Early ultrastructural changes in skeletal muscle biopsies from patients with mitochondrial myopathy

To ascertain the effects of sprint and endurance exercise on the time course of skeletal muscle mitochondrial changes, an ultrastructural study was conducted on four Thoroughbred horses. Skeletal muscle biopsies were taken at various intervals during and after the exercise. Transient mitochondrial alterations of varying degrees were observed following both types of exercise and were considered to be related to the development of fatigue. The degree of distortion of mitochondrial structure is considered not to represent the in vivo condition but the state of responsiveness to the fixation medium.

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Some Observations on Intra-Mitochondrial Crystals

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100079486 ◽

1977 ◽

Vol 35 ◽

pp. 406-407

Author(s):

J. A. Clarke ◽

D. N. Landon ◽

P. R. Ward

Keyword(s):

Cytochrome B ◽

Mitochondrial Myopathy ◽

Crystallographic Analysis ◽

Mitochondrial Membranes ◽

Electron Microscopes ◽

Muscle Biopsies

Intra-mitochondrial crystals have been noted in muscle biopsies from patients in a wide variety of diseased states. As far as we are aware, none of these crystals have been subjected to detailed crystallographic analysis. Recently, similar crystals were observed in a biopsy from a patient with a mitochondrial myopathy, characterised by a deficiency in reducible cytochrome b (Morgan-Hughes, J. A., Darveniza, P., Kahn, S. N., Landon, D. N., Sherratt, R. M., Land, J. M. and Clark, J. B., 1977, Brain, In Press). Aldehyde-fixed, osmicated resin imbedded material was examined using Siemens, JEOL and Phillips electron microscopes with goniometer specimen stages. The crystals generally lay between the outer and inner mitochondrial membranes and measured 1 - 3 μm in length and 0.1 - 0.3 μm in width. Characteristically, these crystals revealed specific periodicities.

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Studies of the halothane-cooling contractures of skeletal muscle

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-115 ◽

1987 ◽

Vol 65 (4) ◽

pp. 697-703 ◽

Cited By ~ 3

Author(s):

Roberto T. Sudo ◽

Gisele Zapata ◽

Guilherme Suarez-Kurtz

Keyword(s):

Skeletal Muscle ◽

Synergistic Effects ◽

Rabbit Muscle ◽

Slow Twitch ◽

Fast Twitch ◽

Dose Dependent ◽

Muscle Biopsies ◽

Ca Homeostasis ◽

Potential Use

The characteristics of transient contractures elicited by rapid cooling of frog or mouse muscles perfused in vitro with solutions equilibrated with 0.5–2.0% halothane are reviewed. The data indicate that these halothane-cooling contractures are dose dependent and reproducible, and their amplitude is larger in muscles containing predominantly slow-twitch type fibers, such as the mouse soleus, than in muscles in which fast-twitch fibers predominate, such as the mouse extensor digitorum longus. The halothane-cooling contractures are potentiated in muscles exposed to succinylcholine. The effects of Ca2+-free solutions, of the local anesthetics procaine, procainamide, and lidocaine, and of the muscle relaxant dantrolene on the halothane-cooling contractures are consistent with the proposal that the halothane-cooling contractures result from synergistic effects of halothane and low temperature on Ca sequestration by the sarcoplasmic reticulum. Preliminary results from skinned rabbit muscle fibers support this proposal. The halothane concentrations required for the halothane-cooling contractures of isolated frog or mouse muscles are comparable with those observed in serum of patients during general anesthesia. Accordingly, fascicles dissected from muscle biopsies of patients under halothane anesthesia for programmed surgery develop large contractures when rapidly cooled. The amplitude of these halothane-cooling contractures declined with the time of perfusion of the muscle fascicles in vitro with halothane-free physiological solutions. It is suggested that the halothane-cooling contractures could be used as a simple experimental model for the investigation of the effects of halothane on Ca homeostasis and contractility in skeletal muscle and for study of drugs of potential use in the management of the contractures associated with the halothane-induced malignant hyperthermia syndrome. It is shown that salicylates, but not indomethacin or mefenamic acid, inhibit the halothane-cooling contractures.

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Ultrastructural changes in skeletal muscle capillaries caused by snake venom and two of its fractions

Toxicon ◽

10.1016/0041-0101(85)90307-1 ◽

1985 ◽

Vol 23 (4) ◽

pp. 603

Keyword(s):

Skeletal Muscle ◽

Snake Venom ◽

Ultrastructural Changes ◽

Muscle Capillaries

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Pro- and macroglycogenolysis: relationship with exercise intensity and duration

Journal of Applied Physiology ◽

10.1152/jappl.2001.90.3.873 ◽

2001 ◽

Vol 90 (3) ◽

pp. 873-879 ◽

Cited By ~ 33

Author(s):

T. E. Graham ◽

K. B. Adamo ◽

J. Shearer ◽

I. Marchand ◽

B. Saltin

Keyword(s):

Skeletal Muscle ◽

Metabolic Regulation ◽

Human Skeletal Muscle ◽

Exercise Period ◽

Group 3 ◽

Group 2 ◽

Male Subjects ◽

Muscle Biopsies ◽

Over Time ◽

Group 1

We examined the net catabolism of two pools of glycogen, proglycogen (PG) and macroglycogen (MG), in human skeletal muscle during exercise. Male subjects ( n = 21) were assigned to one of three groups. Group 1 exercised 45 min at 70% maximal O2 uptake (V˙o 2 max) and had muscle biopsies at rest, 15 min, and 45 min. Group 2 exercised at 85%V˙o 2 max to exhaustion (45.4 ± 3.4 min) and had biopsies at rest, 10 min, and exhaustion. Group 3 performed three 3-min bouts of exercise at 100%V˙o 2 max separated by 6 min of rest. Biopsies were taken at rest and after each bout. Group 1 had small MG and PG net glycogenolysis rates (ranging from 3.8 ± 1.0 to 2.4 ± 0.6 mmol glucosyl units · kg−1 · min−1) that did not change over time. In group 2, the MG glycogenolysis rate remained low and unchanged over time, whereas the PG rate was initially elevated (11.3 ± 2.3 mmol glucosyl units · kg−1 · min−1) and declined ( P ≤ 0.05) with time. During the first 10 min, PG concentration ([PG]) declined ( P ≤ 0.05), whereas MG concentration ([MG]) did not. Similarly, in group 3, in both the first and the second bouts of exercise [PG] declined ( P ≤ 0.05) and [MG] did not, although by the end of the second exercise period the [MG] was lower ( P ≤ 0.05) than the rest level. The net catabolic rates for PG in the first two exercises were 22.6 ± 6.8 and 21.8 ± 8.2 mmol glucosyl units · kg−1 · min−1, whereas the corresponding values for MG were 17.6 ± 6.0 and 10.8 ± 5.6. The MG pool appeared to be more resistant to mobilization, and, when activated, its catabolism was inhibited more rapidly than that of PG. This suggests that the metabolic regulation of the two pools must be different.

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Regulation of glycogen phosphorylase and PDH during exercise in human skeletal muscle during hypoxia

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2000.278.3.e522 ◽

2000 ◽

Vol 278 (3) ◽

pp. E522-E534 ◽

Cited By ~ 41

Author(s):

Michelle L. Parolin ◽

Lawrence L. Spriet ◽

Eric Hultman ◽

Melanie G. Hollidge-Horvat ◽

Norman L. Jones ◽

...

Keyword(s):

Skeletal Muscle ◽

Glycogen Phosphorylase ◽

Lactate Production ◽

Muscle Metabolism ◽

Lactate Accumulation ◽

Pyruvate Oxidation ◽

Reduced Rate ◽

Rate Limiting ◽

Muscle Biopsies ◽

Elevated Lactate

The present study examined the acute effects of hypoxia on the regulation of skeletal muscle metabolism at rest and during 15 min of submaximal exercise. Subjects exercised on two occasions for 15 min at 55% of their normoxic maximal oxygen uptake while breathing 11% O2 (hypoxia) or room air (normoxia). Muscle biopsies were taken at rest and after 1 and 15 min of exercise. At rest, no effects on muscle metabolism were observed in response to hypoxia. In the 1st min of exercise, glycogenolysis was significantly greater in hypoxia compared with normoxia. This small difference in glycogenolysis was associated with a tendency toward a greater concentration of substrate, free Pi, in hypoxia compared with normoxia. Pyruvate dehydrogenase activity (PDHa) was lower in hypoxia at 1 min compared with normoxia, resulting in a reduced rate of pyruvate oxidation and a greater lactate accumulation. During the last 14 min of exercise, glycogenolysis was greater in hypoxia despite a lower mole fraction of phosphorylase a. The greater glycogenolytic rate was maintained posttransformationally through significantly higher free [AMP] and [Pi]. At the end of exercise, PDHawas greater in hypoxia compared with normoxia, contributing to a greater rate of pyruvate oxidation. Because of the higher glycogenolytic rate in hypoxia, the rate of pyruvate production continued to exceed the rate of pyruvate oxidation, resulting in significant lactate accumulation in hypoxia compared with no further lactate accumulation in normoxia. Hence, the elevated lactate production associated with hypoxia at the same absolute workload could in part be explained by the effects of hypoxia on the activities of the rate-limiting enzymes, phosphorylase and PDH, which regulate the rates of pyruvate production and pyruvate oxidation, respectively.

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A pattern-based approach to the interpretation of skeletal muscle biopsies

Modern Pathology ◽

10.1038/s41379-018-0164-x ◽

2018 ◽

Vol 32 (4) ◽

pp. 462-483 ◽

Cited By ~ 6

Author(s):

Chunyu Cai ◽

Douglas C. Anthony ◽

Peter Pytel

Keyword(s):

Skeletal Muscle ◽

Muscle Biopsies

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A single bout of exercise activates matrix metalloproteinase in human skeletal muscle

Journal of Applied Physiology ◽

10.1152/japplphysiol.00822.2006 ◽

2007 ◽

Vol 102 (6) ◽

pp. 2346-2351 ◽

Cited By ~ 89

Author(s):

E. Rullman ◽

H. Rundqvist ◽

D. Wågsäter ◽

H. Fischer ◽

P. Eriksson ◽

...

Keyword(s):

Skeletal Muscle ◽

Matrix Metalloproteinase ◽

Vastus Lateralis ◽

Tissue Expression ◽

Tissue Inhibitor Of Metalloproteinase ◽

Vastus Lateralis Muscle ◽

Protein Levels ◽

Single Bout ◽

Exercise Induced ◽

Muscle Biopsies

The aims of this study were 1) to characterize changes in matrix metalloproteinase (MMP), endostatin, and vascular endothelial growth factor (VEGF)-A expression in skeletal muscle in response to a single bout of exercise in humans; and 2) to determine if any exchange of endostatin and VEGF-A between circulation and the exercising leg is associated with a change in the tissue expression or plasma concentration of these factors. Ten healthy males performed 65 min of cycle exercise, and muscle biopsies were obtained from the vastus lateralis muscle at rest and immediately and 120 min after exercise. In the muscle biopsies, measurements of mRNA expression levels of MMP-2, MMP-9, MMP-14, and tissue inhibitor of metalloproteinase; VEGF and endostatin protein levels; and MMP activities were performed. Femoral arterial and venous concentrations of VEGF-A and endostatin were determined before, during, and 120 min after exercise. A single bout of exercise increased MMP-9 mRNA and activated MMP-9 protein in skeletal muscle. No measurable increase of endostatin was observed in the skeletal muscle or in plasma following exercise. A concurrent increase in skeletal muscle VEGF-A mRNA and protein levels was induced by exercise, with no signs of peripheral uptake from the circulation. However, a decrease in plasma VEGF-A concentration occurred following exercise. Thus 1) a single bout of exercise activated the MMP system without any resulting change in tissue endostatin protein levels, and 2) the increased VEGF-A protein levels are due to changes in the skeletal muscle tissue itself. Other mechanisms are responsible for the observed exercise-induced decrease in VEGF-A in plasma.

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