Attenuated hepatosplanchnic uptake of lactate during intense exercise in humans

2002 ◽  
Vol 92 (4) ◽  
pp. 1677-1683 ◽  
Author(s):  
H. B. Nielsen ◽  
J. O. Clemmesen ◽  
C. Skak ◽  
P. Ott ◽  
N. H. Secher

We evaluated whether the increase in blood lactate with intense exercise is influenced by a low hepatosplanchnic blood flow as assessed by indocyanine green dye elimination and blood sampling from an artery and the hepatic vein in eight men. The hepatosplanchnic blood flow decreased from a resting value of 1.6 ± 0.1 to 0.7 ± 0.1 (SE) l/min during exercise. Yet the hepatosplanchnic O2uptake increased from 67 ± 3 to 93 ± 13 ml/min, and the output of glucose increased from 1.1 ± 0.1 to 2.1 ± 0.3 mmol/min ( P < 0.05). Even at the lowest hepatosplanchnic venous hemoglobin O2 saturation during exercise of 6%, the average concentration of glucose in arterial blood was maintained close to the resting level (5.2 ± 0.2 vs. 5.5 ± 0.2 mmol/l), whereas the difference between arterial and hepatic venous blood glucose increased to a maximum of 22 mmol/l. In arterial blood, the concentration of lactate increased from 1.1 ± 0.2 to 6.0 ± 1.0 mmol/l, and the hepatosplanchnic uptake of lactate was elevated from 0.4 ± 0.06 to 1.0 ± 0.05 mmol/min during exercise ( P < 0.05). However, when the hepatosplanchnic venous hemoglobin O2 saturation became low, the arterial and hepatosplanchnic venous blood lactate difference approached zero. Even with a marked reduction in its blood flow, exercise did not challenge the ability of the liver to maintain blood glucose homeostasis. However, it appeared that the contribution of the Cori cycle decreased, and the accumulation of lactate in blood became influenced by the reduced hepatosplanchnic blood flow.

2012 ◽  
Vol 303 (8) ◽  
pp. R843-R849 ◽  
Author(s):  
Peter M. Christensen ◽  
Nikolai Baastrup Nordsborg ◽  
Lars Nybo ◽  
Stefan P. Mortensen ◽  
Mikael Sander ◽  
...  

In response to hypoxic breathing most studies report slower pulmonary oxygen uptake (V̇o2) kinetics at the onset of exercise, but it is not known if this relates to an actual slowing of the V̇o2 in the active muscles. The aim of the present study was to evaluate whether thigh V̇o2 is slowed at the onset of intense exercise during acute exposure to hypoxia. Six healthy male subjects (25.8 ± 1.4 yr, 79.8 ± 4.0 kg, means ± SE) performed intense (100 ± 6 watts) two-legged knee-extensor exercise for 2 min in normoxia (NOR) and hypoxia [fractional inspired oxygen concentration (FiO2) = 0.13; HYP]. Thigh V̇o2 was measured by frequent arterial and venous blood sampling and blood flow measurements. In arterial blood, oxygen content was reduced ( P < 0.05) from 191 ± 5 ml O2/l in NOR to 180 ± 5 ml O2/l in HYP, and oxygen pressure was reduced ( P < 0.001) from 111 ± 4 mmHg in NOR to 63 ± 4 mmHg in HYP. Thigh blood flow was the same in NOR and HYP, and thigh oxygen delivery was consequently reduced ( P < 0.05) in HYP, but femoral arterial-venous oxygen difference and thigh V̇o2 were similar in NOR and HYP. In addition, muscle lactate release was the same in NOR and HYP, and muscle lactate accumulation during the first 25 s of exercise determined from muscle biopsy sampling was also similar (0.35 ± 0.07 and 0.36 ± 0.07 mmol·kg dry wt−1·s−1 in NOR and HYP). Thus the increase in thigh V̇o2 was not attenuated at the onset of intense knee-extensor exercise despite a reduction in oxygen delivery and pressure.


1987 ◽  
Vol 252 (5) ◽  
pp. G648-G653
Author(s):  
S. Gelman ◽  
E. Dillard ◽  
D. A. Parks

The present study was performed on eight young pigs to test the hypothesis that glucagon increases hepatic oxygen supply to a greater extent than hepatic oxygen uptake, providing a better hepatic oxygen supply-demand relationship. The experiments were performed under pentobarbital sodium anesthesia and controlled ventilation. Splanchnic blood flow was studied using radioactive microspheres. Glucagon was administered in doses of 1 and 5 micrograms X kg-1 X min-1. During glucagon infusion, hepatic arterial blood flow substantially increased, splenic and pancreatic blood flows increased moderately, while stomach and intestinal blood flows, as well as portal blood flow did not change significantly. Shunting of both 9- and 15-micron spheres through preportal tissues did not change significantly. Oxygen content in arterial or portal venous blood did not change significantly, while it increased in hepatic venous blood by 30%. There were no differences in the effects between the doses of glucagon administered. There was no correlation found between changes in hepatic oxygen supply and cardiac output or blood pressure. The changes observed during glucagon administration resulted in an increase in oxygen delivery to the liver and hepatic oxygen supply-uptake ratio.


2007 ◽  
Vol 47 (4) ◽  
pp. 150 ◽  
Author(s):  
M. Tatang Puspanjono ◽  
Abdul Latief ◽  
Alan R. Tumbelaka ◽  
Sudigdo Sastroasmoro ◽  
Hartono Gunardi

Background Dengue shock syndrome (DSS) mortality is still high.Monitoring of blood lactate level is important to evaluate shock.Objectives The study were to review the difference between bloodlactate level of DSS and that of dengue hemorrhagic fever (DHF),to correlate blood lactate level with hypoxia state as shock riskfactors (PaO 2 , oxygen saturation, and anion gap) and to determinethe cut-off point of blood lactate level to predict shock.Methods The study was carried out at the Department of ChildHealth, Medical School, University of Indonesia, CiptoMangunkusumo Hospital, Jakarta, from January until July 2006.Three mL venous blood specimen was collected from all subjectsfor peripheral blood, blood gasses, serology, and blood lactateexaminations. This study consisted of a retrospective cohort anda cross sectional method. Data were analyzed with Chi-squaretest. Continous data tested using Mann-Whitney method. Toknow the correlation between blood lactate level and shock riskfactors we use logistic regression test.Results In DSS group, 73% shows hyperlactatemia (lactate =2mmol/L). Conversion of lactate means between two groups issignificantly different from day one to day two and three. Therewas a negative correlation between lactate level and pO 2 andoxygen saturation. Oxygen saturation is the only value that hasclinical correlation. Regressions analysis can be applied using Y= 7.05–0.05 X equation. The cut-off point of lactate level asmarker for shock by using ROC curve is 32.015 mmol/L with 70%sensitivity and 83.3% specificity.Conclusions Hyperlactatemia in DSS can be considered as a signfor unappropriate treatment of shock. Blood lactate level can beused as a biochemical marker for tissue hypoxia, to assess severityof the disease, as monitoring of treatment, and has prognosticvalue of DHF cases.


1963 ◽  
Vol 18 (5) ◽  
pp. 933-936 ◽  
Author(s):  
P. Harris ◽  
T. Bailey ◽  
M. Bateman ◽  
M. G. Fitzgerald ◽  
J. Gloster ◽  
...  

The concentrations of lactic acid, pyruvic acid, glucose, and free fatty acids have been measured simultaneously in the blood from the pulmonary and brachial arteries at rest and during exercise in a group of patients with acquired heart disease. The arteriovenous differences in the concentration of lactate, pyruvate, and free fatty acid were such as could be attributed to chance. The average concentration of glucose was slightly but significantly higher in the brachial arterial blood than in the mixed venous blood. cardiac output; lung metabolism; exercise Submitted on January 15, 1963


2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.


1988 ◽  
Vol 255 (1) ◽  
pp. E94-E98 ◽  
Author(s):  
S. L. Lehman ◽  
W. C. Stanley

When a substrate appears in and disappears from an unmeasured (tissue) compartment, the proper sites for tracer infusion and sampling to measure tracee turnover become controversial. We analyze a three-compartment model representing arterial blood, tissue, and venous blood. The desired quantity, tracee turnover, is the ratio of the steady-state infusion rate to tissue specific activity. However, specific activity in the tissue compartment is unknown. We assume infusion of tracer into the arterial pool at a constant rate and consider sampling of specific activity of either blood compartment in the steady state. We obtain estimates of tissue specific activity from measurement of concentrations of tracer and tracee in blood samples in two extreme cases. In case I, tracee is assumed to appear in the venous compartment but to disappear from the tissue pool. Then tissue specific activity is equal to arterial specific activity. In case II, both appearance and disappearance are from the tissue pool. Tissue specific activity is then less than arterial or venous specific activity. We give formulas for the difference in each case. We discuss the relationship of our models to actual tracer experiments and define physiological locations for our three compartments. Appearance of substrates is probably intermediate between our extreme cases. A numerical estimate of turnover for the substrate lactate in resting humans reveals an error bound of approximately 30%. We discuss sites of infusion and sampling consistent with our model, the effects of relaxing some of our modeling constraints, and experimental necessities for getting beyond the steady state.


1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
Author(s):  
J. N. Benoit ◽  
B. Zimmerman ◽  
A. J. Premen ◽  
V. L. Go ◽  
D. N. Granger

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.


1997 ◽  
Vol 272 (3) ◽  
pp. G617-G625 ◽  
Author(s):  
A. J. Makin ◽  
R. D. Hughes ◽  
R. Williams

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.


1961 ◽  
Vol 16 (2) ◽  
pp. 348-350 ◽  
Author(s):  
Florian Nykiel ◽  
Vincent V. Glaviano

In dogs with left adrenal cannulation, administration of 1 mg/kg of purified E. coli endotoxin resulted in a decrease in mean blood pressure and adrenal blood flow. These changes were accompanied by significant increases in levels of epinephrine in adrenal venous blood. Release of epinephrine by the adrenals in endotoxin shock was due to a neurogenic mechanism, since sectioning of the splanchnic nerves prevented secretion of epinephrine. The rise in epinephrine output from an intact adrenal was noted to occur only in the presence of a significant decrease in arterial blood pressure; therefore endotoxin causes adrenal stimulation from reflexes initiated by the hypothalamus or peripheral baroreceptors. Submitted on September 20, 1960


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