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AB Introduction: The pulsatile secretion pattern of growth hormone (GH) is an important parameter of GH action at peripheral tissues, and more information is needed on how exercise impacts GH secretion. This study hypothesized that both aerobic and resistance exercise would exhibit dose-response relationships with respect to exercise duration and 20-h postexercise GH secretion. Methods: Eight healthy men randomly completed five separate conditions: 1) control (no exercise; CON), 2) a moderate-duration (1-h) aerobic exercise session (MA), 3) a long-duration (2-h) aerobic exercise session (LA), 4) a moderate-duration (1-h) resistance exercise session (MR), and 5) a long-duration (2-h) resistance exercise session (LR). Exercise intensity, diet, sleep, and physical activity were strictly controlled during each condition, and blood was sampled postexercise every 20 min for 20 h, and GH secretion parameters were analyzed via cluster and deconvolution analyses. Results: Only the 2-h aerobic exercise bout resulted in a significant amplification of GH secretion as evidenced by increases in GH burst peak amplitude (~100%), basal GH secretion rate (~127%), total GH basal secretion (~120%), total pulsatile secretion (~88%), and total GH secretion (~89%) over the control (i.e., no exercise) condition. GH secretions for the resistance exercise conditions were not different from control. Conclusions: The fact that the 2-h aerobic exercise condition resulted in higher energy expenditure than the other exercise conditions could offer a partial explanation for the greater GH amplification because of the metabolic effects that GH exerts in stimulating postexercise lipolysis. We conclude that extending the duration of aerobic exercise, but not resistance exercise, from 1- to 2-h significantly amplifies GH secretion during a 20-h period.

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.

The purpose of this investigation was to determine the test-retest reliability and coefficient of variation of 2 novel physical performance tests. Ten healthy men (22.0 +/- 3.0 years, 87.0 +/- 8.0 kg, 20.0 +/- 5.0% body fat) performed 30 continuous and dynamic jump squats (JS) and bench throws (BT) on 4 separate occasions. The movements were performed under loaded conditions utilizing 30% of subject's predetermined 1 repetition maximum in the back squat and bench press. Mean power (MP; W), peak power (PP; W), mean velocity (MV; m.s(-1)), peak velocity (PV; m.s(-1)), and total work (TW; J) were assessed using a ballistic measurement system (Innervations Inc., Muncie, IN). Data were analyzed using repeated measures analysis of variance with Duncan's post hoc test when mean differences were p < or = 0.05. Intraclass correlation coefficient (ICC) and within-subject coefficient of variation (CV%) were also calculated. All values are presented as mean +/- SE. BT variables were statistically similar across the 4 sessions: MP (350.0 +/- 13.9 W), PP (431.4 +/- 18.5 W) MV (1.6 +/- 0.03 m.s(-1)), PV (2.0 +/- 0.03 m.s(-1)), and TW (199.1 +/- 7.2 J). For JS, session 3 PP (1,669.8 +/- 111.2 W) was significantly greater vs. sessions 1, 2, and 4 (1,601.2 +/- 58.4 W). Session 4 MP (1,403.2 +/- 88.6 W) and MV (1.9 +/- 0.1 m.s(-1)) for JS were significantly lower during sessions 1, 2, and 3 (MP: 1,479.4.5 +/- 44.8 W, MV: 2.0 +/- 0.05 m.s(-1)). TW (834.7 +/- 24.3 J) and PV (2.2 +/- 0.04 m.s(-1)) were statistically similar during all sessions for JS. The CVs ranged from 3.0 to 7.6% for the BT and 3.2 to 5.7% for the JS. ICCs for MP, PP, MV, PV, and TW were 0.92, 0.95, 0.94, 0.91, and 0.95, respectively, during BT. ICCs during JS for MP, PP, MV, PV, and TW were 0.96, 0.98, 0.94, 0.94, and 0.89, respectively. The results of the current study support the use of a 30 continuous and dynamic BT protocol as a reliable upper-body physical performance test, which can be administered with minimal practice. Slightly greater variability for JS was observed, although the test had high reliability.

AB Introduction: This study examined the effects of short-term physical training on the acute hormonal response (i.e., growth hormone, total and free insulin-like growth factor I [IGF-I], and IGF binding proteins [IGFBP]-1, IGFBP-2, and IGFBP-3) to resistance exercise (RE) in women. Methods: Forty-six women (20.3 +/- 0.3 yr, mass = 64.1 +/- 7.3 kg, height = 165.7 +/- 1.0 cm) were randomly assigned to an endurance training (E), resistance training (R), combined training (R + E), or control (C) group for 8 wk. Subjects completed a standardized bout of RE (six sets of back squats at 10 repetition maximum) before and after training. Blood samples were obtained at rest (PRE), after the third set, immediately postexercise (POST), and at 15 min and 30 min after exercise. Results: Acute RE significantly increased (P < 0.05) serum growth hormone (mean +/- SD; change from PRE to POST = +10.9 +/- 7.5 [mu]g[middle dot]L-1), total IGF-I (+66.1 +/- 25.4 [mu]g[middle dot]L-1), IGFBP-1 (+2.5 +/- 3.1 [mu]g[middle dot]L-1), IGFBP-2 (+86.0 +/- 86.8 [mu]g[middle dot]L-1), and IGFBP-3 (+0.69 +/- 0.25 mg[middle dot]L-1) concentrations and decreased free IGF-I concentrations (-0.14 +/- 0.21 [mu]g[middle dot]L-1). After 8 wk of training, total IGF-I concentrations were significantly increased (change in POST concentrations from week 0 to week 8 = +82.5 +/- 120.8 [mu]g[middle dot]L-1), and IGFBP-1 concentrations were significantly decreased (-6.7 +/- 13.6 [mu]g[middle dot]L-1) during exercise in groups that participated in resistance training (R and R + E); no significant changes were seen after E or C. Conclusions: Participation in resistance training increased total IGF-I and reduced IGFBP-1 concentrations during acute RE, indicating exercise mode-specific adaptations in the circulating IGF-I system.

This study hypothesized that insulin-like growth factor-binding protein (IGFBP), rather than insulin-like growth factor I (IGF-I) itself, would be more responsive to acute exercise stress in a dose-dependent fashion.Eight men (24 +/- 5 yr, 87 +/- 9 kg, 182 +/- 6 cm, 21 +/- 5% body fat) had blood drawn every 4 h after exercise for 24 h and assayed for IGF-I, IGFBP-1, -3, -6, the acid labile subunit (ALS), insulin, glucose, and nonesterified free fatty acids on five occasions: no exercise (control, C), moderate-duration resistance exercise (MDRE; 25, 5-10 repetition maximum (RM) sets), long-duration resistance exercise (LDRE; 50, 5-10 RM sets), moderate-duration aerobic exercise (MDAE; three 15-min cycling bouts at approximately 70% (.)VO2peak), and long-duration aerobic exercise (LDAE; six 15-min cycling bouts at approximately 70% (.)VO2peak). Energy requirements were determined from resting metabolic rate, age, and a physical activity factor. Dietary control was implemented by providing all meals during the experimental trials. A two-way ANOVA with repeated measures (P0.05) was used for statistical analysis.Significant exercise effects were observed for IGFBP-1 (C: 14.0 +/- 2.7MDRE: 35.9 +/- 8.6 = LDRE: 45.2 +/- 10.6 = MDAE: 34.2 +/- 7.4 = LDAE: 47.0 +/- 11.8 ng x mL(-1) and insulin (C: 26.0 +/- 9LDRE: 13.2 +/- 6 ng x mL). In addition, a dose-response relationship was observed for the IGFBP-1 response (long-duration exercise (46 +/- 10 ng x mL(-1))moderate-duration exercise (35 +/- 7 ng x mL(-1)). There were no exercise effects for total IGF-I, IGFBP-3, and ALS. Effects of time of day were observed for all variables except ALS.For the circulating IGF-I system components measured, only IGFBP-1 seems to be a sensitive biomarker capable of assessing the physiological strain of acute physical exercise.

Purpose: To test the hypothesis that the appearance of disulfide-linked growth hormone (GH) aggregates during and after an acute resistance exercise test (ARET) in men could be influenced by chronic physical training. Methods: Fourteen men (28 +/- 1 yr) underwent two different 8-wk physical training programs designed to improve military performance. Before and after chronic training, subjects performed an ARET (six sets of 10 repetition-maximum squat) and had venous blood drawn pre-, mid-, and post-ARET (0, 15, and 30 min postexercise). To determine whether GH molecules were disulfide-linked, serum samples were chemically reduced via glutathione (GSH). Serum immunoreactive GH (IRGH) and immunofunctional GH (IFGH) concentrations were determined using two specific immunoassays, in nonreduced (-GSH) and reduced (+GSH) states. Data were analyzed using repeated-measures ANOVA. Results: No differences were observed in the GH responses of the two training programs; therefore, training group data were combined for analysis. GSH reduction increased the mean GH signal (-GSH: 1.4 +/- 0.3 [mu]g[middle dot]L-1 vs +GSH: 1.7 +/- 0.3 [mu]g[middle dot]L-1; P < 0.01) only when quantifying IRGH. Post hoc testing indicated that serum contained IRGH disulfide-linked GH aggregates at the mid, 0-, 15-, and 30-min posttime points of the ARET (P < 0.01), whereas GSH reduction did not affect IFGH concentrations. Chronic physical training had no effect on the ARET-induced GH response. Conclusion: Acute resistance exercise leads to the appearance of disulfide-linked IRGH aggregates, and this response does not appear to be affected by 8 wk of chronic physical training. The physiological significance of increased proportions of disulfide-linked GH aggregates postexercise remains uncertain; however, structural alterations in GH moieties after acute exercise may represent important regulatory steps in mediating GH biological activity at selected target tissues.

Purpose: Soldiers are expected to maintain a high degree of physical readiness as operational demands can severely degrade performance capabilities. This study examined the physiological consequences of U.S. Army Ranger training on strength, power, body composition, and somatotrophic hormones. Methods: In an intensive 8-wk military training course that included an average daily energy deficit of 1000 kcal·d-1, lower-body power output, maximal lifting strength, body composition, and serum concentrations of several somatotrophic hormones were measured in 50 male soldiers (24.6 ± 4.4 y; 176.1 ± 7.8 cm; 78.4 ± 8.7 kg; 14.7 ± 4.2% body fat) before and after the course. Results: Vertical jump height (-16%), explosive power output (-21%), maximal lifting strength. (-20%), body mass (-13%), fat-free mass (-6%), and fat mass (-50%) declined (P < 0.05) after the training course. Circulating total testosterone and insulin-like growth factor-I (IGF-I) experienced significant (P < 0.05) declines, and cortisol was significantly increased. Lower-body power output, but not maximal lifting strength, correlated with changes in fat-free mass. IGF-I and cortisol, but not total testosterone, were correlated with losses of tissue mass. Conclusion: Lower-body power output, estimated from vertical jump height and body mass, is a sensitive and field expedient measure that can be used to assess the influence of caloric deficit on physical performance after 8 wk of U.S. Army Ranger training. With severe weight loss (=13% of body mass), IGF-I and cortisol correlate more closely with soft-tissue tissue adaptations than does testosterone.

Insulin-like growth factor (IGF)-I is a biomarker that may have greater utility than other conventional nutritional biomarkers in assessing nutritional, health, and fitness status. We hypothesized that the IGF-I system would directionally track a short-term energy deficit and would be more related to changes in body composition than other nutritional biomarkers. Thirty-five healthy men (24 ± 0.3 yr) underwent 8 days of exercise and energy imbalance. Total and free IGF-I, IGF binding proteins-1, -2, and -3, the acid labile subunit, transferrin, ferritin, retinol binding protein, prealbumin, testosterone, triiodothyronine, thyroxine, and leptin responses were measured. Dual-energy X-ray absorptiometry assessed changes in body mass and composition. Repeated-measures ANOVA, correlation analysis, and receiver operator characteristic curves were used for statistical analyses ( P ≤ 0.05). Body mass (−3.8%), fat-free mass (−2.2%), and fat mass (−12.9%) all decreased. Total and free IGF-I, IGF binding protein-3, and the acid labile subunit and prealbumin, but not transferrin, retinol-binding protein, and ferritin, directionally tracked the energy deficit and losses in body composition. The correlation ( r = 0.43) between changes in free IGF-I and body and fat-free mass was the only significant association observed. Receiver operator characteristic curve analysis revealed that a baseline value < 1.67 for the molar volume ratio of IGF-I to acid labile subunit had an area under the curve of 0.745 and was a significant discriminator for those subjects losing >5% body mass. The IGF-I system is an important adjunct in the overall assessment of adaptation to stress imposed by high levels of physical activity superimposed on energy and sleep restriction and is more closely associated with losses in body mass and fat-free mass than other conventional nutritional biomarkers.