Gender Impact on the GH Response to Exercise

Wideman, Laurie; Weltman, Judy Y.; Shah, N.; Story, E. Shannon; Bowers, Cyril Y.; Veldhuis, Johannes D.; Weltman, Arthur

doi:10.1007/978-1-4612-1546-2_26

Sex-Steroid Interactions With Growth Hormone 1999

DOI: 10.1007/978-1-4612-1546-2_26

|View full text |Cite

Gender Impact on the GH Response to Exercise

Laurie Wideman¹,

Judy Y. Weltman²,

N. Shah³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2000

2004

Publication Types

Select...

Article3

Relationship

Self Cite1

Independent2

Authors

Journals

Cited by 3 publications

(1 citation statement)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…centrations (2,6,8,10,19,21,23,29,33,37,38,39,41,42), few quantitative correlates are available to link central nervous-system activation with growth hormone (GH) release to greater exercise intensities. We recently reported a linear dose-response relationship between exercise intensity and incremental GH release in young men across a wide span of exertional intensities beginning below the lactate threshold (LT) (29).…”

mentioning

confidence: 99%

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow

Weltman¹,

Pritzlaff²,

Wideman³

et al. 2000

Journal of Applied Physiology

Self Cite

View full text Add to dashboard Cite

To test the hypothesis that heightened sympathetic outflow precedes and predicts the magnitude of the growth hormone (GH) response to acute exercise (Ex), we studied 10 men [age 26.1 +/- 1.7 (SE) yr] six times in randomly assigned order (control and 5 Ex intensities). During exercise, subjects exercised for 30 min (0900-0930) on each occasion at a single intensity: 25 and 75% of the difference between lactate threshold (LT) and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT). Mean values for peak plasma epinephrine (Epi), plasma norepinephrine (NE), and serum GH concentrations were determined [Epi: 328 +/- 93 (SE), 513 +/- 76, 584 +/- 109, 660 +/- 72, and 2,614 +/- 579 pmol/l; NE: 2. 3 +/- 0.2, 3.9 +/- 0.4, 6.9 +/- 1.0, 10.7 +/- 1.6, and 23.9 +/- 3.9 nmol/l; GH: 3.6 +/- 1.5, 6.6 +/- 2.0, 7.0 +/- 2.0, 10.7 +/- 2.4, and 13.7 +/- 2.2 microg/l for 0.25, 0.75, 1.0, 1.25, and 1.75LT, respectively]. In all instances, the time of peak plasma Epi and NE preceded peak GH release. Plasma concentrations of Epi and NE always peaked at 20 min after the onset of Ex, whereas times to peak for GH were 54 +/- 6 (SE), 44 +/- 5, 38 +/- 4, 38 +/- 4, and 37 +/- 2 min after the onset of Ex for 0.25-1.75LT, respectively. ANOVA revealed that intensity of exercise did not affect the foregoing time delay between peak NE or Epi and peak GH (range 17-24 min), with the exception of 0.25LT (P < 0.05). Within-subject linear regression analysis disclosed that, with increasing exercise intensity, change in (Delta) GH was proportionate to both DeltaNE (P = 0.002) and DeltaEpi (P = 0.014). Furthermore, within-subject multiple-regression analysis indicated that the significant GH increment associated with an antecedent rise in NE (P = 0.02) could not be explained by changes in Epi alone (P = 0.77). Our results suggest that exercise intensity and GH release in the human may be coupled mechanistically by central adrenergic activation.

show abstract

mentioning

confidence: 99%

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow

Weltman¹,

Pritzlaff²,

Wideman³

et al. 2000

Journal of Applied Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

Sex-Steroid Hormone Modulation of the Tripeptidyl Control of the Human Somatotropic Axis

Veldhuis

Evans

Anderson

et al. 2002

Journal of Anti-Aging Medicine

View full text Add to dashboard Cite

Contrasting Negative-Feedback Control of Endogenously Driven and Exercise-Stimulated Pulsatile Growth Hormone Secretion in Women and Men

Veldhuis

Patrie²,

Wideman³

et al. 2004

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

GH represses its own secretion via rapid and reversible feedback exerted at key hypothalamic loci. The primary mechanisms include stimulation of somatostatin release and inhibition of GHRH outflow. Autoinhibition is prominent in the adult male rat but diminutive in the female animal. The sex contrast reflects important differences in central neuropeptide signaling in this species. No comparable insights into gender-specific control of GH autofeedback are available in the human. To examine this issue, we quantitated acute recombinant human (rh)GH-induced inhibition of baseline (resting) and aerobic exercise-stimulated GH secretion in healthy young men (n = 8) and early follicular-phase women (n = 6). Each subject underwent four fasting, morning inpatient infusion studies in a prospectively randomized, placebo-controlled, double-blind, within-subject cross-over design. The feedback paradigm comprised 6-min bolus iv infusion of saline or rhGH (10 microg/kg) followed in 120 min by rest or submaximal aerobic (individually calibrated) bicycle ergometry for 30 min. Concomitantly, blood was sampled every 10 min for 6 h, and sera were submitted to immunochemiluminometric GH assay (sensitivity 0.005 microg/liter). Biexponential deconvolution analysis was applied to estimate stimulated GH secretory-burst mass (microg/liter per 90 min after onset of exercise or rest). Women and men had statistically comparable serum estradiol but unequal testosterone concentrations. Repeated-measures ANOVA documented a significant three-way interaction among gender, stimulus type (rest or exercise), and feedback status (saline or rhGH injection) in determining GH secretory-burst mass (P = 0.008). There were prominent two-factor interactions among gender and exercise (P < 0.001); gender and rhGH-induced negative feedback (P = 0.002); and exercise and rhGH feedback (P = 0.006). Gender comparisons disclosed that women, compared with men, maintain 20-fold higher GH secretory-burst mass at rest (P < 0.001); 40-fold less stimulation of pulsatile GH release by exercise than rest (P < 0.001); and 20-fold greater inhibition of GH secretory-burst mass by rhGH than saline at rest (P < 0.05). Observed feedback contrasts by sex were specific, inasmuch as gender did not affect absolute estimates of exercise-stimulated GH secretion (microg/liter/90 min); nadir GH concentrations (microg/liter) enforced by rhGH infusion; and the time latency (min) to manifest maximal inhibition after rhGH injection. In summary, the present clinical investigation unmasks: 1) markedly greater fractional feedback inhibition of pulsatile GH secretion by rhGH in young women than men; and 2) partial resistance of the aerobic-exercise stimulus to GH autofeedback in both women and men. We postulate that sex-steroid-specific control of somatostatin and GHRH outflow may mediate the former gender contrasts, whereas unknown (gender-independent) factors may determine the capability of exercise to significantly antagonize GH autoinhibition.

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

hi@scite.ai

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Gender Impact on the GH Response to Exercise

Cited by 3 publications

References 59 publications

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow

Sex-Steroid Hormone Modulation of the Tripeptidyl Control of the Human Somatotropic Axis

Contrasting Negative-Feedback Control of Endogenously Driven and Exercise-Stimulated Pulsatile Growth Hormone Secretion in Women and Men

Contact Info

Product

Resources

About