Fatigue and phosphocreatine depletion during carbon dioxide-induced acidosis in rat muscle

1983 ◽  
Vol 245 (1) ◽  
pp. C15-C20 ◽  
Author(s):  
K. Sahlin ◽  
L. Edstrom ◽  
H. Sjoholm

Isolated extensor digitorum longus muscles from rat were exposed to atmospheres of 30% CO2 (high-CO2 muscles) or 6.5% CO2 (control muscles) in O2 for 95 min. Muscle contraction characteristics were studied before and after the incubation. Tetanic tension decreased in high-CO2 muscles to 55% of initial value but remained unchanged in control muscles. Relaxation time was prolonged in high-CO2 muscles but not in control muscles. Intracellular pH was 6.67 +/- 0.04 (SD) in high-CO2 muscles and 7.01 +/- 0.04 in control muscles. CO2-induced acidosis had a marked influence on the intermediary energy metabolism as shown by a fourfold increase of glucose 6-phosphate, a 14% increase of ADP, and a decrease of phosphocreatine to 44% of the control value. Lactate and pyruvate contents were unchanged. The observed metabolic changes can be explained by an effect of H+ on the activity of phosphofructokinase and on the creatine kinase equilibrium. It can be concluded that H+ concentration causes muscular fatigue. It is, however, uncertain whether this is an effect of increased H+ per se or by high-energy phosphate depletion induced by acidosis.

1986 ◽  
Vol 6 (4) ◽  
pp. 455-462 ◽  
Author(s):  
D. B. Kintner ◽  
J. L. Kao ◽  
R. D. Woodson ◽  
D. D. Gilboe

The use of canine erythrocytes suspended in artificial plasma to maintain the isolated brain was investigated in 18 preparations. Two plasmas were studied: One (AP1) contained electrolytes, amino acids, and albumin; the other (AP2) was similar to CSF and contained a mixture of 37 organic nutrients plus electrolytes and albumin. The CMRO2, CMRglu, and cerebral vascular resistance (CVR) were measured during 2 h of perfusion, and tissue high-energy phosphates were measured at the end of perfusion. The AP1 and AP2 groups were compared with control preparations perfused with canine red blood cells suspended in buffy coat-poor canine plasma. Both CMRO2 and ATP decreased to 60% of the control value; CVR increased to 187% of the control value in both groups following 2 h of perfusion. After 2 h of perfusion, the calculated value of intracellular pH (pHi)—based on creatine kinase equilibrium—remained normal (6.96) for the control brains, but decreased to 6.49 and 6.63, respectively, for the AP1- and AP2-perfused brains. Thus, there appears to be an eventual disruption of normal oxidative metabolism resulting in energy failure, possibly caused by the absence of an essential nutrient from the artificial plasma. For studies of intermediary metabolism in isolated normothermic brain, diluted whole blood appears to be the perfusate of choice.


1991 ◽  
Vol 260 (3) ◽  
pp. E430-E435 ◽  
Author(s):  
I. Raz ◽  
A. Katz ◽  
M. K. Spencer

The effect of epinephrine (E) infusion on insulin-mediated glucose metabolism in humans has been studied. Eight glucose-tolerant 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. Glucose disposal, correcting for endogenous glucose production, was 36 +/- 3 and 18 +/- 2 (SE) mumol.kg fat-free mass (FFM)-1.min-1 during the last 40 min of UH and UHE, respectively (P less than 0.001). Nonoxidative glucose disposal (presumably glycogenesis) averaged 23.0 +/- 3.0 and 4.0 +/- 1.1 (P less than 0.001), whereas carbohydrate oxidation (which is proportional to glycolysis) averaged 13.1 +/- 1.4 and 15.3 +/- 1.1 mumol.kg FFM-1.min-1 (P less than 0.05) during UH and UHE, respectively. UHE resulted in significantly higher contents of UDP-glucose, hexose monophosphates, postphosphofructokinase intermediates, and glucose 1,6-bisphosphate (G-1,6-P2) in muscle (P less than 0.05-0.001), but there were no significant differences in high-energy phosphates or fructose 2,6-bisphosphate (F-2,6-P2) between treatments. Fractional activities of phosphorylase increased (P less than 0.01), and glycogen synthase decreased (P less than 0.001) during UHE. It is concluded that E inhibits insulin-mediated glycogenesis because of an inactivation of glycogen synthase and an activation of glycogenolysis. E also appears to inhibit insulin-mediated glucose utilization, at least partly, because of an increase in G-6-phosphate (which inhibits hexokinase) and enhances glycolysis by G-1,6-P2-, fructose 6-phosphate-, and F-1,6-P2-mediated activation of PFK.


1992 ◽  
Vol 52 (5) ◽  
pp. 483-488 ◽  
Author(s):  
Robert H. Messier ◽  
Patrick W. Domkowski ◽  
Hamdy M. Aly ◽  
Anwar S. Abd-Elfattah ◽  
Donald G. Crescenzo ◽  
...  

2013 ◽  
Vol 28 (2) ◽  
pp. 68-71 ◽  
Author(s):  
Thomas N. Blanton ◽  
Debasis Majumdar

In an effort to study an alternative approach to make graphene from graphene oxide (GO), exposure of GO to high-energy X-ray radiation has been performed. X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), and atomic force microscopy (AFM) have been used to characterize GO before and after irradiation. Results indicate that GO exposed to high-energy radiation is converted to an amorphous carbon phase that is conductive.


1989 ◽  
Vol 263 (2) ◽  
pp. 347-353 ◽  
Author(s):  
J F Nagelkerke ◽  
P Dogterom ◽  
H J G M De Bont ◽  
G J Mulder

Isolated rat hepatocytes were incubated with ATP to induce high intracellular free Ca2+ concentrations as determined with the Quin-2 method. Immediately after addition of ATP, the intracellular concentration of Ca2+ rose from 200 nM to more than 2.5 microM. It stayed at this value during the first 1/2 h; the rise was absolutely dependent on extracellular Ca2+. After the first 1/2 h the Ca2+ concentration decreased to 1-2 microM (5-10 times the control value). These high intracellular free Ca2+ concentrations did not lead to an immediate loss of cell viability. Only after 2 h of incubation a substantial number of cells lost viability. This was preceded by a decrease in cellular NADH (greater than 40%) and accompanied by a sharp increase in the intracellular Ca2+ concentration. Under these conditions the NADPH concentration was not affected. Cellular GSH was decreased to 30% of the initial value, but no lipid peroxidation or protein-thiol depletion was observed. Intracellular ATP, ADP and AMP were increased in the presence of extracellular ATP. Ca2+-dependent proteases seemed not to be involved in cell death. These observations are consistent with a collapse of mitochondrial functions as a final trigger of cell death.


2020 ◽  
Vol 635 ◽  
pp. A167 ◽  
Author(s):  
◽  
H. Abdalla ◽  
R. Adam ◽  
F. Aharonian ◽  
F. Ait Benkhali ◽  
...  

Aims. Colliding wind binary systems have long been suspected to be high-energy (HE; 100 MeV < E < 100 GeV) γ-ray emitters. η Car is the most prominent member of this object class and is confirmed to emit phase-locked HE γ rays from hundreds of MeV to ~100 GeV energies. This work aims to search for and characterise the very-high-energy (VHE; E >100 GeV) γ-ray emission from η Car around the last periastron passage in 2014 with the ground-based High Energy Stereoscopic System (H.E.S.S.). Methods. The region around η Car was observed with H.E.S.S. between orbital phase p = 0.78−1.10, with a closer sampling at p ≈ 0.95 and p ≈ 1.10 (assuming a period of 2023 days). Optimised hardware settings as well as adjustments to the data reduction, reconstruction, and signal selection were needed to suppress and take into account the strong, extended, and inhomogeneous night sky background (NSB) in the η Car field of view. Tailored run-wise Monte-Carlo simulations (RWS) were required to accurately treat the additional noise from NSB photons in the instrument response functions. Results. H.E.S.S. detected VHE γ-ray emission from the direction of η Car shortly before and after the minimum in the X-ray light-curve close to periastron. Using the point spread function provided by RWS, the reconstructed signal is point-like and the spectrum is best described by a power law. The overall flux and spectral index in VHE γ rays agree within statistical and systematic errors before and after periastron. The γ-ray spectrum extends up to at least ~400 GeV. This implies a maximum magnetic field in a leptonic scenario in the emission region of 0.5 Gauss. No indication for phase-locked flux variations is detected in the H.E.S.S. data.


1982 ◽  
Vol 242 (6) ◽  
pp. F699-F704 ◽  
Author(s):  
N. Brautbar ◽  
R. Baczynski ◽  
C. Carpenter ◽  
S. Moser ◽  
P. Geiger ◽  
...  

The effects of phosphate depletion (PD) of 4, 8, and 12 wk duration on myocardial energy metabolism were studied in rats fed a phosphate-deficient diet and compared with rats pair-fed a normal phosphate diet. Myocardial biopsies were examined for high-energy phosphate bonds. The results show that PD causes a significant reduction in myocardial concentration of inorganic phosphorus at 4 wk of PD and creatine phosphate at 8 wk of PD, while adenine nucleotides were significantly reduced only after 12 wk of PD. The changes in cellular inorganic phosphorus and creatine phosphate displayed a significant correlation with serum phosphorus levels. Mitochondrial respiration was impaired early in PD. Total cellular, mitochondrial, and myofibrillar creatine kinase activities were significantly reduced at 4 wk of PD and fell further at 8 and 12 wk. These data show that chronic PD is associated with reduced mitochondrial capacity to produce ATP, impaired transport via the creatine phosphate shuttle, and reduced myofibrillar ability to utilize ATP. These abnormalities indicate that all steps of myocardial energetics are impaired in PD and provide the molecular basis for the altered myocardial function seen in PD.


1998 ◽  
Vol 275 (6) ◽  
pp. C1548-C1554 ◽  
Author(s):  
Gordon S. Lynch ◽  
John A. Faulkner

We tested the null hypothesis that the severity of injury to single muscle fibers following a single pliometric (lengthening) contraction is not dependent on the velocity of stretch. Each single permeabilized fiber obtained from extensor digitorum longus muscles of rats was maximally activated and then exposed to a single stretch of either 5, 10, or 20% strain [% of fiber length ( L f)] at a velocity of 0.5, 1.0, or 2.0 L f /s. The force deficit, the difference between maximum tetanic isometric force (Po) before and after the stretch expressed as a percentage of the control value for Po before the stretch, provided an estimate of the magnitude of muscle injury. Despite a fourfold range from the lowest to the highest velocities, force deficits were not different among stretches of the same strain. At stretches of 20% strain, even an eightfold range of velocities produced no difference in the force deficit, although 40% of the fibers were torn apart at a velocity of 4 L f /s. We conclude that, within the range of velocities tolerated by single permeabilized fibers, the severity of contraction-induced injury is not related to the velocity of stretch.


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