Non-Release of Lactic Acid from Anaerobic Swimming Muscle of Plaice Pleuronectes Platessa L.: A Stress Reaction

1978 ◽  
Vol 77 (1) ◽  
pp. 141-155 ◽  
Author(s):  
C. S. WARDLE
Keyword(s):  
Lactic Acid ◽  
Blood Lactate ◽  
Muscle Glycogen ◽  
Blood Stream ◽  
Stress Reaction ◽  
Release Mechanism ◽  
Exhausting Exercise ◽  
Adrenergic Block ◽  
Lactate Levels ◽  
Blood Lactate Levels

1. Plaice caught by trawl net and plaice exercised in laboratory tanks all show high levels of lactic acid (33–44 mmol/kg) in the anaerobic swimming muscle. During exhausting exercise 2 moles of lactate are formed from 1 mole of glycogen glucose. After an 8 h rest 50–80% of the muscle glycogen is restored. 2. Blood lactate levels remain low (0.5-2 mmol/1) in the majority of plaice caught by trawl. In a small number of plaice, peak levels over 5 mmol/1 are reached 2-4 h after capture. Low blood lactate levels could be guaranteed in all fish exercised 24 h after the stress of capture and in tank-adapted fish exercised and injected with the β-adrenergic stimulating drug, isoxsuprine hydrochloride. The blood lactate in plaice, tank-adapted for more than 8 days and then exercised, may reach peak levels up to 5 mmol/l 2-4 h later. 3. High blood lactate levels were obtained by injecting the β-adrenergic block propranolol to stressed exercised fish. The α-adrenergic block did not have this effect. All plaice with blood lactate levels reaching 5–12 mmol/l died. 4. The results indicate that the muscle cells regulate the release or nonrelease of their lactate load to the blood stream and increases in the blood circulating to the muscle do not influence this release. The non-release mechanism may be actived by a catecholamine circulated in the blood stream following a stress.

Amelioration of hypoxia-induced lactic acidosis by superimposed hypercapnea or hydrochloric acid infusion

1986 ◽  
Vol 250 (4) ◽  
pp. F702-F709 ◽  
Author(s):  
S. Abu Romeh ◽  
R. L. Tannen
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Lactic Acidosis ◽  
Blood Lactate ◽  
Acid Production ◽  
Lactic Acid Production ◽  
Respiratory Acidosis ◽  
Control Mechanisms ◽  
Lactate Levels ◽  
Blood Lactate Levels

Recent studies have shown that ketoacid production is exquisitely sensitive to changes in systemic pH, with a decrease inhibiting and an increase stimulating the production rate. To determine whether inhibition of net endogenous acid production is a widely applicable mechanism for the defense of acid-base homeostasis, we examined the effect of superimposed acidosis on lactic acid production by hypoxic rats. Anesthetized paralyzed mechanically ventilated rats with normocapnia increased blood lactate progressively in response to a fractional inspired O2 (FIO2) of 8% (PaO2, 35-38 mmHg) and achieved a level of 7.0 +/- 1.2 mM at 3 h. Superimposition of either mild respiratory acidosis (PCO2, 59 mmHg) or exogenous inorganic metabolic acidosis (intra-arterial HCl sufficient to decrease pH from 7.33 to 7.23) after 1 h of hypoxia dramatically diminished the rise in blood lactate. At the end of the third hour, blood lactate levels averaged 1.7 +/- 0.6 mM with superimposed respiratory acidosis and 2.7 +/- 0.4 mM with superimposed metabolic acidosis, both values being significantly less than the hypoxic controls. Termination of the superimposed respiratory acidosis resulted in a rapid increase in blood lactate levels, demonstrating the reversibility of the pH modulation of lactic acid production. Thus systemic acidosis appears to feed back in a protective fashion to inhibit net lactic acid production in rats with hypoxia-induced lactic acidosis. These findings suggest that finely tuned feedback control mechanisms that keep systemic pH within a narrow range operate under both major conditions of enhanced endogenous acid production (i.e., keto- and lactic acidosis).

scholarly journals Effects of whole-body neuromuscular electrical stimulation device on hemodynamics, arrhythmia, and sublingual microcirculation

2021 ◽  
Author(s):  
Megumi Hoshiai ◽  
Kaori Ochiai ◽  
Yuma Tamura ◽  
Tomoki Tsurumi ◽  
Masato Terashima ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Blood Glucose ◽  
Blood Lactate ◽  
Neuromuscular Electrical Stimulation ◽  
Whole Body ◽  
Left Ventricular Ejection ◽  
Sublingual Microcirculation ◽  
Blood Fluidity ◽  
Lactate Levels ◽  
Blood Lactate Levels

AbstractNeuromuscular electrical stimulation has been used to treat cardiovascular diseases and other types of muscular dysfunction. A novel whole-body neuromuscular electrical stimulation (WB-NMES) wearable device may be beneficial when combined with voluntary exercises. This study aimed to investigate the safety and effects of the WB-NMES on hemodynamics, arrhythmia, and sublingual microcirculation. The study included 19 healthy Japanese volunteers, aged 22–33 years, who were not using any medication. Electrocardiogram (ECG), echocardiography, and blood sampling were conducted before a 20-min WB-NMES session and at 0 and 10 min after termination of WB-NMES. Their tolerable maximum intensity was recorded using numeric rating scale. Arrhythmia was not detected during neuromuscular electrical stimulation or during 10 min of recovery. Blood pressure, heart rate, left ventricular ejection fraction, and diastolic function remained unchanged; however, mild mitral regurgitation was transiently observed during WB-NMES in a single male participant. A decrease in blood glucose and an increase in blood lactate levels were observed, but no changes in blood fluidity, sublingual microcirculation, blood levels of noradrenaline, or oxidative stress were shown. WB-NMES is safe and effective for decreasing blood glucose and increasing blood lactate levels without changing the blood fluidity or microcirculation in healthy people.

The response of the kidney of the freshwater rainbow trout to true metabolic acidosis

1980 ◽  
Vol 84 (1) ◽  
pp. 227-244 ◽  
Author(s):  
K. A. Kobayashi ◽  
C. M. Wood
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Blood Lactate ◽  
Renal Excretion ◽  
Total Acid ◽  
Time Courses ◽  
Lactate Levels ◽  
Urinary Acid ◽  
Proton Load ◽  
Lactate Excretion

Infusion of lactic acid into the bloodstream of trout produced a short-lived depression of blood pH and a long-lasting elevation of blood lactate. The lactate injected was distributed in a volume of 198 ml/kg. Renal excretion of lactate anion and total acid increased by approximately equal amounts during the period of high blood lactate levels, but total renal loss over 72 h accounted for only 2% of the lactate load and 6% of the proton load. Comparable differences in the time courses of blood lactate and pH changes occurred when lactacidosis was induced endogenously by normocapnic hypoxia. The immediate response of the kidney was similar to that with lactic acid infusion, but there was a long-lasting (12–72 + h) elevation of urinary acid efflux that was not associated with lactate excretion. Following hypoxia, renal excretion over 72 h accounted for 1% of the estimated lactate load and 12–25% of the proton load. A renal lactate threshold of 4–10 muequiv/ml prevents significant urinary lactate excretion. The response of the trout kidney to true metabolic acidosis is similar to that of the mammalian kidney.

scholarly journals Serial blood lactate levels as a prognostic factor for sepsis mortality

2014 ◽  
Vol 54 (3) ◽  
pp. 168
Author(s):  
Keswari Aji Patriawati ◽  
Nurnaningsih Nurnaningsih ◽  
Purnomo Suryantoro
Keyword(s):  
Blood Lactate ◽  
Lactate Clearance ◽  
Major Health Problem ◽  
Major Health ◽  
Serial Blood ◽  
Factors Associated ◽  
Relative Risks ◽  
Increased Risk ◽  
Lactate Levels ◽  
Blood Lactate Levels

Background Sepsis is a major health problem in children and aleading cause of death. In recent decades, lactate has been studiedas a biomarker for sepsis, and as an indicator of global tissuehypoxia, increased glycolysis, endotoxin effect, and anaerobicmetabolism. Many studies h ave shown both high levels andincreased serial blood lactate level measurements to be associatedwith increased risk of sepsis mortality.Objective To evaluate serial blood lactate levels as a prognosticfactor for sepsis mortality.Methods We performed an observational, prospective study in thePediatric Intensive Care Unit (PICU) at DR. Sardjito Hospital,Yogyakarta from July to November 2012. We collected serialblood lactate specimens of children with sepsis, first at the time ofadmission, followed by 6 and 24 hours later. The outcome measurewas mortality at the end ofintensive care. Relative risks and 95%confidence intervals of the factors associated with mortality werecalculated using univariate and multivariate analyses.Results Sepsis was found in 91 (50.3%) patients admitted tothe PIW , of whom 75 were included in this study. Five patients(6. 7%) died before the 24-hour lactate collection and 39 patients(52.0%) died during the study. Blood lactate levels of ~ 4mmol;Lat the first and 24-hour specimens were associated with mortality(RR 2.9; 95%CI 1.09 to 7 .66 and RR 4.92; 95%CI 1.77 to 13.65,respectively). Lactate clearance of less than 10% at 24 hours(adjusted RR 5.3; 95% CI 1.1 to 24.5) had a significantly greaterrisk fo llowed by septic shock (adjusted RR 1.54; 95%CI 1.36 to6.4 7) due to mortality.Conclusion In children with sepsis there is a greater risk of mortalityin those with increasing or persistently high serial blood lactatelevels, as shown by less than 10% lactate clearance at 24-hours afterPIW admission.

Oxamate Enhances the Anti-Inflammatory and Insulin-Sensitizing Effects of Metformin in Diabetic Mice

Pharmacology ◽  
2017 ◽  
Vol 100 (5-6) ◽  
pp. 218-228 ◽  
Author(s):  
Mu-chao Wu ◽  
Wei-ran Ye ◽  
Yi-jia Zheng ◽  
Shan-shan Zhang
Keyword(s):  
Blood Lactate ◽  
Cell Mass ◽  
Lactate Production ◽  
Beta Cell Mass ◽  
Serum Lactate ◽  
Blood Levels ◽  
Anti Inflammatory ◽  
Lactate Levels ◽  
Blood Lactate Levels

Metformin (MET) is the first-line drug for treating type 2 diabetes mellitus (T2DM). However, MET increases blood lactate levels in patients with T2DM. Lactate possesses proinflammatory properties and causes insulin resistance (IR). Oxamate (OXA), a lactate dehydrogenase inhibitor, can decrease tissue lactate production and blood lactate levels. This study was conducted to examine the effects of the combination of OXA and MET on inflammation, and IR in diabetic db/db mice. Supplementation of OXA to MET led to lowered tissue lactate production and serum lactate levels compared to MET alone, accompanied with further decreased tissue and blood levels of pro-inflammatory cytokines, along with better insulin sensitivity, beta-cell mass, and glycemic control in diabetic db/db mice. These results show that OXA enhances the anti-inflammatory and insulin-sensitizing effects of MET through the inhibition of tissue lactate production in db/db mice.

Muscle glycogen repletion during active postexercise recovery

1987 ◽  
Vol 253 (3) ◽  
pp. E305-E311 ◽  
Author(s):  
E. M. Peters Futre ◽  
T. D. Noakes ◽  
R. I. Raine ◽  
S. E. Terblanche
Keyword(s):  
Blood Lactate ◽  
Muscle Glycogen ◽  
High Intensity ◽  
Active Recovery ◽  
Muscle Lactate ◽  
Glycogen Resynthesis ◽  
Passive Recovery ◽  
Lactate Removal ◽  
Glycogen Repletion ◽  
Lactate Levels

High-intensity intermittent bicycle exercise was used to deplete muscle glycogen levels by 70% and elevate blood lactate levels to greater than 13.0 mmol/l. Thereafter subjects either cycled with one leg for 45 min followed by 45 min of passive recovery (partially active recovery) or rested for 90 min (passive recovery). During the first 45 min of partially active recovery 1) blood lactate (P less than 0.05) and pH levels (P less than 0.05) returned more rapidly to preexercise values than during passive recovery, 2) the rate of net glycogen resynthesis (0.28 mumol . g-1 . min-1) was the same in both legs, and 3) muscle lactate levels were significantly lower (P less than 0.05) in the passive than in the active leg. Thereafter the rate of net muscle glycogen resynthesis was unchanged (0.26 mumol . g-1 . min-1) and lactate removal could theoretically account for only 18% of the glycogen resynthesized. Overall, the rate of muscle glycogen resynthesis and muscle lactate removal was not different from that measured during passive recovery. After high-intensity exercise 1) glycogen repletion is not impeded by light exercise, and 2) blood glucose is an important substrate for glycogen resynthesis.

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