scholarly journals Lactate metabolism in the perfused rat hindlimb

1984 ◽  
Vol 222 (2) ◽  
pp. 281-292 ◽  
Author(s):  
M Shiota ◽  
S Golden ◽  
J Katz
Keyword(s):  
Glycogen Synthesis ◽  
Lactate Concentration ◽  
Specific Radioactivity ◽  
Bicarbonate Buffer ◽  
Glucose Carbon ◽  
Lactate Turnover ◽  
Net Uptake ◽  
Lactate Uptake ◽  
Glycogen Deposition ◽  
Fast Twitch

A preparation of isolated rat hindleg was perfused with a medium consisting of bicarbonate buffer containing Ficoll and fluorocarbon, containing glucose and/or lactate. The leg was electrically prestimulated to deplete partially muscle glycogen. The glucose was labelled uniformly with 14C and with 3H in positions 2, 5 or 6, and lactate uniformly with 14C and with 3H in positions 2 or 3. Glucose carbon was predominantly recovered in glycogen, and to a lesser extent in lactate. The 3H/14C ration in glycogen from [5-3H,U-14C]- and [6-3H,U-14C]-glucose was the same as in glucose. Nearly all the utilized 3H from [2-3H]glucose was recovered as water. Insulin increased glucose uptake and glycogen synthesis 3-fold. When the muscle was perfused with a medium containing 10 mM-glucose and 2 mM-lactate, there was little change in lactate concentration. 14C from lactate was incorporated into glycogen. There was a marked exponential decrease in lactate specific radioactivity, much greater with [3H]- than with [14C]-lactate. The ‘apparent turnover’ of [U-14C]lactate was 0.28 mumol/min per g of muscle, and those of [2-3H]- and [3-3H]-lactate were both about 0.7 mumol/min per g. With 10 mM-lactate as sole substrate, there was a net uptake of lactate, at a rate of about 0.15 mumol/min per g, and the apparent turnover of [U-14C]lactate was 0.3 mumol/min per g. The apparent turnover of [3H]lactate was 3-5 times greater. When glycogen synthesis was low (no prestimulation, no insulin), the incorporation of lactate carbon into glycogen exceeded that from glucose, but at high rates of glycogen deposition the incorporation of lactate carbon was much less than that of glucose. Lactate incorporation into glycogen was similar in fast-twitch white and fast-twitch red muscle, but was very low in slow-twitch red fibres. We find that (a) pyruvate in muscle is incorporated into glycogen without randomization of carbon, and synthesis is not inhibited by mercaptopicolinate or cycloserine; (b) there is extensive lactate turnover in the absence of net lactate uptake, and there is a large dilution of 14C-labelled lactate from endogenous supply; (c) there is extensive detritiation of [2-3H]- and [3-3H]-lactate in excess of 14C utilization.

Net lactate uptake during progressive steady-level contractions in canine skeletal muscle

1991 ◽  
Vol 71 (2) ◽  
pp. 514-520 ◽  
Author(s):  
L. B. Gladden
Keyword(s):  
Skeletal Muscle ◽  
Lactic Acid ◽  
Metabolic Rate ◽  
Blood Lactate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Steady Level ◽  
Net Uptake ◽  
Anesthetized Dogs ◽  
Lactate Uptake

The purpose of this study was to determine the changes in net lactate uptake (L) by skeletal muscle with a constant elevated blood lactate concentration during steady-level contractions of increasing intensity. The gastrocnemius-plantaris muscle group was isolated in situ in 11 anesthetized dogs. An infusion of lactate/lactic acid at a pH of 3.5–3.7 established a blood lactate concentration of approximately 9 mM while maintaining normal blood gas/pH status. L was measured during three consecutive 30-min periods during which the muscles 1) rested, 2) contracted at 1 Hz, and 3) contracted at 4 Hz. L was always positive, indicating net uptake throughout the lactate/lactic acid infusion. Steady-level O2 uptake averaged 10.9 +/- 2.2 ml.kg-1.min-1 (0.49 +/- 0.10 mmol.kg-1.min-1) at rest, 39.3 +/- 2.1 (1.75 +/- 0.09) at 1 Hz, and 127.8 +/- 9.2 (5.70 +/- 0.41) at 4 Hz. Steady-level L increased with the metabolic rate from 0.113 +/- 0.058 mmol.kg-1.min-1 at rest to 0.329 +/- 0.026 at 1 Hz and 0.715 +/- 0.108 at 4 Hz. The increase in L from rest to 1 Hz was accomplished mainly by an increase in arteriovenous lactate difference, whereas the increase from 1 to 4 Hz was entirely due to a large increase in blood flow. These results support the idea that skeletal muscle is not simply a producer of lactate but can be a significant consumer of lactate even during contractions with a large elevation in metabolic rate.

Skeletal muscle lactate release and glycolytic intermediates during hypercapnia

1986 ◽  
Vol 60 (2) ◽  
pp. 568-575 ◽  
Author(s):  
T. E. Graham ◽  
J. K. Barclay ◽  
B. A. Wilson
Keyword(s):  
Lactate Concentration ◽  
Respiratory Acidosis ◽  
Dihydroxyacetone Phosphate ◽  
Muscle Lactate ◽  
Concentration Difference ◽  
Tension Development ◽  
Lactate Release ◽  
Net Uptake ◽  
Anesthetized Dogs ◽  
Lactate Uptake

The effects of respiratory acidosis on glycolysis in the autoperfused canine gastrocnemius-plantaris were studied using anesthetized dogs that were ventilated either with air (n = 30) or with 4% CO2–21% O2–75% N2 (n = 30). The left muscle group was stimulated at 3 Hz for up to 20 min, after which the active and the contralateral resting muscles were removed and frozen in liquid N2. Blood flow, VO2, Vco2, and tension development were unaffected by CO2. Glycogen catabolism was not affected, but lactate release (La) was lower (P less than 0.05) during activity with CO2; and greater fructose 6-phosphate, fructose 6-phosphate/fructose 1,6-diphosphate, and alpha-glycerophosphate/dihydroxyacetone phosphate ratios resulted (P less than 0.05). With respiratory acidosis, muscle lactate tended to accumulate early in contractions, but a net lactate uptake occurred during the last 10 min of contractions. Thus, respiratory acidosis reduced lactate efflux and there was a net uptake late in the contraction period. Glycogen phosphorylase did not appear to be affected by the respiratory acidosis, but there was evidence of inhibition at the phosphofructokinase step as well as a tendency for lactate to accumulate within the muscle. La often occurred in a direction contrary to the muscle-venous lactate concentration difference with either air or CO2 and La also decreased far more rapidly over time than did the arterial-venous H+.

scholarly journals Lactate metabolism in resting and contracting canine skeletal muscle with elevated lactate concentration

2002 ◽  
Vol 93 (3) ◽  
pp. 865-872 ◽  
Author(s):  
Kevin M. Kelley ◽  
Jason J. Hamann ◽  
Christine Navarre ◽  
L. Bruce Gladden
Keyword(s):  
Skeletal Muscle ◽  
Glycogen Synthesis ◽  
Resting Metabolic Rate ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Lactate Metabolism ◽  
Anesthetized Dogs ◽  
Lactate Uptake ◽  
A Site ◽  
Elevated Lactate

This study was undertaken to quantitatively account for the metabolic disposal of lactate in skeletal muscle exposed to an elevated lactate concentration during rest and mild-intensity contractions. The gastrocnemius plantaris muscle group (GP) was isolated in situ in seven anesthetized dogs. In two experiments, the muscles were perfused with an artificial perfusate with a blood lactate concentration of ∼9 mM while normal blood gas/pH status was maintained with [U-14C]lactate included to follow lactate metabolism. Lactate uptake and metabolic disposal were measured during two consecutive 40-min periods, during which the muscles rested or contracted at 1.25 Hz. Oxygen consumption averaged 10.1 ± 2.0 μmol · 100 g−1 · min−1 (2.26 ± 0.45 ml · kg−1 · min−1) at rest and 143.3 ± 16.2 μmol · 100 g−1 · min−1 (32.1 ± 3.63 ml · kg−1 · min−1) during contractions. Lactate uptake was positive during both conditions, increasing from 10.5 μmol · 100 g−1 · min−1 at rest to 25.0 μmol · 100 g−1 · min−1during contractions. Oxidation and glycogen synthesis represented minor pathways for lactate disposal during rest at only 6 and 15%, respectively, of the [14C]lactate removed by the muscle. The majority of the [14C]lactate removed by the muscle at rest was recovered in the muscle extracts, suggesting that quiescent muscle serves as a site of passive storage for lactate carbon during high-lactate conditions. During contractions, oxidation was the dominant means for lactate disposal at >80% of the [14C]lactate removed by the muscle. These results suggest that oxidation is a limited means for lactate disposal in resting canine GP exposed to elevated lactate concentrations due to the muscle's low resting metabolic rate.

Lactate removal is not enhanced in nonstimulated perfused skeletal muscle after endurance training

2001 ◽  
Vol 90 (4) ◽  
pp. 1307-1313 ◽  
Author(s):  
Ken D. Sumida ◽  
Casey M. Donovan
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Glycogen Synthesis ◽  
Venous Blood ◽  
Muscle Lactate ◽  
Bicarbonate Buffer ◽  
Muscle Glycogen Synthesis ◽  
Lactate Removal ◽  
Lactate Uptake ◽  
And Control

The effects of endurance training (running 40 m/min, 10% grade for 60 min, 5 days/wk for 8 wk) on skeletal muscle lactate removal was studied in rats by utilizing the isolated hindlimb perfusion technique. Hindlimbs were perfused (single-pass) with Krebs-Henseleit bicarbonate buffer, fresh bovine erythrocytes (hematocrit ∼30%), 10 mM lactate, and [U-14C]lactate (30,000 dpm/ml). Arterial and venous blood samples were collected every 10 min for the duration of the experiment to assess lactate uptake. During perfusions, no significant differences in skeletal muscle lactate uptake were observed between trained (7.31 ± 0.20 μmol/min) and control hindlimbs (6.98 ± 0.43 μmol/min). In support, no significant differences were observed for [14C]lactate uptake in trained (22,776 ± 370 dpm/min) compared with control hindlimbs (21,924 ± 1,373 dpm/min). Concomitant with these observations, no significant differences were observed between groups for oxygen consumption (4.93 ± 0.18 vs. 4.92 ± 0.13 μmol/min), net skeletal muscle glycogen synthesis (7.1 ± 0.4 vs. 6.5 ± 0.3 μmol · 40 min−1 · g−1), or14CO2 production (2,203 ± 185 vs. 2,098 ± 155 dpm/min), trained and control, respectively. These findings indicate that endurance training does not affect lactate uptake or alter the metabolic fate of lactate in quiescent skeletal muscle.

Lactate uptake by inactive forearm during progressive leg exercise

1978 ◽  
Vol 45 (6) ◽  
pp. 835-839 ◽  
Author(s):  
J. R. Poortmans ◽  
J. Delescaille-Vanden Bossche ◽  
R. Leclercq
Keyword(s):  
Lactate Concentration ◽  
Arterial Concentration ◽  
Significant Difference ◽  
Net Uptake ◽  
Leg Exercise ◽  
Lactate Uptake ◽  
Male Subjects ◽  
Arteriovenous Difference

Eleven male subjects were studied during graded leg exercise from 60 to 270 W. Arterial and venous lactate concentrations were measured from the resting forearm during the exercise and recovery periods. Lactate concentration rose regularly during the work and declined slowly to basal levels after the exercise. The arteriovenous difference rapidly became positive during the exercise, indicating a net uptake of lactate by the nonexercising muscles. The uptake of lactate by the muscle correlated directly with the arterial concentration. After the 5th min of recovery, there was no longer any significant difference between arterial and venous lactate concentrations. It is concluded that 1) nonexercising muscles play a small role in the removal of lactate during exercise and 2) significant removal of lactate from the blood by nonexercising muscles stops soon after the cessation of exercise.

Effect of lactate concentration and metabolic rate on net lactate uptake by canine skeletal muscle

1994 ◽  
Vol 266 (4) ◽  
pp. R1095-R1101 ◽  
Author(s):  
L. B. Gladden ◽  
R. E. Crawford ◽  
M. J. Webster
Keyword(s):  
Metabolic Rate ◽  
Glycogen Synthesis ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Metabolic Rates ◽  
Arterial Inflow ◽  
Anesthetized Dogs ◽  
Exponential Equations ◽  
Lactate Uptake ◽  
Series Of Experiments

This study addressed two questions: 1) Does net lactate uptake (L) by muscle approach a saturation limit with increasing blood lactate concentration ([La])? 2) Is the muscle net L response to increasing blood [La] affected by metabolic rate (VO2)? The gastrocnemius plantaris muscle group (GP) was isolated in situ in 20 anesthetized dogs. In three series of experiments, a lactate-lactic acid solution was infused into the arterial inflow of the GP to produce five different plasma [La] values: approximately 3, 9, 16, 22, and 30 mM, each of them maintained for 30 min. In one series, the GP remained at rest, whereas in the second series it contracted at 1 Hz and in the third series at 4 Hz. VO2 averaged approximately 3, 43, and 100 ml.kg-1.min-1 at rest and at 1 and 4 Hz, respectively. Within each of the three metabolic rates, increasing plasma [La] resulted in an increase in net L, which was well described (R > 0.98) by exponential equations. These equations predicted net L asymptotic values of 0.80, 0.72, and 1.09 mmol.kg-1.min-1 for rest and for 1 and 4 Hz, respectively. The corresponding plasma [La]s for half-maximal net L from the exponential equations were 16, 10, and 12 mM. Glucose uptake, pyruvate uptake/output, and alanine output by the muscles were not affected by the increasing [La] (and concomitant increases in net L) at any of the metabolic rates. Neither net glycogen synthesis nor depletion was changed by increasing [La].(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The determination of lactate turnover in vivo with 3H- and 14C-labelled lactate. The significance of sites of tracer administration and sampling

1981 ◽  
Vol 194 (2) ◽  
pp. 513-524 ◽  
Author(s):  
J Katz ◽  
F Okajima ◽  
M Chenoweth ◽  
A Dunn
Keyword(s):  
Specific Radioactivity ◽  
Vena Cava ◽  
Turnover Rates ◽  
High Turnover ◽  
Glucose Carbon ◽  
Lactate Turnover ◽  
Carbon Recycling ◽  
Kinetics Of

L-[3-3H,U-14C]Lactate was administered to starved rats either as a bolus or by continuous infusion. Tracer administration was performed two ways: injection into the vena cava and sampling from the aorta (V-A mode), or injection into the aorta and sampling from the vena cava (A-VC mode). The specific-radioactivity curves after infusion or injection differed markedly with the two procedures. However, the specific radioactivities of 14C-labelled glucose derived from [U-14C]lactate were similar in the two modes. The apparent turnover rates of lactate calculated from the 3H specific-radioactivity curves in the V-A mode were about half those obtained from the 3H specific-radioactivity curves in the A-VC mode. The apparent contribution of lactate carbon to glucose carbon calculated from specific-radioactivity curves of the A-VC mode was greater than that obtained from the V-A mode. The apparent recycling of lactate carbon calculated from the specific radioactivities for [U-14C]- and [3-3H]-lactate was greater in the A-VC mode than the V-A mode. [U-14C] Glucose was administered in the two modes, but in contrast with lactate the specific radioactivities were only slightly different. An analysis to account for these observations is presented. It is shown that the two modes represent sampling from different pools of lactate. The significance of sites of tracer administration and sampling for the interpretation of tracer kinetics of compounds present in intracellular and extracellular spaces, and with a high turnover rate, is discussed. We propose that for such compounds, including lactate, alanine and glycerol, the widely used V-A mode leads to a marked underestimate of replacement, mass and carbon recycling, and that the A-VC mode is the preferred method for the assessment of these parameters.

scholarly journals Glycogen synthesis in the perfused liver of adrenalectomized rats

1976 ◽  
Vol 156 (3) ◽  
pp. 585-592 ◽  
Author(s):  
P D Whitton ◽  
D A Hems
Keyword(s):  
Intact Animal ◽  
Glycogen Synthesis ◽  
Hepatic Metabolism ◽  
Hepatic Glycogen ◽  
Perfused Liver ◽  
Short Term ◽  
Glycogen Accumulation ◽  
Glycogen Deposition ◽  
Adrenalectomized Rats

1. A total loss of capacity for net glycogen synthesis was observed in experiments with the perfused liver of starved adrenalectomized rats. 2. This lesion was corrected by insulin or cortisol in vivo (over 2-5h), but not by any agent tested in perfusion. 3. The activity of glycogen synthetase a, and its increase during perfusion, in the presence of glucose plus glucogenic substrates, were proportional to the rate of net glycogen accumulation. 4. This complete inherent loss of capacity for glycogen synthesis after adrenalectomy is greater than any defect in hepatic metabolism yet reported in this situation, and is not explicable by a decrease in the rate of gluconegenesis (which supports glycogen synthesis in the liver of starved rats). The short-term (2-5h) stimulatory effect of glucocorticoids in the intact animal, on hepatic glycogen deposition, may be mediated partly through insulin action, although neither insulin or cortisol appear to act directly on the liver to stimulate glycogen synthesis.

scholarly journals Ethanol and glycogen synthesis in cardiothoracic and skeletal muscles following glucose re-feeding after starvation in the rat

1992 ◽  
Vol 288 (2) ◽  
pp. 445-450 ◽  
Author(s):  
D Xu ◽  
R Thambirajah ◽  
T N Palmer
Keyword(s):  
Blood Glucose ◽  
Skeletal Muscles ◽  
Glycogen Synthesis ◽  
Ethanol Administration ◽  
Ethanol Treatment ◽  
Glycaemic Response ◽  
Glucose Administration ◽  
Glycogen Deposition ◽  
Dose Dependent ◽  
Glucose Availability

The pattern of glycogen deposition in individual cardiothoracic and skeletal muscles in response to oral and intraperitoneal glucose administration was examined in 40 h-starved rats. Rates of glycogen synthesis were consistently higher in oxidative muscles than in non-oxidative muscles. Intragastric ethanol administration was associated with an impaired glycaemic response and the almost total abolition of glycogen deposition in oxidative muscles in response to oral or intraperitoneal glucose re-feeding. This effect was dose-dependent and differential, in that ethanol produced no equivalent impairment in glycogen deposition in non-oxidative muscles. Ethanol treatment also selectively promoted glycogenolysis in oxidative muscles in the starved state. There was positive correlation (P < 0.001) between the decrease in glycogen levels in soleus and diaphragm muscles in response to increasing ethanol doses and blood glucose and lactate concentrations after intraperitoneal glucose administration, implying that the basis for the impairment in glycogen synthesis may be diminished glucose availability. The mechanism whereby ethanol may differentially compromise carbohydrate metabolism in oxidative muscles is discussed.

scholarly journals Leg and arm lactate and substrate kinetics during exercise

2003 ◽  
Vol 284 (1) ◽  
pp. E193-E205 ◽  
Author(s):  
G. van Hall ◽  
M. Jensen-Urstad ◽  
H. Rosdahl ◽  
H.-C. Holmberg ◽  
B. Saltin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Uptake ◽  
Muscle Mass ◽  
Lactate Concentration ◽  
Whole Body ◽  
Glucose Turnover ◽  
Lactate Oxidation ◽  
Arterial Lactate ◽  
Lactate Uptake ◽  
High Lactate

To study the role of muscle mass and muscle activity on lactate and energy kinetics during exercise, whole body and limb lactate, glucose, and fatty acid fluxes were determined in six elite cross-country skiers during roller-skiing for 40 min with the diagonal stride (Continuous Arm + Leg) followed by 10 min of double poling and diagonal stride at 72–76% maximal O2 uptake. A high lactate appearance rate (Ra, 184 ± 17 μmol · kg−1 · min−1) but a low arterial lactate concentration (∼2.5 mmol/l) were observed during Continuous Arm + Leg despite a substantial net lactate release by the arm of ∼2.1 mmol/min, which was balanced by a similar net lactate uptake by the leg. Whole body and limb lactate oxidation during Continuous Arm + Leg was ∼45% at rest and ∼95% of disappearance rate and limb lactate uptake, respectively. Limb lactate kinetics changed multiple times when exercise mode was changed. Whole body glucose and glycerol turnover was unchanged during the different skiing modes; however, limb net glucose uptake changed severalfold. In conclusion, the arterial lactate concentration can be maintained at a relatively low level despite high lactate Ra during exercise with a large muscle mass because of the large capacity of active skeletal muscle to take up lactate, which is tightly correlated with lactate delivery. The limb lactate uptake during exercise is oxidized at rates far above resting oxygen consumption, implying that lactate uptake and subsequent oxidation are also dependent on an elevated metabolic rate. The relative contribution of whole body and limb lactate oxidation is between 20 and 30% of total carbohydrate oxidation at rest and during exercise under the various conditions. Skeletal muscle can change its limb net glucose uptake severalfold within minutes, causing a redistribution of the available glucose because whole body glucose turnover was unchanged.

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