Abstract

IGF-I is an anabolic peptide responsive to changes in nutritional and physiological status. Energy and/or protein restriction decreases circulating IGF-I and increases IGF-I clearance from the circulation. Whether decreases in IGF-I associated with restricted energy intake can be attenuated by the intake of additional dietary protein is unclear. PURPOSE: To evaluate the effect of two different levels of protein intake on IGF-I system responses during seven days of negative energy balance achieved by increases in physical activity. METHODS: Fourteen men (age 23±6 yr, VO2max 60±9 ml kg−1. min−1, 14±7% body fat) completed a 4 day (D1-D4) baseline period of controlled energy balance followed by a 1,000 kcal.d-−1 exercise-induced energy deficit for 7 days (D5-D11). Seven volunteers received an adequate protein diet (AP) containing 0.9 g·kg−1 body weight, and seven volunteers received a high protein diet (HP) containing 1.8 g·kg−1 body weight. Daily energy expenditure was assessed periodically using closed circuit spirometry. Morning fasting blood draws were performed on days 3, 5, 6, 11, and 12 and IGF-I, IGFBP-1, IGFBP-2, and IGFBP-3 were analyzed by immunoassays. A repeated measures ANOVA (p < 0.05) was used for statistical analysis. RESULTS: Mean energy intake for the entire 11 day period was 3,683±737 kcal d−1, while energy expenditure was 3,712±732 kcal·d−1 during D1-D4 and increased to 4,691±743 kcal·d−1 during D5-D11. Both the AP (D3: 63.3±5.2 kg vs. D12: 61.8±5.0 kg) and HP (D3: 73.1±7.5 kg vs. D12: 71.8±7.7 kg) groups lost 2.4% of lean body mass. No interaction or group effects were observed for the IGF-I system. Time effects were observed for IGF-I, IGFBP-1, IGFBP-2, and IGFBP-3.TableCONCLUSIONS: Exercise-induced negative energy balance resulted in a hierarchy of temporal changes within the IGF-I system (IGFBP-1>IGFBP-2=IGF-I>IGFBP-3). With a moderate, exercise induced energy deficit of 1,000 kcal·d−1, increasing dietary protein (0.9 vs. 1.8 g.kg−1 body mass) beyond adequate levels does not appear to affect the loss of lean body mass or attenuate alterations in the IGF-I system.

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