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.