Bradley C Nindl1, Joseph A Alemany2, Kevin R Rarick3, Shawn R Eagle4, Mathew E Darnell5, Katelyn F Allison5, Everett A Harman3. 1. Neuromuscular Research Laboratory/Warrior Human Performance Research Center, Department of Sports Medicine and Nutrition, School of Health and Rehabilitation Sciences, University of Pittsburgh, Pittsburgh, PA 15203, United States; Military Performance Division, US Army Research Institute of Environmental Medicine, Natick, MA 17063, United States. 2. Military Performance Division, US Army Research Institute of Environmental Medicine, Natick, MA 17063, United States; Injury Prevention Program, Epidemiology and Disease Surveillance, U.S. Army Public Health Center (Provisional), Aberdeen Proving Ground, MD 21010, United States. 3. Military Performance Division, US Army Research Institute of Environmental Medicine, Natick, MA 17063, United States. 4. Neuromuscular Research Laboratory/Warrior Human Performance Research Center, Department of Sports Medicine and Nutrition, School of Health and Rehabilitation Sciences, University of Pittsburgh, Pittsburgh, PA 15203, United States. Electronic address: seagle@pitt.edu. 5. Neuromuscular Research Laboratory/Warrior Human Performance Research Center, Department of Sports Medicine and Nutrition, School of Health and Rehabilitation Sciences, University of Pittsburgh, Pittsburgh, PA 15203, United States.
Abstract
OBJECTIVE: The purpose of this study was to: 1) evaluate differential responses of the IGF-I system to either a calisthenic- or resistance exercise-based program and 2) determine if this chronic training altered the IGF-I system during an acute resistance exercise protocol. DESIGN:Thirty-two volunteers were randomly assigned into a resistance exercise-based training (RT) group (n=15, 27±5y, 174±6cm, 81±12kg) or a calisthenic-based training group (CT) (n=17, 29±5y, 179±8cm, 85±10kg) and all underwent 8weeks of exercise training (1.5h/d, 5d/wk). Basal blood was sampled pre- (Week 0), mid- (Week 4) and post-training (Week 8) and assayed for IGF-I system analytes. An acute resistance exercise protocol (AREP) was conducted preand post-training consisting of 6 sets of 10 repetitions in the squat with two minutes of rest in between sets and the IGF-I system analytes measured. A repeated measures ANOVA (p≤0.05) was used for statistical analysis. RESULTS: No interaction or within-subject effects were observed for basal total IGF-I, free IGF-I, or IGFBP-1. IGFBP-2 (pre; 578.6±295.7<mid; 828.6±104.2=post; 833.7±481.2ng/mL; p=0.008) and Acid Labile Subunit (ALS) changed over the exercise training (pre-; 16.2±1.3=mid-; 17.6±1.8>post-training; 14.3±1.9μg/mL; p=0.01). An interaction was observed for the RT group as IGFBP-3 increased from pre to mid (3462.4±216.4 vs. 3962.2±227.9ng/mL), but was not significant at the post-training time point (3770.3±228.7ng/mL). AREP caused all analytes except free IGF-I (40% decrease) to increase (17-27%; p=0.001) during exercise, returning to baseline concentration into recovery. CONCLUSION:Post-training, bioavailable IGF-I recovered more rapidly post-exercise. 8wks of chronic physical training resulted in increased basal IGFBP-2 and IGFBP-3, decreased ALS, increased pre-AREP free IGF-I and a more rapid free IGF-I recovery post-AREP. While total IGF-I was insensitive to chronic physical training, changes were observed with circulating IGFBPs and bioavailable IGF-I. To glean the most robust information on the effects of exercise training, studies must move beyond relying solely on total IGF-I measures and should consider IGFBPs and bioavailable IGF-I as these components of the circulating IGF-I system are essential determinants of IGF-I physiological action.
RCT Entities:
OBJECTIVE: The purpose of this study was to: 1) evaluate differential responses of the IGF-I system to either a calisthenic- or resistance exercise-based program and 2) determine if this chronic training altered the IGF-I system during an acute resistance exercise protocol. DESIGN: Thirty-two volunteers were randomly assigned into a resistance exercise-based training (RT) group (n=15, 27±5y, 174±6cm, 81±12kg) or a calisthenic-based training group (CT) (n=17, 29±5y, 179±8cm, 85±10kg) and all underwent 8weeks of exercise training (1.5h/d, 5d/wk). Basal blood was sampled pre- (Week 0), mid- (Week 4) and post-training (Week 8) and assayed for IGF-I system analytes. An acute resistance exercise protocol (AREP) was conducted preand post-training consisting of 6 sets of 10 repetitions in the squat with two minutes of rest in between sets and the IGF-I system analytes measured. A repeated measures ANOVA (p≤0.05) was used for statistical analysis. RESULTS: No interaction or within-subject effects were observed for basal total IGF-I, free IGF-I, or IGFBP-1. IGFBP-2 (pre; 578.6±295.7<mid; 828.6±104.2=post; 833.7±481.2ng/mL; p=0.008) and Acid Labile Subunit (ALS) changed over the exercise training (pre-; 16.2±1.3=mid-; 17.6±1.8>post-training; 14.3±1.9μg/mL; p=0.01). An interaction was observed for the RT group as IGFBP-3 increased from pre to mid (3462.4±216.4 vs. 3962.2±227.9ng/mL), but was not significant at the post-training time point (3770.3±228.7ng/mL). AREP caused all analytes except free IGF-I (40% decrease) to increase (17-27%; p=0.001) during exercise, returning to baseline concentration into recovery. CONCLUSION: Post-training, bioavailable IGF-I recovered more rapidly post-exercise. 8wks of chronic physical training resulted in increased basal IGFBP-2 and IGFBP-3, decreased ALS, increased pre-AREP free IGF-I and a more rapid free IGF-I recovery post-AREP. While total IGF-I was insensitive to chronic physical training, changes were observed with circulating IGFBPs and bioavailable IGF-I. To glean the most robust information on the effects of exercise training, studies must move beyond relying solely on total IGF-I measures and should consider IGFBPs and bioavailable IGF-I as these components of the circulating IGF-I system are essential determinants of IGF-I physiological action.
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