Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.99.3 (acyl-CoA dehydrogenase)
 1,425 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is not known whether cellular adaptations of the ventilatory muscles are induced by increased respiratory loads. A chronic respiratory load was produced in rats by tracheal banding. Five weeks after the imposition of this increased load, biochemical and histochemical analyses were performed on the diaphragm and intercostal muscles. The oxidative capacity, as indicated by succinate dehydrogenase (SDH) activity, increased 38% in the diaphragm. The capacity for beta-oxidation fatty acids, as indicated by 3-hydroxy-acyl-CoA dehydrogenase (HADH) activity, increased 29%. The glycolytic capacity, as indicated by phosphofructokinase (PFK) activity, did not change. Similar enzymatic adaptations were observed in the intercostal muscles. The proportion of slow-twitch muscle fibers, as indicated by the myofibrillar adenosine triphosphatase (ATPase) stain, increased in the diaphragm, but not in the intercostal muscles. Thus, these ventilatory muscles responded with an increase in their oxidative capacity, and the diaphragm reponded with an increase in the proportion of muscle fibers having the myofibriller ATPase staining characteristic of slow-twich fibers. We conclude that cellular adaptations are induced in the ventilatory muscles by chronic increased respiratory loads.
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PMID:Cellular adaptations of the ventilatory muscles to a chronic increased respiratory load. 14 78

Muscle biopsy samples were collected from the middle gluteal muscle of seven horses undergoing a nine-month endurance training programme. Samples were collected before the programme began and again after three, six and nine months of training. A fifth sample was collected three months after training ceased. Serial muscle sections were reacted histochemically for myosin adenosine triphosphatase after either acid (pH 4.3 and 4.6) or alkaline (pH 10.3) pre-incubation, and muscle fibres identified as type I, IIA, IIB or IIC. The oxidative capacity of individual fibres was assessed, using the reduced nicotinamide dinucleotide tetrazolium reductase stain, and the number of intermyofibrillar capillaries adjacent to each fibre was counted after staining, using the alpha-amylase periodic acid Schiff technique. Biochemical analyses involved the fluorometric measurement of the enzymes citrate synthase, 3-hydroxy acyl CoA dehydrogenase and lactate dehydrogenase as markers of end terminal oxidative, beta oxidative and glycolytic potential, respectively. There was an increase in the percentage of type IIB fibres having high nicotinamide dinucleotide tetrazolium reductase staining after three months training. This increase persisted throughout the period of training and during the period without training. There was an increase in the number of capillaries adjacent to type IIB fibres after six and nine months training. These had returned to near pre-training numbers after three months without training. There were increases in the activities of citrate synthase and 3-hydroxy acyl CoA dehydrogenase after three months training. The activities of both enzymes continued to rise throughout training and the highest activities were attained after nine months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of a nine-month endurance training programme on muscle composition in the horse. 367 37