title: Glucocorticoid-induced alterations in the rate of diaphragmatic fatigue.
abstract: These experiments tested the hypothesis that in vitro diaphragmatic fatigue resistance is enhanced in animals treated with glucocorticoids. Female Sprague-Dawley rats (4 months old) were randomly assigned to a control (N =12) or glucocorticoid treatment group (N =12). Treatment animals were injected daily for 8 days with prednisolone (5 mg kg(-1)); control animals were injected with the same volume of the vehicle. Twenty-four hours after the last injection, the following in vitro diaphragmatic contractile properties were examined in costal diaphragm strips: maximal twitch (P(t)) half time to peak tension (1/2 TPT), half relaxation time (1/2 RT), force-frequency relationship, and the rate of fatigue development. Diaphragmatic fatigue was assessed by monitoring the decrease in force production (measured as percent of initial force) over a 60-min contractile period. The in vitro fatigue protocol incorporated a supramaximal stimulus delivered at 30 Hz every 2 s with a train duration of 250 ms (duty cycle 12.5%). Citrate synthase (CS), superoxide dismutase (SOD), and water content of the costal diaphragm were also determined. Glucocorticoid administration induced an 18.9% (P<0.05) decrease in animal body weight when compared to the control. Similar weight losses also occurred in the diaphragm with a decrease (P<0.05) in mass of 16.5% compared to the control. Furthermore, prednisolone treatment resulted in a significant reduction in the cross-sectional area (CSA) of type IIb fibres with no change in the CSA area of type I and IIa fibres. 1/2 TPT and 1/2 RT were significantly prolonged (P<0.05) in the glucocorticoid treated rats whereas the force-frequency curve was unaltered (P>0.05). Fatigue resistance was greater in the glucocorticoid group (P<0.05); the relative force production differed between groups at the end of 1 min of contractions and remained different throughout the 60-min fatigue protocol. Citrate synthase, SOD, and water content were not different between groups. These experiments support the hypothesis that costal diaphragm strips of glucocorticoid-treated rats possess a greater resistance to fatigue. We postulate that this fatigue resistance is due to glucocorticoid-induced changes muscle fibre type composition.
authors.affiliation: Department of Exercise and Sport Sciences and Physiology, University of Florida, Gainesville 32611, USA.
authors.forename: L K
authors.initials: LK
authors.lastname: Fletcher
authors.forename: S K
authors.initials: SK
authors.lastname: Powers
authors.forename: J S
authors.initials: JS
authors.lastname: Coombes
authors.forename: H
authors.initials: H
authors.lastname: Demirel
authors.forename: H
authors.initials: H
authors.lastname: Vincent
authors.forename: S L
authors.initials: SL
authors.lastname: Dodd
authors.forename: J
authors.initials: J
authors.lastname: Mclaughlin
mesh_terms: D000818:Animals; D001284:Atrophy; D001835:Body Weight / Q000187:drug effects; D003964:Diaphragm / Q000187:drug effects / Q000473:pathology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology*; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects; D018763:Muscle Fatigue / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D013482:Superoxide Dismutase