LACTATE METABOLISM IN RAINBOW TROUT

1993 ◽  
Vol 180 (1) ◽  
pp. 175-193 ◽  
Author(s):  
C. L. Milligan ◽  
S. S. Girard

We have investigated the metabolic fate of blood lactate in resting rainbow trout and in fish recovering from a bout of exhaustive exercise. At rest and during recovery from exercise, the majority of blood lactate was oxidized, the proportion increasing with increasing oxygen consumption. It is estimated that, during recovery from exhaustive exercise, lactate released from the muscle has the potential to fuel a significant portion of oxidative metabolism. The bulk of the remaining blood lactate reappeared in the muscle lactate pool, probably via direct uptake by the muscle. There was a significant incorporation of blood lactate into the muscle glycogen pool, providing strong evidence for in situ glycogenesis as the mode for muscle glycogen replenishment. To investigate the role of the liver in blood lactate clearance, trout were functionally hepatectomized by ligation of the hepatic portal circulation. The exercise performance of hepatectomized fish was equal to that of sham- operated fish and controls, indicating that muscle relies primarily on endogenous fuel stores. Furthermore, blood lactate levels immediately after exercise were greater and muscle metabolic recovery was faster in hepatectomized fish than in sham-operated fish and controls. These observations suggest that glycogen resynthesis in trout muscle may be retarded because of a non- recoverable loss of substrate (i.e. lactate) from the muscle, because the lactate released is utilized by the liver. These results are discussed in view of what is known about these processes in other ectothermic vertebrates.

1987 ◽  
Vol 253 (3) ◽  
pp. E305-E311 ◽  
Author(s):  
E. M. Peters Futre ◽  
T. D. Noakes ◽  
R. I. Raine ◽  
S. E. Terblanche

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.


1992 ◽  
Vol 167 (1) ◽  
pp. 155-169 ◽  
Author(s):  
M. Scarabello ◽  
G. J. Heigenhauser ◽  
C. M. Wood

Juvenile rainbow trout (approximately 6 g) were exercised to exhaustion in two 5 min bouts given 6 h apart. Resting levels of whole-body lactate and glycogen were restored prior to the second bout. The rate of O2 consumption increased about threefold 5 min after each bout of exercise, while recovery time decreased from 4 h after the first bout to 2–3 h after the second. The excess post-exercise oxygen consumption, i.e. ‘oxygen debt’, was significantly reduced by 40% after the second exercise bout, despite almost identical rates of lactate clearance and glycogen resynthesis. The rates of CO2 and ammonia excretion increased sixfold and threefold, and recovery times decreased from 4–6 h to 3 h and from 3 h to 1.5 h, respectively. After the first bout, whole-body lactate levels peaked at 5 min post-exercise at about 8.5 times pre-exercise levels. After the second bout, lactate levels peaked at 0 min post-exercise and fell more rapidly during recovery. Whole-body glycogen levels decreased by 70% and 80% and ATP levels decreased by 75% and 65% after the first and second bouts, respectively, while glucose levels increased about 1.5-fold immediately after both bouts. Creatine phosphate levels decreased by 70% and 80% after the first and second bouts, respectively. After 6 h of recovery, creatine phosphate levels were higher after the second bout than after the first. These findings suggest that exhaustive exercise may cause a ‘non-specific’ increase in metabolic rate not directly related to the processing of metabolites, which is reduced upon a subsequent exercise bout. This is in contrast with the classical ‘oxygen debt hypothesis’, which states that the oxygen debt and lactate clearance are linked. Furthermore, it appears that two sequential exercise bouts are sufficient to induce a ‘training effect’, i.e. improved rates of metabolic recovery.


1991 ◽  
Vol 161 (1) ◽  
pp. 489-508 ◽  
Author(s):  
A. Pagnotta ◽  
C. L. Milligan

The role of blood-borne glucose in the restoration of white muscle glycogen following exhaustive exercise in the active, pelagic rainbow trout (Oncorhynchus mykiss) and the more sluggish, benthic winter flounder (Pseudopleuronectes americanus) were examined. During recovery from exhaustive exercise, the animals were injected with a bolus of universally labelled [14C]glucose via dorsal aortic (trout) or caudal artery (flounder) catheters. The bulk of the injected label (50–70%) remained as glucose in the extracellular fluid in both species. The major metabolic fates of the injected glucose were oxidation to CO2 (6–8%) and production of lactate (6–8%), the latter indicative of continued anaerobic metabolism post-exercise. Oxidation of labelled glucose could account for up to 40% and 15% of the post-exercise MO2 in trout and flounder, respectively. Exhaustive exercise resulted in a reduction of muscle glycogen stores and accumulation of muscle lactate. Glycogen restoration in trout began 2–4h after exercise, whereas in flounder, glycogen restoration began within 2h. Despite a significant labelling of the intramuscular glucose pool, less than 1% of the infused labelled glucose was incorporated into muscle glycogen. This suggests that blood-borne glucose does not contribute significantly to the restoration of muscle glycogen following exhaustive exercise in either trout or flounder and provides further evidence against a prominent role for the Cori cycle in these species.


1966 ◽  
Vol 23 (4) ◽  
pp. 471-485 ◽  
Author(s):  
E. Don Stevens ◽  
Edgar C. Black

The effect of intermittent severe exercise of short duration on carbohydrate metabolism was examined using unanesthetized, intact rainbow trout. The levels of muscle glycogen, muscle lactate, blood lactate, and liver glycogen were determined in fish sampled immediately after severe exercise of 3 sec to 5 min, after recovery of 3 min to 60 min, and after re-exercise of 3 sec to 5 min. It appears that rainbow trout are not well adapted to tolerate frequent exercise of short duration.


2014 ◽  
Vol 54 (3) ◽  
pp. 168
Author(s):  
Keswari Aji Patriawati ◽  
Nurnaningsih Nurnaningsih ◽  
Purnomo Suryantoro

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.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 928-928
Author(s):  
Philip Murphy ◽  
Edel Mullen ◽  
Stephen Bergin ◽  
Geraldine Healy ◽  
Michelle Lavin ◽  
...  

Abstract Red Blood Cells from COVID-19 Patients Show Evidence of Increased Oxidative Stress and Increased Lactate Influx Corona Disease 19 (COVID-19) is caused by SARS-CoV-2, a novel, highly infectious, single stranded RNA virus. In severe cases, excess oxidative stress produced by a 'cytokine storm' may generate excess reactive oxygen species (ROS) and lead to tissue damage in the lungs and elsewhere. As the potential role of RBCs in the pathophysiology of COVID-19 remains controversial (1), we investigated for evidence of increased oxidative stress and increased thrombotic tendency in RBCs from patients with COVID-19 infection. Following ethical approval and written informed consent, we used flow cytometry (BD FACSCanto II) to measure baseline RBC ROS following incubation with 2'-7'-dichlorofluorescein diacetate (DCF). RBC ROS were also measured following pre-incubation with hydrogen peroxide (H2O2) (2mM) +/- antioxidant N-acetyl cysteine (NAC) (0.6mM). We also measured RBC surface expression of adhesion molecules CD44, CD47 and CD242, as well as CD147. Results were expressed as mean +/- standard deviation (SD). RBC ROS were measured in 22 COVID-19 positive patients and in 10 age matched healthy controls. One patient died from respiratory failure, whilst only 3 others required ITU admission for continuous positive airway pressure (CPAP) or intubation. There was no statistical difference in mean basal RBC DCF mean fluorescence intensity (MFI) levels between COVID-19 positive patients and controls. However, mean increase in RBC DCF MFI following H2O2 incubation was significantly higher in the COVID-19 positive group (1105.7+/-336.3) compared to the control group (843.4+/-256.7)( p= 0.042). The increase in RBC DCF MFI in the COVID-19 positive group correlated with CRP (p=0.014) but not with D-dimer, serum ferritin or any complete blood count (CBC) parameters. Incubation of RBC with 0.6 mM NAC for 30 minutes prior to H2O2 exposure caused a mean reduction in DCF MFI of 26.7% in the COVID-19 positive group. RBC expression of CD44, CD47, CD242 and CD147 were measured In a separate cohort of COVID-19 positive patients (n=32), and in 22 age matched controls. There were no statistically significant differences in mean expression levels of CD44, CD47 and CD242 between the 2 groups. However, mean RBC CD147 MFI expression was higher in the COVID-19 group (1319.64+/-374.76) compared to controls (1061.59+/-253.33) (p=0.018). There was no significant correlation between RBC CD147 MFI and D-dimer, CRP, serum ferritin or any CBC parameters in the COVID-19 positive group. However, 21 of the 32 COVID-19 positive patients had blood lactate levels measured and there was a positive correlation between CD147 MFI expression and blood lactate (R=0.56, p=0.0077). Induction of oxidative stress by H2O2 resulted in a greater increase in ROS in RBCs from COVID-19 patients compared to controls and with correlation to CRP, despite the fact that there were very few patients with severe disease in the study. This suggests a role for oxidative stress in disease pathogenesis. Pre-incubation with NAC attenuated this increase in ROS, suggesting a possible role for antioxidants in therapy. Increased RBC cell surface expression of adhesion molecules CD44, CD47 and CD242 can facilitate RBC interaction with platelets and/or endothelial cells, potentially contributing to thrombosis. We found no increase in their expression in COVID-19 patients compared to controls although RBCs may contribute to thrombosis in COVID-19 infection by other means (1). CD147 is tightly associated with and enables proper expression of monocarboxylate transporter 1, the lactate transporter for RBCs. We found increased surface expression of CD147 on RBCs of COVID-19 patients, whilst CD147 expression showed a moderate correlation with serum lactate levels, suggesting that RBCs in COVID-19 infection may be acting as a lactate sink to protect against lactic acidosis. In summary, our study suggests that COVID-19 infection causes increased oxidative stress and increased lactate influx in RBCs. Further studies are warranted into the role of RBCs in COVID-19 infection. Reference: (1) Murphy P, Glavey S, Quinn J. Anemia and red blood cell abnormalities in COVID-19. Leuk Lymphoma 2021;62:1539 Disclosures Quinn: Takeda: Honoraria. Glavey: Abbvie: Research Funding; Celgene and BMS company: Research Funding; Janssen: Honoraria, Research Funding; Amgen: Honoraria, Research Funding.


1989 ◽  
Vol 147 (1) ◽  
pp. 471-491 ◽  
Author(s):  
D. G. MCDONALD ◽  
Y. TANG ◽  
R. G. BOUTILIER

Rainbow trout, fitted with arterial catheters, were exercised to exhaustion by manual chasing and then injected with either saline (controls), the β-agonist isoproterenol or the β-antagonist propranolol. Blood acid-base status, branchial unidirectional and net fluxes of Na+ and Cl−, and net fluxes of ammonia and acidic equivalents (JHnet) were monitored over the subsequent 4 h of recovery. These same parameters were also monitored in normoxic, resting fish following isoproterenol injection and in exercised fish following acute post-exercise elevation of external NaCl concentration. In addition to confirming an important role for β-adrenoreceptors in the regulation of branchial gas exchange and red cell oxygenation and acid-base status, we find a significant β-adrenergic involvement in the flux of lactic acid from muscle and in JHnet across the gills. Both isoproterenol infusion (into nonexercised fish) and exhaustive exercise were found to cause net acid excretion. The post-exercise JHnet was further augmented by elevating [NaCl] but was not affected, in this instance, either by β-stimulation or blockade, indicating that JHnet was not entirely regulated by a β-adrenergic mechanism. On the basis of a detailed analysis of unidirectional Na+ and Cl− fluxes, we conclude that the increase in JHnet following exercise arose mainly from increased Na+/H+(NH4+) exchange and that the upper limit on JHnet was set by the supply of external counterions and by the increase in branchial ionic permeability that invariably accompanies exhaustive exercise.


1987 ◽  
Vol 62 (6) ◽  
pp. 2237-2240 ◽  
Author(s):  
R. W. Stevenson ◽  
D. R. Mitchell ◽  
G. K. Hendrick ◽  
R. Rainey ◽  
A. D. Cherrington ◽  
...  

Muscle glycogen levels in the perfused rat hemicorpus preparation were reduced two-thirds by electrical stimulation plus exposure to epinephrine (10(-7) M) for 30 min. During the contraction period muscle lactate concentrations increased from a control level of 3.6 +/- 0.6 to a final value of 24.1 +/- 1.6 mumol/g muscle. To determine whether the lactate that had accumulated in muscle during contraction could be used to resynthesize glycogen, glycogen levels were determined after 1–3 h of recovery from the contraction period during which time the perfusion medium (flow-through system) contained low (1.3 mmol/l) or high (10.5 or 18 mmol/l) lactate concentrations but no glucose. With the low perfusate lactate concentration, muscle lactate levels declined to 7.2 +/- 0.8 mumol/g muscle by 3 h after the contraction period and muscle glycogen levels did not increase (1.28 +/- 0.07 at 3 h vs. 1.35 +/- 0.09 mg glucosyl U/g at end of exercise). Lactate disappearance from muscle was accounted for entirely by output into the venous effluent. With the high perfusate lactate concentrations, muscle lactate levels remained high (13.7 +/- 1.7 and 19.3 +/- 2.0 mumol/g) and glycogen levels increased by 1.11 and 0.86 mg glucosyl U/g, respectively, after 1 h of recovery from exercise. No more glycogen was synthesized when the recovery period was extended. Therefore, it appears that limited resynthesis of glycogen from lactate can occur after the contraction period but only when arterial lactate concentrations are high; otherwise the lactate that builds up in muscle during contraction will diffuse into the bloodstream.


Author(s):  
Mohamed Ali ◽  
Khaled Morsy ◽  
Mai Helal ◽  
Rasha Ahmed

1976 ◽  
Vol 33 (1) ◽  
pp. 173-176 ◽  
Author(s):  
William R. Driedzic ◽  
Joe W. Kiceniuk

Rainbow trout (Salmo gairdneri) were exercised to fatigue in a series of 60-min stepwise increasing velocity increments. There was no increase in blood lactate concentration, serially sampled during swimming by means of indwelling dorsal and ventral aortic catheters, at velocities as high as 93% of critical velocity of individuals. The data show that under these conditions the rate of production of lactate by white muscle, at less than critical velocities, is minimal or that the rate of elimination of lactate from white muscle is equal to its rate of utilization elsewhere. Immediately following fatigue blood lactate level increases rapidly. During the recovery period there appears to be a net uptake of lactate by the gills.


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