scholarly journals PGC-1^|^alpha; increases skeletal muscle lactate uptake by increasing the expression of MCT1 but not MCT2 or MCT4

2009 ◽  
Vol 58 (1) ◽  
pp. 49-49
Author(s):  
YUKO YOSHIDA ◽  
CARLEY R. BENTON ◽  
JAMES LALLY ◽  
XIAO-XIA HAN ◽  
HIDEO HATTA ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Lactate ◽  
Lactate Uptake

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.

Contribution of liver and skeletal muscle to alanine and lactate metabolism in humans

1990 ◽  
Vol 259 (5) ◽  
pp. E677-E684 ◽  
Author(s):  
A. Consoli ◽  
N. Nurjhan ◽  
J. J. Reilly ◽  
D. M. Bier ◽  
J. E. Gerich
Keyword(s):  
Skeletal Muscle ◽  
Plasma Glucose ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Lactate Metabolism ◽  
Muscle Lactate ◽  
Acid Cycle ◽  
Principal Source ◽  
Lactate Uptake ◽  
Uptake And Release

To quantitate alanine and lactate gluconeogenesis in postabsorptive humans and to test the hypothesis that muscle is the principal source of these precursors, we infused normal volunteers with [3–14C]lactate, [3–13C]alanine, and [6-3H]glucose and calculated alanine and lactate incorporation into plasma glucose corrected for tricarboxylic acid cycle carbon exchange, the systemic appearance of these substrates, and their forearm fractional extraction, uptake, and release. Forearm alanine and lactate fractional extraction averaged 37 +/- 3 and 27 +/- 2%, respectively; muscle alanine release (2.94 +/- 0.27 mumol.kg body wt-1.min-1) accounted for approximately 70% of its systemic appearance (4.18 +/- 0.31 mumol.kg body wt-1.min-1); muscle lactate release (5.51 +/- 0.42 mumol.kg body wt-1.min-1) accounted for approximately 40% of its systemic appearance (12.66 +/- 0.77 mumol.kg body wt-1.min-1); muscle alanine and lactate uptake (1.60 +/- 0.7 and 3.29 +/- 0.36 mumol.kg body wt-1.min-1, respectively) accounted for approximately 30% of their overall disappearance from plasma, whereas alanine and lactate incorporation into plasma glucose (1.83 +/- 0.20 and 4.24 +/- 0.44 mumol.kg body wt-1.min-1, respectively) accounted for approximately 50% of their disappearance from plasma. We therefore conclude that muscle is the major source of plasma alanine and lactate in postabsorptive humans and that factors regulating their release from muscle may thus exert an important influence on hepatic gluconeogenesis.

Evidence for facilitated lactate uptake in lizard skeletal muscle

2001 ◽  
Vol 204 (23) ◽  
pp. 4099-4106
Author(s):  
E. R. Donovan ◽  
T. T. Gleeson
Keyword(s):  
Skeletal Muscle ◽  
Transport System ◽  
Uptake Rate ◽  
Lactate Metabolism ◽  
Muscle Lactate ◽  
Uptake Rates ◽  
Monocarboxylate Transport ◽  
Net Uptake ◽  
Lactate Uptake ◽  
Inhibition Studies

SUMMARY To understand more fully lactate metabolism in reptilian muscle, lactate uptake in lizard skeletal muscle was measured and its similarities to the monocarboxylate transport system found in mammals were examined. At 2 min, uptake rates of 15 mmol l–1 lactate into red iliofibularis (rIF) were 2.4- and 2.2-fold greater than white iliofibularis (wIF) and mouse soleus, respectively. α-Cyano-4-hydroxycinnamate (15 mmol l–1) caused little inhibition of uptake in wIF but caused a 42–54 % reduction in the uptake rate of lactate into rIF, suggesting that much of the lactate uptake by rIF is via protein-mediated transport. N-ethymaleimide (ETH) (10 mmol l–1) also caused a reduction in the rate of uptake, but measurements of adenylate and phosphocreatine concentrations show that ETH had serious effects on rIF and wIF and may not be appropriate for transport inhibition studies in reptiles. The higher net uptake rate by rIF than by wIF agrees with the fact that rIF shows much higher rates of lactate utilization and incorporation into glycogen than wIF. This study also suggests that lactate uptake by reptilian muscle is similar to that by mammalian muscle and that, evolutionarily, this transport system may be relatively conserved even in animals with very different patterns of lactate metabolism.

scholarly journals Training intensity-dependent and tissue-specific increases in lactate uptake and MCT-1 in heart and muscle

1998 ◽  
Vol 84 (3) ◽  
pp. 987-994 ◽  
Author(s):  
Steven K. Baker ◽  
Karl J. A. McCullagh ◽  
Arend Bonen
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Monocarboxylate Transporter ◽  
Moderate Intensity ◽  
Training Intensity ◽  
Trained Group ◽  
Muscle Lactate ◽  
Monocarboxylate Transporter 1 ◽  
Lactate Uptake ◽  
Intensity Training

We investigated the effects of 3 wk of moderate- (21 m/min, 8% grade) and highintensity treadmill training (31 m/min, 15% grade) on 1) monocarboxylate transporter 1 (MCT-1) content in rat hindlimb muscles and the heart and 2) lactate uptake in isolated soleus (Sol) muscles and perfused hearts. In the moderately trained group MCT-1 was not increased in any of the muscles [Sol, extensor digitorum longus (EDL), and red (RG) and white gastrocnemius (WG)] ( P > 0.05). Similarly, lactate uptake in Sol strips was also not increased ( P > 0.05). In contrast, in the heart, MCT-1 (+36%, P < 0.05) and lactate uptake (+72%, P < 0.05) were increased with moderate training. In the highly trained group, MCT-1 (+70%, P < 0.05) and lactate uptake (+79%, P < 0.05) were increased in Sol. MCT-1 was also increased in RG (+94%, P < 0.05) but not in WG and EDL ( P > 0.05). In the highly trained group, heart MCT-1 (+44%, P < 0.05) and lactate uptake (+173%, P < 0.05) were increased. In conclusion, it has been shown that 1) in both heart and skeletal muscle lactate uptake is increased only when MCT-1 is increased; 2) training-induced increases in MCT-1 occurred at a lower training intensity in the heart than in skeletal muscle; 3) in the heart, lactate uptake was increased much more after high-intensity training than after moderate-intensity training, despite similar increases in heart MCT-1 with these two training intensities; and 4) the increases in MCT-1 occurred independently of any changes in the heart’s oxidative capacity (as measured by citrate synthase activity).

PGC-1α increases skeletal muscle lactate uptake by increasing the expression of MCT1 but not MCT2 or MCT4

2008 ◽  
Vol 35 (1) ◽  
pp. 45-54 ◽  
Author(s):  
Carley R. Benton ◽  
Yuko Yoshida ◽  
James Lally ◽  
Xiao-Xia Han ◽  
Hideo Hatta ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
Positive Association ◽  
Strong Relationship ◽  
Muscle Lactate ◽  
Hindlimb Muscles ◽  
Metabolic Genes ◽  
Lactate Uptake ◽  
Strong Positive Association

We examined the relationship between PGC-1α protein; the monocarboxylate transporters MCT1, 2, and 4; and CD147 1) among six metabolically heterogeneous rat muscles, 2) in chronically stimulated red (RTA) and white tibialis (WTA) muscles (7 days), and 3) in RTA and WTA muscles transfected with PGC-1α-pcDNA plasmid in vivo. Among rat hindlimb muscles, there was a strong positive association between PGC-1α and MCT1 and CD147, and between MCT1 and CD147. A negative association was found between PGC-1α and MCT4, and CD147 and MCT4, while there was no relationship between PGC-1α or CD147 and MCT2. Transfecting PGC-1α-pcDNA plasmid into muscle increased PGC-1α protein (RTA +23%; WTA +25%) and induced the expression of MCT1 (RTA +16%; WTA +28%), but not MCT2 and MCT4. As a result of the PGC-1α-induced upregulation of MCT1 and its chaperone CD147 (+29%), there was a concomitant increase in the rate of lactate uptake (+20%). In chronically stimulated muscles, the following proteins were upregulated, PGC-1α in RTA (+26%) and WTA (+86%), MCT1 in RTA (+61%) and WTA (+180%), and CD147 in WTA (+106%). In contrast, MCT4 protein expression was not altered in either RTA or WTA muscles, while MCT2 protein expression was reduced in both RTA (−14%) and WTA (−10%). In these studies, whether comparing oxidative capacities among muscles or increasing their oxidative capacities by PGC-1α transfection and chronic muscle stimulation, there was a strong relationship between the expression of PGC-1α and MCT1, and PGC-1α and CD147 proteins. Thus, MCT1 and CD147 belong to the family of metabolic genes whose expression is regulated by PGC-1α in skeletal muscle.

Point: Muscle lactate and H+ production do have a 1:1 association in skeletal muscle

2011 ◽  
Vol 110 (5) ◽  
pp. 1487-1489 ◽  
Author(s):  
Kalyan C. Vinnakota ◽  
Martin J. Kushmerick
Keyword(s):  
Skeletal Muscle ◽  
Muscle Lactate

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.

Contraction duration affects metabolic energy cost and fatigue in skeletal muscle

1998 ◽  
Vol 274 (3) ◽  
pp. E397-E402 ◽  
Author(s):  
Michael C. Hogan ◽  
Erica Ingham ◽  
S. Sadi Kurdak
Keyword(s):  
Skeletal Muscle ◽  
Short Duration ◽  
Energy Cost ◽  
Lactate Concentration ◽  
Metabolic Energy ◽  
Muscle Lactate ◽  
Contracting Muscle ◽  
Contraction Duration ◽  
Long Duration ◽  
The Difference

It has been suggested that during a skeletal muscle contraction the metabolic energy cost at the onset may be greater than the energy cost related to holding steady-state force. The purpose of the present study was to investigate the effect of contraction duration on the metabolic energy cost and fatigue process in fully perfused contracting muscle in situ. Canine gastrocnemius muscle ( n = 6) was isolated, and two contractile periods (3 min of isometric, tetanic contractions with 45-min rest between) were conducted by each muscle in a balanced order design. The two contractile periods had stimulation patterns that resulted in a 1:3 contraction-to-rest ratio, with the difference in the two contractile periods being in the duration of each contraction: short duration 0.25-s stimulation/0.75-s rest vs. long duration 1-s stimulation/3-s rest. These stimulation patterns resulted in the same total time of stimulation, number of stimulation pulses, and total time in contraction for each 3-min period. Muscle O2 uptake, the fall in developed force (fatigue), the O2 cost of developed force, and the estimated total energy cost (ATP utilization) of developed force were significantly greater ( P < 0.05) with contractions of short duration. Lactate efflux from the working muscle and muscle lactate concentration were significantly greater with contractions of short duration, such that the calculated energy derived from glycolysis was three times greater in this condition. These results demonstrate that contraction duration can significantly affect both the aerobic and anaerobic metabolic energy cost and fatigue in contracting muscle. In addition, it is likely that the greater rate of fatigue with more rapid contractions was a result of elevated glycolytic production of lactic acid.

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