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Aerobic Capacity and Growth Hormone Deficiency after Traumatic Brain Injury

Department of Physical Therapy (K.A.M.) and Medicine (C.R.G., R.J.U.), University of Texas Medical Branch, Galveston, Texas 77555; and Transitional Learning Center (B.E.M.), Galveston, Texas 77550

Address all correspondence and requests for reprints to: Kurt A. Mossberg, P.T., Ph.D., Department of Physical Therapy, University of Texas Medical Branch, 301 University Boulevard, Galveston, Texas 77555-1144. E-mail: kmossber{at}utmb.edu.

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 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.

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.