Load-matched acute and chronic exercise induce changes in mitochondrial biogenesis and metabolic markers

2021 ◽  
Author(s):  
Natalia Almeida Rodrigues ◽  
Claudio Alexandre Gobatto ◽  
Lucas Dantas Maia Forte ◽  
Filipe Antônio de Barros Sousa ◽  
Adriana Souza Torsoni ◽  
...  
Keyword(s):  
Aerobic Capacity ◽  
Skeletal Muscles ◽  
Acute Exercise ◽  
Citrate Synthase ◽  
Liver Glycogen ◽  
Chronic Exercise ◽  
Total Load ◽  
Metabolic Markers ◽  
Target Proteins ◽  
Glycogen Stores

We investigated the effects of the acute and chronic exercise, prescribed in different intensity zones, but with total load-matched on mitochondrial markers (COX-IV, Tfam, and citrate synthase (CS) activity in skeletal muscles, heart, and liver), glycogen stores, aerobic capacity and anaerobic index in swimming rats. For this, two experimental designs were performed (acute and chronic efforts). Load-matched exercises were prescribed below and above and on the anaerobic threshold (AnT), determined by the Lactate Minimum test. In chronic programs, two training prescription strategies were assessed (monotonous and linear periodized model). Results show changes in glycogen stores but no modification in the COX-IV and Tfam contents after acute exercises. In the chronic protocols, COX-IV and Tfam proteins and CS adaptations were intensity and tissue dependents. Monotonous training promoted better adaptations than the periodized model. Training at 80% of the AnT improved both performance variables, emphasizing the anaerobic index, concomitant to CS and COX-IV improvement (soleus muscle). The aerobic capacity and CS activity (gastrocnemius) were increased after 120% AnT training. In conclusion, acute exercise protocol did not promote responses in mitochondrial target proteins. An intensity and tissue dependence are reported in the chronic protocols, highlighting training at 80 and 120% of the AnT. Novelty: • Load-matched acute exercise did not enhance COX-IV and Tfam contents in skeletal muscles, heart, and liver. • In chronic exercise, COX-IV, Tfam, and citrate synthase activity adaptations were intensity and tissue dependents. •Monotonous training was more efficient than the periodized linear model in adaptations of target proteins and enzymatic activity.

scholarly journals Effects of Acute Exercise and Chronic Exercise on the Liver Leptin-AMPK-ACC Signaling Pathway in Rats with Type 2 Diabetes

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Xuejie Yi ◽  
Shicheng Cao ◽  
Bo Chang ◽  
Dalin Zhao ◽  
Haining Gao ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Lipid Metabolism ◽  
Signaling Pathway ◽  
Acute Exercise ◽  
Leptin Receptor ◽  
Liver Glycogen ◽  
Diabetic Rats ◽  
Chronic Exercise ◽  
Glucose And Lipid Metabolism

Aim. To investigate the effects of acute and chronic exercise on glucose and lipid metabolism in liver of rats with type 2 diabetes caused by a high fat diet and low dose streptozotocin (STZ).Methods. Animals were classified into control (CON), diabetes (DC), diabetic chronic exercise (DCE), and diabetic acute exercise (DAE) groups.Results. Compared to CON, the leptin levels in serum and liver and ACC phosphorylation were significantly higher in DC, but the levels of liver leptin receptor, AMPKα1/2, AMPKα1, and ACC proteins expression and phosphorylation were significantly lower in DC. In addition, the levels of liver glycogen reduced significantly, and the levels of TG and FFA increased significantly in DC compared to CON. Compared to DC, the levels of liver AMPKα1/2, AMPKα2, AMPKα1, and ACC phosphorylation significantly increased in DCE and DAE. However, significant increase of the level of liver leptin receptor and glycogen as well as significant decrease of the level of TG and FFA were observed only in DEC.Conclusion. Our study demonstrated that both acute and chronic exercise indirectly activated the leptin-AMPK-ACC signaling pathway and increased insulin sensitivity in the liver of type 2 diabetic rats. However, only chronic and long-term exercise improved glucose and lipid metabolism of the liver.

Adaptations to a high-fat diet that increase exercise endurance in male rats

1984 ◽  
Vol 56 (1) ◽  
pp. 78-83 ◽  
Author(s):  
W. C. Miller ◽  
G. R. Bryce ◽  
R. K. Conlee
Keyword(s):  
High Fat Diet ◽  
Citrate Synthase ◽  
Lactate Production ◽  
Liver Glycogen ◽  
Normal Diet ◽  
Male Rats ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Glycogen Stores

Eighty-seven male Sprague-Dawley rats (245–300 g) were randomly assigned to one of two experimental groups. The first group consumed a diet high in fat and low in carbohydrate (LCD), whereas the second group ate a normal diet (ND). After either 1 or 5 wk on the diets, rats from each group were killed either before or after an exhausting run on a rodent treadmill (35 m X min-1, 0% grade). The LCD animals ran significantly longer before exhaustion at both week 1 (44.9 +/- 5.1 vs. 41.6 +/- 4.2 min) and week 5 (47.1 +/- 3.6 vs. 35.5 +/- 3.1 min) (P less than 0.05). Adaptations to the LCD included lower muscle and liver glycogen content, decreased rate of glycogen breakdown during exercise, decreased lactate production, and elevated blood ketone levels. In addition to these substrate changes, the LCD caused increased enzyme activities of muscular 3-hydroxyacyl-CoA dehydrogenase (35–110%) and citrate synthase (15–20%). These data indicate that rats exposed to a high-fat diet are capable of prolonged intense exercise in spite of limited glycogen stores. This improved capacity for exercise appears to be partially the result of muscular adaptations to the diet, which apparently increase the ability to oxidize fat and concomitantly spare glycogen.

Temporal patterns of tissue glycogen, glucose, and glycogen phosphorylase activity prior to hibernation in freeze-tolerant chorus frogs, Pseudacris triseriata

2008 ◽  
Vol 86 (10) ◽  
pp. 1095-1100 ◽  
Author(s):  
Steve C. Dinsmore ◽  
David L. Swanson
Keyword(s):  
Glycogen Phosphorylase ◽  
Threshold Level ◽  
Liver Glycogen ◽  
Critical Threshold ◽  
Hepatic Glycogen ◽  
Phosphorylase Activity ◽  
Continuous Increase ◽  
Glycogen Accumulation ◽  
Chorus Frogs ◽  
Glycogen Stores

Freezing survival may differ among winters in chorus frogs ( Pseudacris triseriata (Wied-Neuwied, 1838)), and low freezing survival is associated with low hepatic glycogen stores. The pattern of prehibernation liver glycogen accumulation in chorus frogs is unknown. Frogs might accumulate hepatic glycogen stores until a threshold level sufficient for winter survival is attained, after which frogs enter hibernation (critical threshold hypothesis). According to this model, frogs active late in the season should only be those with low hepatic glycogen stores. Alternatively, hepatic glycogen levels might continue to increase throughout the fall as long as frogs remain active (continuous increase hypothesis). We tested these hypotheses by measuring liver and leg muscle glycogen, glucose, and glycogen phosphorylase activities in chorus frogs throughout the fall prehibernation period in southeastern South Dakota. Hepatic glycogen levels were significantly related to date and increased throughout the fall period, consistent with the continuous increase hypothesis. This suggests that hepatic glycogen levels do not serve as a cue for entrance into hibernation. Liver phosphorylase activity did not vary significantly with progression of the fall season and activity was lower than in winter, suggesting that the winter increment of phosphorylase activity requires some stimulus during hibernation (e.g., low temperatures).

The relationship between human skeletal muscle pyruvate dehydrogenase phosphatase activity and muscle aerobic capacity

2011 ◽  
Vol 111 (2) ◽  
pp. 427-434 ◽  
Author(s):  
Lorenzo K. Love ◽  
Paul J. LeBlanc ◽  
J. Greig Inglis ◽  
Nicolette S. Bradley ◽  
Jon Choptiany ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Content ◽  
Endurance Training ◽  
Aerobic Capacity ◽  
Pyruvate Dehydrogenase ◽  
Human Skeletal Muscle ◽  
Citrate Synthase ◽  
Tricarboxylic Acid Cycle ◽  
Carbohydrate Oxidation ◽  
Pyruvate Dehydrogenase Phosphatase

Pyruvate dehydrogenase (PDH) is a mitochondrial enzyme responsible for regulating the conversion of pyruvate to acetyl-CoA for use in the tricarboxylic acid cycle. PDH is regulated through phosphorylation and inactivation by PDH kinase (PDK) and dephosphorylation and activation by PDH phosphatase (PDP). The effect of endurance training on PDK in humans has been investigated; however, to date no study has examined the effect of endurance training on PDP in humans. Therefore, the purpose of this study was to examine differences in PDP activity and PDP1 protein content in human skeletal muscle across a range of muscle aerobic capacities. This association is important as higher PDP activity and protein content will allow for increased activation of PDH, and carbohydrate oxidation. The main findings of this study were that 1) PDP activity ( r2 = 0.399, P = 0.001) and PDP1 protein expression ( r2 = 0.153, P = 0.039) were positively correlated with citrate synthase (CS) activity as a marker for muscle aerobic capacity; 2) E1α ( r2 = 0.310, P = 0.002) and PDK2 protein ( r2 = 0.229, P =0.012) are positively correlated with muscle CS activity; and 3) although it is the most abundant isoform, PDP1 protein content only explained ∼18% of the variance in PDP activity ( r2 = 0.184, P = 0.033). In addition, PDP1 in combination with E1α explained ∼38% of the variance in PDP activity ( r2 = 0.383, P = 0.005), suggesting that there may be alternative regulatory mechanisms of this enzyme other than protein content. These data suggest that with higher muscle aerobic capacity (CS activity) there is a greater capacity for carbohydrate oxidation (E1α), in concert with higher potential for PDH activation (PDP activity).

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).

Acute Exercise Increases the Expression of KIR2DS4 by Promoter Demethylation in NK Cells

2018 ◽  
Vol 40 (01) ◽  
pp. 62-70 ◽  
Author(s):  
Alexander Schenk ◽  
Walter Pulverer ◽  
Christine Koliamitra ◽  
Claus Bauer ◽  
Suzana Ilic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Nk Cells ◽  
Promoter Methylation ◽  
Acute Exercise ◽  
Nk Cell ◽  
Epigenetic Modifications ◽  
Control Group ◽  
Chronic Exercise ◽  
Positive Effects

AbstractPositive effects of exercise on cancer prevention and progression have been proposed to be mediated by stimulating natural killer (NK) cells. Because NK cell receptors are regulated by epigenetic modifications, we investigated whether acute aerobic exercise and training change promoter DNA methylation and gene expression of the activating KIR2DS4 and the inhibiting KIR3DL1 gene. Sixteen healthy women (50–60 years) performed a graded exercise test (GXT) and were randomized into either a passive control group or an intervention group performing a four-week endurance exercise intervention. Blood samples (pre-, post-GXT and post-training) were used for isolation of DNA/RNA of NK cells to assess DNA promoter methylation by targeted deep-amplicon sequencing and gene expression by qRT-PCR. Potential changes in NK cell subsets were determined by flow cytometry. Acute and chronic exercise did not provoke significant alterations of NK cell proportions. Promoter methylation decreased and gene expression increased for KIR2DS4 after acute exercise. A high gene expression correlated with a low methylation of CpGs that were altered by acute exercise. Chronic exercise resulted in a minor decrease of DNA methylation and did not alter gene expression. Acute exercise provokes epigenetic modifications, affecting the balance between the activating KIR2DS4 and the inhibiting KIR3DL1, with potential benefits on NK cell function.

Glucose responses to acute and chronic exercise during pregnancy: a systematic review and meta-analysis

2018 ◽  
Vol 52 (21) ◽  
pp. 1357-1366 ◽  
Author(s):  
Margie H Davenport ◽  
Frances Sobierajski ◽  
Michelle F Mottola ◽  
Rachel J Skow ◽  
Victoria L Meah ◽  
...  
Keyword(s):  
Systematic Review ◽  
Blood Glucose ◽  
Glycaemic Control ◽  
Acute Exercise ◽  
Exercise Intervention ◽  
Meta Analysis ◽  
Fasting Blood Glucose ◽  
Chronic Exercise ◽  
Prenatal Exercise ◽  
Frequency Intensity

ObjectiveTo perform a systematic review and meta-analysis to explore the relationship between prenatal exercise and glycaemic control.DesignSystematic review with random-effects meta-analysis and meta-regression.Data sourcesOnline databases were searched up to 6 January 2017.Study eligibility criteriaStudies of all designs were included (except case studies and reviews) if they were published in English, Spanish or French, and contained information on the population (pregnant women without contraindication to exercise), intervention (subjective or objective measures of frequency, intensity, duration, volume or type of acute or chronic exercise, alone (‘exercise-only’) or in combination with other intervention components (eg, dietary; ‘exercise+cointervention’) at any stage of pregnancy), comparator (no exercise or different frequency, intensity, duration, volume and type of exercise) and outcome (glycaemic control).ResultsA total of 58 studies (n=8699) were included. There was ‘very low’ quality evidence showing that an acute bout of exercise was associated with a decrease in maternal blood glucose from before to during exercise (6 studies, n=123; mean difference (MD) −0.94 mmol/L, 95% CI −1.18 to −0.70, I2=41%) and following exercise (n=333; MD −0.57 mmol/L, 95% CI −0.72 to −0.41, I2=72%). Subgroup analysis showed that there were larger decreases in blood glucose following acute exercise in women with diabetes (n=26; MD −1.42, 95% CI −1.69 to −1.16, I2=8%) compared with those without diabetes (n=285; MD −0.46, 95% CI −0.60 to −0.32, I2=62%). Finally, chronic exercise-only interventions reduced fasting blood glucose compared with no exercise postintervention in women with diabetes (2 studies, n=70; MD −2.76, 95% CI −3.18 to −2.34, I2=52%; ‘low’ quality of evidence), but not in those without diabetes (9 studies, n=2174; MD −0.05, 95% CI −0.16 to 0.05, I2=79%).ConclusionAcute and chronic prenatal exercise reduced maternal circulating blood glucose concentrations, with a larger effect in women with diabetes.

Liver Glycogen Reserves of Interacting Resident and Introduced Trout Populations

1961 ◽  
Vol 18 (1) ◽  
pp. 125-135 ◽  
Author(s):  
P. W. Hochachka
Keyword(s):  
Population Density ◽  
Liver Glycogen ◽  
Salmo Gairdneri ◽  
Recovery Rates ◽  
Introduced Populations ◽  
Wild Trout ◽  
Low Levels ◽  
Glycogen Stores ◽  
Salmo Clarki

Three groups of trout, two introduced populations of Salmo gairdneri and a resident Salmo clarki, were studied in stream sections. Liver glycogen deposits, which were reduced to low levels during transportation to the stream, were restored in 2 to 3 weeks in all groups, with recovery rates being approximately inverse to the population density. Within the hatchery groups, larger fish laid down greater glycogen stores. Wild trout maintained their high glycogen reserves throughout the experiment.

Exercise increases the plasma membrane content of the Na+ -K+ pump and its mRNA in rat skeletal muscles

1996 ◽  
Vol 80 (2) ◽  
pp. 699-705 ◽  
Author(s):  
T. Tsakiridis ◽  
P. P. Wong ◽  
Z. Liu ◽  
C. D. Rodgers ◽  
M. Vranic ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Plasma Membrane ◽  
Skeletal Muscles ◽  
Plasma Membranes ◽  
Acute Exercise ◽  
Treadmill Running ◽  
Type I ◽  
Mrna Levels ◽  
Subunit Mrna ◽  
White Type

Muscle fibers adapt to ionic challenges of exercise by increasing the plasma membrane Na+-K+ pump activity. Chronic exercise training has been shown to increase the total amount of Na+-K+ pumps present in skeletal muscle. However, the mechanism of adaptation of the Na+-K+ pump to an acute bout of exercise has not been determined, and it is not known whether it involves alterations in the content of plasma membrane pump subunits. Here we examine the effect of 1 h of treadmill running (20 m/min, 10% grade) on the subcellular distribution and expression of Na+-K+ pump subunits in rat skeletal muscles. Red type I and IIa (red-I/IIa) and white type IIa and IIb (white-IIa/IIb) hindlimb muscles from resting and exercised female Sprague-Dawley rats were removed for subcellular fractionation. By homogenization and gradient centrifugation, crude membranes and purified plasma membranes were isolated and subjected to gel electrophoresis and immunoblotting by using pump subunit-specific antibodies. Furthermore, mRNA was isolated from specific red type I (red-I) and white type IIb (white-IIb) muscles and subjected to Northern blotting by using subunit-specific probes. In both red-I/IIa and white-IIa/IIb muscles, exercise significantly raised the plasma membrane content of the alpha1-subunit of the pump by 64 +/- 24 and 55 +/- 22%, respectively (P < 0.05), and elevated the alpha2-polypeptide by 43 +/- 22 and 94 +/- 39%, respectively (P < 0.05). No significant effect of exercise could be detected on the amount of these subunits in an internal membrane fraction or in total membranes. In addition, exercise significantly increased the alpha1-subunit mRNA in red-I muscle (by 50 +/- 7%; P < 0.05) and the beta2-subunit mRNA in white-IIb muscles (by 64 +/- 19%; P < 0.01), but the alpha2- and beta1-mRNA levels were unaffected in this time period. We conclude that increased presence of alpha1- and alpha2-polypeptides at the plasma membrane and subsequent elevation of the alpha1- and beta2-subunit mRNAs may be mechanisms by which acute exercise regulates the Na+-K+ pump of skeletal muscle.

VARIATIONS IN GLUCAGON RESPONSE AMONG JUVENILE DIABETICS

PEDIATRICS ◽  
1963 ◽  
Vol 32 (6) ◽  
pp. 1002-1006
Author(s):  
Donnell D. Etzwiler
Keyword(s):  
Blood Glucose ◽  
Good Control ◽  
Liver Glycogen ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Juvenile Diabetics ◽  
Glycogen Stores ◽  
Initial Blood ◽  
Hyperglycemic Effect

Glucagon or a placebo preparation was administered to 65 juvenile diabetics on 74 separate occasions. When the initial blood glucose of these children showed them to be in reasonably good control, glucagon produced a hyperglycemic effect. However, when the blood glucose levels were markedly elevated, the effect of glucagon was less predictable. The depletion of liver glycogen stores and the possible effect of contaminating insulin in glucagon preparations are discussed.

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