Glucocorticoid-induced alterations in the rate of diaphragmatic fatigue

Fletcher, Louise, Powers, Scott K., Coombes, Jeff S., Demirel, Haydar, Vincent, Heather, Dodd, Stephen L. and McLaughlin, James (2000) Glucocorticoid-induced alterations in the rate of diaphragmatic fatigue. Pharmacological Research, 42 1: 61-68. doi:10.1006/phrs.1999.0658

Author Fletcher, Louise
Powers, Scott K.
Coombes, Jeff S.
Demirel, Haydar
Vincent, Heather
Dodd, Stephen L.
McLaughlin, James
Title Glucocorticoid-induced alterations in the rate of diaphragmatic fatigue
Journal name Pharmacological Research   Check publisher's open access policy
ISSN 1043-6618
Publication date 2000-07
Sub-type Article (original research)
DOI 10.1006/phrs.1999.0658
Volume 42
Issue 1
Start page 61
End page 68
Total pages 8
Place of publication London, United Kingdom
Publisher Academic Press
Language eng
Formatted abstract
These experiments tested the hypothesis that in vitro diaphragmaticfatigue 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 (Pt) 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.
Keyword Glucocorticoid
Costal diaphragm
Half time to peak tension
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Human Movement and Nutrition Sciences Publications
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Citation counts: TR Web of Science Citation Count  Cited 3 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 4 times in Scopus Article | Citations
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Created: Wed, 09 Mar 2011, 08:53:09 EST