Effects of prior exercise on insulin‐mediated and noninsulin‐mediated glucose uptake in horses during a hyperglycaemic clamp

Abstract

There is limited information about factors regulating glucose utilisation post exercise in horses. To determine the effects of a single bout of moderate intensity exercise on measures of insulin-mediated (IMGU) and noninsulin-mediated (NIMGU) glucose uptake during a hyperglycaemic clamp (HC). Hyperglycaemic clamps were administered in random order to 8 Standardbreds under 4 conditions: 1) rest, insulinopenia (R-L); 2) rest, hyperinsulinaemia (R-H); 3) post exercise (45 min at ∼ 50% VO2peak), insulinopenia (Ex-L) and 4) post exercise, hyperinsulinaemia (Ex-H). In the R-L and Ex-L trials, somatostatin was infused to suppress insulin secretion and induce insulinopenia. After 30 min, a 2 h HC was initiated with plasma glucose concentrations maintained at ∼ 10 mmol/l by variable glucose infusion. In R-H and Ex-H, regular insulin (1.0 mu/kg bwt/min) was also administered to induce physiological hyperinsulinaemia. Serum insulin and C-peptide concentrations were measured in samples obtained at 10 min intervals. Glucose uptake was calculated from mean glucose infusion rate (GIR) during the last 60 min of the HC. In all HCs C-peptide remained below baseline concentrations, evidence of suppression of insulin secretion by somatostatin. Overall, mean ± s.e. insulin concentrations during the final 60 min of the HC in R-L and Ex-L were 5.7 ± 1.1 and 6.9 ± 1.9 mu/l respectively, and corresponding values in R-H and Ex-H were 64.1 ± 11.1 and 61.2 ± 10.9 mu/l. Prior exercise affected IMGU but not NIMGU. Over the final 60 min of the HC, mean GIR was higher (P < 0.001) in Ex-H (5.6 ± 1.1 mg/kg bwt/min) than in R-H (3.3 ± 0.9 mg/kg bwt/min), whereas mean GIR did not differ (P = 0.26) between R-L (1.2 ± 0.3 mg/kg bwt/min) and Ex-L (1.8 ± 0.5 mg/kg bwt/min). A single bout of moderate intensity exercise increased glucose uptake during a hyperglycaemic clamp under hyperinsulinaemic conditions but not under somatostatin-induced insulinopenia.