Effect of overwork during reinnervation of rat muscle

Herbison, Gerald J.; Jaweed, M.M.; Ditunno, John F.; Scott, Carolyn

doi:10.1016/0014-4886(73)90176-3

Cited by 53 publications

(33 citation statements)

References 18 publications

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“…Accordingly, increased exercise can protect such fibers from glucocorticoids, and it can even induce muscle hypertrophy in fasted animals (14). By contrast, the dark type I fibers high in PGC-1␣ content become sensitive to glucocorticoid-induced atrophy, and they show the greatest atrophy after denervation, when PGC-1␣ expression falls (24). Thus, together with the exercise-induced production of IGF-1, the exerciseinduced changes in PGC-1␣ in muscle seem to be critical factors by which contractile activity determines muscle size as well as its enzymatic composition (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…During fasting (18) or exposure to glucocorticoids (19,20), sepsis (21), and cancer cachexia (22,23), type II glycolytic muscle fibers show greater atrophy than the type I oxidative fibers. On the other hand, during unloading or denervation, the fatigueresistant, slow-contracting, dark muscles show more pronounced atrophy than fast-contracting, glycolytic, pale ones (24). These differences appear to be caused by greater activity of neurons innervating the dark muscles (19).…”

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confidence: 95%

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PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription

Sandri

Lin

Handschin

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

908

871

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Maintaining muscle size and fiber composition requires contractile activity. Increased activity stimulates expression of the transcriptional coactivator PGC-1␣ (peroxisome proliferator-activated receptor ␥ coactivator 1␣), which promotes fiber-type switching from glycolytic toward more oxidative fibers. In response to disuse or denervation, but also in fasting and many systemic diseases, muscles undergo marked atrophy through a common set of transcriptional changes. FoxO family transcription factors play a critical role in this loss of cell protein, and when activated, FoxO3 causes expression of the atrophy-related ubiquitin ligases atrogin-1 and MuRF-1 and profound loss of muscle mass. To understand how exercise might retard muscle atrophy, we investigated the possible interplay between PGC-1␣ and the FoxO family in regulation of muscle size. Rodent muscles showed a large decrease in PGC-1␣ mRNA during atrophy induced by denervation as well as by cancer cachexia, diabetes, and renal failure. Furthermore, in transgenic mice overexpressing PGC-1␣, denervation and fasting caused a much smaller decrease in muscle fiber diameter and a smaller induction of atrogin-1 and MuRF-1 than in control mice. Increased expression of PGC-1␣ also increased mRNA for several genes involved in energy metabolism whose expression decreases during atrophy. Transfection of PGC-1␣ into adult fibers reduced the capacity of FoxO3 to cause fiber atrophy and to bind to and transcribe from the atrogin-1 promoter. Thus, the high levels of PGC-1␣ in dark and exercising muscles can explain their resistance to atrophy, and the rapid fall in PGC-1␣ during atrophy should enhance the FoxO-dependent loss of muscle mass.denervation ͉ fasting ͉ muscle fiber ͉ energy metabolism ͉ mitochondria

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 95%

PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription

Sandri

Lin

Handschin

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

908

871

View full text Add to dashboard Cite

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“…In rat sciatic nerve repair, range of motion impedes the functional nerve recovery by decreasing endoneural collagenization and decreasing angiogenesis [2]. Other animal studies also confirm the deleterious effects of early exercise on the healing of peripheral nerves in rats, but these studies involved high intensity exercises and negative reinforcements [3][4][5][6][7].…”

Section: Range Of Motion Exercisesmentioning

confidence: 97%

Physical Therapy Following Peripheral Nerve Surgeries

Bond

Lundy

2006

Clinics in Podiatric Medicine and Surgery

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“…As a first step we studied the effect of overwork, induced by tenotomy of synergistic muscles, on reinnervating rat soleus and plantaris muscles (Herbison et al, 1973a, b;Herbison et al, 1974a;. The overwork of muscles accomplished by elimination of synergistic muscles two and three weeks after sciatic nerve crush (Herbison et al, 1973b;Herbison et al, 1974b) yielded a decrease in the content of muscle proteins in the former and a significant increase of non-collagenous proteins in the latter. This was interpreted to mean that muscle might be damaged when stressed too soon in or before the reinnervation period.…”

mentioning

confidence: 99%

“…This was interpreted to mean that muscle might be damaged when stressed too soon in or before the reinnervation period. Because of these findings, we formulated the following hypothesis: muscle damage might occur during the course of reinnervation when the number of contractile units (NCU) are too few or the intensity (I) of exercise is too great (Herbison et al, 1973b). This can be expressed as a ratio: NCU/I = C, where C is a limiting value below which reinnervating muscle would be damaged.…”

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confidence: 99%

Effect of swimming on reinnervation of rat skeletal muscle

Herbison

Jaweed

Ditunno

1974

Journal of Neurology, Neurosurgery & Psychiatry

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SYNOPSIS There are no studies that define the optimum intensity or time to begin exercising reinnervating muscle. Exercise is a basic therapeutic procedure in the management of neuromuscular disease, yet far less is known of its applications than, say) chemotherapeutic agents in infectious disease. Fundamental knowledge is lacking in areas one would deem crucial. What should be the intensity of exercises in a given type of impairment? What is the proper duration of exercise ? One hears opinions regarding these variables but nowhere can one find solid principles.Several reports have indicated that patients with disease of the lower motoneurone lost strength after excessive activity (Lovett, 1917;Kendall and Kendall, 1939;Lundervold, 1942;Green, 1949;Seddon, 1949;Hyman, 1953;Mitchell, 1953;Bennett and Knowlton, 1958;Hnik, 1962). Clinical studies designed to determine the effect of exercise after neuronal damage have indicated that exercise does not damage muscle but, on the contrary, they have consistently borne out the efficacy of brief repetitive therapeutic exercises (Delorme et al

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Effect of overwork during reinnervation of rat muscle

Cited by 53 publications

References 18 publications

PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription

PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription

Physical Therapy Following Peripheral Nerve Surgeries

Effect of swimming on reinnervation of rat skeletal muscle

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