title: Exercise and glucocorticoid-induced diaphragmatic myopathy.
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.affiliation: Department of Exercise and Sport Sciences, University of Florida, Gainesville 32611.
authors.forename: F K
authors.initials: FK
authors.lastname: Lieu
authors.forename: S K
authors.initials: SK
authors.lastname: Powers
authors.forename: R A
authors.initials: RA
authors.lastname: Herb
authors.forename: D
authors.initials: D
authors.lastname: Criswell
authors.forename: D
authors.initials: D
authors.lastname: Martin
authors.forename: C
authors.initials: C
authors.lastname: Wood
authors.forename: W
authors.initials: W
authors.lastname: Stainsby
authors.forename: C L
authors.initials: CL
authors.lastname: Chen
mesh_terms: D000311:Adrenal Glands / Q000473:pathology; D000818:Animals; D001284:Atrophy / Q000473:pathology; D001834:Body Water / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D003964:Diaphragm / Q000201:enzymology / Q000503:physiopathology*; D005260:Female; D009124:Muscle Proteins / Q000378:metabolism; D009132:Muscles / Q000473:pathology / Q000503:physiopathology; D009135:Muscular Diseases / Q000139:chemically induced / Q000201:enzymology / Q000503:physiopathology*; D009210:Myofibrils / Q000378:metabolism / Q000648:ultrastructure; D009929:Organ Size / Q000502:physiology; D010805:Physical Conditioning, Animal; D011239:Prednisolone; D051381:Rats; D017207:Rats, Sprague-Dawley; D012132:Respiratory Muscles / Q000473:pathology / Q000503:physiopathology; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
chemical_list: D009124:Muscle Proteins; D011239:Prednisolone