scholarly journals LACTATE AND PYRUVATE IN BLOOD AND URINE AFTER EXERCISE

1937 ◽  
Vol 118 (2) ◽  
pp. 427-432
Author(s):  
R.E. Johnson ◽  
H.T. Edwards
Keyword(s):  
1977 ◽  
Vol 55 (6) ◽  
pp. 625-629 ◽  
Author(s):  
G. J. Murray ◽  
G. E. D. Clark ◽  
M. A. Parniak ◽  
T. Viswanatha

The conversion of L-lysine to its corresponding ε-N-hydroxy derivative has been achieved for the first time by cell-free extracts of Aerobacter aerogenes 62-1. Partial fractionation by differential centrifugation (at 12 000 × g) revealed that both supernatant and pellet are essential for maximum enzymatic activity. The ω-N-hydroxylase (EC 1.14.99) was found to function optimally at pH 7–7.5 and exhibited an apparent Km of about 75 μM for L-lysine. L(+)-Lactate or DL-lactate and pyruvate greatly stimulate the ω-N-hydroxylase activity. The system is strongly inhibited by arsenite and sulfite.


PEDIATRICS ◽  
1958 ◽  
Vol 22 (4) ◽  
pp. 773-773

Recently considerable interest has been directed at the comparative rates of utilization of glucose and fructose, administered intravenously. The present study was designed to carry out such a comparison using intakes of the carbohydrates which would provide sufficient calories to meet the maintenance requirements. The observations included a comparison of the extent of accumulation of certain acid metabolites and disturbances of the acid-base equilibrium which result from the rapid infusion of glucose and fructose. It was found that infusions of glucose and fructose in solution with electrolytes at 1 gm/kg/hr enabled both sugars to be utilized completely, without significant differences in the excretion of water, sodium and potassium. When the sugars were infused at a rate of 2 gm/kg/hr, 20% of the glucose and 9.9% of the fructose were excreted in the urine. Excretion of sodium in the urine with infusions of glucose led to loss of 79% of the intake, while for fructose the urinary excretion was 127% of intake, although no significant differences in excretion of water and potassium were noted. Infusions of fructose were accompanied by much greater increases of lactate and pyruvate in the blood than were caused by infusions of glucose. The urinary excretion of lactic acid was also greater with fructose than with glucose. It is stated that the superior utilization of fructose at rapid rates of infusion is not entirely advantageous because of the accompanying acidosis, which is of sufficient severity to make limitation of the rate of its infusion advisable.


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.


2001 ◽  
Vol 91 (3) ◽  
pp. 1099-1104 ◽  
Author(s):  
François Désy ◽  
Yan Burelle ◽  
Patrice Bélanger ◽  
Marielle Gascon-Barré ◽  
Jean-Marc Lavoie

The present study was conducted to examine the effect of a single bout of exercise (rodent treadmill, 60 min at 26 m/min, 0% grade) on the gluconeogenic activity of periportal hepatocytes (PP-H) and perivenous hepatocytes (PV-H) in fasted (18 h) rats. Isolated PP-H and PV-H, obtained by selective destruction following liver perfusion with digitonin and collagenase, were incubated with saturating concentrations of alanine (Ala; 20 mM) or a mixture of lactate and pyruvate (Lac+Pyr; 20:2 mM) to determine the glucose production flux ( J glucose) in the incubation medium. Results show that, in the resting conditions, J glucose from all exogenous substrates was significantly higher ( P < 0.01) in PP-H than in PV-H. Exercise, compared with rest, resulted in a higher J glucose ( P < 0.01) from Lac+Pyr substrate in the PV-H but not in the PP-H, resulting in the disappearance of the difference in J glucosebetween PP-H and PV-H. Exercise, compared with rest, led to a higher J glucose ( P < 0.01) from Ala substrate in both PP-H and PV-H. However, the exercise-induced increase in J glucose (gluconeogenic activity) from Ala substrate was higher in PV-H than in PP-H, resulting, as from Lac+Pyr substrate, in the disappearance ( P > 0.05) of the difference of J glucose between PP-H and PV-H. It is concluded that exercise differentially stimulates the gluconeogenic activity of PV-H to a larger extent than PP-H, indicative of a heterogenous metabolic response of hepatocytes to exercise.


1965 ◽  
Vol 209 (3) ◽  
pp. 604-610 ◽  
Author(s):  
Stephen M. Cain

Ten anesthetized, splenectomized dogs were made progressively anemic by replacement of blood with warmed dextran to approximate hematocrits of 30, 20, 15, and 10%. A second group of 10 dogs was made progressively hypoxic by having them inspire 11.4, 9.5, 8.0, and 5.9% O2 in N2. Blood gas contents, pH, and gas tensions were measured in arterial and mixed venous bloods. Cardiac output was calculated from the arteriovenous O2 difference and the O2 uptake. Excess lactate was calculated from measured levels of lactate and pyruvate in blood water. Excess lactate appeared at higher mixed venous Po2 in anemic animals than in hypoxic, 40 mm Hg versus 20 mm Hg. When related to total oxygen transport, however, excess lactate appeared at about the same point (12 ml/kg per min) in both groups. Because liver has been shown to reduce its oxygen uptake with any lowering of perfusate oxygen content, it was suggested that the excess lactate measured during both anemic and hypoxic hypoxia in anesthetized dogs is largely the result of liver dysfunction with respect to lactate.


2018 ◽  
Vol 62 (3) ◽  
pp. 443-454 ◽  
Author(s):  
Sara Boenzi ◽  
Daria Diodato

Biomarkers are an indicator of biologic or pathogenic processes, whose function is indicating the presence/absence of disease or monitoring disease course and its response to treatment. Since mitochondrial disorders (MDs) can represent a diagnostic challenge for clinicians, due to their clinical and genetic heterogeneity, the identification of easily measurable biomarkers becomes a high priority. Given the complexity of MD, in particular the primary mitochondrial respiratory chain (MRC) diseases due to oxidative phosphorylation (OXPHOS) dysfunction, a reliable single biomarker, relevant for the whole disease group, could be extremely difficult to find, most of times leading the physicians to better consider a ‘biosignature’ for the diagnosis, rather than a single biochemical marker. Serum biomarkers like lactate and pyruvate are largely determined in the diagnostic algorithm of MD, but they are not specific to this group of disorders. The concomitant determination of creatine (Cr), plasma amino acids, and urine organic acids might be helpful to reinforce the biosignature in some cases. In recent studies, serum fibroblast growth factor 21 (sFGF21) and serum growth differentiation factor 15 (sGDF15) appear to be promising molecules in identifying MD. Moreover, new different approaches have been developed to discover new MD biomarkers. This work discusses the most important biomarkers currently used in the diagnosis of MRC diseases, and some approaches under evaluation, discussing both their utility and weaknesses.


Sign in / Sign up

Export Citation Format

Share Document