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).

Short-term training increases human muscle MCT1 and femoral venous lactate in relation to muscle lactate

1998 ◽  
Vol 274 (1) ◽  
pp. E102-E107 ◽  
Author(s):  
A. Bonen ◽  
K. J. A. McCullagh ◽  
C. T. Putman ◽  
E. Hultman ◽  
N. L. Jones ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vastus Lateralis ◽  
Venous Blood ◽  
Maximal Oxygen Consumption ◽  
Bicycle Ergometer ◽  
Monocarboxylate Transporter ◽  
Short Term ◽  
Bicycle Ergometry ◽  
Muscle Lactate ◽  
Monocarboxylate Transporter 1

We examined the effects of increasing a known lactate transporter protein, monocarboxylate transporter 1 (MCT1), on lactate extrusion from human skeletal muscle during exercise. Before and after short-term bicycle ergometry training [2 h/day, 7 days at 65% maximal oxygen consumption (V˙o 2 max)], subjects ( n = 7) completed a continuous bicycle ergometer ride at 30%V˙o 2 max (15 min), 60%V˙o 2 max (15 min), and 75% V˙o 2 max (15 min). Muscle biopsy samples (vastus lateralis) and arterial and femoral venous blood samples were obtained before exercise and at the end of each workload. After 7 days of training the MCT1 content in muscle was increased (+18%; P < 0.05). The concentrations of both muscle lactate and femoral venous lactate were reduced during exercise ( P < 0.05) that was performed after training. High correlations were observed between muscle lactate and venous lactate before training ( r = 0.92, P < 0.05) and after training ( r = 0.85, P < 0.05), but the slopes of the regression lines between these variables differed markedly. Before training, the slope was 0.12 ± 0.01 mM lactate ⋅ mmol lactate−1 ⋅ kg muscle dry wt−1, and this was increased by 33% after training to 0.18 ± 0.02 mM lactate ⋅ mmol lactate−1 ⋅ kg muscle dry wt−1. This indicated that after training the femoral venous lactate concentrations were increased for a given amount of muscle lactate. These results suggest that lactate extrusion from exercising muscles is increased after training, and this may be associated with the increase in skeletal muscle MCT1.

Effect of two different intense training regimens on skeletal muscle ion transport proteins and fatigue development

2007 ◽  
Vol 292 (4) ◽  
pp. R1594-R1602 ◽  
Author(s):  
Magni Mohr ◽  
Peter Krustrup ◽  
Jens Jung Nielsen ◽  
Lars Nybo ◽  
Martin Krøyer Rasmussen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Ion Transport ◽  
Metabolic Response ◽  
Transport Proteins ◽  
Treadmill Running ◽  
Monocarboxylate Transporter ◽  
Transport Systems ◽  
Muscle Lactate ◽  
Monocarboxylate Transporter 1 ◽  
Response To Exercise

This study examined the effect of two different intense exercise training regimens on skeletal muscle ion transport systems, performance, and metabolic response to exercise. Thirteen subjects performed either sprint training [ST; 6-s sprints ( n = 6)], or speed endurance training [SET; 30-s runs ∼130% V̇o2 max, n = 7]. Training in the SET group provoked higher ( P < 0.05) plasma K+ levels and muscle lactate/H+ accumulation. Only in the SET group was the amount of the Na+/H+ exchanger isoform 1 (31%) and Na+-K+-ATPase isoform α2 (68%) elevated ( P < 0.05) after training. Both groups had higher ( P < 0.05) levels of Na+-K+-ATPase β1-isoform and monocarboxylate transporter 1 (MCT1), but no change in MCT4 and Na+-K+-ATPase α1-isoform. Both groups had greater ( P < 0.05) accumulation of lactate during exhaustive exercise and higher ( P < 0.05) rates of muscle lactate decrease after exercise. The ST group improved ( P < 0.05) sprint performance, whereas the SET group elevated ( P < 0.05) performance during exhaustive continuous treadmill running. Improvement in the Yo-Yo intermittent recovery test was larger ( P < 0.05) in the SET than ST group (29% vs. 10%). Only the SET group had a decrease ( P < 0.05) in fatigue index during a repeated sprint test. In conclusion, turnover of lactate/H+ and K+ in muscle during exercise does affect the adaptations of some but not all related muscle ion transport proteins with training. Adaptations with training do have an effect on the metabolic response to exercise and specific improvement in work capacity.

Exercise training increases branched-chain oxoacid dehydrogenase kinase content in human skeletal muscle

2007 ◽  
Vol 293 (3) ◽  
pp. R1335-R1341 ◽  
Author(s):  
Krista R. Howarth ◽  
Kirsten A. Burgomaster ◽  
Stuart M. Phillips ◽  
Martin J. Gibala
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Protein Content ◽  
Human Skeletal Muscle ◽  
Acute Exercise ◽  
Citrate Synthase ◽  
Muscle Protein ◽  
Moderate Intensity ◽  
Main Effect ◽  
Branched Chain

The branched-chain oxoacid dehydrogenase complex (BCOAD) is rate determining for the oxidation of branched-chain amino acids (BCAAs) in skeletal muscle. Exercise training blunts the acute exercise-induced activation of BCOAD (BCOADa) in human skeletal muscle (McKenzie S, Phillips SM, Carter SL, Lowther S, Gibala MJ, Tarnopolsky MA. Am J Physiol Endocrinol Metab 278: E580–E587, 2000); however, the mechanism is unknown. We hypothesized that training would increase the muscle protein content of BCOAD kinase, the enzyme responsible for inactivation of BCOAD by phosphorylation. Twenty subjects [23 ± 1 yr; peak oxygen uptake (V̇o2peak) = 41 ± 2 ml·kg−1·min−1] performed 6 wk of either high-intensity interval or continuous moderate-intensity training on a cycle ergometer ( n = 10/group). Before and after training, subjects performed 60 min of cycling at 65% of pretraining V̇o2peak, and needle biopsy samples (vastus lateralis) were obtained before and immediately after exercise. The effect of training was demonstrated by an increased V̇o2peak, increased citrate synthase maximal activity, and reduced muscle glycogenolysis during exercise, with no difference between groups (main effects, P < 0.05). BCOADa was lower after training (main effect, P < 0.05), and this was associated with a ∼30% increase in BCOAD kinase protein content (main effect, P < 0.05). We conclude that the increased protein content of BCOAD kinase may be involved in the mechanism for reduced BCOADa after exercise training in human skeletal muscle. These data also highlight differences in models used to study the regulation of skeletal muscle BCAA metabolism, since exercise training was previously reported to increase BCOADa during exercise and decrease BCOAD kinase content in rats (Fujii H, Shimomura Y, Murakami T, Nakai N, Sato T, Suzuki M, Harris RA. Biochem Mol Biol Int 44: 1211–1216, 1998).

Exercise training alleviates MCT1 and MCT4 reductions in heart and skeletal muscles of STZ-induced diabetic rats

2003 ◽  
Vol 94 (6) ◽  
pp. 2433-2438 ◽  
Author(s):  
Taisuke Enoki ◽  
Yuko Yoshida ◽  
Hideo Hatta ◽  
Arend Bonen
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Skeletal Muscles ◽  
Diabetic Rats ◽  
Monocarboxylate Transporter ◽  
Sedentary Control ◽  
Monocarboxylate Transporter 1

We compared the changes in monocarboxylate transporter 1 (MCT1) and 4 (MCT4) proteins in heart and skeletal muscles in sedentary control and streptozotocin (STZ)-induced diabetic rats (3 wk) and in trained (3 wk) control and STZ-induced diabetic animals. In nondiabetic animals, training increased MCT1 in the plantaris (+51%; P < 0.01) but not in the soleus (+9%) or the heart (+14%). MCT4 was increased in the plantaris (+48%; P < 0.01) but not in the soleus muscles of trained nondiabetic animals. In sedentary diabetic animals, MCT1 was reduced in the heart (−30%), and in the plantaris (−31%; P < 0.01) and soleus (−26%) muscles. MCT4 content was also reduced in sedentary diabetic animals in the plantaris (−52%; P < 0.01) and soleus (−25%) muscles. In contrast, in trained diabetic animals, MCT1 and MCT4 in heart and/or muscle were similar to those of sedentary, nondiabetic animals ( P > 0.05) but were markedly greater than in the sedentary diabetic animals [MCT1: plantaris +63%, soleus +51%, heart +51% ( P > 0.05); MCT4: plantaris +107%, soleus +17% ( P > 0.05)]. These studies have shown that 1) with STZ-induced diabetes, MCT1 and MCT4 are reduced in skeletal muscle and/or the heart and 2) exercise training alleviated these diabetes-induced reductions.

Cardiac and skeletal muscle mitochondria have a monocarboxylate transporter MCT1

1999 ◽  
Vol 87 (5) ◽  
pp. 1713-1718 ◽  
Author(s):  
George A. Brooks ◽  
Marcia A. Brown ◽  
C. E. Butz ◽  
James P. Sicurello ◽  
Hervé Dubouchaud
Keyword(s):  
Skeletal Muscle ◽  
Striated Muscle ◽  
Lactic Dehydrogenase ◽  
Monocarboxylate Transporter ◽  
Lactate Oxidation ◽  
Western Blots ◽  
Lactate Shuttle ◽  
Muscle Mitochondria ◽  
Monocarboxylate Transporter 1 ◽  
Skeletal Muscle Mitochondria

To evaluate the potential role of monocarboxylate transporter-1 (MCT1) in tissue lactate oxidation, isolated rat subsarcolemmal and interfibrillar cardiac and skeletal muscle mitochondria were probed with an antibody to MCT1. Western blots indicated presence of MCT1 in sarcolemmal membranes and in subsarcolemmal and interfibrillar mitochondria. Minimal cross-contamination of mitochondria by cell membrane fragments was verified by probing for the sarcolemmal protein GLUT-1. In agreement, immunolabeling and electron microscopy showed mitochondrial MCT1 in situ. Along with lactic dehydrogenase, the presence of MCT1 in striated muscle mitochondria permits mitochondrial lactate oxidation and facilitates function of the “intracellular lactate shuttle.”

Non-oxidative Energy Supply Correlates with Lactate Transport and Removal in Trained Rowers

2020 ◽  
Vol 41 (13) ◽  
pp. 936-943
Author(s):  
Hugo Maciejewski ◽  
Muriel Bourdin ◽  
Léonard Féasson ◽  
Hervé Dubouchaud ◽  
Laurent André Messonnier
Keyword(s):  
Blood Lactate ◽  
Energy Supply ◽  
Citrate Synthase ◽  
Monocarboxylate Transporter ◽  
Oxygen Deficit ◽  
Muscle Lactate ◽  
Lactate Accumulation ◽  
Accumulated Oxygen Deficit ◽  
Lactate Removal ◽  
Exercise Muscle

AbstractThis study aimed to test if the non-oxidative energy supply (estimated by the accumulated oxygen deficit) is associated with an index of muscle lactate accumulation during exercise, muscle monocarboxylate transporter content and the lactate removal ability during recovery in well-trained rowers. Seventeen rowers completed a 3-min all-out exercise on rowing ergometer to estimate the accumulated oxygen deficit. Blood lactate samples were collected during the subsequent passive recovery to assess individual blood lactate curves, which were fitted to the bi-exponential time function: La(t)= [La](0)+A1·(1–e–γ 1 t)+A2·(1–e–γ 2 t), where the velocity constants γ1 and γ2 (min–1) denote the lactate exchange and removal abilities during recovery, respectively. The accumulated oxygen deficit was correlated with the net amount of lactate released from the previously active muscles (r =0.58, P<0.05), the monocarboxylate transporters MCT1 and MCT4 (r=0.63, P<0.05) and γ2 (r=0.55, P<0.05). γ2 and the lactate release rate at exercise completion were negatively correlated with citrate synthase activity. These findings suggest that the capacity to supply non-oxidative energy during supramaximal rowing exercise is associated with muscle lactate accumulation and transport, as well as lactate removal ability.

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

The Effect of Exercise Training Intensity on Quality of Life in Heart Failure Patients: A Systematic Review and Meta-Analysis

Cardiology ◽  
2016 ◽  
Vol 136 (2) ◽  
pp. 79-89 ◽  
Author(s):  
Cecilia Ostman ◽  
Daniel Jewiss ◽  
Neil A. Smart
Keyword(s):  
Quality Of Life ◽  
Heart Failure ◽  
Resistance Training ◽  
Exercise Training ◽  
Left Ventricular ◽  
Moderate Intensity ◽  
Training Intensity ◽  
Medline Search ◽  
Intensity Training

Objectives: To establish if exercise training intensity produces different effect sizes for quality of life in heart failure. Background: Exercise intensity is the primary stimulus for physical and mental adaptation. Methods: We conducted a MEDLINE search (1985 to February 2016) for exercise-based rehabilitation trials in heart failure using the search terms ‘exercise training', ‘left ventricular dysfunction', ‘peak VO2', ‘cardiomyopathy', and ‘systolic heart dysfunction'. Results: Twenty-five studies were included; 4 (16%) comprised high-, 10 (40%) vigorous-, 9 (36%) moderate- and 0 (0%) low-intensity groups; two studies were unclassified. The 25 studies provided a total of 2,385 participants, 1,223 exercising and 1,162 controls (36,056 patient-hours of training). Analyses reported significant improvement in total Minnesota living with heart failure (MLWHF) total score [mean difference (MD) -8.24, 95% CI -11.55 to -4.92, p < 0.00001]. Physical MLWHF scorewas significantly improved in all studies (MD -2.89, 95% CI -4.27 to -1.50, p < 0.00001). MLWHF total score was significantly reduced after high- (MD -13.74, 95% CI -21.34 to -6.14, p = 0.0004) and vigorous-intensity training (MD -8.56, 95% CI -12.77 to -4.35, p < 0.0001) but not moderate-intensity training. A significant improvement in the total MLWHF score was seen after aerobic training (MD -3.87, 95% CI -6.97 to -0.78, p = 0.01), and combined aerobic and resistance training (MD -9.82, 95% CI -15.71 to -3.92, p = 0.001), but not resistance training. Conclusions: As exercise training intensity rises, so may the magnitude of improvement in quality of life in exercising patients. Aerobic-only or combined aerobic and resistance training may offer the greatest improvements in quality of life.

scholarly journals Rethinking the Citric Acid Cycle: Connecting Pyruvate Carboxylase and Citrate Synthase to the Flow of Energy and Material

2021 ◽  
Vol 22 (2) ◽  
pp. 604
Author(s):  
Dirk Roosterman ◽  
Graeme Stuart Cottrell
Keyword(s):  
Lactate Dehydrogenase ◽  
Citric Acid ◽  
Pyruvate Carboxylase ◽  
Citric Acid Cycle ◽  
Citrate Synthase ◽  
Monocarboxylate Transporter ◽  
Acid Cycle ◽  
Oxaloacetic Acid ◽  
Monocarboxylate Transporter 1 ◽  
Original Concept

In 1937, Sir H. A Krebs first published the Citric Acid Cycle, a unidirectional cycle with carboxylic acids. The original concept of the Citric Acid Cycle from Krebs’ 1953 Nobel Prize lecture illustrates the unidirectional degradation of lactic acid to water, carbon dioxide and hydrogen. Here, we add the heart lactate dehydrogenase•proton-linked monocarboxylate transporter 1 complex, connecting the original Citric Acid Cycle to the flow of energy and material. The heart lactate dehydrogenase•proton-linked monocarboxylate transporter 1 complex catalyses the first reaction of the Citric Acid Cycle, the oxidation of lactate to pyruvate, and thus secures the provision of pyruvic acid. In addition, we modify Krebs’ original concept by feeding the cycle with oxaloacetic acid. Our concept enables the integration of anabolic processes and allows adaption of the organism to recover ATP faster.

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