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This version published online on April 15, 2008
Journal of Clinical Endocrinology & Metabolism , doi:10.1210/jc.2008-0368
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*Substance via MeSH
Medline Plus Health Information
*Exercise for Children
*Exercise and Physical Fitness
*Traumatic Brain Injury

Submitted on February 14, 2008
Accepted on April 4, 2008

Aerobic Capacity and Growth Hormone Deficiency after Traumatic Brain Injury

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

Department of Physical Therapy, University of Texas Medical Branch, Galveston, TX; Transitional Learning Center, Galveston, TX; Department of Medicine, University of Texas Medical Branch, Galveston, TX

* To whom correspondence should be addressed. E-mail: kmossber{at}utmb.edu.

Context: Growth hormone (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 growth hormone deficiency by the glucagon stimulation test and performed a maximal treadmill exercise test. Setting: Patients were studied in the post-acute 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: None. Main Outcome Measure: Aerobic capacity was assessed by measuring expired gases during a graded treadmill exercise test. One-way and two-way analyses of variance (ANOVA) were carried out on all peak and submaximal cardiorespiratory variables, respectively. Appropriate post hoc comparisons followed as necessary. Results: Significantly higher peak VO2 was found in traumatic brain injury subjects with GH normal versus GH insufficient and deficient (26.4 ± 6.9, 20.8 ± 4.6 and 19.7 ± 5.0; respectively (p<0.05)). Submaximal VO2 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.







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