را به ورزش طولاني مدت در دوچرخه سواران تمرين كرده از بين مي برد IGFBP-1 هيپرگليسمي و هيپرانسولينمي ، واكنش

Will IGFBP - 1 Response to Endurance Exercise Be Abolished in Effect of Hyperglycemia and Hyperinsulinemia?

Prolonged exercise increases plasma insulin growth factor binding protein-I (IGFBP-1) in response to a decline in plasma insulin and glucose. In a previous study, it was speculated that factors of exercise per se might also regulate aIGFBP-I secretion, as values increased despite euglycaemia under carbohydrate feeding. Therefore, to determine the effect of exercise per se on circulation of IGFBP-I, the present study undertook prolonged exercise during hyperglycemic and hyperinsulinemic clamps. Eight trained male cyclists cycled at 70% VO2max for 120 min on two separate occasions under either an intravenous glucose clamp (G) at 10 mmol/l, or a glucose (10 mmol/l) and insulin clamp (GI) at 40 mUlsgm/min. Fasting venous blood samples taken at rest both befor and after clamp and also during exercise were analyzed for IGFI, IGFBP-1 and IGFBP-3 using specific radio immunoassay. Plasma glucose was maintained at 10 mmol/l in both trials. Plasma insulin averaged 32 It. 7.3 and 102 ± 16.6 mU/ml during exercise in G and GI trials respectively. Plasma IGFBP-1 was not changed 30 min after either clamps, but significantly decreased after 60 min and 120 min exercise in both trials (P<0.001). It would appear from these findings that the high levels of exogenous glucose and insulin completely suppress IGFBP-1 secretion during the execise and / or enhance IGFBP-I clearance from the circulation. We conclude that insulin is the primary regulator of IGFBP-I and that there is no effect of exercise on IGFBP-l regulation.