Abstract

This study was undertaken to determine whether regular endurance running, of the type known to attenuate glucocorticoid-induced muscle atrophy, produces a reversal of the glucocorticoid-mediated suppression of myosin heavy chain (MHC) synthesis. Female rats were assigned to one of four groups. There were two sedentary groups that received either a vehicle or cortisol acetate for 11 consecutive days and two exercise (treadmill running 29 m/min, 90 min/day, for 11 consecutive days) groups that received the activity simultaneously with either vehicle or steroid treatments. Protein synthesis measurements were performed by constant infusion of (3H)leucine. Fractional synthesis rates of MHC were determined from the leucyl-tRNA precursor pool, which was similar in all groups. Exercise prevented 30 of the plantaris muscle mass loss as the result of cortisol acetate treatment. MHC synthesis rates (/day) in plantaris muscles of sedentary animals were reduced by glucocorticoid treatment to 65 (6.2/9.5) of the vehicle-treated group. Exercise did not alter this depression of MHC synthesis. The combination of exercise and glucocorticoid treatment reduced the calculated MHC breakdown rate to 80 (-8.0/-10.1) of the rate resulting from hormone treatment alone and 60 (-8.0/-13.3) of the rate resulting from exercise alone. These results show that endurance exercise does not reverse the glucocorticoid inhibition of MHC synthesis in muscle but may act through reducing MHC breakdown. Verf.-Referat