scholarly journals Alterations in Lactate Dehydrogenase of the Brain, Heart, Skeletal Muscle, and Liver of Rats of Various Ages

1968 ◽  
Vol 243 (17) ◽  
pp. 4526-4529
Author(s):  
S N Singh ◽  
M S Kanungo
Keyword(s):  
Skeletal Muscle ◽  
Lactate Dehydrogenase ◽  
The Brain

Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

1974 ◽  
Vol 32 ◽  
pp. 148-149
Author(s):  
D. E. Philpott ◽  
A. Takahashi
Keyword(s):  
Skeletal Muscle ◽  
Endothelial Cells ◽  
Salivary Gland ◽  
Carotid Artery ◽  
Basement Membrane ◽  
Coronary Vessels ◽  
Ruthenium Red ◽  
E Coli ◽  
Old Rats ◽  
The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

scholarly journals Lack of Skeletal Muscle Serotonin Impairs Physical Performance

2021 ◽  
Vol 14 ◽  
pp. 117864692110031
Author(s):  
Marion Falabrègue ◽  
Anne-Claire Boschat ◽  
Romain Jouffroy ◽  
Marieke Derquennes ◽  
Haidar Djemai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Physical Performance ◽  
Depressive Disorders ◽  
Tryptophan Metabolism ◽  
Long Distance ◽  
Positive Effects ◽  
Tryptophan Metabolites ◽  
The Brain ◽  
Deficient Mice

Low levels of the neurotransmitter serotonin have been associated with the onset of depression. While traditional treatments include antidepressants, physical exercise has emerged as an alternative for patients with depressive disorders. Yet there remains the fundamental question of how exercise is sensed by the brain. The existence of a muscle–brain endocrine loop has been proposed: according to this scenario, exercise modulates metabolization of tryptophan into kynurenine within skeletal muscle, which in turn affects the brain, enhancing resistance to depression. But the breakdown of tryptophan into kynurenine during exercise may also alter serotonin synthesis and help limit depression. In this study, we investigated whether peripheral serotonin might play a role in muscle–brain communication permitting adaptation for endurance training. We first quantified tryptophan metabolites in the blood of 4 trained athletes before and after a long-distance trail race and correlated changes in tryptophan metabolism with physical performance. In parallel, to assess exercise capacity and endurance in trained control and peripheral serotonin–deficient mice, we used a treadmill incremental test. Peripheral serotonin–deficient mice exhibited a significant drop in physical performance despite endurance training. Brain levels of tryptophan metabolites were similar in wild-type and peripheral serotonin–deficient animals, and no products of muscle-induced tryptophan metabolism were found in the plasma or brains of peripheral serotonin–deficient mice. But mass spectrometric analyses revealed a significant decrease in levels of 5-hydroxyindoleacetic acid (5-HIAA), the main serotonin metabolite, in both the soleus and plantaris muscles, demonstrating that metabolization of tryptophan into serotonin in muscles is essential for adaptation to endurance training. In light of these findings, the breakdown of tryptophan into peripheral but not brain serotonin appears to be the rate-limiting step for muscle adaptation to endurance training. The data suggest that there is a peripheral mechanism responsible for the positive effects of exercise, and that muscles are secretory organs with autocrine-paracrine roles in which serotonin has a local effect.

scholarly journals Exercise Inducible Lactate Dehydrogenase B Regulates Mitochondrial Function in Skeletal Muscle

2016 ◽  
Vol 291 (49) ◽  
pp. 25306-25318 ◽  
Author(s):  
Xijun Liang ◽  
Lin Liu ◽  
Tingting Fu ◽  
Qian Zhou ◽  
Danxia Zhou ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lactate Dehydrogenase ◽  
Mitochondrial Function

scholarly journals THE DISTRIBUTION OF LACTATE DEHYDROGENASE ISOZYMES IN HUMAN SKELETAL MUSCLE FIBERS

1964 ◽  
Vol 12 (8) ◽  
pp. 608-614 ◽  
Author(s):  
M. VAN WIJHE ◽  
M. C. BLANCHAER ◽  
S. ST. GEORGE-STUBBS
Keyword(s):  
Skeletal Muscle ◽  
Lactate Dehydrogenase ◽  
Human Skeletal Muscle ◽  
Muscle Fibers ◽  
Isozyme Pattern ◽  
Electrophoretic Separation ◽  
Lactate Dehydrogenase Isozymes ◽  
Dehydrogenase Isozyme ◽  
Lactate Dehydrogenase Isozyme ◽  
Normal Human

A study of the distribution of lactate dehydrogenase isozymes in single fibers from normal human skeletal muscle is presented. The fibers were classified into red, intermediate and white types on histochemical grounds and their lactate dehydrogenase isozyme content assessed by electrophoretic separation in veronal buffered agar. The results generally agreed with previous homogenate studies on animal skeletal muscle, in that the white fibers contained almost exclusively isozymes IV and V, whereas red fibers were rich in isozymes I, II and III, but IV and V also appeared indigenous to these fibers. The intermediate fibers had an isozyme pattern combining the features of red and white fibers. The metabolic implications of these findings are discussed.

Skeletal muscle biochemical adaptations to exercise training in miniature swine

1997 ◽  
Vol 82 (6) ◽  
pp. 1862-1868 ◽  
Author(s):  
Richard M. McAllister ◽  
Brian L. Reiter ◽  
John F. Amann ◽  
M. Harold Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Lactate Dehydrogenase ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Oxidative Capacity ◽  
Treadmill Running ◽  
Miniature Swine ◽  
Endurance Exercise Training ◽  
Hydroxyacyl Coa Dehydrogenase

McAllister, Richard M., Brian L. Reiter, John F. Amann, and M. Harold Laughlin. Skeletal muscle biochemical adaptations to exercise training in miniature swine. J. Appl. Physiol. 82(6): 1862–1868, 1997.—The primary purpose of this study was to test the hypothesis that endurance exercise training induces increased oxidative capacity in porcine skeletal muscle. To test this hypothesis, female miniature swine were either trained by treadmill running 5 days/wk over 16–20 wk (Trn; n = 35) or pen confined (Sed; n = 33). Myocardial hypertrophy, lower heart rates during submaximal stages of a maximal treadmill running test, and increased running time to exhaustion during that test were indicative of training efficacy. A variety of skeletal muscles were sampled and subsequently assayed for the enzymes citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactate dehydrogenase and for antioxidant enzymes. Fiber type composition of a representative muscle was also determined histochemically. The largest increase in CS activity (62%) was found in the gluteus maximus muscle (Sed, 14.7 ± 1.1 μmol ⋅ min−1 ⋅ g−1; Trn, 23.9 ± 1.0; P < 0.0005). Muscles exhibiting increased CS activity, however, were located primarily in the forelimb; ankle and knee extensor and respiratory muscles were unchanged with training. Only two muscles exhibited higher 3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed. Lactate dehydrogenase activity was unchanged with training, as were activities of antioxidant enzymes. Histochemical analysis of the triceps brachii muscle (long head) revealed lower type IIB fiber numbers in Trn (Sed, 42 ± 6%; Trn, 10 ± 4; P < 0.01) and greater type IID/X fiber numbers (Sed, 11 ± 2; Trn, 22 ± 3; P < 0.025). These findings indicate that porcine skeletal muscle adapts to endurance exercise training in a manner similar to muscle of humans and other animal models, with increased oxidative capacity. Specific muscles exhibiting these adaptations, however, differ between the miniature swine and other species.

Differential energetic response of brain vs. skeletal muscle upon glycemic variations in healthy humans

2008 ◽  
Vol 294 (1) ◽  
pp. R12-R16 ◽  
Author(s):  
Kerstin M. Oltmanns ◽  
Uwe H. Melchert ◽  
Harald G. Scholand-Engler ◽  
Maria C. Howitz ◽  
Bernd Schultes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Underlying Mechanism ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
High Energy Phosphate ◽  
Available Energy ◽  
Healthy Humans ◽  
High Energy Phosphate Metabolism ◽  
The Brain

The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using 31P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by 31P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain ( P = 0.013), while there was a similar trend in the hypopglycemic condition ( P = 0.055). Skeletal muscle content remained constant in both conditions ( P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to −4%) revealed clear divergent effects in both conditions ( P < 0.05). These effects were reflected by PCr/Pi ratio ( P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia ( P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.

Hippocampal glutamine synthetase: insensitivity to glucocorticoids and stress

1990 ◽  
Vol 258 (5) ◽  
pp. E894-E897 ◽  
Author(s):  
G. C. Tombaugh ◽  
R. M. Sapolsky
Keyword(s):  
Skeletal Muscle ◽  
Central Nervous System ◽  
Nervous System ◽  
Glutamine Synthetase ◽  
Glutamate Metabolism ◽  
Glutamatergic Synapses ◽  
Adult Rats ◽  
Glucocorticoid Induction ◽  
The Central Nervous System ◽  
The Brain

Glucocorticoids enhance the neurotoxic potential of several insults to the rat hippocampus that involve overactivation of glutamatergic synapses. These hormones also stimulate the synthesis of glutamine synthetase (GS) in peripheral tissue. Because this enzyme helps regulate glutamate metabolism in the central nervous system, glucocorticoid induction of GS in the brain may underlie the observed synergy. We have measured GS activity in the hippocampus and skeletal muscle (plantaris) of adult rats after bilateral adrenalectomy (ADX), corticosterone (Cort) replacement, or stress. No significant changes in GS were observed in hippocampal tissue, whereas muscle GS was significantly elevated after Cort treatment or stress and was reduced after ADX. These results suggest that Cort-induced shifts in GS activity probably do not explain Cort neurotoxicity, although the stress-induced rise in muscle GS may be relevant to certain types of myopathy.

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