The validity of anaerobic threshold determination by a Douglas bag method compared with arterial blood lactate concentration

1981 ◽  
Vol 46 (4) ◽  
pp. 423-430 ◽  
Author(s):  
Takayoshi Yoshida ◽  
Akira Nagata ◽  
Masuo Muro ◽  
Naofumi Takeuchi ◽  
Yoshihiro Suda
1993 ◽  
Vol 75 (3) ◽  
pp. 1070-1074 ◽  
Author(s):  
B. Kayser ◽  
G. Ferretti ◽  
B. Grassi ◽  
T. Binzoni ◽  
P. Cerretelli

The aim of the present study was to test the hypothesis that the net maximal blood lactate accumulation ([La]max) during heavy exercise in lowlanders acclimatized to chronic hypoxia may be limited by the reduced bicarbonate stores. Six men [age 32 +/- 4 (SD) yr] performed supramaximal exercise until voluntary exhaustion at sea level (204 +/- 54 W) and after sojourning for 1 mo at 5,050 m (175 +/- 23 W), without (C) and with (B) oral sodium-bicarbonate loading (0.3 g/kg body wt). Exhaustion time, arterial blood lactate concentration, arterial pH (pHa), arterial PCO2, and intramuscular pH were measured at rest and after exercise. At sea level, exhaustion time increased from 6.5 +/- 2.8 min in C to 7.5 +/- 2.7 min in B (P < 0.05). At altitude, exhaustion times were similar to the sea level C values and the same in C and B. At sea level, resting pHa increased from 7.41 +/- 0.02 in C to 7.46 +/- 0.03 in B (P < 0.001); the corresponding values at altitude were 7.46 +/- 0.04 and 7.55 +/- 0.03 (P < 0.001). Postexercise pHa at sea level was 7.22 +/- 0.02 in C and 7.25 +/- 0.08 in B (NS). After exercise at altitude, pHa was 7.32 +/- 0.04 and 7.44 +/- 0.03 in C and B, respectively (P < 0.001). [La]max increased from 12.86 +/- 1.45 mM in C to 16.63 +/- 1.76 mM in B (P < 0.01) at sea level and from 6.85 +/- 1.40 mM in C to 7.95 +/- 1.74 mM in B (NS) at altitude.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Author(s):  
Giuseppe Nardi ◽  
Gianfranco Sanson ◽  
Lucia Tassinari ◽  
Giovanna Guiotto ◽  
Antonella Potalivo ◽  
...  

ABSTRACTObjectiveIn physiological conditions arterial blood lactate concentration is equal or lower than central venous. The aim of this study was to explore if the COVID-19 induced lung cells damage was mirrored by an arterial lactatemia higher than the central venous one; then if the administration of immunosuppressant drugs (i.e. canakinumab) could normalize such abnormal lactate a-cv difference.MethodsProspective cohort study started on March 25th 2020 for a duration of 10 days, enrolling 21 patients affected by severe COVID-19 pneumonia undergoing mechanical ventilation consecutively admitted to the ICU of the Rimini Hospital, Italy.Arterial and central venous blood samples were contemporary collected to calculate the difference between arterial and central venous lactate (Delta a-cv lactate) concentration within 24 h from tracheal intubation (T0), and 24 hours after canakinumab administration (T1).ResultsAt the T0 19/21 (90.5%) patients showed a pathologic Delta a-cv lactate (median 0.22 mmol/L; IQR 0.07–0.36), suggesting severe inflammation. In the 13 patients undergoing canakinumab administration, at the T1 Delta a-cv lactate decreased in 92.3% of cases, being the decrease statistically significant (T0: median 0.15, IQR 0.07–0.25 mmol/L; T1: median −0.01, IQR 0.09–0.04 mmol/L; p=0.002).ConclusionA reversed Delta a-cv lactate is likely to be one of the effects of COVID-19 related cytokine storm, that could reflect a derangement in the lung cells mitochondrial metabolism induced by inflammation or other uncoupling mediators. Delta a-cv lactate decrease may reflect the anti-inflammatory activity of canakinumab. Our preliminary findings need to be confirmed by larger outcome studies.


1981 ◽  
Vol 51 (4) ◽  
pp. 840-844 ◽  
Author(s):  
B. A. Stamford ◽  
A. Weltman ◽  
R. Moffatt ◽  
S. Sady

The purpose of this study was to determine the effects of resting and exercise recovery above [70% of maximum O2 uptake (VO2 max)] and below [40% of VO2 max] anaerobic threshold (AT) on blood lactate disappearance following maximal exercise. Blood lactate concentrations at rest (0.9 mM) and during exercise at 40% (1.3 mM) and 70% (3.5 mM) of VO2 max without preceding maximal exercise were determined on separate occasions and represented base lines for each condition. The rate of blood lactate disappearance from peak values was ascertained from single-component exponential curves fit for each individual subject for each condition using both the determined and resting base lines. When determined base lines were utilized, there were no significant differences in curve parameters between the 40 and 70% of VO2 max recoveries, and both were significantly different from the resting recovery. When a resting base line (0.9 mM) was utilized for all conditions, 40% of VO2 max demonstrated a significantly faster half time than either 70% of VO2 max or resting recovery. No differences were found between 70% of VO2 max and resting recovery. It was concluded that interpretation of the effectiveness of exercise recovery above and below AT with respect to blood lactate disappearance is influenced by the base-line blood lactate concentration utilized in the calculation of exponential half times.


2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Maria Schollin-Borg ◽  
Pär Nordin ◽  
Henrik Zetterström ◽  
Joakim Johansson

Lactate has been thoroughly studied and found useful for stratification of patients with sepsis, in the Intensive Care Unit, and trauma care. However, little is known about lactate as a risk-stratification marker in the Medical Emergency Team- (MET-) call setting. We aimed to determine whether the arterial blood lactate level at the time of a MET-call is associated with increased 30-day mortality. This is an observational study on a prospectively gathered cohort at a regional secondary referral hospital. All MET-calls during the two-year study period were eligible. Beside blood lactate, age and vital signs were registered at the call. Among the 211 calls included, there were 64 deaths (30.3%). Median lactate concentration at the time of the MET-call was 1.82 mmol/L (IQR 1.16–2.7). We found differences between survivors and nonsurvivors for lactate and oxygen saturation, a trend for age, but no significant correlations between mortality and systolic blood pressure, respiratory rate, and heart rate. As compared to normal lactate (<2.44 mmol/L), OR for 30-day mortality was 3.54 (p<0.0006) for lactate 2.44–5.0 mmol/L and 4.45 (p<0.0016) for lactate > 5.0 mmol/L. The present results support that immediate measurement of blood lactate in MET call patients is a useful tool in the judgment of illness severity.


1983 ◽  
Vol 54 (5) ◽  
pp. 1254-1260 ◽  
Author(s):  
L. B. Gladden ◽  
J. W. Yates

This study had two purposes: 1) to determine the effects of varying the pH of lactic acid infusion solutions on the acid-base status of anesthetized dogs, and 2) to determine the effect of elevated blood lactate concentration on muscle lactate concentration. The experiments were performed on the in situ gastro cnemius-plantaris muscle group in 14 mongrel dogs. The infusions increased the arterial blood lactate concentration to 11.0 +/- 0.5 (SE) mM after 20 min. Above an infusate pH of 4.4, the arterial pH increased by 0.118–0.167 during infusion; the arterial pH was unchanged when the infusate pH was between 3.4 and 4.0; and the arterial pH decreased as infusate pH decreased below 3.0. The effect of lactic acid infusion on blood pH appears to be the result of two opposing effects: 1) an acidifying effect due to its weak acid properties, and 2) an alkalinizing effect due to the metabolism of sodium lactate. The estimated ratio between intracellular muscle lactate and venous plasma water lactate averaged 0.647 +/- 0.038, indicative of a substantial gradient between blood and muscle. The infusion produced a significant change from lactate output to lactate uptake by the muscles. The infusion also transiently increased muscle blood flow and oxygen uptake.


1985 ◽  
Vol 63 (12) ◽  
pp. 1570-1576
Author(s):  
Mitchell L. Halperin ◽  
Ching B. Chen ◽  
Surinder Cheema-Dhadli

It appears that glutamine and lactate are the principal substrates for the kidney in dogs with chronic metabolic acidosis. Accordingly, the purpose of this study was to determine if a higher or lower rate of renal lactate extraction would influence the rate of glutamine extraction at a constant rate of renal ATP turnover. The blood lactate concentration was 0.9 ± 0.01 mM in 15 acidotic dogs. However, eight dogs with chronic metabolic acidosis had a spontaneous blood lactate concentration of 0.5 mM or lower. The kidneys of these dogs extracted considerably less lactate from the arterial blood (19 vs. 62 μmol/100 mL glomerular filtration rate (GFR)). Nevertheless, glutamine, alanine, citrate, and ammonium metabolism were not significantly different in these two groups of dogs. Renal ATP balance in acidotic dogs with a low blood lactate could only be achieved if a substrate other than additional glutamine were oxidized in that segment of the nephron which normally oxidized lactate; presumably a fat-derived substrate and (or) lactate derived from glucose was now the metabolic fuel at these more distal sites. When the blood lactate concentration was greater than 1.9 mM, lactate extraction rose to 219 μmol/100 mL GFR. Glutamine, alanine, citrate, and ammonium metabolism were again unchanged; in this case, ATP balance required substrate flux to products other than carbon dioxide, presumably, gluconeogenesis. It appears that renal ammoniagenesis is a proximal event and is independent of the rate of renal lactate extraction.


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