AENDO Apr. 39/4

Farrell, Peter A., Mark J. Fedele, Thomas C. Vary, Scot R. Kimball, Charles H. Lang, and Leonard S. Jefferson. Regulation of protein synthesis after acute resistance exercise in diabetic rats. Am. J. Physiol. 276 (Endocrinol. Metab. 39): E721–E727, 1999.—These studies determined whether insulin-like growth factor-I (IGF-I) involvement in exercise-stimulated anabolic processes becomes more evident during hypoinsulinemia. Male SpragueDawley rats (n 5 6–12/group) were made diabetic (blood glucose > 300 mg/dl) by partial pancreatectomy (PPX) or remained nondiabetic (glucose > 144 mg/dl). Rats performed acute resistance exercise by repetitive standing on the hindlimbs with weighted backpacks (ex), or they remained sedentary (sed). Resistance exercise caused increases in rates of protein synthesis (nmol Phe incorporated·g muscle21 ·h21, measured for gastrocnemius muscle in vivo 16 h after exercise) for both nondiabetic [sed 5 154 6 6 (SE) vs. ex 5 189 6 7] and diabetic rats (PPXsed 5 152 6 11 vs. PPXex 5 202 6 14, P , 0.05). Arterial plasma insulin concentrations in diabetic rats, >180 pM, were less than one-half those found in nondiabetic rats, >444 pM, (P , 0.05). The activity of eukaryotic initiation factor 2B (eIF2B; pmol GDP exchanged/ min) was higher (P , 0.05) in ex rats (sed 5 0.028 6 0.006 vs. ex 5 0.053 6 0.015; PPXsed 5 0.033 6 0.013 vs. PPXex 5 0.047 6 0.009) regardless of diabetic status. Plasma IGF-I concentrations were higher in ex compared with sed diabetic rats (P , 0.05). In contrast, plasma IGF-I was not different in nondiabetic ex or sed rats. Muscle IGF-I (ng/g wet wt) was similar in ex and sed nondiabetic rats, but in diabetic rats was 2to 3-fold higher in ex (P , 0.05) than in sed rats. In conclusion, moderate hypoinsulinemia that is sufficient to alter glucose homeostasis does not inhibit an increase in rates of protein synthesis after acute moderate-intensity resistance exercise. This preserved response may be due to a compensatory increase in muscle IGF-I content and a maintained ability to activate eIF2B.