Relationship between O2 consumption, high energy phosphates and the kinetics of the O2 debt in exercise

1968 ◽  
Vol 304 (1) ◽  
pp. 11-19 ◽  
Author(s):  
P. E. di Prampero ◽  
R. Margaria
Keyword(s):  
High Energy ◽  
High Energy Phosphates ◽  
O2 Consumption ◽  
Kinetics Of ◽  
O2 Debt

scholarly journals DEGRADATION KINETICS OF HIGH ENERGY PHOSPHATES IN THE RABBIT BRIN USING NMR-SPECTROSCOPY

1985 ◽  
Vol 19 (10) ◽  
pp. 1073-1073
Author(s):  
N Herschkowitz ◽  
F Stocker ◽  
E Bossi ◽  
M Stoller ◽  
W Aue ◽  
...  
Keyword(s):  
Nmr Spectroscopy ◽  
Degradation Kinetics ◽  
High Energy ◽  
High Energy Phosphates ◽  
Kinetics Of

scholarly journals Respiratory gas exchange at lungs, gills and tissues: mechanisms and adjustments.

1982 ◽  
Vol 100 (1) ◽  
pp. 5-22 ◽  
Author(s):  
J Piiper
Keyword(s):  
Gas Exchange ◽  
Metabolic Rate ◽  
High Energy ◽  
Tissue Level ◽  
High Energy Phosphates ◽  
Amphibian Skin ◽  
Physiological Adjustments ◽  
Pressure Changes ◽  
Hydrolysis Of ◽  
O2 Debt

(1) A general model for external gas exchange organs of vertebrates is presented, in which the main parameters are the ventilatory, diffusive and perfusive conductances for O2 and CO2. The relevant properties of the external medium (air or water) and of the internal medium (blood) are analysed in terms of capacitance coefficients (effective solubilities) for O2 and CO2. The models for the main types of gas exchange organs (fish gills, amphibian skin, and avian and mammalian lungs) are compared in terms of their intrinsic gas exchange efficacy. The adjustments to increased metabolic rate or to hypoxia are achieved by increasing the conductances. (2) The gas exchange at tissue level is analysed using the Krogh cylinder and a simplified model containing a diffusive and a perfusive conductance. The adjustments to increased load (exercise, hypoxia) consist in both increased local blood flow and in improvement of diffusion conditions (enlargement and recruitment of capillaries). (3) Some particular features of respiration in transitional (unsteady) states, such as occurring at the beginning of exercise and of hypoxia, are examined. The additional physical variables are the O2 (and CO2) stores acting according to their capacitances and partial pressure changes. Delayed increase in O2 uptake at the beginning of exercise is due to the limited speed of physiological adjustments. The ensuing O2 debt is energetically covered by anoxidative energy releasing processes (hydrolysis of high-energy phosphates and anaerobic glycolysis). Finally, the reduction of metabolic rate as adjustment to hypoxia is discussed.

scholarly journals Unchanged mitochondrial organization and compartmentation of high-energy phosphates in creatine-deficient GAMT−/− mouse hearts

2013 ◽  
Vol 305 (4) ◽  
pp. H506-H520 ◽  
Author(s):  
Jelena Branovets ◽  
Mervi Sepp ◽  
Svetlana Kotlyarova ◽  
Natalja Jepihhina ◽  
Niina Sokolova ◽  
...  
Keyword(s):  
Pyruvate Kinase ◽  
Energy Homeostasis ◽  
Three Dimensional ◽  
High Energy ◽  
Regulation Of Respiration ◽  
High Energy Phosphates ◽  
Gamt Deficiency ◽  
Intracellular Compartmentation ◽  
Kinetics Of ◽  
Deficient Mice

Disruption of the creatine kinase (CK) system in hearts of CK-deficient mice leads to changes in the ultrastructure and regulation of mitochondrial respiration. We expected to see similar changes in creatine-deficient mice, which lack the enzyme guanidinoacetate methyltransferase (GAMT) to produce creatine. The aim of this study was to characterize the changes in cardiomyocyte mitochondrial organization, regulation of respiration, and intracellular compartmentation associated with GAMT deficiency. Three-dimensional mitochondrial organization was assessed by confocal microscopy. On populations of permeabilized cardiomyocytes, we recorded ADP and ATP kinetics of respiration, competition between mitochondria and pyruvate kinase for ADP produced by ATPases, ADP kinetics of endogenous pyruvate kinase, and ATP kinetics of ATPases. These data were analyzed by mathematical models to estimate intracellular compartmentation. Quantitative analysis of morphological and kinetic data as well as derived model fits showed no difference between GAMT-deficient and wild-type mice. We conclude that inactivation of the CK system by GAMT deficiency does not alter mitochondrial organization and intracellular compartmentation in relaxed cardiomyocytes. Thus, our results suggest that the healthy heart is able to preserve cardiac function at a basal level in the absence of CK-facilitated energy transfer without compromising intracellular organization and the regulation of mitochondrial energy homeostasis. This raises questions on the importance of the CK system as a spatial energy buffer in unstressed cardiomyocytes.

Blood flow and high-energy phosphates in microregions of left ventricular subendocardium

1981 ◽  
Vol 240 (5) ◽  
pp. H804-H810 ◽  
Author(s):  
H. D. Kleinert ◽  
H. R. Weiss
Keyword(s):  
Blood Flow ◽  
Linear Relationship ◽  
Tissue Perfusion ◽  
High Energy ◽  
Left Ventricular ◽  
Significant Loss ◽  
Tissue Blood Flow ◽  
High Energy Phosphates ◽  
Tissue Samples ◽  
Heterogeneous Distribution

Blood flow and high-energy phosphate (HEP) content were determined simultaneously in multiple microregions of left ventricular subendocardium in 29 normal anesthetized open-chest rabbits by use of a new micromethod to determine whether a direct linear relationship existed between these parameters. Tissue samples weighed 1-2 mg. ATP and creatine phosphate (CP) content were quantitated in quick-frozen hearts by fluorometry at sites where tissue perfusion was measured by H2 clearance by use of bare-tipped platinum electrodes. A series of validation studies were conducted to ensure that 1) no significant damage to the tissue surrounding the electrode occurred during the period of experimentation and 2) no significant loss of biochemical constituents had occurred due to labile processes during freezing or storage of the tissue. Blood flow, ATP, and CP values averaged 79.1 +/- 24.1 (SD) ml.min-1.100 g-1, 4.9 +/- 1.3 mumol/g tissue, and 8.0 +/- 3.0 mumol/g tissue, respectively, and are similar to those reported in studies using larger tissue samples. Correlation between the heterogeneous distribution of tissue perfusion and HEP revealed no direct linear relationship between these parameters in the normal unstressed rabbit subendocardium.

Manipulating the intracellular environment of hippocampal slices: pH and high-energy phosphates

1989 ◽  
Vol 28 (1-2) ◽  
pp. 83-91 ◽  
Author(s):  
Tim S. Whittingham ◽  
Eduardo Warman ◽  
Hussein Assaf ◽  
Thomas J. Sick ◽  
Joseph C. LaManna
Keyword(s):  
Hippocampal Slices ◽  
High Energy ◽  
High Energy Phosphates ◽  
Intracellular Environment

Reduced substrate oxidation in postischemic myocardium: 13C and 31P NMR analyses

1990 ◽  
Vol 258 (5) ◽  
pp. H1357-H1365 ◽  
Author(s):  
E. D. Lewandowski ◽  
D. L. Johnston
Keyword(s):  
Steady State ◽  
31P Nmr ◽  
Tca Cycle ◽  
High Energy ◽  
Substrate Oxidation ◽  
High Energy Phosphates ◽  
Atp Content ◽  
And Control ◽  
13C And 31P Nmr ◽  
Postischemic Myocardium

13C and 31P nuclear magnetic resonance (NMR) spectra were used to assess substrate oxidation and high-energy phosphates in postischemic (PI) isolated rabbit hearts. Phosphocreatine (PCr) increased in nonischemic controls on switching from glucose perfusion to either 2.5 mM [3-13C]pyruvate (120%, n = 7) or [2-13C]acetate (114%, n = 8, P less than 0.05). ATP content, oxygen consumption (MVO2), and hemodynamics (dP/dt) were not affected by substrate availability in control or PI hearts. dP/dt was 40-60% lower in PI hearts during reperfusion after 10 min ischemia. Hearts reperfused with either pyruvate (n = 11) or acetate (n = 8) regained preischemic PCr levels within 45 s. Steady-state ATP levels were 55-70% of preischemia with pyruvate and 52-60% with acetate. Percent maximum [4-13C]glutamate signal showed reduced conversion of pyruvate to glutamate via the tricarboxylic acid (TCA) cycle at 4-min reperfusion (PI = 24 +/- 4%, means +/- SE; Control = 48 +/- 4%). The increase in 13C signal from the C-4 position of glutamate was similar to control hearts within 10.5 min. The increase in [4-13C]glutamate signal from acetate was not different between PI and control hearts. The ratio of [2-13C]Glu:[4-13C]Glu, reflecting TCA cycle activity, was reduced in PI hearts with acetate for at least 10 min (Control = 0.76 +/- 0.03; PI = 0.51 +/- 0.09) until steady state was reached. Despite rapid recovery of oxidative phosphorylation, contractility remained impaired and substrate oxidation was significantly slowed in postischemic hearts.

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