Lactate kinetics in resting and exercising forearms during moderate-intensity supine leg exercise

1993 ◽  
Vol 74 (1) ◽  
pp. 435-443 ◽  
Author(s):  
P. G. Catcheside ◽  
G. C. Scroop

Arterial blood lactate was elevated by supine leg exercise (20 min at approximately 65% maximal oxygen uptake) in five untrained male subjects, and the contribution to blood lactate removal from passive uptake vs. metabolic disposal was compared in resting and lightly exercising (15% maximal voluntary contraction static handgrip) forearm skeletal muscle. An integrated form of the Fick equation was used to predict venous lactate levels resulting solely from passive equilibration of lactate between incoming arterial blood and the forearm muscles. In the resting forearm, predicted and measured venous lactate levels were closely correlated during the exercise period (r = 0.995, P < 0.001), indicating that lactate removal could be accounted for in terms of passive uptake alone. In the lightly exercising forearm, measured venous lactate levels were higher than both the arterial and predicted venous levels, indicating net lactate production. It was concluded that most of the blood lactate generated by moderate-intensity supine leg exercise is taken up passively and not metabolized by resting skeletal muscle and that the rate of lactate disposal is unlikely to be enhanced in lightly exercising muscle.

Pharmacology ◽  
2017 ◽  
Vol 100 (5-6) ◽  
pp. 218-228 ◽  
Author(s):  
Mu-chao Wu ◽  
Wei-ran Ye ◽  
Yi-jia Zheng ◽  
Shan-shan Zhang

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.


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.


1989 ◽  
Vol 257 (5) ◽  
pp. E782-E789 ◽  
Author(s):  
C. M. Donovan ◽  
M. J. Pagliassotti

Constant infusions of cold molar lactate (178.0 +/- 1.6 mumol.kg-1.min-1), [U-14C]lactate (0.50 muCi/min), and [6-3H]glucose (0.5 muCi/min) were employed to study the effects of endurance training (running 1 h/day, at 38 m/min, 10% grade) on lactate clearance in resting, hyperlactatemic rats. Before infusion, resting blood lactate levels were not significantly different between controls, 1.10 +/- 0.04 mM, and trained animals, 1.16 +/- 0.04 mM. Lactate levels increased significantly during the infusion period, attaining steady-state mixed venous concentrations of 11.32 +/- 0.24 mM and 5.44 +/- 0.09 mM, respectively, for controls and trained animals. Lactate clearance rates, based on net lactate removal (i.e., not tracer-estimated lactate removal), were twofold greater in trained animals vs. controls, 33.0 +/- 0.7 and 15.4 +/- 0.4 ml.kg-1. min-1, respectively. Lactate specific activity values during the infusion period were not significantly different between controls, 22,243 +/- 236 dpm/mumol, and trained animals, 21,270 +/- 374 dpm/mumol, indicating similar endogenous dilution of the pyruvate-lactate pool. For both control and trained animals, essentially 100% of the 14C infused as lactate was recovered as either glucose or CO2; however, trained animals demonstrated a 25% greater rate of gluconeogenesis. At a given lactate production rate, trained animals maintain lower lactate levels through enhanced clearance via gluconeogenesis and oxidation.


1958 ◽  
Vol 192 (3) ◽  
pp. 585-591 ◽  
Author(s):  
Norman R. Alpert ◽  
Herbert Kayne ◽  
Winona Haslett

An experiment was designed to test the ‘O2debt’ hypothesis. Oxygen consumption and plasma lactate were measured before, during and following hypoixa in unanesthetized spinally transected dogs. The O2 consumption was depressed during hypoxia and returned toward control levels during recovery. Lactate levels increased during the hypoxia and returned to the control during recovery. Oxygen missed was correlated with the excess consumption of recovery. A highly significant relationship was found which indicated that the larger the depression in O2 consumption during hypoxia, the greater was the depression during the recovery period and the more prolonged the return to control levels. Oxygen missed during hypoxia was compared to lactate production. A significant relationship was found. Lactate removal was compared to excess consumption of recovery. No correlation existed between lactate removal and recovery O2 consumption. The authors postulate the presence of a metabolic governor which controls the rate of O2 uptake.


1998 ◽  
Vol 275 (4) ◽  
pp. E655-E664 ◽  
Author(s):  
Amy E. Halseth ◽  
Nathalie Rhéaume ◽  
Allison B. Messina ◽  
Erica K. Reed ◽  
Mahesh G. Krishna ◽  
...  

The goal of this study was to determine how liver glutamine (Gln) metabolism adapts to acute exercise in the 18-h-fasted dogs ( n = 7) and in dogs that were glycogen depleted by a 42-h fast ( n = 8). For this purpose, sampling (carotid artery, portal vein, and hepatic vein) and infusion (vena cava) catheters and Doppler flow probes (portal vein, hepatic artery) were implanted under general anesthesia. At least 16 days later an experiment, consisting of a 120-min equilibration period, a 30-min basal sampling period, and a 150-min exercise period was performed. At the start of the equilibration period, a constant-rate infusion of [5-15N]Gln was initiated. Arterial Gln flux was determined by isotope dilution. Gut and liver Gln release into and uptake from the blood were calculated by combining stable isotopic and arteriovenous difference methods. The results of this study show that 1) in the 18-h-fasted dog, ∼10% and ∼35% of the basal Gln appearance in arterial blood is due to Gln release from the gut and liver, respectively, whereas ∼30% and ∼25% of the basal Gln disappearance is due to removal by these tissues; 2) extending the fast to 42 h does not affect basal arterial Gln flux or the contribution of the gut to arterial Gln fluxes but decreases hepatic Gln release, causing a greater retention of gluconeogenic carbon by the liver; 3) moderate-intensity exercise increases hepatic Gln removal from the blood regardless of fast duration but does not affect the hepatic release of Gln; and 4) Gln plays an important role in channeling nitrogen into the ureagenic pathway in the basal state, and this role is increased by ∼80% in response to exercise. These studies illustrate the quantitative importance of the splanchnic bed contribution to arterial Gln flux during exercise and the ability of the liver to acutely adapt to changes in metabolic requirements induced by the combined effects of fasting and exercise.


1980 ◽  
Vol 48 (4) ◽  
pp. 689-694 ◽  
Author(s):  
T. T. Gleeson

Gas exchange (VO2 and VCO2) and blood lactate concentration were measured in the lizard Amblyrhynchus cristatus at 25 and 35 degrees C during resting, running, and recovery after exhaustion (less than or equal to 180 min) to analyze the temperature dependency of metabolic recovery in this lizard. Amblyrhynchus exhausted twice as fast (4.2 vs. 8.8 min) at 25 degrees C than when running at the same speed at 35 degrees C. At both temperatures, VO2 and VCO2 increased rapidly during activity and declined toward resting levels during recovery in a manner similar to other vertebrates. Respiratory quotients (R, where R = VCO2/VO2) exceeded 2.0 after exhaustion at both temperatures. Extensive lactate production occurred during activity; blood lactate concentrations ranged from 1.0 to 1.7 mg lactate/ml blood after activity. Net lactate removal exhibited a temperature dependence. Blood lactate concentrations remained elevated hours after VO2 returned to normal. Endurance was reduced in lizards that had recovered aerobically but still possessed high lactate concentrations. The temporal separation of the excess oxygen consumption and lactate removal suggests that the concept of the lactacid oxygen debt is not applicable to this animal. The temperature dependence of total metabolic recovery suggests a benefit for Amblyrhynchus that select warm basking temperatures following strenuous activity.


1993 ◽  
Vol 84 (5) ◽  
pp. 565-571 ◽  
Author(s):  
Paul L. Greenhaff ◽  
Anna Casey ◽  
Anthony H. Short ◽  
Roger Harris ◽  
Karin Soderlund ◽  
...  

1. The present experiment was undertaken to investigate the influence of oral creatine supplementation, shown previously to increase the total creatine content of human skeletal muscle (Harris RC, Soderlund K, Hultman E. Clin Sci 1992; 83: 367–74), on skeletal muscle isokinetic torque and the accumulation of plasma ammonia and blood lactate during five bouts of maximal exercise. 2. Twelve subjects undertook five bouts of 30 maximal voluntary isokinetic contractions, interspersed with 1 min recovery periods, before and after 5 days of placebo (4 × 6 g of glucose/day, n = 6) or creatine (4 × 5 g of creatine plus 1 g of glucose/day, n = 6) oral supplementation. Muscle torque production and plasma ammonia and blood lactate accumulation were measured during and after exercise on each treatment 3. No difference was seen when comparing muscle peak torque production during exercise before and after placebo ingestion. After creatine ingestion, muscle peak torque production was greater in all subjects during the final 10 contractions of exercise bout 1 (P <0.05), throughout the whole of exercise bouts 2 (P <0.01), 3 (P <0.05) and 4 (P = 0.057) and during contractions 11–20 of the final exercise bout (P <0.05), when compared with the corresponding measurements made before creatine ingestion. Plasma ammonia accumulation was lower during and after exercise after creatine ingestion. No differences were found when comparing blood lactate levels. 4. There is evidence to suggest that the decrease in the degree of muscle torque loss after dietary creatine supplementation may be a consequence of a creatine-induced acceleration of skeletal muscle phosphocreatine resynthesis. It is postulated that an increased availability of phosphocreatine would maintain better the required rate of ATP demand during contraction. This is supported by the observed lower accumulation of plasma ammonia during exercise after creatine ingestion.


1994 ◽  
Vol 76 (2) ◽  
pp. 846-852 ◽  
Author(s):  
C. Duan ◽  
W. W. Winder

Endurance training attenuates exercise-induced increases in blood lactate at the same submaximal work rate. Three intramuscular compounds that influence muscle lactate production were measured in fasted non-trained (NT) and endurance-trained (T) rats. The T rats were subjected to a progressive endurance-training program. At the end of the program (11 wk), they were running 2 h/day at 31 m/min up a 15% grade 5 days/wk. NT and T rats were fasted for 24 h and then anesthetized (pentobarbital, iv) at rest or after running for 30 min at 21 m/min (15% grade). Blood lactate levels were significantly lower in the T rats than in the NT rats after 30 min of running (2.3 +/- 0.2 vs. 3.9 +/- 0.2 mM). The lower blood lactate concentration was accompanied by lower plasma epinephrine (2.8 +/- 0.4 vs. 6.0 +/- 0.8 nM), adenosine 3′, 3′,5′-cyclic monophosphate (0.36 +/- 0.02 vs. 0.50 +/- 0.03 pmol/mg), mg), glucose 1,6-diphosphate (26 +/- 2 vs. 40 +/- 5 pmol/mg), and fructose 2,6-diphosphate (3.2 +/- 0.2 vs. 4.3 +/- 0.3 pmol/mg) in white quadriceps muscle in T than in NT rats. Red quadriceps muscle glucose 1,6-diphosphate and adenosine 3′,5′-cyclic monophosphate were also lower in T than in NT rats. These adaptations may be responsible in part for the lower exercise-induced blood lactate in fasted rats as a consequence of endurance training.


2019 ◽  
Vol 25 (1) ◽  
pp. 30-34 ◽  
Author(s):  
Francisco Sérgio Lopes Vasconcelos Filho ◽  
Mateus Bastos de Souza ◽  
Jefferson Pacheco Amaral Fortes ◽  
Karla Camila Lima de Souza ◽  
Mayara Rangel Araújo Carneiro ◽  
...  

ABSTRACT Objective: To propose a duathlon model adapted for rats (associated swimming and running training) and compare it with the individual activities carried out separately, considering the glucose uptake and serum lactate production mechanism. Methods: Twenty-eight 90-day-old Wistar rats with a mean weight of 150-200 g were used. The animals were divided into four groups: control group, swimming group, running group, and swimming/running group. These animals were adapted to their respective training programs for three days and underwent the 4-week training protocol soon afterwards. Pre- and post-training blood lactate and blood glucose analyses were performed at the end of each week. Statistical difference was considered when the p value was less than 0.01 (p <0.01). Results: There was a decrease in glycemic levels and an increase in lactate levels in the swimming and swimming/running groups throughout the training period, which did not occur in the running group. Conclusion: The duathlon model adapted for rats proved satisfactory in terms of the production and stabilization of blood lactate levels. Level of evidence II; Therapeutic Studies - Investigating the Results of Treatment.


1976 ◽  
Vol 40 (1) ◽  
pp. 1-5 ◽  
Author(s):  
A. H. Harken

Oxygen utilization (VO2) and lactate production by an isolated perfused canine hindlimb was evaluated at various hydrogen ion concentrations. A membrane lung perfusion system was established such that blood flow and temperature could be fixed at normal levels. Oxygen, nitrogen, and carbon dioxide (CO2) gas flows to the membrane lung were independently regulated to provide a fixed arterial oxygen content (CaO2). By changing CO2 flow, the pH of the arterial blood was varied between 6.9 and 7.6 at 10-min intervals. The mean O2 delivery (CaO2 X blood flow) was between 16.3 ML O2/min and 20.5 ml O2/min. Standard error of the mean in each dog, however, was less than 0.4 ml O2/min. VO2 was linearly related to the pH of the perfusing blood: VO2% = 100.1 pH - 643 (r = 0.866). Oxygen consumption was inversely related to PCO2: VO2% = -0.62 PCO2 + 124, but the correlation was less good (r = 0.729). Lactate production was linearly related to the pH of the perfusing blood (above a pH of 7.4): lactate produced = 22.5 pH - 162.5 (r = 0.75). At a pH below 7.4, lactate was not produced. Oxygen consumption of skeletal muscle appears critically dependent on extracellular fluid pH. A change in pH of 0.1 alters VO2 almost exactly 10%. Alkalosis is a potent stimulus to lactic acid production by skeletal muscle.


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