keith1569
New Member
On my trt since I run a lot I either always have low dose Deca or EQ.. Definitely helps
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Anabolic Steroids
Joints/Tendons/Bone
- Thread starter pauladrive
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Anabolic Steroids As A Strategy In Reversing Denervation Atrophy
Isaacs J, Loveland K, Mallu S, Adams S, Wodicka R. The use of anabolic steroids as a strategy in reversing denervation atrophy after delayed nerve repair. Hand (N Y) 2011;6(2):142-8. Hand, Volume 6, Number 2 - SpringerLink
BACKGROUND: Denervation atrophy is one factor contributing to suboptimal motor recovery following major nerve repair. The hypertrophic effects of anabolic steroids may have a potential role in improving reinnervated muscle strength after delayed repair.
METHODS: Forty-five immature female Sprague-Dawley rats underwent three surgeries and final testing. The tibial nerve was transected in the hind limb of the experimental (n = 13) and control (n = 14) animals and exposed, but not transected in the sham (n = 15) group animals. Three months later, once denervation atrophy was established, all transected nerves underwent repair using an autograft from the contralateral limb. After waiting an additional month to allow axonal regeneration to the gastrocnemius muscles, the rodents were implanted with a subcutaneous infusion pump. For the experimental group, nandrolone was administered over the next 30 days via this pump, while the control and sham group pumps were filled with carrier only.
RESULTS: Final testing, 6 weeks later, showed improved muscle contraction strength in the steroid-treated animals (72% of sham group strength) compared to control animals (57% of sham group strength, p < 0.5). A trend towards increased weight and muscle belly diameter in the steroid-treated group was not statistically significant.
CONCLUSIONS: These findings support the potential role of anabolic steroids in improving recovery of atrophic muscle after delayed reinnervation.
Isaacs J, Loveland K, Mallu S, Adams S, Wodicka R. The use of anabolic steroids as a strategy in reversing denervation atrophy after delayed nerve repair. Hand (N Y) 2011;6(2):142-8. Hand, Volume 6, Number 2 - SpringerLink
BACKGROUND: Denervation atrophy is one factor contributing to suboptimal motor recovery following major nerve repair. The hypertrophic effects of anabolic steroids may have a potential role in improving reinnervated muscle strength after delayed repair.
METHODS: Forty-five immature female Sprague-Dawley rats underwent three surgeries and final testing. The tibial nerve was transected in the hind limb of the experimental (n = 13) and control (n = 14) animals and exposed, but not transected in the sham (n = 15) group animals. Three months later, once denervation atrophy was established, all transected nerves underwent repair using an autograft from the contralateral limb. After waiting an additional month to allow axonal regeneration to the gastrocnemius muscles, the rodents were implanted with a subcutaneous infusion pump. For the experimental group, nandrolone was administered over the next 30 days via this pump, while the control and sham group pumps were filled with carrier only.
RESULTS: Final testing, 6 weeks later, showed improved muscle contraction strength in the steroid-treated animals (72% of sham group strength) compared to control animals (57% of sham group strength, p < 0.5). A trend towards increased weight and muscle belly diameter in the steroid-treated group was not statistically significant.
CONCLUSIONS: These findings support the potential role of anabolic steroids in improving recovery of atrophic muscle after delayed reinnervation.
Very interesting Dr S
Andersson T, Eliasson P, Aspenberg P. Growth hormone does not stimulate early healing in rat tendons. Int J Sports Med 2012;33(3):240-3. https://www.thieme-connect.com/DOI/DOI?10.1055/s-0031-1291324
Growth Hormone stimulates bone growth and fracture repair. It acts mainly by increasing the systemic levels of IGF-1. Local treatment with IGF-1 appears to stimulate tendon healing. We therefore hypothesized that systemic treatment with Growth Hormone would also stimulate tendon healing. Rat Achilles tendons were transected and left to heal. 4 groups were studied. Intramuscular injections of botulinum toxin A (Botox) were used to reduce loading in 2 groups. The animals were randomized to twice daily injections of Growth Hormone (n=2x10) or saline (n=2x10), and killed after 10 days. Healing was assessed by mechanical testing. Muscle paralysis induced by Botox reduced the strength of the healing tendon by two thirds. Growth Hormone increased femoral and tibial length in the unloaded, and femoral and tibial weight in the loaded group. Body weight and muscle weight were increased in both. In contrast, there was no increase in the strength of the healing tendons, regardless of mechanical loading status. An increase in peak force of the loaded healing tendons by more than 5% could be excluded with 95% confidence. In spite of its stimulatory effects on other tissues, Growth Hormone did not appear to stimulate tendon or tendon repair.
Growth Hormone stimulates bone growth and fracture repair. It acts mainly by increasing the systemic levels of IGF-1. Local treatment with IGF-1 appears to stimulate tendon healing. We therefore hypothesized that systemic treatment with Growth Hormone would also stimulate tendon healing. Rat Achilles tendons were transected and left to heal. 4 groups were studied. Intramuscular injections of botulinum toxin A (Botox) were used to reduce loading in 2 groups. The animals were randomized to twice daily injections of Growth Hormone (n=2x10) or saline (n=2x10), and killed after 10 days. Healing was assessed by mechanical testing. Muscle paralysis induced by Botox reduced the strength of the healing tendon by two thirds. Growth Hormone increased femoral and tibial length in the unloaded, and femoral and tibial weight in the loaded group. Body weight and muscle weight were increased in both. In contrast, there was no increase in the strength of the healing tendons, regardless of mechanical loading status. An increase in peak force of the loaded healing tendons by more than 5% could be excluded with 95% confidence. In spite of its stimulatory effects on other tissues, Growth Hormone did not appear to stimulate tendon or tendon repair.
NO ONE on Meso locates more relevant articles than you Dr.S
Thx
Thx
Marqueti RC, Heinemeier KM, Durigan JL, et al. Gene expression in distinct regions of rat tendons in response to jump training combined with anabolic androgenic steroid administration. Eur J Appl Physiol 2012;112(4):1505-15. European Journal of Applied Physiology, Volume 112, Number 4 - SpringerLink
The aim of this study was to evaluate the expression of key genes responsible for tendon remodeling of the proximal and distal regions of calcaneal tendon (CT), intermediate and distal region of superficial flexor tendon (SFT) and proximal, intermediate and distal region of deep flexor tendon (DFT) submitted to 7 weeks of jumping water load exercise in combination with AAS administration. Wistar male rats were grouped as follows: sedentary (S), trained (jumping water load exercise) (T), sedentary animals treated with AAS (5 mg/kg, twice a week) and animals treated with AAS and trained (AAST). mRNA levels of COL1A1, COL3A1, TIMP-1, TIMP-2, MMP-2, IGF-IEa, GAPDH, CTGF and TGF-beta-1 were evaluated by quantitative PCR. Our main results indicated that mRNA levels alter in different regions in each tendon of sedentary animals. The training did not alter the expression of COL1A1, COL3A, IGF-IEa and MMP-2 genes, while AAS administration or its combination with training reduced their expression. This study indicated that exercise did not alter the expression of collagen and related growth factors in different regions of rat tendon. Moreover, the pattern of gene expression was distinct in the different tendon regions of sedentary animals. Although, the RNA yield levels of CT, SFT and DFT were not distinct in each region, these regions possess not only the structural and biochemical difference, but also divergence in the expression of key genes involved in tendon adaptation.
The aim of this study was to evaluate the expression of key genes responsible for tendon remodeling of the proximal and distal regions of calcaneal tendon (CT), intermediate and distal region of superficial flexor tendon (SFT) and proximal, intermediate and distal region of deep flexor tendon (DFT) submitted to 7 weeks of jumping water load exercise in combination with AAS administration. Wistar male rats were grouped as follows: sedentary (S), trained (jumping water load exercise) (T), sedentary animals treated with AAS (5 mg/kg, twice a week) and animals treated with AAS and trained (AAST). mRNA levels of COL1A1, COL3A1, TIMP-1, TIMP-2, MMP-2, IGF-IEa, GAPDH, CTGF and TGF-beta-1 were evaluated by quantitative PCR. Our main results indicated that mRNA levels alter in different regions in each tendon of sedentary animals. The training did not alter the expression of COL1A1, COL3A, IGF-IEa and MMP-2 genes, while AAS administration or its combination with training reduced their expression. This study indicated that exercise did not alter the expression of collagen and related growth factors in different regions of rat tendon. Moreover, the pattern of gene expression was distinct in the different tendon regions of sedentary animals. Although, the RNA yield levels of CT, SFT and DFT were not distinct in each region, these regions possess not only the structural and biochemical difference, but also divergence in the expression of key genes involved in tendon adaptation.
MANWHORE
Subscriber
Didn't know this post was hear when I started
the other one on collagen synth
I gotta read this one
the other one on collagen synth
I gotta read this one
Piovesan RF, Fernandes KP, Alves AN, et al. Effect of Nandrolone Decanoate on Skeletal Muscle Repair. Int J Sports Med. https://www.thieme-connect.de/ejournals/abstract/10.1055/s-0032-1311652
This study analyzed the effect of nandrolone decanoate (ND) on muscle repair and the expression of myogenic regulatory factors following cryoinjury in rat skeletal muscle. Adult male Wistar rats were randomly divided into 4 groups: control group, sham group, cryoinjured group treated with ND and non-injured group treated with ND. Treatment consisted of subcutaneous injections of ND (5 mg/kg) twice a week. After sacrifice, the tibialis anterior muscle was removed for the isolation of total RNA and analysis of myogenic regulatory factors using real-time PCR as well as morphological analysis using the hematoxylin-eosin assay. There was a significant increase in MyoD mRNA after 7 days and in myogenin mRNA after 21 days in the cryoinjured ND group in comparison to other groups in the same period. The morphological analysis revealed no edema or myonecrosis after 7 days as well as no edema or inflammatory infiltrate after 14 days in the cryoinjured ND group.
In conclusion, the anabolic steroid nandrolone decanoate can modulate the muscle repair process in rats following cryoinjury by influencing the expression of regulatory myogenic factors and phases of muscle repair.
This study analyzed the effect of nandrolone decanoate (ND) on muscle repair and the expression of myogenic regulatory factors following cryoinjury in rat skeletal muscle. Adult male Wistar rats were randomly divided into 4 groups: control group, sham group, cryoinjured group treated with ND and non-injured group treated with ND. Treatment consisted of subcutaneous injections of ND (5 mg/kg) twice a week. After sacrifice, the tibialis anterior muscle was removed for the isolation of total RNA and analysis of myogenic regulatory factors using real-time PCR as well as morphological analysis using the hematoxylin-eosin assay. There was a significant increase in MyoD mRNA after 7 days and in myogenin mRNA after 21 days in the cryoinjured ND group in comparison to other groups in the same period. The morphological analysis revealed no edema or myonecrosis after 7 days as well as no edema or inflammatory infiltrate after 14 days in the cryoinjured ND group.
In conclusion, the anabolic steroid nandrolone decanoate can modulate the muscle repair process in rats following cryoinjury by influencing the expression of regulatory myogenic factors and phases of muscle repair.
Sworder
Member
After 10 days? Obviously we would expect 100% recovery 10 days after treatment started which is why most guys run 10 day hGH cycles........
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I am really starting to wonder the potential implications of Nandrolone use for arthritis. I suspect its MUCH more than a simple "watering of the lawn". One question is going to be real side effects of prolonged Deca use. But more importantly - just how little would it take to benefit? This seems like a drug that does a lot of bang for the buck.!
I could be as simple as this. In many rhelms of life. The principles of repeated conditions are what wind up causing the damage. WHAT IF, just a once per year application of Nandrolone for just a couple of months (or injections) could totally prevent osteo arthritis from effecting its damage? What if..? While after all osteoarthritis appears to be the result of the skeletal system's heal and repair process, and related to the eventual accumulation of scar tissue inhibiting this process. The collagen activity associated with Nandrolone could perhaps keep these ligaments "soft enough" to extend the normal wear conditions of heal and repair potentially just by the "watering effect". The notion of simple "pain masking" which has been cast upon steroids in the witch blasting incurred due to fear and ignorance, MUST be incorrect. I see no indications that the CNS is effectively altered in ways that prevent our perceived "Feelings", thus it must be incorrect. While its nice to "feel good" as a result of the anabolic activity associated with "steroids", "feeling good" must still remain and "being good". It must.
And funny just as proof of the scope and MAGNITUDE of the medical failure and ball dropped in the steroid area is that Deca is poor in muscle growth and androgenic activity and the last choice of an educated "super villain". Ridiculous and exemplary of the damage done to science via the power of politics and ignorance. The same powers now suffering too as a result of this failure..
I could be as simple as this. In many rhelms of life. The principles of repeated conditions are what wind up causing the damage. WHAT IF, just a once per year application of Nandrolone for just a couple of months (or injections) could totally prevent osteo arthritis from effecting its damage? What if..? While after all osteoarthritis appears to be the result of the skeletal system's heal and repair process, and related to the eventual accumulation of scar tissue inhibiting this process. The collagen activity associated with Nandrolone could perhaps keep these ligaments "soft enough" to extend the normal wear conditions of heal and repair potentially just by the "watering effect". The notion of simple "pain masking" which has been cast upon steroids in the witch blasting incurred due to fear and ignorance, MUST be incorrect. I see no indications that the CNS is effectively altered in ways that prevent our perceived "Feelings", thus it must be incorrect. While its nice to "feel good" as a result of the anabolic activity associated with "steroids", "feeling good" must still remain and "being good". It must.
And funny just as proof of the scope and MAGNITUDE of the medical failure and ball dropped in the steroid area is that Deca is poor in muscle growth and androgenic activity and the last choice of an educated "super villain". Ridiculous and exemplary of the damage done to science via the power of politics and ignorance. The same powers now suffering too as a result of this failure..
Sworder
Member
If the "Watering of the lawn" theory was correct wouldn't estrogen also water the lawn?
I believe there to be a positive effect on tendons/joints from Nandrolone, whether it is increased collagen synthesis or something else. The preventative measure you mention is interesting and I would guinea-pig myself if I believed myself to be prone to arthritis.
I believe there to be a positive effect on tendons/joints from Nandrolone, whether it is increased collagen synthesis or something else. The preventative measure you mention is interesting and I would guinea-pig myself if I believed myself to be prone to arthritis.
Sworder
Member
Does Nandrolone increase synovial fluid? Does estrogen?
Gerber C, Meyer DC, Von Rechenberg B, Hoppeler H, Frigg R, Farshad M. Rotator Cuff Muscles Lose Responsiveness to Anabolic Steroids After Tendon Tear and Musculotendinous Retraction: An Experimental Study in Sheep. Am J Sports Med. Rotator Cuff Muscles Lose Responsiveness to Anabolic Steroids After Tendon Tear and Musculotendinous Retraction
BACKGROUND: Long-standing rotator cuff tendon tearing is associated with retraction, loss of work capacity, irreversible fatty infiltration, and atrophy of the rotator cuff muscles. Although continuous musculotendinous relengthening can experimentally restore muscular architecture, restoration of atrophy and fatty infiltration is hitherto impossible.
HYPOTHESIS: Continuous relengthening with pharmacological stimulation of muscle growth using an anabolic steroid or insulin-like growth factor (IGF) can reverse atrophy and fatty infiltration as well as improve the work capacity of chronically retracted rotator cuff muscles in sheep.
STUDY DESIGN: Controlled laboratory study.
METHODS: Sixteen weeks after tenotomy of the infraspinatus (ISP) tendon, atrophy and fatty infiltration had developed in the retracted ISP muscle. The musculotendinous unit was continuously relengthened in 14 sheep during 6 weeks: Four sheep were treated without pharmacological stimulation, 4 with intramuscular administration of an anabolic steroid, and 6 with IGF before final repair and rehabilitation (12 weeks). Changes were documented by intraoperative measurements of muscle work capacity, histology, and computed tomography/magnetic resonance imaging.
RESULTS: Musculotendinous relengthening by continuous traction resulted in gains of length ranging from 0.7 cm in the IGF group to 1.3 cm in the control group. Fatty infiltration progressed in all groups, and the muscle's cross-sectional area ranged from 71% to 74% of the contralateral side at sacrifice and did not show any differences between groups in weight, volume, histological composition, or work capability of the muscle. The contralateral muscles in the anabolic steroid group, however, showed significantly higher (mean +/- standard deviation) muscle work capacity of 10 +/- 0.9 N.m than the contralateral muscles of the control group (6.8 +/- 2.4 N.m) (P < .05). This was accompanied by an increased mean muscle fiber area as well as by an unusual gain in the animals' weight after injection of the anabolic steroid.
CONCLUSION: Subcutaneous continuous relengthening of a chronically retracted musculotendinous unit is feasible and advances the retracted musculotendinous junction toward its original position. This does not change the muscle work capacity. Whereas anabolic steroids have been shown to be effective in preventing classic degenerative muscle changes after tendon tears, neither an anabolic steroid nor IGF contributes to regeneration of the muscle once degenerative changes are established.
CLINICAL RELEVANCE: The findings demonstrate that muscle cells lose reactiveness to an anabolic steroid and IGF once retraction has led to fatty infiltration and atrophy of the muscle. Retraction of the muscle after tendon tears must be avoided by early repair, particularly in an athlete, as no regeneration can be achieved by mechanical or pharmacological means at this time.
BACKGROUND: Long-standing rotator cuff tendon tearing is associated with retraction, loss of work capacity, irreversible fatty infiltration, and atrophy of the rotator cuff muscles. Although continuous musculotendinous relengthening can experimentally restore muscular architecture, restoration of atrophy and fatty infiltration is hitherto impossible.
HYPOTHESIS: Continuous relengthening with pharmacological stimulation of muscle growth using an anabolic steroid or insulin-like growth factor (IGF) can reverse atrophy and fatty infiltration as well as improve the work capacity of chronically retracted rotator cuff muscles in sheep.
STUDY DESIGN: Controlled laboratory study.
METHODS: Sixteen weeks after tenotomy of the infraspinatus (ISP) tendon, atrophy and fatty infiltration had developed in the retracted ISP muscle. The musculotendinous unit was continuously relengthened in 14 sheep during 6 weeks: Four sheep were treated without pharmacological stimulation, 4 with intramuscular administration of an anabolic steroid, and 6 with IGF before final repair and rehabilitation (12 weeks). Changes were documented by intraoperative measurements of muscle work capacity, histology, and computed tomography/magnetic resonance imaging.
RESULTS: Musculotendinous relengthening by continuous traction resulted in gains of length ranging from 0.7 cm in the IGF group to 1.3 cm in the control group. Fatty infiltration progressed in all groups, and the muscle's cross-sectional area ranged from 71% to 74% of the contralateral side at sacrifice and did not show any differences between groups in weight, volume, histological composition, or work capability of the muscle. The contralateral muscles in the anabolic steroid group, however, showed significantly higher (mean +/- standard deviation) muscle work capacity of 10 +/- 0.9 N.m than the contralateral muscles of the control group (6.8 +/- 2.4 N.m) (P < .05). This was accompanied by an increased mean muscle fiber area as well as by an unusual gain in the animals' weight after injection of the anabolic steroid.
CONCLUSION: Subcutaneous continuous relengthening of a chronically retracted musculotendinous unit is feasible and advances the retracted musculotendinous junction toward its original position. This does not change the muscle work capacity. Whereas anabolic steroids have been shown to be effective in preventing classic degenerative muscle changes after tendon tears, neither an anabolic steroid nor IGF contributes to regeneration of the muscle once degenerative changes are established.
CLINICAL RELEVANCE: The findings demonstrate that muscle cells lose reactiveness to an anabolic steroid and IGF once retraction has led to fatty infiltration and atrophy of the muscle. Retraction of the muscle after tendon tears must be avoided by early repair, particularly in an athlete, as no regeneration can be achieved by mechanical or pharmacological means at this time.
Nice study, especially since I've had both RCs repaired one requiring a relengthening procedure. Have you seen any human-rotator cuff repair studies where steroids were the independent variable?
regular
New Member
Doessing S, Heinemeier KM, Holm L, Mackey AL, Schjerling P, Rennie M, Smith K, Reitelseder S, Kappelgaard AM, Rasmussen MH, Flyvbjerg A, Kjaer M. Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis. J Physiol. 2010 January 15; 588(Pt 2): 341–351. Growth hormone stimulates the collagen synthesis in human tendon and skeletal muscle without affecting myofibrillar protein synthesis
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 microg 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.
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 microg 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.
regular
New Member
Vestergaard PF, Jorgensen JO, Olesen JL, Bosnjak E, Holm L, Frystyk J, Langberg H, Kjaer M, Hansen M. LOCAL ADMINISTRATION OF GROWTH HORMONE STIMULATES TENDON COLLAGEN SYNTHESIS IN ELDERLY MEN. J Appl Physiol. 2012 Sep 6. [Epub ahead of print] LOCAL ADMINISTRATION OF GROWTH HORMONE STIMUL... [J Appl Physiol. 2012] - PubMed - NCBI
Tendon collagen content and circulating growth hormone (GH) is reduced in elderly. In a placebo-controlled, double-blinded study we examined if local injections of rhGH enhance collagen synthesis in healthy elderly men (61±1 yrs). Two injections of rhGH or saline (control) were injected into each of their patellar tendons, respectively. Subsequently, tendon collagen fractional synthesis rate (FSR) and an indirect marker of type I collagen synthesis (PINP) were measured. Within the first 6 hours after the last injections a tendency towards a higher tendon collagen FSR was observed in 10 out of 12 subjects (P=0.08). Similarly, PINP was higher 3 to 4 hours after the last GH injection (P=0.05). Serum IGF-I did not change from baseline, whereas peritendinous bioactive IGF-I was higher in the GH leg vs. control (P=0.05). In conclusion, local injections of rhGH increase tendon collagen synthesis in humans, either directly or indirectly by increasing local bioactive IGF-I.
Tendon collagen content and circulating growth hormone (GH) is reduced in elderly. In a placebo-controlled, double-blinded study we examined if local injections of rhGH enhance collagen synthesis in healthy elderly men (61±1 yrs). Two injections of rhGH or saline (control) were injected into each of their patellar tendons, respectively. Subsequently, tendon collagen fractional synthesis rate (FSR) and an indirect marker of type I collagen synthesis (PINP) were measured. Within the first 6 hours after the last injections a tendency towards a higher tendon collagen FSR was observed in 10 out of 12 subjects (P=0.08). Similarly, PINP was higher 3 to 4 hours after the last GH injection (P=0.05). Serum IGF-I did not change from baseline, whereas peritendinous bioactive IGF-I was higher in the GH leg vs. control (P=0.05). In conclusion, local injections of rhGH increase tendon collagen synthesis in humans, either directly or indirectly by increasing local bioactive IGF-I.
The Anabolic Steroid Nandrolone Enhances Motor and Sensory Functional Ghizoni MF, Bertelli JA, Grala CG, da Silva RM. The Anabolic Steroid Nandrolone Enhances Motor and Sensory Functional Recovery in Rat Median Nerve Repair With Long Interpositional Nerve Grafts. Neurorehabil Neural Repair. The Anabolic Steroid Nandrolone Enhances Motor and Sensory Functional Recovery in Rat Median Nerve Repair With Long Interpositional Nerve Grafts
BACKGROUND: Recovery from peripheral nerve repair is frequently incomplete. Hence drugs that enhance nerve regeneration are needed clinically.
OBJECTIVES: To study the effects of nandrolone decanoate in a model of deficient reinnervation in the rat.
METHODS: In 40 rats, a 40-mm segment of the left median nerve was removed and interposed between the stumps of a sectioned right median nerve. Starting 7 days after nerve grafting and continuing over a 6-month period, we administered nandrolone at a dose of 5 mg/kg/wk to half the rats (n = 20). All rats were assessed behaviorally for grasp function and nociceptive recovery for up to 6 months. At final assessment, reinnervated muscles were tested electrophysiologically and weighed.
RESULTS: were compared between rats that had received versus not received nandrolone and versus 20 nongrafted controls. Results. Rats in the nandrolone group recovered finger flexion faster. At 90 days postsurgery, they had recovered 42% of normal grasp strength versus just 11% in rats grafted but not treated with nandrolone. At 180 days, the average values for grasp strength recovery in the nandrolone and no-nandrolone groups were 40% and 33% of normal values for controls, respectively. At 180 days, finger flexor muscle twitch strength was 16% higher in treated versus nontreated rats. Thresholds for nociception were not detected in either group 90 days after nerve grafting. At 180 days, nociceptive thresholds were significantly lower in the nandrolone group.
CONCLUSIONS: Nandrolone decanoate improved functional recovery in a model of deficient reinnervation.
BACKGROUND: Recovery from peripheral nerve repair is frequently incomplete. Hence drugs that enhance nerve regeneration are needed clinically.
OBJECTIVES: To study the effects of nandrolone decanoate in a model of deficient reinnervation in the rat.
METHODS: In 40 rats, a 40-mm segment of the left median nerve was removed and interposed between the stumps of a sectioned right median nerve. Starting 7 days after nerve grafting and continuing over a 6-month period, we administered nandrolone at a dose of 5 mg/kg/wk to half the rats (n = 20). All rats were assessed behaviorally for grasp function and nociceptive recovery for up to 6 months. At final assessment, reinnervated muscles were tested electrophysiologically and weighed.
RESULTS: were compared between rats that had received versus not received nandrolone and versus 20 nongrafted controls. Results. Rats in the nandrolone group recovered finger flexion faster. At 90 days postsurgery, they had recovered 42% of normal grasp strength versus just 11% in rats grafted but not treated with nandrolone. At 180 days, the average values for grasp strength recovery in the nandrolone and no-nandrolone groups were 40% and 33% of normal values for controls, respectively. At 180 days, finger flexor muscle twitch strength was 16% higher in treated versus nontreated rats. Thresholds for nociception were not detected in either group 90 days after nerve grafting. At 180 days, nociceptive thresholds were significantly lower in the nandrolone group.
CONCLUSIONS: Nandrolone decanoate improved functional recovery in a model of deficient reinnervation.
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