AJP - Endocrinology and Metabolism, Vol 243, Issue 6 512-E521, Copyright © 1982 by American Physiological Society
Glucocorticoid-induced atrophy is not due to impaired excitability of rat muscle
R. L. Ruff, D. Martyn and A. M. Gordon
We explored the possibility that glucocorticoid-induced muscle weakness and
atrophy resulted from impaired muscle membrane excitability. Male
Sprague-Dawley rats received intramuscular injections of dexamethasone,
cortisone acetate (equivalent anti-inflammatory doses), or saline for up to
28 days. Temporal patterns of change in muscle mass, twitch and tetanic
tension, and membrane potential, cable parameters, and excitability were
studied in vitro in the extensor digitorum longus (EDL), soleus (SOL),
omohyoid (OMO), caudofemoralis (CF), and the sternomastoid muscles
(membrane potential only). the membrane properties of EDL fibers were also
studied in vivo (pentobarbital anesthesia). The relative severity of
atrophy was OMO greater than CF greater than EDL greater than SOL.
Reduction in twitch or tetanic tension never preceded atrophy. The twitch
and tetanic tension (per g muscle) increased with glucocorticoid treatment.
There were no significant changes in the time course of the twitch or
tetanus. Dexamethasone produced more severe atrophy and force reduction
than did cortisone acetate. Glucocorticoid treatment produced a
depolarization of EDL muscle fibers measured in vitro at 23 degrees C, but
this did not appear to be physiologically significant because EDL fibers
studied in vivo were not depolarized and had normal action potential
amplitudes and thresholds. Glucocorticoid treatment did not change the
membrane resistance or capacitance. We conclude that glucocorticoid
treatment did not produce muscle weakness by impairing sarcolemmal
excitability or excitation-contraction coupling, but that the weakness
resulted from muscle atrophy.
