Energy Metabolism in Denervated Muscle

Bass, A

doi:10.1007/978-1-4899-4854-0_9

Cited by 14 publications

(4 citation statements)

References 120 publications

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“…An initial hypertrophy and an increase in protein content has been shown in diaphragm muscles (Stewart, 1955). There is evidence for increased oxygen consumption in denervated muscle in vivo and in vitro (Bass, 1962). A change of permeability following denervation is suggested by the increased uptake of labelled decamethonium which has been found in denervated guinea-pig diaphragm (Taylor, Creese, Nedergaard & Case, 1965).…”

Section: Discussionmentioning

confidence: 99%

Sodium movements in denervated muscle and the effects of antimycin A

Creese¹,

El-Shafie²,

Vrbová³

1968

The Journal of Physiology

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SUMMARY1. Fibre sodium in rat diaphragm exchanged at a faster rate in muscles which had been denervated 8 days previously. The half-time was 3-7 min for outward movement in denervated muscles and 5*1 min in controls.2. The inward movement of sodium was also faster in denervated muscle as compared with controls, and the calculated permeability to sodium was approximately doubled.3. In the presence of antimycin A (1-8 x 10-5 M), the outward movement of sodium in denervated diaphragm was slowed and the fibres gained sodium and lost potassium.4. Antimycin markedly reduced the twitch produced by stimulation of denervated diaphragm, and also the response to acetylcholine. Similar effects were found in denervated tibialis anterior of the cat.

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Section: Discussionmentioning

confidence: 99%

Sodium movements in denervated muscle and the effects of antimycin A

Creese¹,

El-Shafie²,

Vrbová³

1968

The Journal of Physiology

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“…The reason for this increase of Oj consumption is not obvious. It might be linked with the increased proteolytic (20,21) or glycolytic (22) activity in the atrophying muscle, or it might be explained by an impairment of oxidative phosphorylation (23). The changes in O 2 and CO 2 tension probably induce vasodilation of the microcirculation, and despite the greatly diminished bulk of the muscular tissue, the vascular bed appears to remain unchanged.…”

Section: Discussionmentioning

confidence: 99%

Blood Flow and Oxygen Consumption in Muscles after Section of Ventral Roots

Hudlická

1967

Circulation Research

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Muscles deprived of somatic motor innervation (sensory and sympathetic motor innervation intact) served as a model for studying the role of vasoconstrictor fibers and skeletal muscle tone in the regulation of skeletal muscle blood flow. Blood flow, vascular resistance and O 2 consumption of the gastrocnemius muscle of the cat were measured 5 to 7, 10 to 16, and 27 to 44 days after unilateral section of ventral roots L 5 to S B in cats and compared to similar measurements in the normal gastrocnemius muscle and in that with its sciatic nerve cut. After section of the peripheral nerve, total blood flow increased and then returned to normal; after section of the ventral roots, total blood flow did not change significantly. In both cases, blood flow per 100 g of muscle increased as atrophy developed. After section of the ventral roots, O 2 consumption and CO 2 production per 100 g of muscle increased earlier than blood flow. Peripheral resistance was calculated before and immediately after acute section of both tibial nerves to evaluate the participation of muscle tone in the regulation of peripheral resistance. At rest, muscle tone appears to be responsible for about 25% of the peripheral resistance. MethodsExperiments were performed on 19 cats weighing 2 to 4.5 kg anesthetized with pentobarbital (0.30 mg/kg body weight, ip). In 13 cats, the ventral roots from L B to S 5 on the left side were cut intradurally under aseptic conditions several days or weeks before measurement of blood flow; in these animals, the gastrocnemius muscle was deprived of its motor nerve supply, but 570

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“…The converse effects occur in type I1 muscle (Drahota and Gutmann, 1963;Bucher and Pette, 1965; Prewitt and Salafsky, 1967;Golisch et al, 1970). Denervation of muscle leads to a rapid reduction of oxidative and glycolytic processes (Bass, 1963) and of histochemical reactions that reflect the activity of enzymes catalyzing these processes (Karpati and Engel, 1968). In addition, oxidative processes or histochemical reactions increase with exercise and electrical stimulation in muscles with a P .…”

mentioning

confidence: 99%

Effects of Denervation and Simple Disuse on Rates of Oxidation and on Activities of Four Mitochondrial Enzymes in Type I Muscle

Nemeth¹,

Meyer

Kark

1980

Journal of Neurochemistry

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To differentiate the effect of muscle contractile activity from that of motor nerve on oxidative processes in type I muscle, oxidative processes were studied in muscle after immobilization and after denervation. The two processes led to similar atrophy of muscle weight and of the mean diameter of muscle fibers. Disuse of soleus muscle (type I) did not affect rates of oxidation of 14C-labeled substrates although these were reduced by disuse of the vastus lateralis (type II). Disuse of the soleus did not affect activities of several mitochondrial enzymes assayed by histochemical or biochemical methods. However, denervation of the soleus did lead to a fall in metabolic rates and enzyme activities. The activity of 3-hydroxybutyrate dehydrogenase fell more than did the activities of succinic dehydrogenase, lipoamide dehydrogenase, or cytochrome-c oxidase in both homogenates and in mitochondrial fractions. These results suggest nerve may regulate mitochondrial enzymes in type I muscle. The mechanism appears to be different from that which regulates oxidative processes in type II muscle.

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Energy Metabolism in Denervated Muscle

Cited by 14 publications

References 120 publications

Sodium movements in denervated muscle and the effects of antimycin A

Sodium movements in denervated muscle and the effects of antimycin A

Blood Flow and Oxygen Consumption in Muscles after Section of Ventral Roots

Effects of Denervation and Simple Disuse on Rates of Oxidation and on Activities of Four Mitochondrial Enzymes in Type I Muscle

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