• Kurt A Mossberg, Brent E Masel, Charles R Gilkison, and Randall J Urban.
• Department of Physical Therapy, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-1144, USA. kmossber@utmb.edu
• J. Clin. Endocrinol. Metab. 2008 Jul 1; 93 (7): 2581-7.

ContextGH deficiency occurs in approximately 20% of all individuals who suffer from a moderate to severe traumatic brain injury.ObjectiveThis study determined whether GH deficiency secondary to traumatic brain injury had an effect on aerobic capacity.DesignSubjects were screened for GH deficiency by the glucagon stimulation test and performed a maximal treadmill exercise test.SettingPatients were studied in the postacute recovery phase after traumatic brain injury.ParticipantsThirty-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).InterventionThere was no intervention.Main Outcome MeasureAerobic 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.ResultsSignificantly higher peak oxygen consumption was found 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.ConclusionsThis 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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