glycogen and Pain

In Delayed Onset Muscle Soreness (DOMS), muscles become sore 24 to 48 hours after eccentric and unaccustomed activity. Fiber stiffness, due to decreased muscle glycogen, may predispose muscle to greater damage during eccentric exercise. This study sought to determine if inadequate carbohydrate intake following a protocol to decrease muscle glycogen would increase DOMS after 15 min of downhill running. Thirty-three male subjects (age, 18-35 years) were randomized into 3 groups for testing over a 7-day period. The depletion (DEP) group (n= 12) underwent a glycogen depletion protocol prior to a 15-min downhill run designed to induce DOMS. The repletion (FED) group (n = 10) underwent a glycogen depletion protocol followed by a carbohydrate repletion protocol (>80% CHO) prior to downhill running. The third (ECC) group (n = 11) performed only the downhill running protocol. Subjective muscle soreness, isometric force production, relaxed knee angle, and thigh circumference were measured pretreatment and on days 1, 2, 3, 4, and 6 post treatment. Subjective muscle soreness for all groups increased from 0 cm pretreatment to 3.05 +/- 0.72 cm (on a 10-cm scale) on day 1 post treatment (p<.05). All groups were significantly different from baseline measurements until day 4 post treatment. Each group experienced a decline in isometric force from 281 +/- 45 N pre- to 253 +/- 13 N on day 1 post treatment (p <.05). The decrease in isometric force persisted in all groups for 4 days post treatment. Increases in thigh circumference and relaxed knee angle elevations in all 3 groups were statistically different (p <.05) from pretreatment until day 4. No differences were noted between groups for any of the parameters examined. In the current study, 15 min of downhill running is sufficient to cause DOMS with the associated functional and morphological changes; however, inadequate carbohydrate intake after a glycogen depleting exercise does not appear to exacerbate DOMS and the associated symptoms.

Topics: Adolescent; Adult; Dietary Carbohydrates; Exercise Test; Glycogen; Humans; Male; Muscle Contraction; Muscle, Skeletal; Pain; Physical Exertion; Running

To examine metabolism during exercise in 2 patients with muscle phosphorylase kinase (PHK) deficiency and to further define the phenotype of this rare glycogen storage disease (GSD).. Patient 1 (39 years old) had mild exercise-induced forearm pain, and EMG showed a myopathic pattern. Patient 2 (69 years old) had raised levels of creatine kinase (CK) for more than 6 months after statin treatment. Both patients had increased glycogen levels in muscle and PHK activity <11% of normal. Two novel pathogenic nonsense mutations were found in the PHKA1 gene. The metabolic response to anaerobic forearm exercise and aerobic cycle exercise was studied in the patients and 5 healthy subjects.. Ischemic exercise showed a normal 5-fold increase in plasma lactate (peak 5.7 and 6.9 mmol/L) but an exaggerated 5-fold increase in ammonia (peak 197 and 171 μmol/L; control peak range 60-113 μmol/L). An incremental exercise test to exhaustion revealed a blunted lactate response (5.4 and 4.8 mmol/L) vs that for control subjects (9.6 mmol/L; range 7.1-14.3 mmol/L). Fat and carbohydrate oxidation rates at 70% of peak oxygen consumption were normal. None of the patients developed a second wind phenomenon or improved their work capacity with an IV glucose infusion.. Our findings demonstrate that muscle PHK deficiency may present as an almost asymptomatic condition, despite a mild impairment of muscle glycogenolysis, raised CK levels, and glycogen accumulation in muscle. The relative preservation of glycogenolysis is probably explained by an alternative activation of myophosphorylase by AMP and P(i) at high exercise intensities.

Topics: Adult; Aged; Ammonia; Biopsy; Carbohydrate Metabolism; Creatine Kinase; Exercise; Exercise Test; Forearm; Genetic Variation; Glycogen; Glycogen Storage Disease; Glycogen Storage Disease Type V; Glycogenolysis; Humans; Ischemia; Lactates; Lipid Metabolism; Male; Muscle, Skeletal; Oxygen Consumption; Pain; Phenotype; Phosphorylase Kinase; Regional Blood Flow

The purpose of this study was to describe the effect of muscle damage and delayed-onset muscle soreness (DOMS) on the metabolic response during a subsequent period of prolonged concentric exercise (120 min, approximately 61% V(.)O(2max), on a cycle ergometer), with ingestion of 3 g of (13)C-glucose/kg body mass. We hypothesized that the oxidation of plasma and exogenous glucose would be reduced, while the oxidation of glucose arising from muscle glycogen would be increased. Six male subjects were studied during exercise in a control situation and 2 days following downhill running, at a time when plasma creatine kinase (CK) activity was increased, and DOMS was present. Carbohydrate and lipid oxidation were computed from indirect respiratory calorimetry corrected for protein oxidation, while the oxidation of plasma glucose and muscle glycogen were computed from V(.)(13)CO(2) and the ratio of (13)C/(12)C in the plasma glucose. All data were presented as the mean and the standard error of the mean. The oxidation of protein (approximately 6% energy yield, in the control and the experimental trial), lipid (approximately 15 and approximately 18%), and carbohydrate (approximately 79 and approximately 76%), as well as that of plasma glucose (approximately 41 and approximately 46%), glucose from the liver (approximately 12 and approximately 14%), and glucose from muscle glycogen (approximately 38 and approximately 31%) were not significantly different between the control and experimental (DOMS) trials. The response of the plasma glucose, insulin, lactate, and free fatty acid concentrations was not modified by the previous eccentric exercise. These results indicate that the metabolic response to prolonged concentric exercise is not modified by muscle damage and DOMS resulting from a bout of eccentric exercise performed 2 days before.

Topics: Adult; Bicycling; Carbohydrate Metabolism; Carbon Isotopes; Glucose; Glycogen; Humans; Male; Muscle, Skeletal; Oxidation-Reduction; Oxygen Consumption; Pain; Physical Endurance; Proteins; Running

Macrophages secrete a variety of chemical mediators that play a central role in the pathophysiology of inflammatory pain. Therefore, the activation or deactivation of these cells in an inflammatory focus could modulate the intensity of the algogenic response. Based on these premises and on our previous demonstration that the calcium-binding protein MRP-14, highly expressed in neutrophils, deactivates activated macrophages in vitro, we decided to investigate the role of MRP-14 and of neutrophils in the control of inflammatory pain in mice. Our results show that this protein is endowed with antinociceptive activity. When tested in the writhing model it was able to inhibit pain response but did not change the behavior of the animals in the hot plate test. This observation indicates that MRP-14 down-regulates inflammatory but not central pain. Using a model of acute neutrophilic peritonitis induced by glycogen, a close correlation between neutrophil migration and antinociception was detected. Surgical adrenalectomy demonstrated that the antinociceptive response induced by glycogen was not due to endogenous liberation of glucocorticoids. The treatment of animals either with a monoclonal antibody anti-MRP-14 or a monoclonal antibody that depletes the animals of neutrophils reverts the antinociceptive response observed in the glycogen-induced peritonitis. These data define the calcium-binding protein MRP-14 as a novel mediator for the control of inflammatory pain and consequently discloses an anti-inflammatory role for the neutrophil.

Topics: Abdomen; Adrenalectomy; Animals; Antibodies, Monoclonal; Antigens, Differentiation; Behavior, Animal; Calcium-Binding Proteins; Calgranulin A; Calgranulin B; Cell Movement; Glycogen; Hot Temperature; Irritants; Macrophages; Male; Mice; Neutrophils; Nociceptors; Pain; Peritonitis

We report a family with McArdle's disease with several affected individuals in two generations. This unusual pedigree for an autosomal recessive disease is explained by the existence of manifesting heterozygotes in the maternal line. The presence of symptoms in heterozygotes seems to be due to a decrease in myophosphorylase activity below a critical threshold, ranging between 30% and 45% of normal mean value. The occurrence of several manifesting heterozygotes in the maternal line only can be explained by compound heterozygosity of a defective allele and a pseudodeficient allele for myophosphorylase, or by a genetic factor which regulates the phenotypic expression of the gene.

Topics: Adolescent; Adult; Densitometry; Electrophoresis, Polyacrylamide Gel; Female; Glycogen; Glycogen Storage Disease Type V; Heterozygote; Humans; Italy; Male; Muscles; Muscular Diseases; Pain; Phenotype; Phosphorylase a

The symptoms of a myopathy permanently affecting limb girdle muscles are reported in a 31-year-old woman who has been presenting an exertional muscle pain syndrome with myoglobinuria for 20 years. Investigations revealed a slightly decreased utilization of glycogen in muscle, while its storage affected only rare type 2 fibers. Active phosphorylase was undetectable and phosphorylase b kinase activity was clearly decreased in muscle cells, but normal in erythocytes, lymphocytes and cultured fibroblasts.

Topics: Adult; Atrophy; Female; Glycogen; Glycogen Storage Disease; Glycolysis; Humans; Microscopy, Electron; Muscles; Muscular Diseases; Pain; Phosphorylase b; Phosphorylase Kinase; Physical Exertion; Syndrome

Marked disorders of energy metabolism in the heart muscle simultaneously with the development of ulcerous lesions of the stomach were revealed in animals which had suffered an emotional-pain stress (EPS). These disorders are displayed in the fact that two hours after EPS, the glycogen reserve in the animal's myocardium diminishes, resynthesis of glycogen and oxidation of the main substrates of the tricarboxylic acid cycle are inhibited, and malate dehydrogenase and possibly other dehydrogenase systems of the mitochondria are partly inactivated. Such decrease in the activity of the metabolic tracts is attended by depression of the force and rate of cardiac contractions revealed on inducing a high rate of contractions. The preliminary administration of sodium gammaoxybutyrate to a considerable extent prevents all the changes in the animal's myocardium occurring due to the effect of EPS.

Topics: Animals; Citric Acid Cycle; Energy Metabolism; Enzyme Activation; Female; gamma-Aminobutyric Acid; Glycogen; Humans; Hydroxybutyrates; Myocardium; Oxidation-Reduction; Pain; Rats; Sodium Oxybate; Stress, Psychological

A 43-year-old male developed abdominal pain and jaundice after the administration of erythromycin estolate. The diagnosis was strongly suspected on clinical grounds, but ultimate confirmation depends upon the demonstration of biochemical and morphological alterations after challenge with the drug.

Topics: Abdomen; Acute Disease; Adult; Bile Ducts; Biopsy, Needle; Endoplasmic Reticulum; Erythromycin; Erythromycin Estolate; Glycogen; Humans; Jaundice; Liver; Liver Function Tests; Male; Microscopy, Electron; Microscopy, Fluorescence; Pain; Pharyngitis; Recurrence

Topics: Astigmatism; Contact Lenses; Cornea; Corneal Dystrophies, Hereditary; Corneal Transplantation; Cysts; Epithelium; Glycogen; Humans; Microscopy, Electron; Ophthalmoscopy; Pain; Visual Acuity

Topics: Blood; Child; Electromyography; Epinephrine; Fructose; Genetics, Medical; Glucose; Glycogen; Glycogen Storage Disease Type V; Histocytochemistry; Humans; Lactates; Muscular Diseases; Pain; Pathology; Phosphotransferases; Physical Exertion; Pyruvates

Topics: Glycogen; Glycogenolysis; Muscles; Musculoskeletal Physiological Phenomena; Pain