scholarly journals Acute melatonin administration improves exercise tolerance and the metabolic recovery after exhaustive effort

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vinícius Silva Faria ◽  
Taciane Maria Melges Pejon ◽  
Claudio Alexandre Gobatto ◽  
Gustavo Gomes de Araujo ◽  
Anabelle Silva Cornachione ◽  
...  
Keyword(s):  
Exercise Tolerance ◽  
Skeletal Muscles ◽  
Glycogen Content ◽  
Substrate Availability ◽  
Maximal Aerobic Capacity ◽  
Incremental Test ◽  
Energy Substrates ◽  
Metabolic Recovery ◽  
Melatonin Administration ◽  
Muscle Energy

AbstractThe present study investigated the effects of acute melatonin administration on the biomarkers of energy substrates, GLUT4, and FAT/CD36 of skeletal muscle and its performance in rats subjected to exhaustive swimming exercise at an intensity corresponding to the maximal aerobic capacity (tlim). The incremental test was performed to individually determine the exercise intensity prescription and 48 h after, the animals received melatonin (10 mg·kg−1) or vehicles 30 min prior to tlim. Afterwards, the animals were euthanized 1 or 3 h after the exhaustion for blood and muscles storage. The experiment 1 found that melatonin increased the content of glycogen and GLUT4 in skeletal muscles of the animals that were euthanized 1 (p < 0.05; 22.33% and 41.87%) and 3 h (p < 0.05; 37.62% and 57.87%) after the last procedures. In experiment 2, melatonin enhanced the tlim (p = 0.01; 49.42%), the glycogen content (p < 0.05; 40.03%), GLUT4 and FAT/CD36 in exercised skeletal muscles (F = 26.83 and F = 25.28, p < 0.01). In summary, melatonin increased energy substrate availability prior to exercise, improved the exercise tolerance, and accelerated the recovery of muscle energy substrates after the tlim, possibly through GLUT4 and FAT/CD36.

scholarly journals Effects of Individualized Treadmill Endurance Training on Oxidative Stress in Skeletal Muscles of Transgenic Sickle Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Etienne Gouraud ◽  
Emmanuelle Charrin ◽  
John J. Dubé ◽  
Solomon F. Ofori-Acquah ◽  
Cyril Martin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endurance Training ◽  
Skeletal Muscles ◽  
Citrate Synthase ◽  
Antioxidant Response ◽  
Oxygen Species ◽  
Cell Disease ◽  
Incremental Test ◽  
Stress Markers ◽  
Maximal Aerobic Speed

Oxidative stress is a key feature in the pathophysiology of sickle cell disease. Endurance training has been shown to reduce oxidative stress in the heart and the liver of sickle mice. However, the effects of endurance training on skeletal muscles, which are major producers of reactive oxygen species during exercise, are currently unknown. The aim of this study was to evaluate the effect of sickle genotype on prooxidant/antioxidant response to individualized endurance training in skeletal muscles of sickle mice. Healthy and homozygous Townes sickle mice were divided into trained or sedentary groups. Maximal aerobic speed and V̇O2 peak were determined using an incremental test on a treadmill. Trained mice ran at 40% to 60% of maximal aerobic speed, 1 h/day, 5 days/week for 8 weeks. Oxidative stress markers, prooxidant/antioxidant response, and citrate synthase enzyme activities were assessed in the gastrocnemius, in the plantaris, and in the soleus muscles. Maximal aerobic speed and V̇O2 peak were significantly reduced in sickle compared to healthy mice (-57% and -17%; p<0.001). NADPH oxidase, superoxide dismutase, and catalase activities significantly increased after training in the gastrocnemius of sickle mice only. A similar trend was observed for citrate synthase activity in sickle mice (p=0.06). In this study, we showed an adaptive response to individualized endurance training on the prooxidant/antioxidant balance in the gastrocnemius, but neither in the plantaris nor in the soleus of trained sickle mice, suggesting an effect of sickle genotype on skeletal muscle response to endurance treadmill training.

scholarly journals Exposure to cigarette smoke induces overexpression of von Hippel-Lindau tumor suppressor in mouse skeletal muscle

2012 ◽  
Vol 303 (6) ◽  
pp. L519-L527 ◽  
Author(s):  
Vladimir T. Basic ◽  
Elsa Tadele ◽  
Ali Ateia Elmabsout ◽  
Hongwei Yao ◽  
Irfan Rahman ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Tumor Suppressor ◽  
Cigarette Smoke ◽  
Muscle Fiber ◽  
Exercise Tolerance ◽  
Skeletal Muscles ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Cross Sectional ◽  
Von Hippel Lindau

Cigarette smoke (CS) is a well-established risk factor in the development of chronic obstructive pulmonary disease (COPD). In contrast, the extent to which CS exposure contributes to the development of the systemic manifestations of COPD, such as skeletal muscle dysfunction and wasting, remains largely unknown. Decreased skeletal muscle capillarization has been previously reported in early stages of COPD and might play an important role in the development of COPD-associated skeletal muscle abnormalities. To investigate the effects of chronic CS exposure on skeletal muscle capillarization and exercise tolerance, a mouse model of CS exposure was used. The 129/SvJ mice were exposed to CS for 6 mo, and the expression of putative elements of the hypoxia-angiogenic signaling cascade as well as muscle capillarization were studied. Additionally, functional tests assessing exercise tolerance/endurance were performed in mice. Compared with controls, skeletal muscles from CS-exposed mice exhibited significantly enhanced expression of von Hippel-Lindau tumor suppressor (VHL), ubiquitin-conjugating enzyme E2D1 (UBE2D1), and prolyl hydroxylase-2 (PHD2). In contrast, hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) expression was reduced. Furthermore, reduced muscle fiber cross-sectional area, decreased skeletal muscle capillarization, and reduced exercise tolerance were also observed in CS-exposed animals. Taken together, the current results provide evidence linking chronic CS exposure and induction of VHL expression in skeletal muscles leading toward impaired hypoxia-angiogenesis signal transduction, reduced muscle fiber cross-sectional area, and decreased exercise tolerance.

scholarly journals Musclin is an activity-stimulated myokine that enhances physical endurance

2015 ◽  
Vol 112 (52) ◽  
pp. 16042-16047 ◽  
Author(s):  
Ekaterina Subbotina ◽  
Ana Sierra ◽  
Zhiyong Zhu ◽  
Zhan Gao ◽  
Siva Rama Krishna Koganti ◽  
...  
Keyword(s):  
Exercise Capacity ◽  
Exercise Tolerance ◽  
Skeletal Muscles ◽  
Molecular Mechanisms ◽  
Mitochondrial Protein ◽  
Guanosine Monophosphate ◽  
Physical Endurance ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor

Exercise remains the most effective way to promote physical and metabolic wellbeing, but molecular mechanisms underlying exercise tolerance and its plasticity are only partially understood. In this study we identify musclin—a peptide with high homology to natriuretic peptides (NP)—as an exercise-responsive myokine that acts to enhance exercise capacity in mice. We use human primary myoblast culture and in vivo murine models to establish that the activity-related production of musclin is driven by Ca2+-dependent activation of Akt1 and the release of musclin-encoding gene (Ostn) transcription from forkhead box O1 transcription factor inhibition. Disruption of Ostn and elimination of musclin secretion in mice results in reduced exercise tolerance that can be rescued by treatment with recombinant musclin. Reduced exercise capacity in mice with disrupted musclin signaling is associated with a trend toward lower levels of plasma atrial NP (ANP) and significantly smaller levels of cyclic guanosine monophosphate (cGMP) and peroxisome proliferator-activated receptor gamma coactivator 1-α in skeletal muscles after exposure to exercise. Furthermore, in agreement with the established musclin ability to interact with NP clearance receptors, but not with NP guanyl cyclase-coupled signaling receptors, we demonstrate that musclin enhances cGMP production in cultured myoblasts only when applied together with ANP. Elimination of the activity-related musclin-dependent boost of ANP/cGMP signaling results in significantly lower maximum aerobic capacity, mitochondrial protein content, respiratory complex protein expression, and succinate dehydrogenase activity in skeletal muscles. Together, these data indicate that musclin enhances physical endurance by promoting mitochondrial biogenesis.

Calf Muscle Metabolism in Venous Insufficiency

1993 ◽  
Vol 8 (2) ◽  
pp. 58-61
Author(s):  
L. J. Hands ◽  
G. J. Kemp ◽  
A. Zukowski ◽  
A. N. Nicolaides ◽  
G. K. Radda
Keyword(s):  
Venous Insufficiency ◽  
Muscle Metabolism ◽  
Calf Muscle ◽  
Resonance Spectroscopy ◽  
Metabolic Recovery ◽  
Glycolytic Activity ◽  
Muscle Energy ◽  
Muscle Energy Metabolism ◽  
Phosphorus Metabolites

Objectives: To study the effect of deep venous insufficiency on calf muscle energy metabolism. Design: A paired study of affected and unaffected calf muscle in seven patients with unilateral lower limb deep venous insufficiency. Investigations: Phosphorus-31 magnetic resonance spectroscopy was used to study changes in vivo in pH, phosphocreatine and other phosphorus metabolites during and after exercise. Results: Glycolytic activity was increased in the affected muscle at the start of exercise but metabolic recovery following exercise was normal. Conclusions: Oxidative phosphorylation is impaired, at least at the start of exercise, but appears normal immediately after exercise. This may be due to inadequate blood flow, perhaps secondary to the rise in intramuscular pressure that occurs with exercise.

scholarly journals Physical Activity-Dependent Regulation of Parathyroid Hormone and Calcium-Phosphorous Metabolism

2020 ◽  
Vol 21 (15) ◽  
pp. 5388 ◽  
Author(s):  
Giovanni Lombardi ◽  
Ewa Ziemann ◽  
Giuseppe Banfi ◽  
Sabrina Corbetta
Keyword(s):  
Parathyroid Hormone ◽  
Skeletal Muscles ◽  
Mineral Metabolism ◽  
The Body ◽  
Phosphate Homeostasis ◽  
Energy Substrates ◽  
Physiological Conditions ◽  
Exercise Induced ◽  
Activity Dependent ◽  
Circulating Levels

Exercise perturbs homeostasis, alters the levels of circulating mediators and hormones, and increases the demand by skeletal muscles and other vital organs for energy substrates. Exercise also affects bone and mineral metabolism, particularly calcium and phosphate, both of which are essential for muscle contraction, neuromuscular signaling, biosynthesis of adenosine triphosphate (ATP), and other energy substrates. Parathyroid hormone (PTH) is involved in the regulation of calcium and phosphate homeostasis. Understanding the effects of exercise on PTH secretion is fundamental for appreciating how the body adapts to exercise. Altered PTH metabolism underlies hyperparathyroidism and hypoparathyroidism, the complications of which affect the organs involved in calcium and phosphorous metabolism (bone and kidney) and other body systems as well. Exercise affects PTH expression and secretion by altering the circulating levels of calcium and phosphate. In turn, PTH responds directly to exercise and exercise-induced myokines. Here, we review the main concepts of the regulation of PTH expression and secretion under physiological conditions, in acute and chronic exercise, and in relation to PTH-related disorders.

Glycogen content and contraction regulate glycogen synthase phosphorylation and affinity for UDP-glucose in rat skeletal muscles

2007 ◽  
Vol 293 (6) ◽  
pp. E1622-E1629 ◽  
Author(s):  
Yu-Chiang Lai ◽  
Jorid Thrane Stuenæs ◽  
Chia-Hua Kuo ◽  
Jørgen Jensen
Keyword(s):  
Skeletal Muscles ◽  
Glycogen Content ◽  
Glycogen Synthase ◽  
Dry Weight ◽  
Kinetic Properties ◽  
Glycogen Accumulation ◽  
Specific Antibodies ◽  
Phosphorylation Pattern ◽  
Gsk 3Β

Glycogen content and contraction strongly regulate glycogen synthase (GS) activity, and the aim of the present study was to explore their effects and interaction on GS phosphorylation and kinetic properties. Glycogen content in rat epitrochlearis muscles was manipulated in vivo. After manipulation, incubated muscles with normal glycogen [NG; 210.9 ± 7.1 mmol/kg dry weight (dw)], low glycogen (LG; 108.1 ± 4.5 mmol/ kg dw), and high glycogen (HG; 482.7 ± 42.1 mmol/kg dw) were contracted or rested before the studies of GS kinetic properties and GS phosphorylation (using phospho-specific antibodies). LG decreased and HG increased GS Km for UDP-glucose (LG: 0.27 ± 0.02 < NG: 0.71 ± 0.06 < HG: 1.11 ± 0.12 mM; P < 0.001). In addition, GS fractional activity inversely correlated with glycogen content ( R = −0.70; P < 0.001; n = 44). Contraction decreased Km for UDP-glucose (LG: 0.14 ± 0.01 = NG: 0.16 ± 0.01 < HG: 0.33 ± 0.03 mM; P < 0.001) and increased GS fractional activity, and these effects were observed independently of glycogen content. In rested muscles, GS Ser641 and Ser7 phosphorylation was decreased in LG and increased in HG compared with NG. GSK-3β Ser9 and AMPKα Thr172 phosphorylation was not modulated by glycogen content in rested muscles. Contraction decreased phosphorylation of GS Ser641 at all glycogen contents. However, contraction increased GS Ser7 phosphorylation even though GS was strongly activated. In conclusion, glycogen content regulates GS affinity for UDP-glucose and low affinity for UDP-glucose in muscles with high glycogen content may reduce glycogen accumulation. Contraction increases GS affinity for UDP-glucose independently of glycogen content and creates a unique phosphorylation pattern.

scholarly journals The fate of the sugar disappearing under the action of insulin

1926 ◽  
Vol 100 (700) ◽  
pp. 32-54 ◽  
Keyword(s):  
Guinea Pigs ◽  
Skeletal Muscles ◽  
Glycogen Content ◽  
Normal Animal ◽  
Liver Glycogen ◽  
Diabetic Animal ◽  
Significant Difference ◽  
Long Time ◽  
Series Of Experiments ◽  
High Level

The apparent disappearance of sugar injected into normal animals has for a long time puzzled physiological investigators (Bang, Meltzer and Kleiner, Palmer, Woodyatt). When insulin was discovered it was apparent that an agent was available by which the normal processes could be exaggerated, and therefore more easily studied. It was soon shown that the administration of sugar and insulin to the diabetic animal resulted in an increased combustion of carbohydrate and the accumulation of glycogen in the depôts. When, however, attempts were made to trace the fate of the sugar which disappears from the blood of the normal animal under the influence of an injection of insulin, difficulties were encountered. McCormick and Macleod (1) studied the effect of insulin on the glycogen reserves of rabbits which had been starved and treated with epinephrin. In some of the experiments glucose was administered subcutaneously during the period of action of insulin. No significant difference between the glycogen content of the muscles of the control animals and of those which received insulin was observed. The glycogen of the livers of the insulin-treated animals was slightly less than that of the control animals. Macleod (2) concluded from these experiments “that less glycogen is deposited both in the muscles and the liver when insulin is given along with sugar to previously starved animals than when the same amounts of sugar are given alone.” In the experiments of Dudley and Marrian (3), in which the effect of insulin on the liver glycogen of mice was studied, a much smaller amount of glycogen was found in the livers of the animals which received insulin than in those which served for controls. In another series of experiments in which insulin was administered to rabbits which had been previously fed on a carbohydrate rich diet, the glycogen content of the liver and skeletal muscles of the insulin-treated animals was again much less than that of the control animals. In both series of experiments the animals were killed after convulsions had supervened. The experiments of Babkin (4) are similar to those of McCormick and Macleod. In some of his experiments Babkin kept the blood sugar of the rabbits at a high level by the administration of sugar. He found no increase in glycogen after insulin. Kuhn and Baur (5), in a study of the effect of insulin on the glycogen content of the skeletal muscles of rabbits and guinea-pigs, found that, after insulin convulsions, the glycogen had practically disappeared from the muscles of these animals. They are undecided as to whether the depletion of glycogen is a primary effect of insulin or is to be attributed to the convulsions.

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