Do growth hormone intakes help heal a tendinopathy?
I wonder whether growth hormone intakes (e.g., through injections) help heal a tendinopathy.
What I have found so far is limited and somewhat contradictory:
(1) shows some positive results but has only 10 human participants
(2) shows some negative results but was performed on rats, and focus on acute tendon injuries
(3) shows some negative results (a higher stimulation of type III collagen production and a lower stimulation of type I collagen production in CTS cells as compared with control cells)
I am mostly interested in epicondylopathy (either lateral or medial, a.k.a. tennis elbow or golfer elbow).
References:
(1) Doessing, Simon, Katja M. Heinemeier, Lars Holm, Abigail L. Mackey, Peter Schjerling, Michael Rennie, Kenneth Smith et al. "Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis." The Journal of physiology 588, no. 2 (2010): 341-351. scholar.google.com/scholar?cluster=3306954158736346801&hl=en&as_sdt=0,22 ; www.ncbi.nlm.nih.gov/pmc/articles/PMC2821728/?report=classic
In skeletal muscle and tendon the extracellular matrix confers important tensile properties and is crucially important for tissue regeneration after injury. Musculoskeletal tissue adaptation is influenced by mechanical loading, which modulates the availability of growth factors, including growth hormone (GH) and insulin-like growth factor-I (IGF-I), which may be of key importance. To test the hypothesis that GH promotes matrix collagen synthesis in musculotendinous tissue, we investigated the effects of 14 day administration of 33–50 ?g kg?1 day?1 recombinant human GH (rhGH) in healthy young individuals. rhGH administration caused an increase in serum GH, serum IGF-I, and IGF-I mRNA expression in tendon and muscle. Tendon collagen I mRNA expression and tendon collagen protein synthesis increased by 3.9-fold and 1.3-fold, respectively (P < 0.01 and P= 0.02), and muscle collagen I mRNA expression and muscle collagen protein synthesis increased by 2.3-fold and 5.8-fold, respectively (P < 0.01 and P= 0.06). Myofibrillar protein synthesis was unaffected by elevation of GH and IGF-I. Moderate exercise did not enhance the effects of GH manipulation. Thus, increased GH availability stimulates matrix collagen synthesis in skeletal muscle and tendon, but without any effect upon myofibrillar protein synthesis. The results suggest that GH is more important in strengthening the matrix tissue than for muscle cell hypertrophy in adult human musculotendinous tissue.
(2) Baumgarten, Keith M., Harvey A. Oliver, Jack Foley, Ding-Geng Chen, Peter Autenried, Shanzhong Duan, and Patrick Heiser. "Human growth hormone may be detrimental when used to accelerate recovery from acute tendon-bone interface injuries." J Bone Joint Surg Am 95, no. 9 (2013): 783-789. scholar.google.com/scholar?cluster=6271717280291194701&hl=en&as_sdt=0,22 ; www.ncbi.nlm.nih.gov/pubmed/23636184
CONCLUSIONS:
In this rat model of acute tendon-bone injury repair, daily subcutaneous postoperative human growth hormone treatment for fourteen days failed to demonstrate a significant difference in any biomechanical parameter compared with placebo. Furthermore, subcutaneous administration of 5 mg/kg of human growth hormone twice daily from seven days preoperatively until twenty-eight days postoperatively demonstrated lower loads to ultimate failure and a higher risk of bone fracture failure compared with placebo.
(3) Allampallam, Krishnan, Joana Chakraborty, and John Robinson. "Effect of ascorbic acid and growth factors on collagen metabolism of flexor retinaculum cells from individuals with and without carpal tunnel syndrome." Journal of occupational and environmental medicine 42, no. 3 (2000): 251-259. ; scholar.google.com/scholar?cluster=235155596236721817&hl=en&as_sdt=0,22 ;
The effects of ascorbic acid and various growth factors on the proliferation rate and collagen metabolism were studied in cells from the flexor retinaculum of individuals with carpal tunnel syndrome (FR-CTS) and without carpal tunnel syndrome (FR control) and in human dermal fibroblasts. Ascorbic acid and four growth factors, including basic fibroblast growth factor, transforming growth factor, platelet-derived growth factor, and epidermal growth factors, were used. Ascorbic acid stimulates type I collagen production more in FR control than in FR-CTS. Growth factor treatment resulted in the following responses by the cells: (1) a higher mitogenic response than in the control cells; (2) a higher stimulation of type III collagen production and a lower stimulation of type I collagen production in CTS cells as compared with control cells; and (3) more ?2(I) than ?1(I) collagen production in CTS cells, unlike in control cells. We concluded that cells of the FR from individuals with CTS are physiologically altered.
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