Aerobic capacity and growth hormone deficiency after traumatic brain injury
Open accessAbstract
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.
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In patients with GHD due to TBI and sports-related head trauma, impaired cognitive functions, quality of life, metabolic parameters, body composition, increased cardiovascular risk factors, and decreased muscle force and aerobic capacity have been demonstrated.
“Recently impaired cognitive functions and quality of life, impaired metabolic parameters, abnormal body composition, increased cardiovascular risk factors, and decreased muscle force and aerobic capacity have been clearly demonstrated in patients with GHD due to TBI and sports-related head trauma (16, 46 -48, 72, 80, 81, 271).”
From Pituitary Dysfunction After Traumatic Brain Injury: A Clinical and Pathophysiological Approach (2015) · cites this paper as [271]
The Results and Conclusions (page unavailable) show reduced aerobic capacity in patients with traumatic brain injury and GH insufficiency or deficiency; the Results also report an association between GH response and body mass index. The paper does not demonstrate the full list of cognitive, quality-of-life, metabolic, cardiovascular-risk, and muscle-force impairments in these patients, and its study population did not include sports-related head trauma. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPTHP is correlated with decreased exercise capacity.
“as well as decreased exercise capacity (30)”
From Post-Traumatic Hypopituitarism—Who Should Be Screened, When, and How? (2018) · cites this paper as [30]
The Results report significantly lower peak oxygen consumption in patients with traumatic brain injury and GH insufficiency or deficiency than in those with a normal GH response. This supports an association with reduced exercise capacity for post-traumatic GH dysfunction, but the study does not establish the claim for post-traumatic hypopituitarism (PTHP) generally. (LLM, conf=0.86)
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References 44 · Cited by 43
- Authors
- Mossberg, K. A., Masel, B. E., Gilkison, C. R., & Urban, R. J.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Transitional Learning Center (US)
- Corresponding author
- Mossberg, Kurt A.
- Venue
- The Journal of Clinical Endocrinology & Metabolism
- Publisher
- The Endocrine Society
- Published
- 2008-07-01
- Volume
- 93
- Issue
- 7
- Pages
- 2581-2587
- ISSN
- 0021-972X (ISSN-L)
- 1945-7197
- PMC
- PMC3214275
- OpenAlex
- W2047592324
- Semantic Scholar
- 7f98f8eb77f22850b9d9deeac1c1c5d5e862f7b2
- Cited by
- 43
- References
- 44
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 1 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 6 · 2018: 4 · 2017: 3 · 2016: 2 · 2015: 5 · 2014: 1 · 2012: 4
- FWCI
- 1.69
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Pfizer
- University of Texas Medical Branch
- National Institutes of Health
- National Center for Research Resources (M01 RR-00073, M01RR000073)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Keywords
- traumatic brain injury, growth hormone deficiency, cardiorespiratory fitness, peak oxygen uptake, submaximal oxygen consumption, glucagon stimulation test, growth hormone replacement therapy
- MeSH terms
- Adolescent, Adult, Brain Injuries, Exercise Test, Humans, Middle Aged, Oxygen Consumption, Exercise, Human Growth Hormone
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