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Exercise and glucocorticoid-induced diaphragmatic myopathy.
J Appl Physiol (1985). 1993 Aug; 75(2):763-71.JA

Abstract

We tested the hypothesis that a chronically active muscle, such as the rat diaphragm, would be more resistant to glucocorticoid-induced myopathy than a less active locomotor skeletal muscle (plantaris). Furthermore, we sought to determine whether endurance exercise could antagonize the glucocorticoid-induced atrophy in the diaphragm. Rats were assigned to one of seven experimental groups (n = 10 per group) and injected daily over a 10-day period with either a sham solution or prednisolone acetate: group 1: control; sedentary and sham injected; group 2: control; exercise trained and sham injected; group 3; sedentary; prednisolone (0.5 mg.kg-1 x day-1); group 4: sedentary; prednisolone (1.0 mg.kg-1 x day-1); group 5: sedentary; prednisolone (2.0 mg.kg-1 x day-1); group 6: sedentary; prednisolone (5.0 mg.kg-1 x day-1); group 7: exercise trained; prednisolone (5.0 mg.kg-1 x day-1). Slope differences in the dose-response curves suggest that prednisolone-induced muscle atrophy in the plantaris was more severe than that in the diaphragm. Furthermore, high doses of prednisolone resulted in a differential effect on muscle bioenergetic enzyme activities in the plantaris and diaphragm. Prednisolone treatment (> or = 2 mg.kg-1 x day-1) resulted in a significant reduction in phosphofructokinase activity (expressed as microM substrate.min-1 x mg protein-1) and an increase in 3-hydroxyacyl-CoA dehydrogenase activity in the plantaris muscle. In contrast, prednisolone treatment did not influence phosphofructokinase activity (P > 0.05) in the diaphragm but decreased (P < 0.05) relative citrate synthase activity. Finally, 90 min daily of endurance exercise did not antagonize prednisolone-induced myopathy in either the diaphragm or the plantaris.

Authors+Show Affiliations

Department of Exercise and Sport Sciences, University of Florida, Gainesville 32611.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8226480

Citation

Lieu, F K., et al. "Exercise and Glucocorticoid-induced Diaphragmatic Myopathy." Journal of Applied Physiology (Bethesda, Md. : 1985), vol. 75, no. 2, 1993, pp. 763-71.
Lieu FK, Powers SK, Herb RA, et al. Exercise and glucocorticoid-induced diaphragmatic myopathy. J Appl Physiol (1985). 1993;75(2):763-71.
Lieu, F. K., Powers, S. K., Herb, R. A., Criswell, D., Martin, D., Wood, C., Stainsby, W., & Chen, C. L. (1993). Exercise and glucocorticoid-induced diaphragmatic myopathy. Journal of Applied Physiology (Bethesda, Md. : 1985), 75(2), 763-71.
Lieu FK, et al. Exercise and Glucocorticoid-induced Diaphragmatic Myopathy. J Appl Physiol (1985). 1993;75(2):763-71. PubMed PMID: 8226480.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Exercise and glucocorticoid-induced diaphragmatic myopathy. AU - Lieu,F K, AU - Powers,S K, AU - Herb,R A, AU - Criswell,D, AU - Martin,D, AU - Wood,C, AU - Stainsby,W, AU - Chen,C L, PY - 1993/8/1/pubmed PY - 1993/8/1/medline PY - 1993/8/1/entrez SP - 763 EP - 71 JF - Journal of applied physiology (Bethesda, Md. : 1985) JO - J Appl Physiol (1985) VL - 75 IS - 2 N2 - We tested the hypothesis that a chronically active muscle, such as the rat diaphragm, would be more resistant to glucocorticoid-induced myopathy than a less active locomotor skeletal muscle (plantaris). Furthermore, we sought to determine whether endurance exercise could antagonize the glucocorticoid-induced atrophy in the diaphragm. Rats were assigned to one of seven experimental groups (n = 10 per group) and injected daily over a 10-day period with either a sham solution or prednisolone acetate: group 1: control; sedentary and sham injected; group 2: control; exercise trained and sham injected; group 3; sedentary; prednisolone (0.5 mg.kg-1 x day-1); group 4: sedentary; prednisolone (1.0 mg.kg-1 x day-1); group 5: sedentary; prednisolone (2.0 mg.kg-1 x day-1); group 6: sedentary; prednisolone (5.0 mg.kg-1 x day-1); group 7: exercise trained; prednisolone (5.0 mg.kg-1 x day-1). Slope differences in the dose-response curves suggest that prednisolone-induced muscle atrophy in the plantaris was more severe than that in the diaphragm. Furthermore, high doses of prednisolone resulted in a differential effect on muscle bioenergetic enzyme activities in the plantaris and diaphragm. Prednisolone treatment (> or = 2 mg.kg-1 x day-1) resulted in a significant reduction in phosphofructokinase activity (expressed as microM substrate.min-1 x mg protein-1) and an increase in 3-hydroxyacyl-CoA dehydrogenase activity in the plantaris muscle. In contrast, prednisolone treatment did not influence phosphofructokinase activity (P > 0.05) in the diaphragm but decreased (P < 0.05) relative citrate synthase activity. Finally, 90 min daily of endurance exercise did not antagonize prednisolone-induced myopathy in either the diaphragm or the plantaris. SN - 8750-7587 UR - https://www.unboundmedicine.com/medline/citation/8226480/Exercise_and_glucocorticoid_induced_diaphragmatic_myopathy_ L2 - https://journals.physiology.org/doi/10.1152/jappl.1993.75.2.763?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -