TY - JOUR
T1 - Multipathway modulation of exercise and glucose stress effects upon GH secretion in healthy men
AU - Veldhuis, Johannes D.
AU - Olson, Thomas P.
AU - Takahashi, Paul Y.
AU - Miles, John M.
AU - Joyner, Michael J.
AU - Yang, Rebecca J.
AU - Wigham, Jean
N1 - Funding Information:
Supported in part via R01 AG019695 , R01 AG029362 , and P30 DK050456 (Metabolic Studies Core of the Minnesota Obesity Center) from the National Institutes of Health (Bethesda, MD). The project described was supported by UL1 TR000135 from the National Center for Advancing Translational Sciences (NCATS).
Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2015/9/1
Y1 - 2015/9/1
N2 - Objective Exercise evokes pulsatile GH release followed by autonegative feedback, whereas glucose suppresses GH release followed by rebound-like GH release (feedforward escape). Here we test the hypothesis that age, sex steroids, insulin, body composition and physical power jointly determine these dynamic GH responses. Methods This was a prospectively randomized glucose-blinded study conducted in the Mayo Center for Advancing Translational Sciences in healthy men ages 19-77 years (N = 23). Three conditions, fasting/rest/saline, fasting/exercise/saline and fasting/rest/iv glucose infusions, were used to drive GH dynamics during 10-min blood sampling for 6 h. Linear correlation analysis was applied to relate peak/nadir GH dynamics to age, sex steroids, insulin, CT-estimated abdominal fat and physical power (work per unit time). Results Compared with the fasting/rest/saline (control) day, fasting/exercise/saline infusion evoked peak GH within 1 h, followed by negative feedback 3-5 h later. The dynamic GH excursion was strongly (R2 = 0.634) influenced by (i) insulin negatively (P = 0.011), (ii) power positively (P = 0.0008), and (iii) E2 positively (P = 0.001). Dynamic glucose-modulated GH release was determined by insulin negatively (P = 0.0039) and power positively (P = 0.0034) (R2 = 0.454). Under rest/saline, power (P = 0.031) and total abdominal fat (P = 0.012) (R2 = 0.267) were the dominant correlates of GH excursions. Conclusion In healthy men, dynamic GH perturbations induced by exercise and glucose are strongly related to physical power, insulin, estradiol, and body composition, thus suggesting a network of regulatory pathways.
AB - Objective Exercise evokes pulsatile GH release followed by autonegative feedback, whereas glucose suppresses GH release followed by rebound-like GH release (feedforward escape). Here we test the hypothesis that age, sex steroids, insulin, body composition and physical power jointly determine these dynamic GH responses. Methods This was a prospectively randomized glucose-blinded study conducted in the Mayo Center for Advancing Translational Sciences in healthy men ages 19-77 years (N = 23). Three conditions, fasting/rest/saline, fasting/exercise/saline and fasting/rest/iv glucose infusions, were used to drive GH dynamics during 10-min blood sampling for 6 h. Linear correlation analysis was applied to relate peak/nadir GH dynamics to age, sex steroids, insulin, CT-estimated abdominal fat and physical power (work per unit time). Results Compared with the fasting/rest/saline (control) day, fasting/exercise/saline infusion evoked peak GH within 1 h, followed by negative feedback 3-5 h later. The dynamic GH excursion was strongly (R2 = 0.634) influenced by (i) insulin negatively (P = 0.011), (ii) power positively (P = 0.0008), and (iii) E2 positively (P = 0.001). Dynamic glucose-modulated GH release was determined by insulin negatively (P = 0.0039) and power positively (P = 0.0034) (R2 = 0.454). Under rest/saline, power (P = 0.031) and total abdominal fat (P = 0.012) (R2 = 0.267) were the dominant correlates of GH excursions. Conclusion In healthy men, dynamic GH perturbations induced by exercise and glucose are strongly related to physical power, insulin, estradiol, and body composition, thus suggesting a network of regulatory pathways.
KW - Age
KW - Body composition
KW - Metabolic
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U2 - 10.1016/j.metabol.2015.05.008
DO - 10.1016/j.metabol.2015.05.008
M3 - Article
C2 - 26028283
AN - SCOPUS:84939573515
SN - 0026-0495
VL - 64
SP - 1022
EP - 1030
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 9
ER -