Aerobic capacity and growth hormone deficiency after traumatic brain injury

Kurt A. Mossberg, Brent E. Masel, Charles R. Gilkison, Randall Urban

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Context: GH deficiency occurs in approximately 20% of all individuals who suffer from a moderate to severe traumatic brain injury. Objective: This study determined whether GH deficiency secondary to traumatic brain injury had an effect on aerobic capacity. Design: Subjects were screened for GH deficiency by the glucagon stimulation test and performed a maximal treadmill exercise test. Setting: Patients were studied in the postacute recovery phase after traumatic brain injury. Participants: Thirty-five individuals were studied. Groups were formed as follows: normal GH axis, greater than 8 ng/ml response (n = 12); insufficient, GH 3-8 ng/ml response (n = 11); and deficient, less than 3 ng/ml response (n = 12). Intervention: There was no intervention. Main Outcome Measure: Aerobic capacity was assessed by measuring expired gases during a graded treadmill exercise test. One-way and two-way ANOVAs were carried out on all peak and submaximal cardiorespiratory variables, respectively. Appropriate post hoc comparisons followed as necessary. Results: Significantly higher peak oxygen consumptionwasfound in traumatic brain injury subjects with GH normal vs. GH insufficient and deficient [26.4 ± 6.9, 20.8 ± 4.6, and 19.7 ± 5.0, respectively (P < 0.05)]. Submaximal oxygen consumption was significantly higher in the GH normal group. All other variables were statistically similar. Conclusions: This study shows that individuals with traumatic brain injury with normal GH secretion have below normal aerobic capacity and those patients who have GH insufficiency/deficiency are further deconditioned. Studies of GH replacement in these subjects should be conducted to assess whether GH therapy can improve cardiorespiratory fitness and prevent secondary disability.

Original languageEnglish (US)
Pages (from-to)2581-2587
Number of pages7
JournalJournal of Clinical Endocrinology and Metabolism
Volume93
Issue number7
DOIs
StatePublished - Jul 2008

Fingerprint

Growth Hormone
Brain
Exercise Test
Exercise equipment
Oxygen
Analysis of variance (ANOVA)
Glucagon
Oxygen Consumption
Analysis of Variance
Gases
Outcome Assessment (Health Care)
Traumatic Brain Injury
Recovery
Therapeutics

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Aerobic capacity and growth hormone deficiency after traumatic brain injury. / Mossberg, Kurt A.; Masel, Brent E.; Gilkison, Charles R.; Urban, Randall.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 93, No. 7, 07.2008, p. 2581-2587.

Research output: Contribution to journalArticle

Mossberg, Kurt A. ; Masel, Brent E. ; Gilkison, Charles R. ; Urban, Randall. / Aerobic capacity and growth hormone deficiency after traumatic brain injury. In: Journal of Clinical Endocrinology and Metabolism. 2008 ; Vol. 93, No. 7. pp. 2581-2587.
@article{e913743059134a51a5f6cac46edbb257,
title = "Aerobic capacity and growth hormone deficiency after traumatic brain injury",
abstract = "Context: GH deficiency occurs in approximately 20{\%} of all individuals who suffer from a moderate to severe traumatic brain injury. Objective: This study determined whether GH deficiency secondary to traumatic brain injury had an effect on aerobic capacity. Design: Subjects were screened for GH deficiency by the glucagon stimulation test and performed a maximal treadmill exercise test. Setting: Patients were studied in the postacute recovery phase after traumatic brain injury. Participants: Thirty-five individuals were studied. Groups were formed as follows: normal GH axis, greater than 8 ng/ml response (n = 12); insufficient, GH 3-8 ng/ml response (n = 11); and deficient, less than 3 ng/ml response (n = 12). Intervention: There was no intervention. Main Outcome Measure: Aerobic capacity was assessed by measuring expired gases during a graded treadmill exercise test. One-way and two-way ANOVAs were carried out on all peak and submaximal cardiorespiratory variables, respectively. Appropriate post hoc comparisons followed as necessary. Results: Significantly higher peak oxygen consumptionwasfound in traumatic brain injury subjects with GH normal vs. GH insufficient and deficient [26.4 ± 6.9, 20.8 ± 4.6, and 19.7 ± 5.0, respectively (P < 0.05)]. Submaximal oxygen consumption was significantly higher in the GH normal group. All other variables were statistically similar. Conclusions: This study shows that individuals with traumatic brain injury with normal GH secretion have below normal aerobic capacity and those patients who have GH insufficiency/deficiency are further deconditioned. Studies of GH replacement in these subjects should be conducted to assess whether GH therapy can improve cardiorespiratory fitness and prevent secondary disability.",
author = "Mossberg, {Kurt A.} and Masel, {Brent E.} and Gilkison, {Charles R.} and Randall Urban",
year = "2008",
month = "7",
doi = "10.1210/jc.2008-0368",
language = "English (US)",
volume = "93",
pages = "2581--2587",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "7",

}

TY - JOUR

T1 - Aerobic capacity and growth hormone deficiency after traumatic brain injury

AU - Mossberg, Kurt A.

AU - Masel, Brent E.

AU - Gilkison, Charles R.

AU - Urban, Randall

PY - 2008/7

Y1 - 2008/7

N2 - Context: GH deficiency occurs in approximately 20% of all individuals who suffer from a moderate to severe traumatic brain injury. Objective: This study determined whether GH deficiency secondary to traumatic brain injury had an effect on aerobic capacity. Design: Subjects were screened for GH deficiency by the glucagon stimulation test and performed a maximal treadmill exercise test. Setting: Patients were studied in the postacute recovery phase after traumatic brain injury. Participants: Thirty-five individuals were studied. Groups were formed as follows: normal GH axis, greater than 8 ng/ml response (n = 12); insufficient, GH 3-8 ng/ml response (n = 11); and deficient, less than 3 ng/ml response (n = 12). Intervention: There was no intervention. Main Outcome Measure: Aerobic capacity was assessed by measuring expired gases during a graded treadmill exercise test. One-way and two-way ANOVAs were carried out on all peak and submaximal cardiorespiratory variables, respectively. Appropriate post hoc comparisons followed as necessary. Results: Significantly higher peak oxygen consumptionwasfound in traumatic brain injury subjects with GH normal vs. GH insufficient and deficient [26.4 ± 6.9, 20.8 ± 4.6, and 19.7 ± 5.0, respectively (P < 0.05)]. Submaximal oxygen consumption was significantly higher in the GH normal group. All other variables were statistically similar. Conclusions: This study shows that individuals with traumatic brain injury with normal GH secretion have below normal aerobic capacity and those patients who have GH insufficiency/deficiency are further deconditioned. Studies of GH replacement in these subjects should be conducted to assess whether GH therapy can improve cardiorespiratory fitness and prevent secondary disability.

AB - Context: GH deficiency occurs in approximately 20% of all individuals who suffer from a moderate to severe traumatic brain injury. Objective: This study determined whether GH deficiency secondary to traumatic brain injury had an effect on aerobic capacity. Design: Subjects were screened for GH deficiency by the glucagon stimulation test and performed a maximal treadmill exercise test. Setting: Patients were studied in the postacute recovery phase after traumatic brain injury. Participants: Thirty-five individuals were studied. Groups were formed as follows: normal GH axis, greater than 8 ng/ml response (n = 12); insufficient, GH 3-8 ng/ml response (n = 11); and deficient, less than 3 ng/ml response (n = 12). Intervention: There was no intervention. Main Outcome Measure: Aerobic capacity was assessed by measuring expired gases during a graded treadmill exercise test. One-way and two-way ANOVAs were carried out on all peak and submaximal cardiorespiratory variables, respectively. Appropriate post hoc comparisons followed as necessary. Results: Significantly higher peak oxygen consumptionwasfound in traumatic brain injury subjects with GH normal vs. GH insufficient and deficient [26.4 ± 6.9, 20.8 ± 4.6, and 19.7 ± 5.0, respectively (P < 0.05)]. Submaximal oxygen consumption was significantly higher in the GH normal group. All other variables were statistically similar. Conclusions: This study shows that individuals with traumatic brain injury with normal GH secretion have below normal aerobic capacity and those patients who have GH insufficiency/deficiency are further deconditioned. Studies of GH replacement in these subjects should be conducted to assess whether GH therapy can improve cardiorespiratory fitness and prevent secondary disability.

UR - http://www.scopus.com/inward/record.url?scp=47549109806&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=47549109806&partnerID=8YFLogxK

U2 - 10.1210/jc.2008-0368

DO - 10.1210/jc.2008-0368

M3 - Article

VL - 93

SP - 2581

EP - 2587

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 7

ER -