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Udgivelsesdato: 2010-Apr-15 Insulin-like growth factor-I (IGF-I) is regulated by a number of IGF-binding proteins (IGFBPs) and proteases that influence IGF-I bioactivity. A specific IGF-I kinase receptor activation assay (KIRA) has been developed that determines the ability of IGF-I to activate the IGF-I receptor by quantification of intracellular receptor autophosphorylation upon IGF-I binding. KIRA-assessed IGF-I bioactivity has not been utilized within the context of chronic exercise training paradigms. This study measured total and free immunoreactive IGF-I, bioactive IGF-I, and IGFBP-1, -2, and -3 pre, mid, and post in young, healthy women who were randomized into one of 4 groups: control (n = 10), resistance (n = 18), aerobic (n = 13), and combined (n = 15) exercise training. Training was on 3 alternating days a week for 8 weeks. The training programs were effective in improving physical fitness specific to the exercise mode engaged in: increases were observed for lean mass (~2%), aerobic fitness (6-7%), and upper (20-24%) and lower (15-48%) body strength (all p-values < 0.05). By contrast, no time, group or interaction effects were observed for the circulating IGF-I system as immunoreactive total (pre = 264+/-16 mug/L; mid = 268+/-17 mug/L; post = 271+/-17 mug/L), free (pre = 0.70+/-0.1 mug/L; mid = 0.63+/-0.1 mug/L; post = 0.63+/-0.2 mug/L) and bioactive (pre = 2.35+/-0.3 mug/L; mid = 2.25+/-0.3 mug/L; post = 2.33+/-0.3 mug/L) IGF-I were unchanged throughout the study. All IGFBP measures were also unchanged. We conclude that increased lean mass, aerobic fitness, and upper and lower body strength resulting from an 8-week exercise training programs can occur without concomitant increases in either circulating bioactive or immunoreactive IGF-I as well as associated IGF binding proteins. In terms of reflecting positive anabolic neuromuscular outcomes, these data support a growing consensus that locally produced IGF-I may be of greater relative importance than endocrine-derived IGF-I.

Energy restriction coupled with high energy expenditure from arduous work is associated with an altered insulin-like growth factor-I (IGF-I) system and androgens that are coincident with losses of fat-free mass. The aim of this study was to determine the effects of two levels of dietary protein content and its effects on IGF-I, androgens, and losses of fat-free mass accompanying energy deficit. We hypothesized that higher dietary protein content would attenuate the decline of anabolic hormones and, thus, prevent losses of fat-free mass. Thirty-four men [24 (SD 0.3) yr, 180.1 (SD 1.1) cm, and 83.0 (SD 1.4) kg] participated in an 8-day military exercise characterized by high energy expenditure (16.5 MJ/day), low energy intake (6.5 MJ/day), and sleep deprivation (4 h/24 h) and were randomly divided into two dietary groups: 0.9 and 0.5 g/kg dietary protein intake. IGF-I system analytes, androgens, and body composition were assessed before and on days 4 and 8 of the intervention. Total, free, and nonternary IGF-I and testosterone declined 50%, 64%, 55%, and 45%, respectively, with similar reductions in both groups. There was, however, a diet × time interaction on day 8 for total IGF-I and sex hormone-binding globulin. Decreases in body mass (3.2 kg), fat-free mass (1.2 kg), fat mass (2.0 kg), and percent body fat (1.5%) were similar in both groups ( P = 0.01). Dietary protein content of 0.5 and 0.9 g/kg minimally attenuated the decline of IGF-I, the androgenic system, and fat-free mass during 8 days of negative energy balance associated with high energy expenditure and low energy intake.

The purpose of this study was to determine the impact of dietary factors and exercise-associated factors on the response of IGF-I and its binding proteins (IGFBPs) during a period of increased physical activity. Twenty-nine men completed a 4-day ( days 1–4) baseline period of a controlled energy balanced diet while maintaining their normal physical activity level followed by 7 days ( days 5–11) of a 1,000 kcal/day increase in physical activity above their normal activity levels. Two subject groups, one sedentary (Sed, mean V̇o2peak: 39 ml·kg−1·min−1, n = 7) and one fit (FIT1, mean V̇o2peak: 56 ml·kg−1·min−1, n = 8) increased energy intake to maintain energy balance throughout the 7-day intervention. In two other fit subject groups (FIT2, n = 7 and FIT3, n = 7), energy intake remained at baseline resulting in a 1,000 kcal/day exercise-induced energy deficit. Of these, FIT2 received an adequate protein diet (0.9 g/kg), and FIT3 received a high-protein diet (1.8 g/kg). For all four groups, IGF-I, IGFBP-3, and the acid labile subunit (ALS) were significantly decreased by day 11 (27 ± 4%, 10 ± 2%, and 19 ± 4%, respectively) and IGFBP-2 significantly increased by 49 ± 21% following day 3. IGFBP-1 significantly increased only in the two negative energy balance groups, FIT2 (38 ± 6%) and FIT3 (46 ± 8%). Differences in initial fitness level and dietary protein intake did not alter the IGF-I system response to an acute increase in physical activity. Decreases in IGF-I were observed during a moderate increase in physical activity despite maintaining energy balance, suggesting that currently unexplained exercise-associated mechanisms, such as increased energy flux, regulate IGF-I independent of energy deficit.