glycogen and Hypertrophy

The astrocyte subtypes in moderate and severe human brain trauma complicated with subdural hematoma or hygroma are described. Clear and dense edematous and hypertrophic reactive astrocytes are distinguished in severe vasogenic brain edema. Swollen perineuronal astrocytes appear compressing and indenting dark, degenerated pyramidal and nonpyramidal nerve cells. Glycogen-depleted and glycogen-rich astrocytes also are seen. Reactive hypertrophic astrocytes exhibit increased amounts of dilated smooth and rough endoplasmic reticulum, microtubules, and gliofilaments. Perisynaptic astrocyte ensheathments of neuropil synaptic contacts are lost, and the perivascular astrocyte end-feet appear dissociated from the capillary basement membrane. The interastrocytary gap junctions appear fragmented.

Topics: Astrocytes; Brain Edema; Cell Size; Cerebral Cortex; Glycogen; Hematoma, Subdural; Humans; Hypertrophy; Microscopy, Electron; Phagocytosis; Severity of Illness Index; Subdural Effusion

Interleukin 6 (IL-6) has received significant attention for its regulatory role in muscle wasting during cachexia. This review examines the role of circulating IL-6 for decreasing muscle mass during cancer and emphasizes some of the indirect actions of IL-6 that may cause muscle wasting.

Topics: Cachexia; Exercise; Glycogen; Humans; Hypertrophy; Inflammation; Interleukin-6; Muscle, Skeletal; Neoplasms; Risk Factors; Signal Transduction

AMP-activated protein kinase (AMPK) is becoming recognized as a critical regulator of energy metabolism in cells. Using a mouse model in which we specifically blocked AMPK activity in muscles, we have demonstrated that activation of AMPK is necessary for the effects of 5-aminoimidazole-4-carboxamide riboside ('AICAR') and hypoxia, and is possibly required for a portion of exercise-induced glucose uptake. These same mice could not maintain sufficient glycogen in their skeletal muscle and it was rapidly depleted when the animals were subjected to mild exercise. Using isolated strips, we observed muscle hypertrophy and increased tiredness in the AMPK-deficient muscle. We also performed microarray analysis and showed dramatic changes of transcription profile in muscles of the lazy mice. These could have a significant impact on muscle function and may contribute to the observed phenotype.

Topics: Aminoimidazole Carboxamide; AMP-Activated Protein Kinases; Animals; Enzyme Inhibitors; Glycogen; Glycogen Synthase; Hypertrophy; Hypoxia; Mice; Multienzyme Complexes; Muscle, Skeletal; Mutation; Phenotype; Physical Conditioning, Animal; Protein Serine-Threonine Kinases; Ribonucleotides; Time Factors; Transcription, Genetic

Concurrent strength and endurance training appears to inhibit strength development when compared with strength training alone. Our understanding of the nature of this inhibition and the mechanisms responsible for it is limited at present. This is due to the difficulties associated with comparing results of studies which differ markedly in a number of design factors, including the mode, frequency, duration and intensity of training, training history of participants, scheduling of training sessions and dependent variable selection. Despite these difficulties, both chronic and acute hypotheses have been proposed to explain the phenomenon of strength inhibition during concurrent training. The chronic hypothesis contends that skeletal muscle cannot adapt metabolically or morphologically to both strength and endurance training simultaneously. This is because many adaptations at the muscle level observed in response to strength training are different from those observed after endurance training. The observation that changes in muscle fibre type and size after concurrent training are different from those observed after strength training provide some support for the chronic hypothesis. The acute hypothesis contends that residual fatigue from the endurance component of concurrent training compromises the ability to develop tension during the strength element of concurrent training. It is proposed that repeated acute reductions in the quality of strength training sessions then lead to a reduction in strength development over time. Peripheral fatigue factors such as muscle damage and glycogen depletion have been implicated as possible fatigue mechanisms associated with the acute hypothesis. Further systematic research is necessary to quantify the inhibitory effects of concurrent training on strength development and to identify different training approaches that may overcome any negative effects of concurrent training.

Topics: Adaptation, Physiological; Glycogen; Humans; Hypertrophy; Muscle Fibers, Skeletal; Muscle, Skeletal; Physical Endurance; Recruitment, Neurophysiological

Skeletal muscle tissue is sensitive to the acute and chronic stresses associated with resistance training. These responses are influenced by the structure of resistance activity (i.e. frequency, load and recovery) as well as the training history of the individuals involved. There are histochemical and biochemical data which suggest that resistance training alters the expression of myosin heavy chains (MHCs). Specifically, chronic exposure to bodybuilding and power lifting type activity produces shifts towards the MHC I and IIb isoforms, respectively. However, it is not yet clear which training parameters trigger these differential expressions of MHC isoforms. Interestingly, many programmes undertaken by athletes appear to cause a shift towards the MHC I isoform. Increments in the cross-sectional area of muscle after resistance training can be primarily attributed to fibre hypertrophy. However, there may be an upper limit to this hypertrophy. Furthermore, significant fibre hypertrophy appears to follow the sequence of fast twitch fibre hypertrophy preceding slow twitch fibre hypertrophy. Whilst some indirect measures of fibre number in living humans suggest that there is no interindividual variation, postmortem evidence suggests that there is. There are also animal data arising from investigations using resistance training protocols which suggest that chronic exercise can increase fibre number. Furthermore, satellite cell activity has been linked to myotube formation in the human. However, other animal models (i.e. compensatory hypertrophy) do not support the notion of fibre hyperplasia. Even if hyperplasia does occur, its effect on the cross-sectional area of muscle appears to be small. Phosphagen and glycogen metabolism, whilst important during resistance activity appear not to normally limit the performance of resistance activity. Phosphagen and related enzyme adaptations are affected by the type, structure and duration of resistance training. Whilst endogenous glycogen reserves may be increased with prolonged training, typical isotonic training for less than 6 months does not seem to increase glycolytic enzyme activity. Lipid metabolism may be of some significance in bodybuilding type activity. Thus, not surprisingly, oxidative enzyme adaptations appear to be affected by the structure and perhaps the modality of resistance training. The dilution of mitochondrial volume and endogenous lipid densities appears mainly because of fibre hypertrophy.

Topics: Exercise; Glycogen; Humans; Hypertrophy; Lipid Metabolism; Muscles; Myosins; Phosphocreatine; Weight Lifting

Topics: Adrenal Insufficiency; Animals; Biomechanical Phenomena; Blood Pressure; Calcium; Cardiac Glycosides; Cardiomegaly; Citric Acid Cycle; Cyclic AMP; Fatty Acids; Glycogen; Glycolysis; Heart; Hemodynamics; Homeostasis; Humans; Hypertrophy; In Vitro Techniques; Intercellular Junctions; Mitochondria, Muscle; Muscle Contraction; Myocardium; NAD; Phosphofructokinase-1; RNA; Ventricular Function

Some studies report greater muscle hypertrophy during resistance exercise (RE) training from supplement timing (i.e., the strategic consumption of protein and carbohydrate before and/or after each workout). However, no studies have examined whether this strategy provides greater muscle hypertrophy or strength development compared with supplementation at other times during the day. The purpose of this study was to examine the effects of supplement timing compared with supplementation in the hours not close to the workout on muscle-fiber hypertrophy, strength, and body composition during a 10-wk RE program.. In a single-blind, randomized protocol, resistance-trained males were matched for strength and placed into one of two groups; the PRE-POST group consumed a supplement (1 g x kg(-1) body weight) containing protein/creatine/glucose immediately before and after RE. The MOR-EVE group consumed the same dose of the same supplement in the morning and late evening. All assessments were completed the week before and after 10 wk of structured, supervised RE training. Assessments included strength (1RM, three exercises), body composition (DEXA), and vastus lateralis muscle biopsies for determination of muscle fiber type (I, IIa, IIx), cross-sectional area (CSA), contractile protein, creatine (Cr), and glycogen content.. PRE-POST demonstrated a greater (P < 0.05) increase in lean body mass and 1RM strength in two of three assessments. The changes in body composition were supported by a greater (P < 0.05) increase in CSA of the type II fibers and contractile protein content. PRE-POST supplementation also resulted in higher muscle Cr and glycogen values after the training program (P < 0.05).. Supplement timing represents a simple but effective strategy that enhances the adaptations desired from RE-training.

Topics: Absorptiometry, Photon; Adult; Biopsy, Needle; Body Composition; Contractile Proteins; Creatine; Dietary Supplements; Glycogen; Humans; Hypertrophy; Male; Muscle Fibers, Skeletal; Muscle Strength; Muscle, Skeletal; Physical Education and Training; Single-Blind Method

Interleukin-6 (IL-6) influences both inflammatory response and anti-inflammatory processes. This cytokine can be released by exercising skeletal muscle, which characterizes it as a myokine. Unlike what is observed in inflammation, IL-6 produced by skeletal muscle is not preceded by the release of other pro-inflammatory cytokines, but it seems to be dependent on the lactate produced during exercise, thus causing different effects from those seen in inflammatory state. After binding to its receptor, myokine IL-6 activates the PI3K-Akt pathway. One consequence of this upregulation is the potentiation of insulin signaling, which enhances insulin sensitivity. IL-6 increases GLUT-4 vesicle mobilization to the muscle cell periphery, increasing the glucose transport into the cell, and also glycogen synthesis. Muscle glycogen provides energy for ATP resynthesis, and regulates Ca2+ release by the sarcoplasmic reticulum, influencing muscle contraction, and, hence, muscle function by multiple pathways. Another implication for the upregulation of the PI3K-Akt pathway is the activation of mTORC1, which regulates mRNA translational efficiency by regulating translation machinery, and translational capacity by inducing ribosomal biogenesis. Thus, IL-6 may contribute to skeletal muscle hypertrophy and function by increasing contractile protein synthesis.

Topics: Adenosine Triphosphate; Anti-Inflammatory Agents; Calcium; Contractile Proteins; Cytokines; Glucose; Glucose Transporter Type 4; Glycogen; Humans; Hypertrophy; Insulin; Insulin Resistance; Interleukin-6; Lactates; Mechanistic Target of Rapamycin Complex 1; Muscle, Skeletal; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; RNA, Messenger

Topics: AMP-Activated Protein Kinases; Animals; Glucose; Glycogen; Hypertrophy; Mice, Transgenic; Muscle, Skeletal; Muscles; Protein Serine-Threonine Kinases

The comprehensive studies done on resveratrol (RES) support that this polyphenol has multiple bioactivities and is widely accepted for dietary supplementation. Furthermore, regular exercise is known to have benefits on health and is considered as a form of preventive medicine. Although the vast majority of prior studies emphasize the efficacy of aerobic exercise in promoting physiological adaptions, other types of exercise, such as resistance exercise and high-intensity interval training (HIIT), may achieve similar or different physiological outcomes. Few studies have looked into the effectiveness of a combinational, synergistic approach to exercise using a weight-loading ladder climbing animal platform. In this study, ICR mice were allocated randomly to the RES and training groups using a two-way ANOVA (RES × Training) design. Exercise capacities, including grip strength, aerobic performance, and anaerobic performance, were assessed and the physiological adaptions were evaluated using fatigue-associated indexes that were implemented immediately after the exercise intervention. In addition, glycogen levels, muscular characteristics, and safety issues, including body composition, histopathology, and biochemistry, were further elucidated. Synergistic effects were observed on grip strength, anaerobic capacities, and exercise lactate, with significant interaction effects. Moreover, the training or RES may have contributed significantly to elevating aerobic capacity, tissue glycogen, and muscle hypertrophy. Toxic and other deleterious effects were also considered to evaluate the safety of the intervention. Resistance exercise in combination with resveratrol supplementation may be applied in the general population to achieve better physiological benefits, promote overall health, and promote participation in regular physical activities.

Topics: Adaptation, Physiological; Anaerobic Threshold; Analysis of Variance; Animals; Body Composition; Fatigue; Glycogen; Hand Strength; Hypertrophy; Lactic Acid; Male; Mice, Inbred ICR; Muscle, Skeletal; Performance-Enhancing Substances; Physical Conditioning, Animal; Plant Extracts; Random Allocation; Resistance Training; Resveratrol

As aerobic exercise (AE) may interfere with adaptations to resistance exercise (RE), this study explored acute and chronic responses to consecutive AE (∼45 min cycling) and RE (4 × 7 maximal knee extensions) vs. RE only. Ten men performed acute unilateral AE + RE interspersed by 15 min recovery. The contralateral leg was subjected to RE. This exercise paradigm was then implemented in a 5-wk training program. Protein phosphorylation, gene expression, and glycogen content were assessed in biopsies obtained from the vastus lateralis muscle of both legs immediately before and 3 h after acute RE. Quadriceps muscle size and in vivo torque were measured, and muscle samples were analyzed for citrate synthase activity and glycogen concentration, before and after training. Acute AE reduced glycogen content (32%; P < 0.05) and increased (P < 0.05) phosphorylation of AMPK (1.5-fold) and rpS6 (1.3-fold). Phosphorylation of p70S6K and 4E-BP1 remained unchanged. Myostatin gene expression was downregulated after acute AE + RE but not RE. Muscle size showed greater (P < 0.05) increase after AE + RE (6%) than RE (3%) training. Citrate synthase activity (18%) and endurance performance (22%) increased (P < 0.05) after AE + RE but not RE. While training increased (P < 0.05) in vivo muscle strength in both legs, normalized and concentric torque increased after RE only. Thus AE activates AMPK, reduces glycogen stores, and impairs the progression of concentric force, yet muscle hypertrophic responses to chronic RE training appear not to be compromised.

Topics: Adaptation, Physiological; Adult; AMP-Activated Protein Kinases; Bicycling; Biomechanical Phenomena; Enzyme Activation; Gene Expression Regulation; Glycogen; Humans; Hypertrophy; Magnetic Resonance Imaging; Male; Muscle Contraction; Muscle Proteins; Muscle Strength; Phosphorylation; Physical Endurance; Quadriceps Muscle; Resistance Training; Time Factors; Torque; Young Adult

In the early recognition of portal vein ligation (PVL) induced tumor progression, positron emission tomography and magnetic resonance imaging (PET/MRI) could improve diagnostic accuracy of conventionally used methods. It is unknown how PVL affects metabolic patterns of tumor free hepatic tissues. The aim of this preliminary study is to evaluate the effect of PVL on glucose metabolism, using PET/MRI imaging in healthy rat liver.. Male Wistar rats (n=30) underwent PVL. 2-deoxy-2-(18F)fluoro-D-glucose (FDG) PET/MRI imaging (nanoScan PET/MRI) and morphological/histological examination were performed before (Day 0) and 1, 2, 3, and 7 days after PVL. Dynamic PET data were collected and the standardized uptake values (SUV) for ligated and non-ligated liver lobes were calculated in relation to cardiac left ventricle (SUVVOI/SUVCLV) and mean liver SUV (SUVVOI/SUVLiver).. PVL induced atrophy of ligated lobes, while non-ligated liver tissue showed compensatory hypertrophy. Dynamic PET scan revealed altered FDG kinetics in both ligated and non-ligated liver lobes. SUVVOI/SUVCLV significantly increased in both groups of lobes, with a maximal value at the 2nd postoperative day and returned near to the baseline 7 days after the ligation. After PVL, ligated liver lobes showed significantly higher tracer uptake compared to the non-ligated lobes (significantly higher SUVVOI/SUVLiver values were observed at postoperative day 1, 2 and 3). The homogenous tracer biodistribution observed before PVL reappeared by 7th postoperative day.. The observed alterations in FDG uptake dynamics should be taken into account during the assessment of PET data until the PVL induced atrophic and regenerative processes are completed.

Topics: Animals; Atrophy; Fluorodeoxyglucose F18; Glycogen; Health; Heart Ventricles; Hypertrophy; Ligation; Liver; Magnetic Resonance Imaging; Male; Multimodal Imaging; Portal Vein; Positron-Emission Tomography; Radioactive Tracers; Rats; Rats, Wistar; Time Factors; Tissue Distribution

This study tested the hypothesis that chronic aerobic and resistance exercise (AE+RE) would elicit greater muscle hypertrophy than resistance exercise only (RE). Ten men (25 ± 4 yr) performed 5 wk unilateral knee extensor AE+RE. The opposing limb was subjected to RE. AE completed 6 hr prior to RE consisted of ~45 min one-legged cycle ergometry. RE comprised 4 × 7 maximal concentric-eccentric knee extensions. Various indexes of in vivo knee extensor function were measured before and after training. Magnetic resonance imaging (MRI) assessed m. quadricep femoris (QF) cross-sectional area (CSA), volume, and signal intensity (SI). Biopsies obtained from m. vastus lateralis determined fiber CSA, enzyme levels, and gene expression of myostatin, atrogin-1, MuRF-1, PGC-1α, and VEGF. Increases (P < 0.05) in isometric strength and peak power, respectively, were comparable in AE+RE (9 and 29%) and RE (11 and 24%). AE+RE showed greater increase (14%; P < 0.05) in QF volume than RE (8%). Muscle fiber CSA increased 17% after AE+RE (P < 0.05) and 9% after RE (P > 0.05). QF SI increased (12%; P < 0.05) after AE+RE, but not RE. Neither AE+RE nor RE showed altered mRNA levels. Citrate synthase activity increased (P < 0.05) after AE+RE. The results suggest that the increased aerobic capacity shown with AE+RE was accompanied by a more robust increase in muscle size compared with RE. Although this response was not carried over to greater improvement in muscle function, it remains that intense AE can be executed prior to RE without compromising performance outcome.

Topics: Adult; Exercise; Gene Expression; Glycogen; Heat-Shock Proteins; Humans; Hypertrophy; Isometric Contraction; Knee Joint; L-Lactate Dehydrogenase; Male; Muscle Fibers, Skeletal; Muscle Proteins; Myostatin; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Resistance Training; RNA, Messenger; SKP Cullin F-Box Protein Ligases; Transcription Factors; Tripartite Motif Proteins; Ubiquitin-Protein Ligases; Vascular Endothelial Growth Factor A; Water

The gastrointestinal tract of neonates is sensitive to dietary manipulations. When nursing mothers use Aloe vera, their babies are at risk of indirect exposure to Aloe vera via breast feeding or directly as health supplements. The effects of orally administered extracts of Aloe vera in unweaned rats were investigated. Six day old Sprague-Dawley rats were gavaged with aqueous or alcohol extracts of Aloe vera (low dose 50mg. kg⁻¹ or high dose 500mg. kg⁻¹) daily for eight days. All data were expressed as mean ± SD and analyzed by one way ANOVA. Pups receiving high doses of either extract had a significantly higher body mass gain than the group receiving lower dose (p < 0.05). Tibial length was significantly increased in the high dose aqueous extract group (15-26%). The differences in growth could not be attributed to circulating insulin-like growth factor-1 as the levels were not significantly different. The caecum was significantly enlarged in the rats that received the high doses of both extracts. Although, there was no significant difference in the non-fasting plasma concentration of glucose and triglycerides, the hepatic lipid and glycogen content were significantly higher (p < 0.001) for the high dose aqueous extract group. The plasma alanine transaminase was not affected by the treatments, however the high doses of the extracts significantly increased plasma alkaline phosphatase activity. Short term administration of Aloe vera extracts resulted in growth promotion, enhanced hepatic storage of metabolic substrates, increased ALP possibly in relation to bone growth and caused hypertrophy of the caecum of neonatal rats. These effects need to be explored further to enhance animal production and health.

Topics: Abdomen; Administration, Oral; Alanine Transaminase; Alkaline Phosphatase; Aloe; Analysis of Variance; Animals; Cecum; Female; Glycogen; Hypertrophy; Lipid Metabolism; Liver; Male; Plant Extracts; Rats; Rats, Sprague-Dawley; Tibia; Weight Gain

11beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regulates local glucocorticoid action in tissues by catalysing conversion of inactive glucocorticoids to active glucocorticoids. 11β-HSD1 inhibition ameliorates obesity and associated co-morbidities. Here, we tested the effect of 11β-HSD inhibitor, carbenoxolone (CBX) on obesity and associated comorbidities in obese rats of WNIN/Ob strain, a new animal model for genetic obesity.. Subcutaneous injection of CBX (50 mg/kg body weight) or volume-matched vehicle was given once daily for four weeks to three month-old WNIN/Ob lean and obese rats (n = 6 for each phenotype and for each treatment). Body composition, plasma lipids and hormones were assayed. Hepatic steatosis, adipose tissue morphology, inflammation and fibrosis were also studied. Insulin resistance and glucose intolerance were determined along with tissue glycogen content. Gene expressions were determined in liver and adipose tissue. CBX significantly inhibited 11β-HSD1 activity in liver and adipose tissue of WNIN/Ob lean and obese rats. CBX significantly decreased body fat percentage, hypertriglyceridemia, hypercholesterolemia, insulin resistance in obese rats. CBX ameliorated hepatic steatosis, adipocyte hypertrophy, adipose tissue inflammation and fibrosis in obese rats. Tissue glycogen content was significantly decreased by CBX in liver and adipose tissue of obese rats. Severe fat loss and glucose- intolerance were observed in lean rats after CBX treatment.. We conclude that 11β-HSD1 inhibition by CBX decreases obesity and associated co-morbidities in WNIN/Ob obese rats. Our study supports the hypothesis that inhibition of 11β-HSD1 is a key strategy to treat metabolic syndrome. Severe fat loss and glucose -intolerance by CBX treatment in lean rats suggest that chronic 11β-HSD1 inhibition may lead to insulin resistance in normal conditions.

Topics: 11-beta-Hydroxysteroid Dehydrogenase Type 1; Adipocytes; Adipose Tissue; Adrenal Glands; Animals; Body Composition; Carbenoxolone; Cholesterol, HDL; Corticosterone; Eating; Enzyme Inhibitors; Fibrosis; Gene Expression Regulation; Glucose Intolerance; Glycogen; Hypertrophy; Liver; Male; Metabolic Syndrome; Obesity; Organ Size; Rats; Signal Transduction; Thinness; Triglycerides

Intact protein, protein hydrolysates, and free amino acids are popular ingredients in contemporary sports nutrition, and have been suggested to augment post-exercise recovery. Protein and/or amino acid ingestion stimulates skeletal muscle protein synthesis, inhibits protein breakdown and, as such, stimulates muscle protein accretion following resistance and endurance type exercise. This has been suggested to lead to a greater adaptive response to each successive exercise bout, resulting in more effective muscle reconditioning. Despite limited evidence, some basic guidelines can be defined regarding the preferred type, amount, and timing of dietary protein that should be ingested to maximize post-exercise muscle protein accretion. Whey protein seems most effective in stimulating muscle protein synthesis during acute post-exercise recovery. This is likely attributable to its rapid digestion and absorption kinetics and specific amino acid composition. Ingestion of approximately 20 g protein during and/or immediately after exercise is sufficient to maximize post-exercise muscle protein synthesis rates. Coingestion of a large amount of carbohydrate or free leucine is not warranted to further augment post- exercise muscle protein synthesis when ample protein is already ingested. Future research should focus on the relevance of the acute anabolic response following exercise to optimize the skeletal muscle adaptive response to exercise training.

Topics: Caseins; Dietary Carbohydrates; Dietary Proteins; Exercise; Glycogen; Humans; Hypertrophy; Leucine; Milk Proteins; Muscle Proteins; Muscle, Skeletal; Musculoskeletal Physiological Phenomena; Physical Endurance; Protein Hydrolysates; Whey Proteins

Maternal nicotine (NIC) exposure during lactation leads to overweight, hyperleptinemia, and hypothyroidism in adult rat offspring. In this model, we analyzed adipocyte morphology, glucose homeostasis (serum insulin and adiponectin; liver and muscle glycogen), serum lipid, and the leptin signaling pathway. After birth, osmotic minipumps were implanted in lactating rats, which were divided into the groups NIC (6 mg/kg per day s.c. for 14 days) and control (C, saline). NIC and C offspring were killed at the age of 180 days. Adult NIC rats showed higher total body fat (+10%, P<0.05), visceral fat mass (+12%, P<0.05), and cross-sectional area of adipocytes (epididymal: +12% and inguinal: +43%, P<0.05). Serum lipid profile showed no alteration except for apolipoprotein AI, which was lower. We detected a lower adiponectin:fat mass ratio (-24%, P<0.05) and higher insulinemia (+56%, P<0.05), insulin resistance index (+43%, P<0.05), leptinemia (+113%, P<0.05), and leptin:adiponectin ratio (+98%, P<0.05) in the adult NIC group. These rats presented lower hypothalamic contents of the proteins of the leptin signaling pathway (leptin receptor (OB-R): -61%, janus tyrosine kinase 2: -41%, and p-signal transducer and activator of transcription 3: -56%, P<0.05), but higher suppressor of cytokine signaling 3 (+81%, P<0.05). Therefore, NIC exposure only during lactation programs rats for adipocyte hypertrophy in adult life, as well as for leptin and insulin resistance. Through the effects of NIC, perinatal maternal cigarette smoking may be responsible for the future development of some components of the metabolic syndrome in the offspring.

Topics: Adipocytes; Adiponectin; Animals; Animals, Newborn; Blood Glucose; Cotinine; Drug Resistance; Female; Glycogen; Homeostasis; Hypertrophy; Hypothalamus; Insulin; Insulin Resistance; Lactation; Leptin; Lipids; Liver; Male; Milk; Muscle, Skeletal; Nicotine; Rats; Signal Transduction

The aim of this study was to investigate effects of albumin and insulin separately as well as in combination on mature muscle fibres during long-term culture. Single muscle fibres were dissected from m. iliofibularis of Xenopus laevis and attached to a force transducer in a culture chamber. Fibres were cultured in a serum-free medium at slack length (mean sarcomere length 2.3 mum) for 8 to 22 days. The medium was supplemented with (final concentrations): (1) bovine insulin (6 nmol/L or 200-600 nmol/L), (2) 0.2% bovine albumin or (3) 0.2% bovine albumin in combination with insulin (120 nmol/L). In culture medium with insulin, 50% of the muscle fibres became in-excitable within 7-12 days, whereas the other 50% were stable. Caffeine contractures of in-excitable muscle fibres produced 80.4 +/- 2.4% of initial peak tetanic force, indicating impaired excitation-contraction (E-C) coupling in in-excitable fibres. In the presence of albumin, all cultured muscle fibres were stable for at least 10 days. Muscle fibres cultured in medium with insulin or albumin exclusively did not hypertrophy or change the number of sarcomeres in series. In contrast, muscle fibres cultured with both albumin and insulin showed an increase in tetanic force and fibre cross-sectional area of 19.6 +/- 2.8% and 32.5 +/- 4.9%, respectively, (means +/- SEM.; P = 0.007) after 16.3 +/- 1.7 days, whereas the number of sarcomeres in series remained unchanged. We conclude that albumin prevents muscle fibre damage and preserves E-C coupling in culture. Furthermore, albumin is important in regulating muscle fibre adaptation by a synergistic action with growth factors like insulin.

Topics: Adenosine Triphosphatases; Albumins; Animals; Cells, Cultured; Cytoplasm; Densitometry; Diffusion Chambers, Culture; Female; Glycogen; Hypertrophy; Hypoglycemic Agents; Immunohistochemistry; Insulin; Lipids; Mitochondria, Muscle; Muscle Contraction; Muscle Fibers, Skeletal; Myofibrils; Sarcomeres; Xenopus laevis

The structural and metabolic characteristics of the pectoralis major (P. major) muscle (i.e., breast muscle) and the quality of the resulting meat were studied in relation to breast muscle fiber development in broiler chickens. Six hundred birds originating from a commercial, grand parental, male heavy line (Hubbard-Europe, Châteaubourg, France) were kept under conventional breeding methods until their usual marketing age of 6 wk. For all birds, the plasma creatine kinase activity and the P. major muscle fiber cross-sectional area (CSA), glycolytic potential, lactate content, pH at 15 min postmortem, as well as the ultimate pH, CIELAB color parameters [lightness (L*), redness (a*), and yellowness (b*)], and drip loss of breast meat, were measured. Increased breast weight and yield were associated with increased fiber CSA, reduced muscle glycolytic potential, and reduced lactate content at 15 min postmortem. Therefore, P. major muscle exhibiting larger fiber CSA exhibited greater pH at 15 min postmortem and ultimate pH, produced breast meat with lower L* and reduced drip loss, and was potentially better adapted to further processing than muscle exhibiting small fiber CSA.

Topics: Animals; Chickens; Creatine Kinase; Female; Glycogen; Glycolysis; Hydrogen-Ion Concentration; Hypertrophy; Lactic Acid; Male; Meat; Muscle Fibers, Skeletal; Pectoralis Muscles; Phenotype; Pigmentation; Sex Factors; Statistics as Topic

Chronic treatment of rats with N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) biosynthesis, results in hypertension mediated partly by enhanced angiotensin-I-converting enzyme (ACE) activity. We examined the influence of L-NAME on rat liver morphology, on hepatic glycogen, cholesterol, and triglyceride content, and on the activities of the cytochrome P450 isoforms CYP1A1/2, CYP2B1/2, CYP2C11, and CYP2E1. Male Wistar rats were treated with L-NAME (20 mg/rat per day via drinking water) for 2, 4, and 8 weeks, and their livers were then removed for analysis. Enzymatic induction was produced by treating rats with phenobarbital (to induce CYP2B1/2), beta-naphthoflavone (to induce CYP1A1/2), or pyrazole (to induce CYP2E1). L-NAME significantly elevated blood pressure; this was reversed by concomitant treatment with enalapril (ACE inhibitor) or losartan (angiotensin II AT(1) receptor antagonist). L-NAME caused vascular hypertrophy in hepatic arteries, with perivascular and interstitial fibrosis involving collagen deposition. Hepatic glycogen content also significantly increased. L-NAME did not affect fasting glucose levels but significantly reduced insulin levels and increased the insulin sensitivity of rats, based on an intraperitoneal glucose tolerance test. Immunoblotting experiments indicated enhanced phosphorylation of protein kinase B and of glycogen synthase kinase 3. All these changes were reversed by concomitant treatment with enalapril or losartan. L-NAME had no effect on hepatic cholesterol or triglyceride content or on the basal or drug-induced activities and protein expression of the cytochrome P450 isoforms. Thus, the chronic inhibition of NO biosynthesis produced hepatic morphological alterations and changes in glycogen metabolism mediated by the renin-angiotensin system. The increase in hepatic glycogen content probably resulted from enhanced glycogen synthase activity following the inhibition of glycogen synthase kinase 3 by phosphorylation.

Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Animals; Chronic Disease; Cytochrome P-450 Enzyme System; Enalapril; Enzyme Activation; Enzyme Inhibitors; Fasting; Glucose; Glycogen; Glycogen Synthase Kinase 3; Hypertension; Hypertrophy; Liver; Liver Cirrhosis; Losartan; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Peptidyl-Dipeptidase A; Phosphorylation; Proto-Oncogene Proteins c-akt; Rats; Rats, Wistar; Renin-Angiotensin System

Although mutations in the gamma-subunit of AMP-activated protein kinase (AMPK) can result in excessive glycogen accumulation and cardiac hypertrophy, the mechanisms by which this occurs have not been well defined. Because >65% of cardiac AMPK activity is associated with the gamma1-subunit of AMPK, we investigated the effects of expression of an AMPK-activating gamma1-subunit mutant (gamma1 R70Q) on regulatory pathways controlling glycogen accumulation and cardiac hypertrophy in neonatal rat cardiac myocytes. Whereas expression of gamma1 R70Q displayed the expected increase in palmitate oxidation rates, rates of glycolysis were significantly depressed. In addition, glycogen synthase activity was increased in cardiac myocytes expressing gamma1 R70Q, due to both increased expression and decreased phosphorylation of glycogen synthase. The inhibition of glycolysis and increased glycogen synthase activity were correlated with elevated glycogen levels in gamma1 R70Q-expressing myocytes. In association with the reduced phosphorylation of glycogen synthase, glycogen synthase kinase (GSK)-3beta protein and mRNA levels were profoundly decreased in the gamma1 R70Q-expressing myocytes. Consistent with GSK-3beta negatively regulating hypertrophy via inhibition of nuclear factor of activated T cells (NFAT), the dramatic downregulation of GSK-3beta was associated with increased nuclear activity of NFAT. Together, these data provide important new information about the mechanisms by which a mutation in the gamma-subunit of AMPK causes altered AMPK signaling and identify multiple pathways involved in regulating both cardiac myocyte metabolism and growth that may contribute to the development of the gamma mutant-associated cardiomyopathy.

Topics: Active Transport, Cell Nucleus; AMP-Activated Protein Kinases; Animals; Animals, Newborn; Cardiomegaly; Cell Size; Cells, Cultured; Glucose; Glycogen; Glycogen Synthase; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Glycolysis; Hypertrophy; Multienzyme Complexes; Mutation; Myocytes, Cardiac; NFATC Transcription Factors; Oxidation-Reduction; Palmitic Acid; Phosphorylation; Protein Serine-Threonine Kinases; Rats; RNA, Messenger; Signal Transduction; Transduction, Genetic

The pathophysiology of urinary retention in women is generally unknown but a subgroup of women with urinary retention have been diagnosed as having so-called primary disorder of sphincter relaxation on the basis of an abnormal urethral sphincter electromyogram. It was suggested this sphincter overactivity could lead to work hypertrophy of the urethral rhabdosphincter and in this study we looked for any evidence of such muscle fiber hypertrophy.. In 9 women 18 to 45 years old (mean age 31.6) with urinary retention and overactive urethral sphincter electromyogram, light and electron microscopy were used to examine core needle biopsies of the urethral rhabdosphincter taken under transvaginal ultrasound control. Of the 9 patients only 5 biopsies processed for light microscopy and 4 processed for electron microscopy contained striated urethral muscle fibers. The results of these biopsies were compared to the morphology of a control specimen from a postmenopausal woman without a history of urinary retention.. On light microscopy the urethral rhabdosphincter fiber diameter did not differ among patients (mean average 7.6 mum), was less than that reported in the literature (15 to 20), but did not differ from that of the control (mean 9.9). In all patients electron microscopy showed excessive peripheral sarcoplasm with lipid and glycogen deposition, and sarcoplasmic accumulation of normal mitochondria. These ultrastructural abnormalities were not seen in the control.. To our knowledge this is the first morphological description of the urethral rhabdosphincter in a subgroup of women with urinary retention. Mean rhabdosphincter fiber diameter was approximately the same in patients and controls. This study does not support the previous theory that urethral sphincter overactivity in a subgroup of women with urinary retention leads to work hyperplasia of urethral rhabdosphincter fibers. An alternative hypothesis is suggested.

Topics: Adolescent; Adult; Biopsy, Needle; Electromyography; Female; Glycogen; Humans; Hypertrophy; Lipids; Microscopy, Electron; Middle Aged; Mitochondria, Muscle; Muscle Fibers, Skeletal; Muscle Fibers, Slow-Twitch; Sarcoplasmic Reticulum; Ultrasonography, Interventional; Urethra; Urinary Retention

Some previous studies have shown that resistance exercise training with venous occlusion causes an enhanced hypertrophy in human muscles. To investigate the effects of blood flow on muscular size at either cellular or subcellular level, we developed an animal model in which several veins from hindlimb muscles of the rat are surgically crush-occluded.. Twenty-four male Wister rats were randomly assigned into either a group for sham operation (sham group) or a group for venous occlusion (experimental group; N = 12 for each group). Fourteen days after the operation, plantaris, soleus, gastrocnemius, extensor digitorum longus, and tibialis anterior muscles were dissected from hindlimbs and subjected to morphological and biochemical analyses.. Fourteen days after the operation, the muscles expect for soleus showed similar increases in wet weight/body weight (by 7-12%) as compared with the sham-operated group (P < 0.05). Further analyses on the plantaris muscle showed increases in muscle dry weight/ body weight (by 10%) and the concentrations of myofibrillar protein (by 23%), glycogen (by 93%) and lactate (by 23%) after the operation (P < 0.05). Mean fiber cross-sectional area was larger by 34% in the experimental group than in the sham-operated group (P < 0.01). The content of HSP-72 increased, whereas that of myostatin protein decreased (P < 0.01). The expression of nitric oxide synthase-1 (NOS-1) mRNA increased (P < 0.01), whereas that of IGF-1 mRNA showed no significant change (P = 0.36). Although the muscle nitric oxide (NO) concentration tended to increase, but the change was not significant (P = 0.10).. Changes in muscle blood flow may affect the muscular size through actions of HSP-72, myostatin, and NOS-1.

Topics: Animals; Base Sequence; Constriction, Pathologic; DNA Primers; Glycogen; Heat-Shock Proteins; HSP72 Heat-Shock Proteins; Hypertrophy; Japan; Lactic Acid; Male; Muscle, Skeletal; Myostatin; Nitric Oxide Synthase; Rats; Rats, Wistar; Transforming Growth Factor beta

How an individual's sex and genetic background modify cardiac adaptation to increased workload is a topic of great interest. We systematically evaluated morphological and physiological cardiac adaptation in response to voluntary and forced exercise. We found that sex/gender is a dominant factor in exercise performance (in two exercise paradigms and two mouse strains) and that females of one of these strains have greater capacity to increase their cardiac mass in response to similar amounts of exercise. To explore the biochemical mechanisms for these differences, we examined signaling pathways previously implicated in cardiac hypertrophy. Ca2+/calmodulin-dependent protein kinase (CaMK) activity was significantly greater in males compared with females and increased after voluntary cage-wheel exposure in both sexes, but the proportional increase in CaMK activity was twofold higher in females compared with males. Phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) was evident after 7 days of cage-wheel exposure in both sexes and remained elevated in females only by 21 days of exercise. Despite moderate increases in myocyte enhancer factor-2 (a downstream effector of CaMK) transcriptional activity and phosphorylation of Akt with exercise, there were no sex differences. Mitogen-activated protein kinase signaling components (p38 mitogen-activated protein kinase and extracellular regulated kinase 1/2) were not different between male and female mice and were not affected by exercise. We conclude that females have increased exercise capacity and increased hypertrophic response to exercise. We have also identified sex-specific differences in hypertrophic signaling within the cardiac myocyte that may contribute to sexual dimorphism in exercise and cardiac adaptation to exercise.

Topics: Adaptation, Physiological; Animals; Calcium; Calcium Signaling; Calmodulin; Cyclic AMP-Dependent Protein Kinases; DNA-Binding Proteins; Female; Glycogen; Heart; Hypertrophy; Male; MEF2 Transcription Factors; Mice; Mice, Inbred C57BL; Myocytes, Cardiac; Myogenic Regulatory Factors; Physical Conditioning, Animal; Physical Exertion; Sex Characteristics; Transcription Factors

Hypertrophic placenta, or placentomegaly, has been reported in cloned cattle and mouse concepti, although their placentation processes are quite different from each other. It is therefore tempting to assume that common mechanisms underlie the impact of somatic cell cloning on development of the trophoblast cell lineage that gives rise to the greater part of fetal placenta. To characterize the nature of placentomegaly in cloned mouse concepti, we histologically examined term cloned mouse placentas and assessed expression of a number of genes. A prominent morphological abnormality commonly found among all cloned mouse placentas examined was expansion of the spongiotrophoblast layer, with an increased number of glycogen cells and enlarged spongiotrophoblast cells. Enlargement of trophoblast giant cells and disorganization of the labyrinth layer were also seen. Despite the morphological abnormalities, in situ hybridization analysis of spatiotemporally regulated placenta-specific genes did not reveal any drastic disturbances. Although repression of some imprinted genes was found in Northern hybridization analysis, it was concluded that this was mostly due to the reduced proportion of the labyrinth layer in the entire placenta, not to impaired transcriptional activity. Interestingly, however, cloned mouse fetuses appeared to be smaller than those of litter size-matched controls, suggesting that cloned mouse fetuses were under a latent negative effect on their growth, probably because the placentas are not fully functional. Thus, a major cause of placentomegaly is expansion of the spongiotrophoblast layer, which consequently disturbs the architecture of the layers in the placenta and partially damages its function.

Topics: Animals; Basic Helix-Loop-Helix Transcription Factors; Blotting, Northern; Cloning, Organism; DNA-Binding Proteins; Embryo Transfer; Female; Fetal Weight; Gene Expression; Genomic Imprinting; Glycogen; Hypertrophy; In Situ Hybridization; Litter Size; Male; Mice; Mice, Inbred C57BL; Mice, Inbred DBA; Nuclear Transfer Techniques; Placenta; Placental Lactogen; Pregnancy; Transcription Factors; Trophoblasts

To study the direct cause of liver enlargement in the Japanese flounder Paralichthys olivaceus infected with Edwardsiella tarda, the fish were challenged with E. tarda and reared without feeding. The liver of fish exposed to the bacteria was markedly enlarged compared to that of the controls while no severe histopathological change appeared in the organ during the experiments. No notable difference was observed in the crude fat, glycogen, and water content of the liver between challenged and control fish. The size of liver cells and nuclei of the challenged fish was apparently larger than that of the controls. Analysis of crude DNA in the liver suggested that the number of liver cells of starved control fish significantly decreased during the experiment while that of the challenged fish was maintained at a level of the initial control. RNA/DNA ratio of the liver of challenged fish clearly increased while it decreased in the control fish during the experiment. These observations suggest that liver enlargement of flounder infected with E. tarda, at least in the early stage of infection, is not a result of any readily observable histopathological changes and that E. tarda infection causes hypertrophy of the cells, as well as preventing decrease in liver cell number.

Topics: Animals; Blood Glucose; DNA, Bacterial; Edwardsiella tarda; Electrophoresis, Polyacrylamide Gel; Enterobacteriaceae Infections; Fish Diseases; Flatfishes; Glycogen; Hypertrophy; Image Processing, Computer-Assisted; Kidney; Liver; Organ Size; RNA, Bacterial; Seawater; Water

Longitudinal bone growth, and hence stature, are functions of growth plate chondrocyte proliferation and hypertrophy. Insulin-like growth factor 1 (Igf1) is reputed to augment longitudinal bone growth by stimulating growth plate chondrocyte proliferation. In this study, however, we demonstrate that chondrocyte numbers and proliferation are normal in Igf1 null mice despite a 35% reduction in the rate of long bone growth. Igf1 null hypertrophic chondrocytes differentiate normally in terms of expressing specialized proteins such as collagen X and alkaline phosphatase, but are smaller than wild-type at all levels of the hypertrophic zone. The terminal hypertrophic chondrocytes, which form the scaffold on which long bone growth extends, are reduced in linear dimension by 30% in Igf1 null mice, accounting for most of their decreased longitudinal growth. The expression of the insulin-sensitive glucose transporter, GLUT4, is significantly decreased and the insulin-regulated enzyme glycogen synthase kinase 3beta (GSK3) is hypo-phosphorylated in Igf1 null chondrocytes. Glycogen levels were significantly decreased and ribosomal RNA levels were reduced by almost 75% in Igf1 null chondrocytes. These data suggest that Igf1 promotes longitudinal bone growth by 'insulin-like' anabolic actions which augment chondrocyte hypertrophy.

Topics: Animals; Cell Division; Chondrocytes; Glucose Transporter Type 4; Glycogen; Growth Plate; Hypertrophy; Insulin; Insulin-Like Growth Factor I; Mice; Monosaccharide Transport Proteins; Muscle Proteins; RNA, Ribosomal

A severe myopathy leading to death or euthanasia was identified in 4 Belgian and 4 Percheron draught horses age 2-21 years. Clinical signs ranged from overt weakness and muscle atrophy in 2 horses age 2 and 3 years, to recumbency with inability to rise in 6 horses age 4-21 years. In 5 horses there was mild to severe increases in muscle enzyme levels. Clinical diagnoses included equine motor neuron disease (2 horses), post anaesthetic myopathy (2 horses), exertional myopathy (2 horses), myopathy due to unknown (one horse), and equine protozoal myelitis (one horse). Characteristic histopathology of muscle from affected horses was the presence of excessive complex polysaccharide and/or glycogen, revealed by periodic acid-Schiff staining in all cases and by electron microscopy in one case. Evaluation of frozen section histochemistry performed on 2 cases indicated that affected fibres were Type 2 glycolytic fibres. Subsarcolemmal and intracytoplasmic vacuoles were most prominent in 3 horses age 2-4 years, and excessive glycogen, with little or no complex polysaccharide, was the primary compound stored in affected muscle in these young horses. Myopathic changes, including fibre size variation, fibre hypertrophy, internal nuclei, and interstitial fat infiltration, were most prominent in 5 horses age 6-21 years, and the accumulation of complex polysaccharide appeared to increase with age. Mild to moderate segmental myofibre necrosis was present in all cases.

Topics: Animals; Atrophy; Female; Glycogen; Glycogen Storage Disease; Histocytochemistry; Horse Diseases; Horses; Hypertrophy; Male; Microscopy, Electron, Scanning Transmission; Muscle Fibers, Skeletal; Muscle, Skeletal; Muscular Diseases; Necrosis; Polysaccharides

Hepatic changes of mice in the subacute phase of streptozotocin (SZ)-induced diabetes were investigated biochemically and pathologically. Biochemically, the contents of serum glucose and of serum and liver lipids increased while the content of liver glycogen decreased in SZ-induced diabetic mice. Histopathologically, hypertrophy of hepatocytes due to an increase in number of intracytoplasmic acidophilic granules was common to SZ-induced diabetic mice. Electron microscopically, these hepatocytes were characterized by a prominent increase in number of mitochondria showing normal structure, a marked decrease of glycogen granules and poorly developed rough endoplasmic reticulum, which were common to so-called oncocytic cells. In some SZ-induced diabetic mice, bile duct hyperplasia with an appearance of cytomegalic hepatocytes was also observed.

Topics: Animals; Blood Glucose; Diabetes Mellitus, Experimental; Endoplasmic Reticulum; Glycogen; Hypertrophy; Lipids; Liver; Male; Mice; Mice, Inbred ICR; Microscopy, Electron; Organ Size; Streptozocin; Weight Gain

Morphometrical and histochemical techniques were used to demonstrate changes to the cartilage layer of the rat temporomandibular joint condyle following chronic exposure to fluoride. An increase in thickness of the cartilage layer was noted in rats given 100 parts per million sodium fluoride in drinking water. No significant changes were observed with either control or low dose (10 parts per million) groups. The observed thickening was attributable to an increase in number and size of cells of the lower hypertrophic zone. Accumulations of glycogen were observed in these cells, which reflects the inhibitory effect of fluoride on glycolysis. Stimulation of chondrocytes by fluoride may have delayed the normal processes of capillary invasion, resulting in thickening of the cartilage layer. No changes to staining patterns of immature or mature types of collagen were observed, nor did the staining pattern of detectable glycosaminoglycans change due to fluoride.

Topics: Animals; Cartilage; Cell Nucleus; Chondroitin Sulfates; Collagen; Cytoplasm; Drug Administration Schedule; Glycogen; Hypertrophy; Inclusion Bodies; Keratan Sulfate; Mandibular Condyle; Microscopy, Electron; Rats; Rats, Inbred Strains; Sodium Fluoride

We investigated the preventive effects of long-term treatment with the angiotensin converting enzyme inhibitor ramipril on myocardial left ventricular hypertrophy and capillary length density in spontaneously hypertensive rats. Rats were treated in utero and subsequently up to 20 weeks of age with a high dose (1 mg/kg per day) or with a low dose (0.01 mg/kg per day) of ramipril. Animals given a high dose of ramipril remained normotensive, whereas those given a low dose developed hypertension in parallel to vehicle-treated controls. At the end of the treatment period, converting enzyme activity in heart tissue was inhibited dose-dependently in the treated groups. Both groups revealed an increase in myocardial capillary length density together with increased myocardial glycogen and reduced citric acid concentrations. Left ventricular mass was reduced only in high dose- but not in low dose-treated animals. Our results demonstrate that early onset treatment with a converting enzyme inhibitor can induce myocardial capillary proliferation, even at doses too low to antagonize the development of hypertension or left ventricular hypertrophy. We hypothesize that potentiation of kinins is responsible for this effect, probably by augmenting myocardial blood flow, which is a well-known trigger mechanism of angiogenesis in the heart.

Topics: Administration, Oral; Age Factors; Analysis of Variance; Angiotensin-Converting Enzyme Inhibitors; Animals; Animals, Newborn; Cardiomyopathy, Hypertrophic; Citrates; Citric Acid; Coronary Vessels; Dose-Response Relationship, Drug; Female; Glycogen; Hypertension; Hypertrophy; Maternal-Fetal Exchange; Microscopy, Electron; Myocardium; Peptidyl-Dipeptidase A; Pregnancy; Ramipril; Rats; Rats, Inbred SHR

In experiments on rats with different resistance to oxygen deficiency (high-resistant--HR, and low-resistant LR animals) the myocardium ultrastructure of nonadapted and adapted rats was studied. It was shown that there were more glycogen granules and lipid drops initially in cardiomyocytes of nonadapted HR animals in comparison with LR ones. After a long-term adaptation to hypoxia the hypertrophia and hyperplasia of mitochondria, the nucleus and endoplasmatic reticulum hypertrophy were observed. Moreover, the increase of glycogen and lipids content was more pronounced in the myocardium of LR rats. Besides, the activation of protein-synthesizing processes was observed not only as a result of long-term adaptation, but also after single acute hypoxic effect. The results of submicroscopic cardiomyocyte studies of HR and LR rats are in good correlation with the peculiarities of energetic metabolism.

Topics: Acute Disease; Adaptation, Physiological; Animals; Cell Nucleus; Endoplasmic Reticulum; Glycogen; Hypertrophy; Hypoxia; Lipid Metabolism; Male; Mitochondria, Heart; Myocardium; Rats; Time Factors

Smooth muscle cell biopsies obtained at pyloromyotomy from 37 children with infantile hypertrophic pyloric stenosis (IHPS) were studied by light and electron microscopy and compared with 6 autopsy control cases without any clinical evidence of this disorder. In cases with IHPS an apparently irregular increase in the number of smooth muscle cells by mitosis was accompanied by an increase of the endoplasmic reticulum, proliferation of mitochondria and regressive changes, such as shrinkage, swelling, necrosis and apoptosis of smooth muscle cells. Other alterations, seen in some but not all cases consisted of large numbers of unusual dense granules some of which were clearly associated with actin filaments and, therefore, regarded as derivatives of the normally occurring dense bodies. Furthermore, intermyofibrillar and subsarcolemmal glycogen accumulations, various nuclear abnormalities and pleomorphic membranous cytoplasmic or nuclear bodies occurred. While smooth muscle cell abnormalities predominated in some cases of IHPS, in others there were more severe axonal changes in the myenteric plexus. It is suggested, therefore, that a primarily myogenic type of IHPS can be distinguished from a predominantly neurogenic type.

Topics: Biopsy; Cytoplasm; Glycogen; Humans; Hypertrophy; Inclusion Bodies; Infant; Infant, Newborn; Microscopy, Electron; Muscle, Smooth; Pyloric Stenosis

1. A single subcutaneous injection of clenbuterol hydrochloride (0.125 mg/kg body wt.) to female Wistar rats produced a rapid increase in muscle cyclic AMP and lactate concentrations and a decrease in muscle glycogen concentrations. These changes are characteristic of muscle beta-adrenoceptor stimulation and were abolished by intraperitoneal injection of propranolol (12.5 mg/kg) 15 min before clenbuterol administration. 2. When this dose of clenbuterol was injected twice daily, the changes in muscle metabolite concentrations which followed its acute administration persisted until day 7 of treatment, and were accompanied by increases in muscle mass, body weight and muscle protein synthesis rate (ks). When the clenbuterol injections were preceded by propranolol injections (12.5 mg/kg administered according to the protocol described above), or if animals were treated with propranolol only, the values of these variables were not significantly different from those of sham-injected controls. 3. In rats fed on a semi-synthetic diet (PW3) supplemented with 2 mg of clenbuterol/kg of diet for 7 days, the muscle mass was greater than that of rats fed on unsupplemented PW3. The increased muscle mass was accompanied by increased muscle lactate and decreased muscle glycogen concentrations. When PW3 was supplemented with 2 mg of clenbuterol/kg and 200 mg of propranolol/kg, the increase in muscle mass remained, but decreased muscle glycogen concentrations and increased muscle lactate concentrations were also observed. 4. These data are consistent with the hypothesis that clenbuterol influences muscle growth via beta-adrenoceptor stimulation.

Topics: Animals; Body Composition; Clenbuterol; Cyclic AMP; Ethanolamines; Female; Glycogen; Heart; Hypertrophy; Lactates; Liver; Muscle Proteins; Muscles; Myocardium; Propranolol; Rats; Rats, Inbred Strains; Receptors, Adrenergic, beta; Reference Values; RNA

1. Rat plantaris muscles were subjected to chronic overload by the surgical removal of the soleus and most of the gastrocnemius muscles. Twelve to 16 wk later whole muscle and motor unit (ventral root dissection technique) contractile properties as well as histochemistry were determined. 2. Motor units were categorized as fast, fatigable (FF), fast, intermediate fatigue-resistant (FI), fast, fatigue-resistant (FR), and slow (S) based on contractile characteristics. Muscle fibers were identified as type I and type II according to myofibrillar ATPase staining. 3. Whole muscles demonstrated increases in wet weight, tetanic force, proportion of type I fibers, and mean cross-sectional areas of both type I and II fibers, as a result of chronic overload. 4. Tetanic tension increased by the same relative magnitude in all motor units whereas twitch tension remained unchanged. A significant change in the proportions of the motor unit types occurred in overloaded muscles, such that the latter contained higher proportions of FF and S units, and lower proportions of FI and FR units, than normal muscles. 5. The fatigue profile of a composite constructed from a summation of motor unit responses revealed that the overloaded plantaris displayed fatigue resistance similar to that of the normal plantaris for a given absolute force output. 6. Glycogen-depleted fibers of hypertrophied single motor units demonstrated uniform myofibrillar ATPase and SDH staining characteristics suggesting that metabolic adaptations among fibers of the same unit were similar after 12-16 wk of overload. 7. The finding that overload caused a uniform increase in the tetanic strength of all motor units, whereas alterations in fatigue resistance varied in degree and direction among unit types, demonstrate that these two properties are not controlled in parallel in this model. The smallest units maintain or even increase their fatigue resistance during the hypertrophic process, whereas high threshold units actually decrease in fatigue resistance.

Topics: Adenosine Triphosphatases; Animals; Electric Stimulation; Female; Glycogen; Hypertrophy; Motor Neurons; Muscle Contraction; Muscles; Myofibrils; Rats; Rats, Inbred Strains; Reference Values; Succinate Dehydrogenase

Previous findings suggest that skeletal muscle that has enlarged as a result of removal of synergistic muscles has a similar metabolic capacity and improved resistance to fatigue compared with normal muscle. The purpose of the present study was to follow blood flow and glycogen loss patterns in hypertrophied rat plantaris plantaris and soleus muscles during treadmill exercise to provide information on the adequacy of perfusion of the muscles during in vivo exercise. Thirty days following surgical removal of gastrocnemius muscle, blood flows (determined with radiolabeled microspheres) and glycogen concentrations were determined in all of the ankle extensor muscles of experimental and sham-operated control rats during preexercise and after 5-6 min of treadmill exercise at 15 m/min. There were no differences (P greater than 0.05) in blood flows per unit mass or glycogen concentrations between control and hypertrophied plantaris or soleus muscles at either time, although both muscles were larger (P less than 0.05) in the experimental group (plantaris: 95%; soleus: 40%). None of the other secondary ankle extensor muscles (tibialis posterior, flexor digitorum longus or flexor hallicus longus) hypertrophied in response to removal of gastrocnemius. These results provide indirect evidence that O2 delivery in the enlarged muscles is not compromised during low-intensity treadmill exercise due to limited perfusion.

Topics: Animals; Aorta; Blood Pressure; Glycogen; Heart Rate; Hypertrophy; Male; Muscles; Physical Exertion; Rats; Rats, Inbred Strains; Regional Blood Flow

The effect of work-induced hypertrophy (without any concomitant change in circulating parameters) on skeletal muscle metabolism was studied in lean mice and in gold-thioglucose-obese mice. Soleus muscle was functionally overloaded in one leg by tenotomy of gastrocnemius muscle 4 days before muscle isolation, muscle in the other leg being used as control. Basal deoxyglucose uptake and glycolysis were markedly increased in overloaded muscles compared with control muscles, together with a ten-fold increase in fructose 2-6 bisphosphate content. In the presence of maximally effective insulin concentrations, deoxyglucose uptake and glycolysis were identical in overloaded and control muscles of lean mice, while the effects of overload and insulin were partly additive in muscles of gold-thioglucose-obese mice. The sensitivity to insulin and insulin binding to muscles were not modified in overloaded muscles. Insulin-stimulated glycogenogenesis was decreased by about 50% probably due to a lower amount of glycogen synthase in overloaded than in control muscles. Thus, in muscles of gold-thioglucose-obese mice work-induced hypertrophy increased the response to maximal insulin concentrations without modifying the altered insulin sensitivity and decreased insulin binding.

Topics: Animals; Aurothioglucose; Body Weight; Deoxyglucose; Fructosediphosphates; Glycogen; Glycolysis; Hypertrophy; Insulin; Insulin Resistance; Male; Mice; Muscles; Obesity; Physical Exertion

The response of hypertrophied soleus and plantaris muscle of rats to endurance training was studied. Hypertrophy was produced by bilateral extirpation of the gastrocnemius muscle. A 13-wk training program of treadmill running initiated 30 days after removal of the gastrocnemius muscle accentuated (P less than 0.01) the hypertrophy. Succinate dehydrogenase activities of the enlarged muscles of sedentary rats were similar to those of normal animals, as were the increases associated with training. Phosphorylase and hexokinase activities were unaltered as a result of the experimental perturbations. Rates of glycogen depletion during exercise were lower (P less than 0.01) in the liver and soleus and plantaris muscles of endurance-trained animals. No difference existed in the rate of glycogen depletion of normal and hypertrophied muscle within the sedentary or trained groups. These data demonstrate that extensively hypertrophied muscle responds to training and exercise in a manner similar to that of normal muscle.

Topics: Adaptation, Physiological; Animals; Female; Glycogen; Hexokinase; Hypertrophy; Liver; Muscles; Phosphorylases; Physical Conditioning, Animal; Physical Endurance; Rats; Rats, Inbred Strains; Succinate Dehydrogenase

Infantile acid maltase deficiency (Pompe's disease, glycogenosis II) is a progressive, severe lysosomal storage disease in which skeletal and cardiac muscle fibers accumulate membrane-bound and free glycogen and are destroyed. New information in this report concerns 1) early hypertrophy of skeletal muscle fibers, 2) absence of size change as glycogen is lost, and 3) the ultrastructure of end-stage fibers empty of glycogen. Muscle fibers enlarge as they accumulate glycogen and then stay large as glycogen is lost. They are so large that, if empty fibers did in fact contain glycogen, over 80% of the muscle would be glycogen instead of 6.3-11.5% (from 37 published determinations). Fibers that have reached "empty" end-stage are shown to be more numerous than all other stages combined in biopsies from infantile acid maltase deficiency. Ultrastructurally, end-stage fibers contain much "empty" space (liquid-filled without fine structure) and various remnants and masses of altered myofibrillar and sarcoplasmic material. Many broken membranes originally enclosing glycogen in storage lysosomes are seen. A single broken membrane can enclose an area larger than the cross section area of a muscle fiber from a normal infant. The results support the proposal of Hers that the disease is due to a deficiency of the single lysosomal enzyme acid maltase. The results also support the lysosomal rupture hypothesis of Griffin, which accounts for muscle fibers being more damaged than are other cells and for the release of glycogen to the sarcoplasm.

Topics: alpha-Glucosidases; Glucan 1,4-alpha-Glucosidase; Glucosidases; Glycogen; Glycogen Storage Disease; Glycogen Storage Disease Type II; Histocytochemistry; Humans; Hypertrophy; Infant; Lysosomes; Microscopy, Electron; Muscles; Staining and Labeling

Topics: Adult; Glycogen; Glycogen Storage Disease; Glycogen Storage Disease Type III; Humans; Hypertrophy; Male; Muscles; Muscular Diseases; Peripheral Nerves; Peripheral Nervous System Diseases

The effects of denervation on the gastrocnemius muscle of the frog were studied by histologic and histochemical methods. Thirteen Rana pipiens underwent unilateral sciatic neurotomy and were sacrificed weekly as long as 46 days. Of the three normal populations of muscle fibers, the small fibers underwent atrophy, the intermediate sized fibers remained unchanged in size, and the large fibers either did not change or underwent hypertrophy between 21 and 46 days. Necrosis of muscle fibers did not occur. Histochemical stains showed persistence of the normal pattern after denervation. The small fibers continued to have a high concentration of both oxidative and glycolytic enzyme activity (NADH-TR, SDH, phosphorylase), and the large fibers continued to have a low concentration of these enzymes. Depletion of glycogen stores was seen with PAS. Hypertrophic muscle fibers had mostly subsarcolemmal nuclei and few internal nuclei, suggesting that they may be physiologically tonic rather than twitch fibers. Achilles tenotomy at the time of denervation prevented the hypertrophy of large fibers. Abnormal inclusions have been demonstrated in mammalian muscle following tenotomy alone, but were not seen in the frog.

Topics: Achilles Tendon; Adenosine Triphosphatases; Animals; Anura; Glycogen; Hypertrophy; Muscle Denervation; Muscles; Muscular Atrophy; Rana pipiens; Time

Topics: Animals; Deoxyribonucleases; Endoplasmic Reticulum; Glycogen; Hypertrophy; Liver; Male; Phenobarbital; Rats; Ribonucleases; Time Factors

The response of the intima-media of the thoracic aorta to 1 to 4 weeks of two-kidney renal hypertension in the rat has been analyzed by morphometric techniques at light and electron microscopic levels. The increased thickness of the aorta that ensues is the result of an increase in the size but not the number of smooth muscle cell layers. The volume fractions of intima occupied by endothelium (26%), internal elastic lamina (37%), and subendothelial space (37%) in normotensive animals are not significantly altered by the hypertension. The percent increases in muscle cross-sectional area is greatest (58 to 60%) in the two innermost layers (M1 and M2). M1 is composed of nearly equal compartments of smooth muscle cells and interstitial space that expand 69% and 50%, respectively, with hypertension. Analysis of the subcellular constituents of the M1 smooth muscle cells indicates that significant changes in absolute volume include increases of caveolae (45%), myofibrils (59%), mitochondria (81%), glycogen (163%), and rough endoplasmic reticulum (221%). Factors contributing to these alterations are discussed.

Topics: Animals; Aorta, Thoracic; Endoplasmic Reticulum; Endothelium; Glycogen; Hypertension, Renal; Hypertrophy; Male; Mitochondria, Muscle; Muscle, Smooth; Myofibrils; Rats

The effects on selected histochemical and morphological parameters of anabolic steroid administration and of high-intensity sprint running, separately, and in combination, were studied in young adult male rats. Dianabol (methandrostenolone) 1 mg/day for 8 weeks had no significant effects on phosphorylase or glycogen staining intensities and on fiber area in skeletal muscles of either trained or sedentary animals. The program of sprint training resulted in significantly decreased intensities of phosphorylase in all ten regions of the gastrocnemius, plantaris, and soleus muscles that were studied. Glycogen localization was significantly increased with training in five regions of the gastrocnemius and plantaris muscles which contained predominantly fast-switch fibers. No changes in fiber area occurred with the training program. We conclude from these results that (a) normal androgen levels in young, healthy male animals are sufficiently high so that the intake of large doses of anabolic steroid does not result in the stimulation of glycogen metabolism or hypertrophy of skeletal muscle; (b) the changes induced by high-intensity, short-duration sprint training suggest that the existing glycolytic capacity of muscle is adequate to supply the muscles energy needs even during the stress of very strenous exercise, and that more fast-twitch fibers were recruited by the exercise regimen than slow-twitch fibers.

Topics: Animals; Biometry; Glycogen; Hypertrophy; Male; Methandrostenolone; Muscles; Phosphorylases; Physical Conditioning, Animal; Rats

In diabetes mellitus abnormal quantiites of glycoprotein may be formed in the basement membrane of the glomerulus and both renal function and size may increase. It is suggested that these changes, of quite different potential significance, have a common origin an increased rate of uridine-triphosphate synthesis resulting from hyperglycemia.

Topics: Animals; Basement Membrane; Diabetes Complications; Diabetes Mellitus; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Glycogen; Glycoproteins; Humans; Hyperglycemia; Hypertrophy; Kidney; Kidney Diseases; Kidney Glomerulus; Rats; RNA; Sclerosis; Uracil Nucleotides

Ultrastructural studies were made of operatively resected crista supraventricularis muscle in 59 patients with congenital heart diseases, or whom 54 had obstruction to right ventricular outflow. Relationships of anatomic diagnosis, age, peripheral arterial oxygen saturation (PAO2), peak right ventricular systolic pressure gradient and right ventricular end-diastolic pressure (RVEDP) to hypertrophic changes, abnormalities of cellular and myofibrillar orientation, and degenerative alterations were determined. Changes directly related to hypertrophy were: cell diameters greater than 20 mu, irregular cell shape, lobulated nuclei, multiple intercalated discs, dilated T tubules, abnormal Z bands, and increased numbers of ribosomes. Abnormalities of cellular or myofibrillar orientation were focal in distribution and occurred in 12 patients, most of whom had elevated RVEDP, decreased PAO2, markedly enlarged cells, and interstitial fibrosis. Interstitial fibrosis was prominent in 19 patients and was associated with cellular hypertrophy, elevation of RVEDP, and increased age of the patients. Degenerative changes (myofibrillar lysis, abnormally small mitochondria, myelin figure formation, and proliferation of sarcoplasmic reticulum in cardiac muscle cells ocurred in six patients and correlated with increased age, decreased PAO2, and elevated RVEDP. Mitochondria containing glycogen deposits were present in 17 patients, most of whom had decreased PAO2. The variability of morphologic manifestations of chronic cardiac hypertrophy and the relationships of hypertrophic changes to orientation abnormalities and degenerative alterations are discussed.

Topics: Adolescent; Adult; Cardiomegaly; Cell Nucleus; Child; Child, Preschool; Collagen; Cytoplasmic Granules; Glycogen; Heart Defects, Congenital; Heart Septal Defects, Ventricular; Humans; Hypertrophy; Microscopy, Electron; Microtubules; Middle Aged; Mitochondria, Muscle; Myocardium; Myofibrils; Pulmonary Valve; Pulmonary Valve Stenosis; Ribosomes; Sarcoplasmic Reticulum; Tetralogy of Fallot

Topics: Adenosine Triphosphatases; Animals; Animals, Newborn; Cats; Cell Differentiation; Glycogen; Histocytochemistry; Hypertrophy; Muscles; Myofibrils; Myosins; Succinate Dehydrogenase; Time Factors

The mammalian ACTH (20 I.U.) injected in Heteropneustes fossilis (Bloch) caused hyperplasia of the adrenocortical tissue. The interrenal as well as chrome cells became vacuolated. The interrenal nuclear size increased by 15% as an average than the control fishes. The glycogen granules were found to be absent from the interrenal cells. The effect of bilateral gonadectomy in both sexes has been marked in the gradual decrease of the interrenal nuclear diameter which 12 weeks after the operation, recorded nearly 25% reduction in size. The glycogen content was reduced considerably. Removal of gonads during maturation period bringing inhibition of hyperplasia of the gland at the time of spawning possibly indicates action of gonadal steroids on the physiological alterations of the interrenal cells.

Topics: Adrenal Cortex; Adrenal Glands; Adrenocorticotropic Hormone; Animals; Castration; Cell Nucleus; Fishes; Glycogen; Gonads; Hypertrophy; Kidney

The effect of ovariectomy on the adrenal gland was studied in the Mongolian gerbil. Castration stimulated cells in the zona fasciculata as well as those in the region between the zona fasciculata and zona reticularis. No alterations occurred in the zona reticularis. The width of the intermediate region was enlarged, the cells were hypertrophic and contained an increased number of concentric whorls of rough endoplasmic reticulum. Smooth endoplasmic reticulum was hypertropic in cells of the zona fasciculata and intermediate region. Many mitochondria in cells of the intermediate region were larger than those in controls. Stimulation of cellular ultrastructure is directly correlated with a significant elevation in plasma cortisol in ovariectomized gerbils.

Topics: Adrenal Cortex; Adrenal Glands; Animals; Castration; Endoplasmic Reticulum; Female; Gerbillinae; Glycogen; Hydrocortisone; Hypertrophy; Mitochondrial Swelling; Ovary

Topics: Animals; Cell Membrane Permeability; DNA; Glycogen; Haplorhini; Hypertrophy; L-Lactate Dehydrogenase; Lactates; Lipid Metabolism; Macaca; Muscle Denervation; Muscle Proteins; Muscles; Muscular Atrophy; Pyruvates; RNA; Species Specificity

Topics: Acromegaly; Adenosine Triphosphatases; Aspartate Aminotransferases; Biopsy; Creatine Kinase; Cytoplasmic Granules; Electromyography; Glycogen; Histocytochemistry; Humans; Hypertrophy; L-Lactate Dehydrogenase; Male; Microscopy, Electron; Middle Aged; Mitochondria, Muscle; Muscles; Myofibrils; Pituitary Neoplasms

Topics: Adaptation, Physiological; Animals; Carbon Dioxide; Carbon Radioisotopes; Cytochrome c Group; Dietary Proteins; Energy Metabolism; Glucose; Glycogen; Hypertrophy; In Vitro Techniques; Leucine; Liver; Male; Mitochondria, Muscle; Muscles; Myofibrils; Organ Size; Oxidation-Reduction; Palmitic Acids; Proteins; Rats; Starvation; Time Factors; Water

Topics: Animals; Cartilage, Articular; Cytoplasmic Granules; Dietary Fats; Endoplasmic Reticulum; Fats, Unsaturated; Femur Head; Glycogen; Golgi Apparatus; Hyperplasia; Hypertrophy; Lysosomes; Male; Mice; Mice, Inbred C57BL; Microscopy, Electron; Microscopy, Phase-Contrast; Mitochondria; Oils; Pinocytosis; Time Factors; Zea mays

Topics: Adrenal Glands; Animals; Biometry; Breeding; Cell Nucleolus; Cell Nucleus; Chromaffin System; Chromatin; Cytoplasmic Granules; Epithelial Cells; Female; Fishes; Glycogen; Hypertrophy; Kidney; Male; Ovary; Ovum; Seasons; Temperature; Testis; Thyroid Gland

Topics: Action Potentials; Child; Child, Preschool; Congenital Hypothyroidism; Creatine Kinase; Electromyography; Female; Fructose-Bisphosphate Aldolase; Glycogen; Humans; Hypertrophy; Hypothyroidism; L-Lactate Dehydrogenase; Lipid Metabolism; Male; Microscopy, Electron; Mitochondria, Muscle; Muscles; Muscular Diseases; Neuromuscular Junction; Sarcoplasmic Reticulum; Syndrome; Thyroxine

Topics: Animals; Animals, Newborn; Calcification, Physiologic; Cartilage; Cytoplasm; Female; Fetus; Glycogen; Histocytochemistry; Hypertrophy; Mandibular Condyle; Mice; Mice, Inbred Strains; Microscopy, Electron; Osteogenesis; Pregnancy

A small population of glycogen-containing mitochondria was found in operatively resected myocardium in 8 of 11 patients with various types of congenital heart diseases associated with right ventricular hypertrophy and muscular (infundibular) obstruction to right ventricular outflow. The presence of intramitochondrial glycogen correlated with the degree of peripheral arterial oxygen desaturation but not with the severity of hemodynamic alterations or with the ages of the patients. The occurrence of intramitochondrial glycogen in myocardium in other conditions is reviewed, and its possible pathogenesis is discussed.

Topics: Adolescent; Adult; Child; Child, Preschool; Female; Glycogen; Heart Defects, Congenital; Heart Ventricles; Humans; Hypertrophy; Male; Microscopy, Electron; Mitochondria; Myocardium; Oxygen; Staining and Labeling

Topics: Animals; Calcitonin; Calcium; Cholecalciferol; Chromatin; Cytoplasm; Dogs; Endoplasmic Reticulum; Epithelial Cells; Female; Glycogen; Histocytochemistry; Hypercalcemia; Hyperplasia; Hypertrophy; Male; Microscopy, Electron; Parathyroid Glands; Thyroid Gland

Topics: Adipose Tissue; Animals; Blood Glucose; Body Weight; Cytoplasmic Granules; Endoplasmic Reticulum; Epididymis; Glycogen; Golgi Apparatus; Hypertrophy; Insulin; Islets of Langerhans; Male; Microscopy, Electron; Microtubules; Obesity; Organ Size; Rats; Time Factors; Triglycerides

Topics: Animals; Blood Urea Nitrogen; Dogs; Female; Glycogen; Hypertrophy; Male; Muscles; Urinary Bladder; Urinary Bladder, Neurogenic

Topics: Animals; Blood Glucose; Blood Urea Nitrogen; Cattle; Cattle Diseases; Creatine Kinase; Epinephrine; Fasting; Female; Glycogen; Humans; Hydrogen-Ion Concentration; Hypertrophy; Lactates; Muscles; Muscular Diseases; Physical Exertion; Stress, Physiological; Stress, Psychological

Topics: Adipose Tissue; Age Factors; Aged; Basement Membrane; Biopsy; Cell Nucleus; Cytoplasmic Granules; Endothelium; Female; Glycogen; Humans; Hypertrophy; Lysosomes; Microscopy, Electron; Mitochondria; Muscles; Muscular Diseases; Myofibrils; Nerve Endings; Neuromuscular Junction; Sarcolemma; Staining and Labeling

Topics: Animals; Autoradiography; Cardiomegaly; Cell Nucleus; Chromatin; DNA; Edema; Glycogen; Histocytochemistry; Hypertrophy; Injections, Intraperitoneal; Isoproterenol; Male; Microscopy; Microscopy, Electron; Mitochondria, Muscle; Myocardium; Necrosis; Rats; Ribosomes; RNA; Sarcoplasmic Reticulum; Time Factors

Topics: Animals; Cartilage, Articular; Cytoplasmic Granules; Endoplasmic Reticulum; Epiphyses; Glycogen; Golgi Apparatus; Hypertrophy; Inclusion Bodies; Mice; Mice, Inbred Strains; Microscopy, Electron; Mitochondria; Ribosomes; Ribs

Topics: Acetanilides; Adrenergic beta-Antagonists; Amino Alcohols; Animals; Blood Glucose; Blood Pressure; Body Weight; Drug Antagonism; Fatty Acids, Nonesterified; Female; Glycogen; Heart Rate; Hypertrophy; Isoproterenol; Lactates; Muscles; Myocardium; Organ Size; Propranolol; Propylamines; Rats; Salivary Gland Diseases; Submandibular Gland; Sympatholytics

Topics: Acute Disease; Animals; Brain; Cerebellum; Cerebral Cortex; Choroid Plexus; Glycogen; Hypertrophy; Inflammation; Macaca; Necrosis; Neuroglia; Protons; Radiation Dosage; Radiation Injuries, Experimental; Spinal Cord

Topics: Animals; Cartilage; Collagen; Diet; Endoplasmic Reticulum; Epiphyses; Glycogen; Golgi Apparatus; Guinea Pigs; Histocytochemistry; Housing, Animal; Hypertrophy; Inclusion Bodies; Lipids; Lysosomes; Microscopy, Electron; Mitochondria; Phagocytosis; Ribosomes; Scurvy; Tibia; Time Factors

Topics: Animals; Female; Glucosephosphate Dehydrogenase; Glycerolphosphate Dehydrogenase; Glycogen; Hexosephosphates; Histocytochemistry; Hydrogen-Ion Concentration; Hypertrophy; L-Lactate Dehydrogenase; Myocardial Infarction; Myocardium; Proteins; Rats; Time Factors

Topics: Alkaline Phosphatase; Aminopropionitrile; Animals; Ascorbic Acid; Calcification, Physiologic; Cartilage; Chick Embryo; Chondroitin; Collagen; Cortisone; Endoplasmic Reticulum; Glycogen; Hypertrophy; Lipids; Skull

Topics: Child, Preschool; Congenital Hypothyroidism; Glycogen; Histocytochemistry; Humans; Hypertrophy; Hypothyroidism; Male; Muscles; Muscular Diseases

Topics: Age Factors; Animals; Body Weight; Chickens; Depression, Chemical; DNA; Drug Antagonism; Electrophoresis; Estradiol; Estrogen Antagonists; Female; Glucose; Glycogen; Hyperplasia; Hypertrophy; Lipid Metabolism; Ovalbumin; Oviducts; Progesterone; Proteins; RNA; Time Factors

Topics: Adult; Alkaline Phosphatase; Castration; Dihydrolipoamide Dehydrogenase; Endometrium; Esterases; Female; Glycogen; Humans; Hypertrophy; Luteinizing Hormone; Menstruation; Mitochondria; Ovary; Oxidoreductases; Phosphoric Monoester Hydrolases; Progesterone; Radioimmunoassay; Time Factors

Topics: Animals; Diaphragm; Glucose; Glucosephosphate Dehydrogenase; Glucosyltransferases; Glycogen; Hexokinase; Hypertrophy; Muscle Denervation; Muscles; Phosphoglucomutase; Rats

Topics: Animals; Body Weight; Cresols; Diet; Fats; Food Additives; Glycogen; Growth; Hepatomegaly; Hyperplasia; Hypertrophy; Liver; Male; Nitrogen; Nucleic Acids; Organ Size; Proteins; Rats; Water

Topics: Aged; Autopsy; Carcinoma, Squamous Cell; Epithelium; Esophageal Diseases; Esophageal Neoplasms; Esophagus; Female; Glycogen; Humans; Hyperplasia; Hypertrophy; Leukoplakia; Male; Middle Aged; Precancerous Conditions

1. Apparatus is described in which rat extensor digitorum longus muscle can be incubated in buffer under conditions of light tension and be subject to contractures induced by electrical stimulation in vitro. Under these conditions the tissue retains its weight, its content of potassium and size of the extracellular space at values similar to those in vivo. 2. Though uptake of glucose was enhanced on addition of insulin, there was little increase in glucose consumption on stimulation. Breakdown of glycogen and enhancement of lactate output were found on stimulation. 3. Incorporation into protein of several labelled amino acids was diminished during stimulation. Accumulation of [(14)C]leucine was enhanced whereas that of glycine was decreased. 4. There were no very consistent changes in the content of free unlabelled amino acids during incubation with or without stimulation. Comparison of actual amino acid concentrations in tissue and incubation mixture with accumulation of (14)C-labelled amino acid indicated that full equilibration of the cell pool of amino amino acids with the medium is slow. 5. Substantial oxidation of several (14)C-labelled acids was observed. 6. The ATP content of the tissue declined a little during incubation and somewhat faster after a period of stimulation. 7. The results are discussed in relation to the way in which exercise can induce muscle hypertrophy.

Topics: Adenine Nucleotides; Adenosine Triphosphate; Amino Acids; Animals; Electric Stimulation; Female; Glucose; Glycine; Glycogen; Hypertrophy; In Vitro Techniques; Insulin; Lactates; Leucine; Muscle Proteins; Muscles; Rats

Topics: Animals; Cardiomegaly; Dogs; Glycogen; Heart Ventricles; Histocytochemistry; Hypertrophy; Microscopy, Electron; Myocardium; Myofibrils; Pulmonary Artery

Topics: Animals; Castration; Cell Nucleolus; Glycogen; Hypertrophy; Male; Microscopy, Electron; Muscles; Muscular Atrophy; Myofibrils; Nitrogen; Pelvis; Rats; Regeneration; Testosterone

Topics: Biopsy; Chemical and Drug Induced Liver Injury; Chronic Disease; Cytoplasmic Granules; Endoplasmic Reticulum; Glycogen; Hemochromatosis; Humans; Hypertrophy; Liver; Liver Cirrhosis; Liver Neoplasms; Microscopy, Electron

Topics: Animals; Bone Marrow; Cartilage; Cartilage, Articular; Cell Nucleus; Endoplasmic Reticulum; Glycogen; Golgi Apparatus; Hypertrophy; Injections, Subcutaneous; Lipids; Male; Mice; Mitochondria; Polysaccharides; Protein Biosynthesis; Tissue Extracts

Topics: Animals; Cardiomegaly; Chick Embryo; DNA; Electrocardiography; Glycogen; Glycogen Storage Disease; Histocytochemistry; Hypertrophy; Microscopy, Electron; Models, Theoretical; Myocardium; Proteins; Temperature

Topics: Adrenal Glands; Animals; Blood Cell Count; Cardiomegaly; Cardiovascular System; Catecholamines; Electrocardiography; Epinephrine; Glycogen; Heart; Hemoglobins; Hyperthyroidism; Hypertrophy; Myocardium; Nitrogen; Norepinephrine; Organ Size; Protein Biosynthesis; Rabbits; Thyroid Hormones; Water-Electrolyte Balance

Topics: Animals; Cholinesterases; Denervation; Diaphragm; Glycogen; Hypertrophy; In Vitro Techniques; Methionine; Peptide Hydrolases; Potassium; Proteins; Rats; RNA

Topics: Glucosidases; Glycogen; Glycogen Storage Disease; Humans; Hyperplasia; Hypertrophy; Infant; Liver Diseases; Metabolic Diseases; Metabolism; Muscular Diseases

Topics: Carbohydrate Metabolism; Glycogen; Hyperplasia; Hypertrophy; Neoplasms; Palate

Topics: Adrenal Glands; Blood; Blood Chemical Analysis; Body Weight; Brain; Brain Chemistry; Carbohydrate Metabolism; Chemical Phenomena; Chemistry; Chlorides; Cold Temperature; Electroshock; Glucose; Glycogen; Hyperglycemia; Hyperplasia; Hypertrophy; Liver; Muscles; Neurochemistry; Physiology; Potassium; Rats; Research; Seizures; Sodium; Thymus Gland; Water

Topics: Animals; Cardiomegaly; Glycogen; Glycogenolysis; Hypertrophy; Myocardium; Rats