 sl. 6. The force produced by contracting muscle was significantly lower at the end of the contraction period after NH4Cl ingestion, 44.6% of initial compared with 55.4% without NH4Cl.

Effect of unweighting on skeletal muscle use during exercise

1995 ◽  
Vol 79 (1) ◽  
pp. 168-175 ◽  
Author(s):  
L. L. Ploutz-Snyder ◽  
P. A. Tesch ◽  
D. J. Crittenden ◽  
G. A. Dudley
Keyword(s):  
Lower Limb ◽  
Weight Bearing ◽  
Muscle Group ◽  
Mr Images ◽  
Cross Sectional ◽  
Quadriceps Femoris Muscle ◽  
Before And After ◽  
Exercise Induced ◽  
The Right ◽  
Femoris Muscle

Exercise-induced spin-spin relaxation time (T2) shifts in magnetic resonance (MR) images were used to test the hypothesis that more muscle would be used to perform a given submaximal task after 5 wk of unweighting. Before and after unilateral lower limb suspension (ULLS), 7 subjects performed 5 sets of 10 unilateral concentric actions with the quadriceps femoris muscle group (QF) at each of 4 loads: 25, 40, 55, and 70% of maximum. T2-weighted MR images of the thigh were collected at rest and after each relative load. ULLS elicited a 20% decrease in strength of the left unweighted QF and a 14% decrease in average cross-sectional area (CSA) with no changes in the right weight-bearing QF. Average CSA of the left or right QF showing exercise-induced T2 shift increased as a function of exercise intensity both before and after ULLS. On average, 12 +/- 1, 15 +/- 2, 18 +/- 2, and 22 +/- 1 cm2 of either QF showed elevated T2 for the 25, 40, 55, and 70% loads, respectively, before ULLS. Average CSA of the left but not the right QF, showing elevated T2 after ULLS, was increased to 16 +/- 2, 23 +/- 3, 31 +/- 7, and 39 +/- 5 cm2, respectively. The results indicated that unweighting increased exercise-induced T2 shift in MR images, presumably due to greater muscle mass involvement in exercise after than before unweighting, suggesting a change in motor control.

Carbohydrate metabolism in human skeletal muscle during exercise is not regulated by G-1,6-P2

1988 ◽  
Vol 65 (1) ◽  
pp. 487-489 ◽  
Author(s):  
A. Katz ◽  
K. Sahlin ◽  
J. Henriksson
Keyword(s):  
Skeletal Muscle ◽  
Human Skeletal Muscle ◽  
Work Load ◽  
Short Term ◽  
Catalytic Function ◽  
Muscle Ph ◽  
Induced Changes ◽  
Femoris Muscle

Glucose 1,6-bisphosphate (G-1,6-P2) is a potent activator of phosphofructokinase (PFK) and an inhibitor of hexokinase in vitro. It has been suggested that increases in G-1,6-P2 are a main means by which PFK can achieve significant catalytic function in vivo despite falling pH and that increases in G-1,6-P2 will inhibit hexokinase in vivo. The purpose of the present study was to determine whether contraction-induced changes in flux through PFK and hexokinase are associated with changes in G-1,6-P2 in skeletal muscle. Ten men performed bicycle exercise for 10 min at 40 and 75% of maximal O2 uptake (VO2max) and to fatigue [4.8 +/- 0.6 (SE) min] at 100% VO2max. Biopsies were obtained from the quadriceps femoris muscle at rest and after each work load and analyzed for G-1,6-P2. G-1,6-P2 averaged 111 +/- 13 mumol/kg dry wt at rest and 121 +/- 16, 123 +/- 15, and 123 +/- 11 mumol/kg dry wt after the low-, moderate-, and high-intensity exercise bouts, respectively (P less than 0.05 for all means vs. rest). Flux through PFK was estimated to increase exponentially as the exercise intensity increased and muscle pH decreased at the higher work loads, whereas flux through hexokinase was estimated to increase during exercise at 40 and 75% VO2max but decrease sharply at 100% VO2max. These data demonstrate that flux through neither PFK nor hexokinase is mediated by changes in G-1,6-P2 in human skeletal muscle during short-term dynamic exercise.

scholarly journals Contraction-mediated inactivation of glycogen synthase is accompanied by inactivation of glycogen synthase phosphatase in human skeletal muscle

1989 ◽  
Vol 259 (3) ◽  
pp. 901-904 ◽  
Author(s):  
Y Kida ◽  
A Katz ◽  
A D Lee ◽  
D M Mott
Keyword(s):  
Skeletal Muscle ◽  
Isometric Contraction ◽  
Human Skeletal Muscle ◽  
Glycogen Synthase ◽  
Active Form ◽  
Human Muscle ◽  
Maximal Voluntary Force ◽  
Before And After ◽  
Muscle Biopsies

Activities of glycogen synthase (GS) and GS phosphatase were determined on human muscle biopsies before and after isometric contraction at 2/3 maximal voluntary force. Total GS activity did not change during contraction (4.92 +/- 0.70 at rest versus 5.00 +/- 0.42 mmol/min per kg dry wt.; mean +/- S.E.M.), whereas both the active form of GS and the ratio of active form to total GS decreased by approximately 35% (P less than 0.01). GS phosphatase was inactivated in all subjects by an average of 39%, from 5.95 +/- 1.30 to 3.63 +/- 0.97 mmol/min per kg dry wt. (P less than 0.01). It is suggested that at least part of the contraction-induced inactivation of GS is due to an inactivation of GS phosphatase.

scholarly journals The effect of platelet concentrate storage temperature on adenine nucleotide metabolism

Blood ◽  
1975 ◽  
Vol 45 (6) ◽  
pp. 749-756
Author(s):  
DJ Filip ◽  
JD Eckstein ◽  
CA Sibley
Keyword(s):  
Storage Temperature ◽  
Adenine Nucleotide ◽  
Nucleotide Metabolism ◽  
Platelet Concentrate ◽  
Release Reaction ◽  
C Storage ◽  
Adenine Nucleotide Metabolism ◽  
Red Cell Count ◽  
Ph Decrease ◽  
Adenine Nucleotide Pool

The effect of platelet concentrate storage temperature (4 degrees C versus 22 degrees C) on platelet adenine nucleotide metabolism was studied. In general, levels of platelet ATP and ADP, the release reaction, and the metabolis nucleotide pool were best preserved for 72 hr by storage of concentrates at 4 degrees C. Storage of concentrates for 72 hr at 22 degrees C was occasionally associated with a pH decrease to less than 6.0, which is incompatible with platelet viability. When the pH fell below 6.0, there was a marked deterioration of platelet adenine nucleotide levels and the release reaction. The results for concentrates stored at 22 degrees C, with a final pH above 6.0, were not inferior to the results for those stored at 4 degrees C. The pH remained above 7.0 in all concentrates stored at 4 degrees C. The pH changes of platelet concentrates stored at 22 degrees C could not solely be attributed to platelet count, red cell count, or bacterial contamination. Storage at both temperatures was associated with conversion of ATP in the metabolic adenine nucleotide pool to hypoxanthine.

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