POST-EXERCISE GLYCOGEN RESYNTHESIS IN RAT SKELETAL MUSCLE IS NOT MEDIATED BY BRADYKININ

Abstract

85 Increasing evidence indicates that insulin action on skeletal muscle glucose metabolism can be modulated by the nonapeptide bradykinin, likely through the interaction of bradykinin with its BK2 receptor on skeletal muscle. The purpose of the present investigation was to determine if the marked resynthesis of glycogen that takes place in rat skeletal muscle immediately following an exhaustive bout of exercise is mediated by bradykinin interaction with BK2 receptors. Young, female Wistar rats swam for a total of 2 hr in order to deplete epitrochlearis muscle glycogen. Thereafter, half of the animals received intraperitoneal injections (100μg/kg body weight, in 0.9% saline) of the specific BK2-antagonist HOE 140 every 30 min, while the other half of the animals received saline only. All animals had free access to chow and a 10% sucrose solution during the recovery period. The exercise bout induced a significant glycogen depletion in the epitrochlearis muscle (21.4 ± 1.4 nmol/mg muscle in sedentary animals vs. 7.7 ± 0.4 nmol/mg in animals immediately after exercise, P<0.05). At 2 hr of recovery, the glycogen concentration in muscle from the saline-treated animals had increased to 31.4 ± 2.0 nmol/mg (P<0.05), while this value in the HOE 140-treated group was slightly, but not significantly, less (27.9 ± 2.5 nmol/mg). The results of this study indicate that the rapid glycogen resynthesis in skeletal muscle that takes place during the first 2 hr following a glycogen-depleting bout of swim exercise is likely not mediated by the nonapeptide bradykinin.