Effect of lactate administration on exercise-induced PGC-1α mRNA expression in Thoroughbreds

2020 ◽  
Vol 16 (4) ◽  
pp. 253-258
Author(s):  
Y. Kitaoka ◽  
K. Mukai ◽  
K. Takahashi ◽  
H. Ohmura ◽  
H. Hatta
Keyword(s):  
Mrna Expression ◽  
Acute Exercise ◽  
Peak Plasma ◽  
Lactate Concentration ◽  
Sodium Lactate ◽  
Treadmill Running ◽  
Peroxisome Proliferator ◽  
Plasma Lactate ◽  
Plasma Lactate Concentration ◽  
Exercise Induced

The aim of this study was to examine the effects of lactate administration on the mRNA response of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) to acute exercise in Thoroughbred skeletal muscle. Five Thoroughbred horses performed treadmill running at 90% of maximal oxygen consumption for 2 min on two separate occasions, either after the administration of two litres of a sodium lactate solution (LAC; 500 mmol/l sodium lactate in 0.9% NaCl) or a saline solution as a control (CON; 0.9% NaCl). Lactate administration significantly elevated the peak plasma lactate concentration during exercise (16.0±2.8 mmol/l in LAC vs 10.8±2.2 mmol/l in CON). The increase in PGC-1α mRNA expression after 4 h of recovery from exercise was similar between treatments. However, there was positive correlation between exercise-induced PGC-1α mRNA response at 4 h after exercise and peak plasma lactate concentration during exercise. These results suggest that the exercise intensity-dependent adaptation of PGC-1α may be attributed, at least in part, to an increased lactate concentration.

90 GENDER DIFFERENCE IN PEAK PLASMA LACTATE CONCENTRATION

1990 ◽  
Vol 22 (2) ◽  
pp. S15
Author(s):  
A. M.P. M. Bovens ◽  
M. A. van Baak ◽  
J. C.P. M. Vrencken ◽  
J. A.C. Wijnen ◽  
F. T.J. Verstappen
Keyword(s):  
Gender Difference ◽  
Peak Plasma ◽  
Lactate Concentration ◽  
Plasma Lactate ◽  
Plasma Lactate Concentration

scholarly journals Endurance training reduces the contraction-induced interleukin-6 mRNA expression in human skeletal muscle

2004 ◽  
Vol 287 (6) ◽  
pp. E1189-E1194 ◽  
Author(s):  
Christian P. Fischer ◽  
Peter Plomgaard ◽  
Anne K. Hansen ◽  
Henriette Pilegaard ◽  
Bengt Saltin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mrna Expression ◽  
Muscle Glycogen ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Glycogen Content ◽  
Knee Extensor ◽  
Exercise Induced ◽  
Response To Exercise ◽  
Resting Muscle

Contracting skeletal muscle expresses large amounts of IL-6. Because 1) IL-6 mRNA expression in contracting skeletal muscle is enhanced by low muscle glycogen content, and 2) IL-6 increases lipolysis and oxidation of fatty acids, we hypothesized that regular exercise training, associated with increased levels of resting muscle glycogen and enhanced capacity to oxidize fatty acids, would lead to a less-pronounced increase of skeletal muscle IL-6 mRNA in response to acute exercise. Thus, before and after 10 wk of knee extensor endurance training, skeletal muscle IL-6 mRNA expression was determined in young healthy men ( n = 7) in response to 3 h of dynamic knee extensor exercise, using the same relative workload. Maximal power output, time to exhaustion during submaximal exercise, resting muscle glycogen content, and citrate synthase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity were all significantly enhanced by training. IL-6 mRNA expression in resting skeletal muscle did not change in response to training. However, although absolute workload during acute exercise was 44% higher ( P < 0.05) after the training period, skeletal muscle IL-6 mRNA content increased 76-fold ( P < 0.05) in response to exercise before the training period, but only 8-fold ( P < 0.05, relative to rest and pretraining) in response to exercise after training. Furthermore, the exercise-induced increase of plasma IL-6 ( P < 0.05, pre- and posttraining) was not higher after training despite higher absolute work intensity. In conclusion, the magnitude of the exercise-induced IL-6 mRNA expression in contracting human skeletal muscle was markedly reduced by 10 wk of training.

scholarly journals Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle

2015 ◽  
Vol 308 (9) ◽  
pp. C710-C719 ◽  
Author(s):  
Anna Vainshtein ◽  
Liam D. Tryon ◽  
Marion Pauly ◽  
David A. Hood
Keyword(s):  
Skeletal Muscle ◽  
Acute Exercise ◽  
Transmembrane Protein ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Lipid Trafficking ◽  
Mitochondrial Transcription Factor ◽  
Energy Demands ◽  
Niemann Pick ◽  
Exercise Induced

Regular exercise leads to systemic metabolic benefits, which require remodeling of energy resources in skeletal muscle. During acute exercise, the increase in energy demands initiate mitochondrial biogenesis, orchestrated by the transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α). Much less is known about the degradation of mitochondria following exercise, although new evidence implicates a cellular recycling mechanism, autophagy/mitophagy, in exercise-induced adaptations. How mitophagy is activated and what role PGC-1α plays in this process during exercise have yet to be evaluated. Thus we investigated autophagy/mitophagy in muscle immediately following an acute bout of exercise or 90 min following exercise in wild-type (WT) and PGC-1α knockout (KO) animals. Deletion of PGC-1α resulted in a 40% decrease in mitochondrial content, as well as a 25% decline in running performance, which was accompanied by severe acidosis in KO animals, indicating metabolic distress. Exercise induced significant increases in gene transcripts of various mitochondrial (e.g., cytochrome oxidase subunit IV and mitochondrial transcription factor A) and autophagy-related (e.g., p62 and light chain 3) genes in WT, but not KO, animals. Exercise also resulted in enhanced targeting of mitochondria for mitophagy, as well as increased autophagy and mitophagy flux, in WT animals. This effect was attenuated in the absence of PGC-1α. We also identified Niemann-Pick C1, a transmembrane protein involved in lysosomal lipid trafficking, as a target of PGC-1α that is induced with exercise. These results suggest that mitochondrial turnover is increased following exercise and that this effect is at least in part coordinated by PGC-1α. Anna Vainshtein received the AJP-Cell 2015 Paper of the Year award. Listen to a podcast with Anna Vainshtein and coauthor David A. Hood at http://ajpcell.podbean.com/e/ajp-cell-paper-of-the-year-2015-award-podcast/ .

Glucose and lactate kinetics after endotoxin administration in dogs.

1977 ◽  
Vol 232 (2) ◽  
pp. E180 ◽  
Author(s):  
R R Wolfe ◽  
D Elahi ◽  
J J Spitzer
Keyword(s):  
Lactate Concentration ◽  
Constant Infusion ◽  
Glucose Turnover ◽  
Metabolic Clearance ◽  
Plasma Lactate ◽  
Metabolic Clearance Rate ◽  
Metabolic Substrate ◽  
E Coli ◽  
Lactate Kinetics ◽  
Plasma Lactate Concentration

We studied the effects of E. coli endotoxin on the glucose and lactate kinetics in dogs by means of the primed constant infusion of [6(-3)H] glucose and Na-L-(+)-[U-14C] lactate. The infusion of endotoxin induced a transient hyperglycemic level, followed by a steady fall in plasma glucose to hypoglycemic levels. The rate of appearance (Ra) and the rate of disappearance (Rd) of glucose were both significantly elevated (P less than .05) for 150 min after endotoxin, after which neither differed from the preinfusion value. The metabolic clearance rate of glucose was significantly elevated at all times 30 min postendotoxin. By 30 min postendotoxin, Ra and Rd of lactate, plasma lactate concentration, and the percent of glucose turnover originating from lactate were significantly elevated and remained so for the duration of the experiment. We concluded that after endotoxin hypoglycemia developed because of an enhanced peripheral uptake of glucose and a failure of the liver to maintain an increased Ra of glucose. We also concluded that lactate became an important precursor for gluconeogenesis and an important metabolic substrate.

Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism

1988 ◽  
Vol 255 (5) ◽  
pp. E629-E635 ◽  
Author(s):  
D. M. Hargrove ◽  
G. J. Bagby ◽  
C. H. Lang ◽  
J. J. Spitzer
Keyword(s):  
Plasma Insulin ◽  
Lactate Concentration ◽  
Insulin Concentration ◽  
Adrenergic Blockade ◽  
Plasma Lactate ◽  
Glucose Kinetics ◽  
Plasma Insulin Concentration ◽  
Beta Adrenergic ◽  
Plasma Lactate Concentration ◽  
Adrenergic Antagonists

Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose appearance (Ra, 83%), disappearance (Rd, 58%), recycling (160%), and metabolic clearance (23%). Adrenergic blockade prevented endotoxin-induced increases in plasma glucose concentration, Ra, Rd, and recycling but not glucose clearance. The increase in plasma lactate concentration was blunted by 35%. After 2 h, endotoxic animals infused with adrenergic antagonists developed hypoglycemia, which may have resulted from an increased plasma insulin concentration. The attenuation of elevated glucose turnover by adrenergic blockade in the endotoxin-treated animals was not due to a reduction in plasma glucagon level or differences in plasma insulin concentration. Administration of the alpha- or beta-adrenergic antagonists separately blunted but did not prevent endotoxin-induced changes in glucose kinetics, and therefore the efficacy of the adrenergic blockade could not be assigned to a single receptor class. These results indicate that catecholamines are important contributory factors to many of the early alterations in carbohydrate metabolism observed during endotoxemia.

scholarly journals Biosynthesis of the Essential Fatty Acid Oxidation Cofactor Carnitine Is Stimulated in Heart and Liver after a Single Bout of Exercise in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Tom L. Broderick ◽  
Frank A. Cusimano ◽  
Chelsea Carlson ◽  
Jeganathan Ramesh Babu
Keyword(s):  
Acute Exercise ◽  
Organic Cation Transporter ◽  
Carnitine Deficiency ◽  
Treadmill Running ◽  
Moderate Intensity ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Single Bout ◽  
Carnitine Uptake

We determined whether one single bout of exercise stimulates carnitine biosynthesis and carnitine uptake in liver and heart. Free carnitine (FC) in plasma was assayed using acetyltransferase and [14C]acetyl-CoA in Swiss Webster mice after 1 hour of moderate-intensity treadmill running or 4 hours and 8 hours into recovery. Liver and heart were removed under the same conditions for measurement of carnitine biosynthesis enzymes (liver butyrobetaine hydroxylase, γ-BBH; heart trimethyllysine dioxygenase, TMLD), organic cation transporter-2 (OCTN2, carnitine transporter), and liver peroxisome proliferator-activated receptor-alpha (PPARα, transcription factor for γ-BBH and OCTN2 synthesis). In exercised mice, FC levels in plasma decreased while heart and liver OCTN2 protein expressed increased, reflecting active uptake of FC. During recovery, the rise in FC to control levels was associated with increased liver γ-BBH expression. Protein expression of PPARα was stimulated in liver after exercise and during recovery. Interestingly, heart TMLD protein was also detected after exercise. Acute exercise stimulates carnitine uptake in liver and heart. The rapid return of FC levels in plasma after exercise indicates carnitine biosynthesis by liver is stimulated to establish carnitine homeostasis. Our results suggest that exercise may benefit patients with carnitine deficiency syndromes.

Plasma lactate and ventilation thresholds in trained and untrained cyclists

1986 ◽  
Vol 60 (3) ◽  
pp. 777-781 ◽  
Author(s):  
J. Simon ◽  
J. L. Young ◽  
D. K. Blood ◽  
K. R. Segal ◽  
R. B. Case ◽  
...  
Keyword(s):  
Lactate Threshold ◽  
Minute Ventilation ◽  
Lactate Concentration ◽  
Work Rate ◽  
Plasma Lactate ◽  
Vo2 Max ◽  
Trained Subjects ◽  
Leg Cycling ◽  
Plasma Lactate Concentration ◽  
Removal Processes

Six trained male cyclists and six untrained sedentary men were studied to determine whether the plasma lactate threshold (PLT) and ventilation threshold (VT) occur at the same work rate in both fit and unfit populations. The PLT was determined from a marked increase in plasma lactate concentration ([La]) and VT from a nonlinear increase in expired minute ventilation (VE) during incremental leg-cycling tests; work rate was increased 30 W every 2 min until volitional exhaustion. The trained subjects' mean VO2 max (63.8 ml O2 X kg-1 X min-1) and VT (65.8% VO2 max) were significantly higher (P less than 0.05) than the untrained subjects' mean VO2max (35.5 ml O2 X kg-1 X min-1) and VT (51.4% VO2 max). The trained subjects' mean PLT (68.8% VO2 max) and VT did not differ significantly, but the untrained subjects' mean PLT (61.6% VO2 max) was significantly higher than their VT. The trained subjects' mean peak [La] (10.5 mmol X l-1) did not differ significantly from the untrained subjects' mean peak [La] (11.5 mmol X l-1). However, the time of appearance of the peak [La] during passive recovery was inversely related to VO2 max. These results suggest that variance in lactate diffusion and/or removal processes between the trained and untrained subjects may account in part for the different relationships between the VT and PLT in each population.

Diving and swimming performance of white whales, Delphinapterus leucas: an assessment of plasma lactate and blood gas levels and respiratory rates.

1997 ◽  
Vol 200 (24) ◽  
pp. 3091-3099 ◽  
Author(s):  
S A Shaffer ◽  
D P Costa ◽  
T M Williams ◽  
S H Ridgway
Keyword(s):  
High Speed ◽  
Swimming Performance ◽  
Lactate Concentration ◽  
Delphinapterus Leucas ◽  
Breath Hold ◽  
Plasma Lactate ◽  
Post Exercise ◽  
Test Platform ◽  
Plasma Lactate Concentration ◽  
Breath Hold Duration

The white whale Delphinapterus leucas is an exceptional diver, yet we know little about the physiology that enables this species to make prolonged dives. We studied trained white whales with the specific goal of assessing their diving and swimming performance. Two adult whales performed dives to a test platform suspended at depths of 5-300 m. Behavior was monitored for 457 dives with durations of 2.2-13.3 min. Descent rates were generally less than 2 m s-1 and ascent rates averaged 2.2-3 m s-1. Post-dive plasma lactate concentration increased to as much as 3.4 mmol l-1 (4-5 times the resting level) after dives of 11 min. Mixed venous PO2 measured during voluntary breath-holds decreased from 79 to 20 mmHg within 10 min; however, maximum breath-hold duration was 17 min. Swimming performance was examined by training the whales to follow a boat at speeds of 1.4-4.2 m s-1. Respiratory rates ranged from 1.6 breaths min-1 at rest to 5.5 breaths min-1 during exercise and decreased with increasing swim speed. Post-exercise plasma lactate level increased to 1.8 mmol l-1 (2-3 times the resting level) following 10 min exercise sessions at swimming speeds of 2.5-2.8 m s-1. The results of this study are consistent with the calculated aerobic dive limit (O2 store/metabolic rate) of 9-10 min. In addition, white whales are not well adapted for high-speed swimming compared with other small cetaceans.

The Effect of Glycemic Index on Plasma Glucose and Lactate Levels during Incremental Exercise

2000 ◽  
Vol 10 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Stephen R. Stannard ◽  
Martin W. Thompson ◽  
Janette C. Brand Miller
Keyword(s):  
Glycemic Index ◽  
Plasma Glucose ◽  
Glucose Concentration ◽  
Lactate Concentration ◽  
Incremental Exercise ◽  
Plasma Glucose Concentration ◽  
Plasma Lactate ◽  
Significant Difference ◽  
Plasma Lactate Concentration ◽  
Lactate Levels

Consumption of low glycemic index (GI) foods before submaximal endurance exercise may be beneficial to performance. To test whether this may also be true for high intensity exercise. 10 trained cyclists began an incremental exercise test to exhaustion 65 min after consuming equal carbohydrate portions of glucose (HGI), pasta (LGI), and a noncarbohydrate control (PL). Time to fatigue did not differ significantly (p = 0.05) between treatments. Plasma glucose concentration was significantly lower after LGI vs. HGI from 15 to 45 min of rest postprandial. During exercise, plasma glucose concentration was significantly lower after HGI vs. LGI from 200 W until exhaustion. Plasma lactate concentration following HGI was significantly higher than PL from 30 min of rest postprandial through to the end of the 200-W workload. Plasma lactate concentration following LGI was significantly lower than after HGI from 45 min of rest postprandial through to the end of the 100-W workload. At higher exercise intensities, there was no significant difference in plasma lactate levels between treatments. These findings suggest that a high GI carbohydrate meal (1 g/kg body wt) 65 min prior to exercise decreases plasma glucose and increases plasma lactate levels compared to a low GI meal, but not enough to be detrimental to incremental exercise performance.

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