Effects on Oxygen Consumption and Metabolic Gene Expression when Determining Experimental Exercise Intensity Based on Exercise Capacity Tests Conducted in Hypoxic and Normoxic Environments

2014 ◽  
Vol 03 (01) ◽  
Author(s):  
Dustin R Slivka
Keyword(s):  
Gene Expression ◽  
Oxygen Consumption ◽  
Exercise Capacity ◽  
Exercise Intensity ◽  
Metabolic Gene ◽  
Metabolic Gene Expression

scholarly journals Activation of PPARδ signaling improves skeletal muscle oxidative metabolism and endurance function in an animal model of ischemic left ventricular dysfunction

2015 ◽  
Vol 308 (9) ◽  
pp. H1078-H1085 ◽  
Author(s):  
Cynthia Zizola ◽  
Peter J. Kennel ◽  
Hirokazu Akashi ◽  
Ruiping Ji ◽  
Estibaliz Castillero ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Oxidative Metabolism ◽  
Ventricular Dysfunction ◽  
Oxidative Capacity ◽  
Muscle Dysfunction ◽  
Metabolic Gene ◽  
Skeletal Muscle Dysfunction ◽  
Metabolic Gene Expression

Exercise intolerance in heart failure has been linked to impaired skeletal muscle oxidative capacity. Oxidative metabolism and exercise capacity are regulated by PPARδ signaling. We hypothesized that PPARδ stimulation reverts skeletal muscle oxidative dysfunction. Myocardial infarction (MI) was induced in C57BL/6 mice and the development of ventricular dysfunction was monitored over 8 wk. Mice were randomized to the PPARδ agonist GW501516 (5 mg/kg body wt per day for 4 wk) or placebo 8 wk post-MI. Muscle function was assessed through running tests and grip strength measurements. In muscle, we analyzed muscle fiber cross-sectional area and fiber types, metabolic gene expression, fatty acid (FA) oxidation and ATP content. Signaling pathways were studied in C2C12 myotubes. FA oxidation and ATP levels decreased in muscle from MI mice compared with sham- operated mice. GW501516 administration increased oleic acid oxidation levels in skeletal muscle of the treated MI group compared with placebo treatment. This was accompanied by transcriptional changes including increased CPT1 expression. Further, the PPARδ-agonist improved running endurance compared with placebo. Cell culture experiments revealed protective effects of GW501516 against the cytokine-induced decrease of FA oxidation and changes in metabolic gene expression. Skeletal muscle dysfunction in HF is associated with impaired PPARδ signaling and treatment with the PPARδ agonist GW501516 corrects oxidative capacity and FA metabolism and improves exercise capacity in mice with LV dysfunction. Pharmacological activation of PPARδ signaling could be an attractive therapeutic intervention to counteract the progressive skeletal muscle dysfunction in HF.

Regulation of myocardial metabolic gene expression in pressure-overload and exercise-induced hypertrophy

2008 ◽  
Vol 56 (S 1) ◽  
Author(s):  
M Schwarzer ◽  
C Riehle ◽  
G Pytel ◽  
H Bugger ◽  
D Blum ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pressure Overload ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Exercise Induced

233-LB: Spinal Cord Injury Inhibited-FGF21 Signaling Is Associated with Dysregulation of Metabolic Gene Expression in Mouse Liver and Adipose Tissue

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 233-LB
Author(s):  
XIN-HUA LIU ◽  
LAUREN HARLOW ◽  
ZACHARY GRAHAM ◽  
JOSHUA F. YARROW ◽  
KENNETH CUSI ◽  
...  
Keyword(s):  
Gene Expression ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Adipose Tissue ◽  
Mouse Liver ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Cord Injury

Effect of carbohydrate ingestion on exercise-induced alterations in metabolic gene expression

2005 ◽  
Vol 99 (4) ◽  
pp. 1359-1363 ◽  
Author(s):  
Laura J. Cluberton ◽  
Sean L. McGee ◽  
Robyn M. Murphy ◽  
Mark Hargreaves
Keyword(s):  
Gene Expression ◽  
Oxygen Uptake ◽  
Pyruvate Dehydrogenase Kinase ◽  
Mrna Levels ◽  
Carbohydrate Ingestion ◽  
Pulmonary Oxygen Uptake ◽  
Metabolic Gene ◽  
Metabolic Gene Expression ◽  
Glucose Ingestion ◽  
Exercise Induced

Skeletal muscle possesses a high degree of plasticity and can adapt to both the physical and metabolic challenges that it faces. An acute bout of exercise is sufficient to induce the expression of a variety of metabolic genes, such as GLUT4, pyruvate dehydrogenase kinase 4 (PDK-4), uncoupling protein-3 (UCP3), and peroxisome proliferator-activated receptor-γ coactivator 1 (PGC-1). Reducing muscle glycogen levels before exercise potentiates the effect of exercise on many genes. Similarly, altered substrate availability induces transcription of many of these genes. The purpose of this study was to determine whether glucose ingestion attenuates the exercise-induced increase in a variety of exercise-responsive genes. Six male subjects (28 ± 7 yr; 83 ± 3 kg; peak pulmonary oxygen uptake = 46 ± 6 ml·kg−1·min−1) performed 60 min of cycling at 74 ± 2% of peak pulmonary oxygen uptake on two separate occasions. On one occasion, subjects ingested a 6% carbohydrate drink. On the other occasion, subjects ingested an equal volume of a sweet placebo. Muscle samples were obtained from vastus lateralis at rest, immediately after exercise, and 3 h after exercise. PDK-4, UCP3, PGC-1, and GLUT4 mRNA levels were measured on these samples using real-time RT-PCR. Glucose ingestion attenuated ( P < 0.05) the exercise-induced increase in PDK-4 and UCP3 mRNA. A similar trend ( P = 0.09) was observed for GLUT4 mRNA. In contrast, PGC-1 mRNA increased following exercise to the same extent in both conditions. These data suggest that glucose availability can modulate the effect of exercise on metabolic gene expression.

scholarly journals Cardiac Raptor Ablation Impairs Adaptive Hypertrophy, Alters Metabolic Gene Expression, and Causes Heart Failure in Mice

Circulation ◽  
2011 ◽  
Vol 123 (10) ◽  
pp. 1073-1082 ◽  
Author(s):  
Pankaj Shende ◽  
Isabelle Plaisance ◽  
Christian Morandi ◽  
Corinne Pellieux ◽  
Corinne Berthonneche ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Metabolic Gene ◽  
Metabolic Gene Expression

Abstract 17010: Metabolic Gene Expression and Mitochondrial Function Are Altered in the Failing Single Ventricle Myocardium

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Anastacia M Garcia ◽  
Kathryn C Chatfield ◽  
Genevieve C Sparagna ◽  
Elisabeth K Phillips ◽  
Anis Karimpour-Fard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mitochondrial Function ◽  
Molecular Mechanisms ◽  
Single Ventricle ◽  
Normal Function ◽  
P Value ◽  
Current Standard ◽  
Illumina Hiseq ◽  
Metabolic Gene ◽  
Metabolic Gene Expression

Introduction: Despite current standard of care, heart failure (HF) remains a leading cause of death and indication for transplant in the single ventricle congenital heart disease (SV) population. However, little is known regarding the molecular mechanisms underlying remodeling and eventual HF in SV patients. The purpose of this study was to characterize the transcriptional profile of SV myocardium in both failing (SVHF) and non-failing (SVNF) SV patients compared to biventricular NF controls (BVNF). Furthermore, we conducted high resolution respirometry to assess mitochondrial function in each of these populations. Methods: Library prep was performed using the TruSeq Ribo Zero rRNA depletion kit, and 2x150 total RNAseq (Illumina HiSEQ 4000) was performed on age-matched explanted RV myocardium from BVNF (n=4 biventricular donors), SVNF (n=8 SV primary transplants, normal function), and SVHF (n=9 SV systolic HF transplants). Samples were aligned to hg19 and were normalized and annotated using the edgeR pipeline. Significant changes in gene expression were calculated using an FDR adjusted p-value (q<0.1; p<0.025). Respiration of myocardial mitochondria was measured using a stepwise protocol to evaluate respiratory capacity in an Oroboros Oxygraph system; n=6 SVHF, n=6 SVNF, n=18 BVNF. Results: RNAseq identified 1,007 differentially expressed genes in SVNF and 2,109 in SVHF myocardium relative to BVNF controls. Transcriptome pathway analysis demonstrated multiple pathways that are similarly dysregulated in SVNF and SVHF, while pathways involved in mitochondrial metabolism and function were significantly dysregulated specifically in the SVHF population. Moreover, mitochondrial oxygen flux was significantly decreased, particularly through complexes I and II, in SVHF relative to BVNF controls. Conclusions: Our results provide new insights into SVHF by identifying unique gene expression changes, including those related to metabolism, and impaired mitochondrial function. Together these data suggest dysregulated metabolic gene expression and mitochondrial dysfunction are phenotypes associated with the failing single ventricle and may serve as potential therapeutic targets for the treatment or prevention of HF in the SV population.

Time course of myogenic and metabolic gene expression in response to acute exercise in human skeletal muscle

2005 ◽  
Vol 98 (5) ◽  
pp. 1745-1752 ◽  
Author(s):  
Yifan Yang ◽  
Andrew Creer ◽  
Bozena Jemiolo ◽  
Scott Trappe
Keyword(s):  
Gene Expression ◽  
Time Course ◽  
Acute Exercise ◽  
Vastus Lateralis ◽  
Gene Induction ◽  
Mrna Levels ◽  
Metabolic Gene ◽  
Expression Studies ◽  
Metabolic Gene Expression ◽  
Gene Expression Studies

The aim of this study was to examine the time course activation of select myogenic (MRF4, Myf5, MyoD, myogenin) and metabolic (CD36, CPT1, HKII, and PDK4) genes after an acute bout of resistance (RE) or run (Run) exercise. Six RE subjects [25 ± 4 yr (mean ± SD), 74 ± 14 kg, 1.71 ± 0.11 m] and six Run subjects (25 ± 4 yr, 72 ± 5 kg, 1.81 ± 0.07 m, 63 ± 8 ml·kg−1·min−1) were studied. Eight muscle biopsies were taken from the vastus lateralis (RE) and gastrocnemius (Run) before, immediately after, and 1, 2, 4, 8, 12 and 24 h after exercise. RE increased mRNA of MRF4 (3.7- to 4.5-fold 2–4 h post), MyoD (5.8-fold 8 h post), myogenin (2.6- and 3.5-fold 8–12 h post), HKII (3.6- to 10.5-fold 2–12 h post), and PDK4 (14- to 26-fold 2–8 h post). There were no differences in Myf5, CD36, and CPT1 mRNA levels 0–24 h post-RE. Run increased mRNA of MyoD (5.0- to 8.0-fold), HKII (12- to 16-fold), and PDK4 (32- to 52-fold) at 8–12 h postexercise. There were no differences in MRF4, Myf5, myogenin, CD36 and CPT1 mRNA levels 0–24 h post-Run. These data indicate a myogenic and metabolic gene induction with RE and Run exercise. The timing of the gene induction is variable and generally peaks 4–8 h postexercise with all gene expression not significantly different from the preexercise levels by 24 h postexercise. These data provide basic information for the timing of human muscle biopsy samples for gene-expression studies involving exercise.

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