scholarly journals Potentiation of cGMP signaling increases oxygen delivery and oxidative metabolism in contracting skeletal muscle of older but not young humans

2015 ◽  
Vol 3 (8) ◽  
pp. e12508 ◽  
Author(s):  
Michael Nyberg ◽  
Peter Piil ◽  
Jon Egelund ◽  
Randy S. Sprague ◽  
Stefan P. Mortensen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Metabolism ◽  
Oxygen Delivery ◽  
Cgmp Signaling

scholarly journals Exercise training improves blood flow to contracting skeletal muscle of older men via enhanced cGMP signaling

2018 ◽  
Vol 124 (1) ◽  
pp. 109-117 ◽  
Author(s):  
Peter Piil ◽  
Tue Smith Jørgensen ◽  
Jon Egelund ◽  
Rasmus Damsgaard ◽  
Lasse Gliemann ◽  
...  
Keyword(s):  
Physical Activity ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Oxidative Metabolism ◽  
Muscle Blood Flow ◽  
Older Men ◽  
Skeletal Muscle Blood Flow ◽  
Cgmp Signaling

Physical activity has the potential to offset age-related impairments in the regulation of blood flow and O2 delivery to the exercising muscles; however, the mechanisms underlying this effect of physical activity remain poorly understood. The present study examined the role of cGMP in training-induced adaptations in the regulation of skeletal muscle blood flow and oxidative metabolism during exercise in aging humans. We measured leg hemodynamics and oxidative metabolism during exercise engaging the knee extensor muscles in young [ n = 15, 25 ± 1 (SE) yr] and older ( n = 15, 72 ± 1 yr) subjects before and after a period of aerobic high-intensity exercise training. To determine the role of cGMP signaling, pharmacological inhibition of phosphodiesterase 5 (PDE5) was performed. Before training, inhibition of PDE5 increased ( P < 0.05) skeletal muscle blood flow and O2 uptake during moderate-intensity exercise in the older group; however, these effects of PDE5 inhibition were not detected after training. These findings suggest a role for enhanced cGMP signaling in the training-induced improvement of regulation of blood flow in contracting skeletal muscle of older men. NEW & NOTEWORTHY The present study provides evidence for enhanced cyclic GMP signaling playing an essential role in the improved regulation of blood flow in contracting skeletal muscle of older men with aerobic exercise training.

Control of oxygen delivery within skeletal muscle

2005 ◽  
pp. 23-24
Author(s):  
Paul McDonough ◽  
Brad Behnke ◽  
Danielle Padilla ◽  
Timothy Musch ◽  
David Poole
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Delivery

METABOLIC RESPONSE TO MALE HORMONE AND THYROID ACTIVITY IN THE INDIAN GARDEN LIZARD, CALOTES VERSICOLOR

1974 ◽  
Vol 61 (2) ◽  
pp. 285-291 ◽  
Author(s):  
ASHA CHANDOLA ◽  
D. SURESH KUMAR ◽  
J. P. THAPLIYAL
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Metabolism ◽  
Environmental Temperature ◽  
Metabolic Response ◽  
Tissue Oxygen ◽  
Thyroid Activity ◽  
Physiological Importance ◽  
Calotes Versicolor ◽  
Isolated Liver ◽  
Male Hormone

SUMMARY Thyroidectomy and orchidectomy led to significant reduction in the oxidative metabolism of isolated liver and skeletal muscle tissue (at 30 °C) in Calotes versicolor. Thyroxine and male hormone were shown to increase this parameter in intact and orchidectomized lizards respectively. The effects of thyroidectomy and orchidectomy on tissue oxygen uptake were not additive. It is supposed that by its effect on oxidative metabolism male hormone may be of a greater physiological importance for reptiles than for other vertebrates. The present results show also that changes in environmental temperature can counteract the depressive effect of orchidectomy on the thyroid of this species of lizard.

scholarly journals The Transcriptional Corepressor RIP140 Regulates Oxidative Metabolism in Skeletal Muscle

2007 ◽  
Vol 6 (3) ◽  
pp. 236-245 ◽  
Author(s):  
Asha Seth ◽  
Jennifer H. Steel ◽  
Donna Nichol ◽  
Victoria Pocock ◽  
Mande K. Kumaran ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxidative Metabolism ◽  
Transcriptional Corepressor

HIF-1α in endurance training: suppression of oxidative metabolism

2007 ◽  
Vol 293 (5) ◽  
pp. R2059-R2069 ◽  
Author(s):  
Steven D. Mason ◽  
Helene Rundqvist ◽  
Ioanna Papandreou ◽  
Roger Duh ◽  
Wayne J. McNulty ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Oxidative Metabolism ◽  
Hypoxia Inducible Factor ◽  
Transcriptional Response ◽  
Oxidative Capacity ◽  
Pyruvate Dehydrogenase Kinase ◽  
Amp Activated Protein Kinase ◽  
Training Protocol

During endurance training, exercising skeletal muscle experiences severe and repetitive oxygen stress. The primary transcriptional response factor for acclimation to hypoxic stress is hypoxia-inducible factor-1α (HIF-1α), which upregulates glycolysis and angiogenesis in response to low levels of tissue oxygenation. To examine the role of HIF-1α in endurance training, we have created mice specifically lacking skeletal muscle HIF-1α and subjected them to an endurance training protocol. We found that only wild-type mice improve their oxidative capacity, as measured by the respiratory exchange ratio; surprisingly, we found that HIF-1α null mice have already upregulated this parameter without training. Furthermore, untrained HIF-1α null mice have an increased capillary to fiber ratio and elevated oxidative enzyme activities. These changes correlate with constitutively activated AMP-activated protein kinase in the HIF-1α null muscles. Additionally, HIF-1α null muscles have decreased expression of pyruvate dehydrogenase kinase I, a HIF-1α target that inhibits oxidative metabolism. These data demonstrate that removal of HIF-1α causes an adaptive response in skeletal muscle akin to endurance training and provides evidence for the suppression of mitochondrial biogenesis by HIF-1α in normal tissue.

Impaired oxygen delivery to muscle in chronic fatigue syndrome

1999 ◽  
Vol 97 (5) ◽  
pp. 603-608 ◽  
Author(s):  
Kevin K. MCCULLY ◽  
Benjamin H. NATELSON
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Time Constant ◽  
Oxidative Metabolism ◽  
Oxygen Delivery ◽  
Specific Effect ◽  
Chronic Fatigue ◽  
Medial Gastrocnemius ◽  
Resonance Spectroscopy ◽  
Activity Levels ◽  
Fatigue Syndrome

The purpose of this study was to determine if chronic fatigue syndrome (CFS) is associated with reduced oxygen delivery to muscles. Patients with CFS according to CDC (Center for Disease Control) criteria (n = 20) were compared with normal sedentary subjects (n = 12). Muscle oxygen delivery was measured as the rate of post-exercise and post-ischaemia oxygen-haem resaturation. Oxygen-haem resaturation was measured in the medial gastrocnemius muscle using continuous-wavelength near-IR spectroscopy. Phosphocreatine resynthesis was measured simultaneously using 31P magnetic resonance spectroscopy. The time constant of oxygen delivery was significantly reduced in CFS patients after exercise (46.5±16 s; mean±S.D.) compared with that in controls (29.4±6.9 s). The time constant of oxygen delivery was also reduced (20.0±12 s) compared with controls (12.0±2.8 s) after cuff ischaemia. Oxidative metabolism was also reduced by 20% in CFS patients, and a significant correlation was found between oxidative metabolism and recovery of oxygen delivery. In conclusion, oxygen delivery was reduced in CFS patients compared with that in sedentary controls. This result is consistent with previous studies showing abnormal autonomic control of blood flow. Reduced oxidative delivery in CFS patients could be specifically related to CFS, or could be a non-specific effect of reduced activity levels in these patients. While these results suggest that reduced oxygen delivery could result in reduced oxidative metabolism and muscle fatigue, further studies will be needed to address this issue.

scholarly journals Skeletal muscle action of estrogen receptor α is critical for the maintenance of mitochondrial function and metabolic homeostasis in females

2016 ◽  
Vol 8 (334) ◽  
pp. 334ra54-334ra54 ◽  
Author(s):  
Vicent Ribas ◽  
Brian G. Drew ◽  
Zhenqi Zhou ◽  
Jennifer Phun ◽  
Nareg Y. Kalajian ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Estrogen Receptor ◽  
Oxidative Metabolism ◽  
Mitochondrial Fission ◽  
Estrogen Receptor Α ◽  
Glucose Disposal ◽  
Mitochondrial Morphology ◽  
Metabolic Dysfunction ◽  
Mtdna Replication ◽  
Primary Tissue

Impaired estrogen receptor α (ERα) action promotes obesity and metabolic dysfunction in humans and mice; however, the mechanisms underlying these phenotypes remain unknown. Considering that skeletal muscle is a primary tissue responsible for glucose disposal and oxidative metabolism, we established that reduced ERα expression in muscle is associated with glucose intolerance and adiposity in women and female mice. To test this relationship, we generated muscle-specific ERα knockout (MERKO) mice. Impaired glucose homeostasis and increased adiposity were paralleled by diminished muscle oxidative metabolism and bioactive lipid accumulation in MERKO mice. Aberrant mitochondrial morphology, overproduction of reactive oxygen species, and impairment in basal and stress-induced mitochondrial fission dynamics, driven by imbalanced protein kinase A–regulator of calcineurin 1–calcineurin signaling through dynamin-related protein 1, tracked with reduced oxidative metabolism in MERKO muscle. Although muscle mitochondrial DNA (mtDNA) abundance was similar between the genotypes, ERα deficiency diminished mtDNA turnover by a balanced reduction in mtDNA replication and degradation. Our findings indicate the retention of dysfunctional mitochondria in MERKO muscle and implicate ERα in the preservation of mitochondrial health and insulin sensitivity as a defense against metabolic disease in women.

Reduced high-energy phosphate levels in rat hearts. I. Effects of alloxan diabetes

1976 ◽  
Vol 230 (6) ◽  
pp. 1744-1750 ◽  
Author(s):  
TB Allison ◽  
SP Bruttig ◽  
Crass MF ◽  
RS Eliot ◽  
JC Shipp
Keyword(s):  
Oxidative Metabolism ◽  
Oxygen Delivery ◽  
Rat Heart ◽  
High Energy ◽  
Diabetic Rat ◽  
High Energy Phosphate ◽  
Atp Production ◽  
Rat Hearts

Significant alterations in heart carbohydrate and lipid metabolism are present 48 h after intravenous injection of alloxan (60 mg/kg) in rats. It has been suggested that uncoupling of oxidative phosphorylation occurs in the alloxanized rat heart in vivo, whereas normal oxidative metabolism has been demonstrated in alloxan-diabetic rat hearts perfused in vitro under conditions of adequate oxygen delivery. We examined the hypothesis that high-energy phosphate metabolism might be adversely affected in the alloxan-diabetic rat heart in vivo. Phosphocreatine and ATP were reduced by 58 and 45%, respectively (P is less than 0.001). Also, oxygen-dissociation curves were shifted to the left by 4 mmHg, and the rate of oxygen release from blood was reduced by 21% (P is less than 0.01). Insulin administration normalized heart high-energy phosphate compounds. ATP production was accelerated in diabetic hearts perfused in vitro with a well-oxygenated buffer. These studies support the hypothesis that oxidative ATP production in the alloxan-diabetic rat heart is reduced and suggest that decreased oxygen delivery may have a regulatory role in the oxidative metabolism of the diabetic rat heart.

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