Unaltered aerobic power and endurance following glucocorticoid-induced muscle atrophy.
The present study was undertaken to evaluate whether the muscle atrophy associated with glucocorticoid excess results in a reduction in maximal oxygen uptake (VO2max) and endurance during exercise. Female rats were administered single subcutaneous injections of cortisone acetate (CA) (100 mg X kg-1 b.w.) or the vehicle (1% carboxymethyl cellulose) for 14 consecutive days. The weights of plantaris muscles (which were used as a marker of the atrophy) of CA-treated rats were 27% less than those of plantaris muscles in the vehicle-treated rats. This condition also produced a 12-fold increase in free serum glucocorticoid concentrations (cortisol) but did not alter serum androgen (testosterone) levels. Peak VO2 (ml X kg-1 X min-1) and endurance were greater in CA-treated vs vehicle-treated animals; however, these effects were shown to be a function of body weight loss. Homogenate oxygen uptakes in the presence of pyruvate or palmitate were also similar in slow-twitch soleus, fast-twitch red vastus, and fast-twitch white vastus lateralis muscles between CA- and vehicle-treated groups. These data provide no evidence to demonstrate that the catabolic actions of glucocorticoids in skeletal muscle result in a decrement in work capacity through at least 14 d of treatment.
D000818:Animals; D001284:Atrophy / Q000139:chemically induced; D003348:Cortisone / Q000031:analogs & derivatives / Q000633:toxicity; D005260:Female; D005938:Glucocorticoids / Q000633:toxicity*; D009132:Muscles / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D010101:Oxygen Consumption / Q000187:drug effects; D010807:Physical Endurance / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains
D005938:Glucocorticoids; D003348:Cortisone