Limited resistance of hypertrophied skeletal muscle to glucocorticoids

R. C. Hickson*, T. M. Galassi, J. A. Capaccio, R. T. Chatterton

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Scopus citations


Male hypophysectomized rats were initially assigned to a control or an overloaded group that underwent compensatory hypertrophy of plantaris muscles to steady-state levels following removal of synergistic musculature. Plantaris muscle mass of overloaded animals was higher than that of controls by 38% (391 ± 8 vs 284 ± 7 mg) and glucocorticoid cytosol specific binding concentrations, using [3H]triamcinolone acetonide (TA) as the labeled steroid, was also significantly higher in hypertrophied muscles (83.3 ± 3.9 fmol · mg protein-1) than in control muscles (56.3 ± 3.9fmol · mg protein-1). Cortisone acetate (CA) was then administered daily subcutaneously in high, 100 mg; intermediate, 10 mg; or low, l.0mg · kg-1 body wt doses. Groups of rats were killed after 1/4, 2 days and 7 days. Absolute muscle mass losses after 7 days of CA treatment were approx 80 mg with high doses and 60 mg with intermediate doses in both hypertrophied and control muscles. The low CA dose did not produce atrophy. The absolute depletion of [3H] TA binding activity with CA treatment was always greater in hypertrophied muscles of high and intermediate dose treated than those of their respective controls, but TA binding capacities remained higher in hypertrophied muscles than in controls at almost all time points in all treatment groups. Unlike previous findings in which the simultaneous initiation of overload prevented glucocorticoid induced muscle wasting, no resistance to the effect of CA treatment was observed when treatment was begun after hypertrophy had occurred.

Original languageEnglish (US)
Pages (from-to)1179-1183
Number of pages5
JournalJournal of Steroid Biochemistry
Issue number6
StatePublished - Jun 1986

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Fingerprint Dive into the research topics of 'Limited resistance of hypertrophied skeletal muscle to glucocorticoids'. Together they form a unique fingerprint.

Cite this