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PubMed1983

Effects of androgenic-anabolic steroids on neuromuscular power and body composition.

The effects of androgenic-anabolic steroids on neuromuscular power and body composition were studied in nine volunteers experienced with progressive-resistance weight training. By use of double-blind procedures, testosterone cypionate, nandrolone decanoate, and sesame oil (placebo) were administered in a repeated-measures design that counterbalanced treatment order. Duration of each treatment condition was 3 wk. Supplemental protein was provided, and dietary records were maintained throughout the study. Subjects were trained with progressive-resistance weight-training exercises. Isokinetic dynamometer testing revealed that peak torque output was not significantly changed between treatments in 7 out of 10 isolated-joint actions. The hydrostatic weighing results revealed insignificant differences in lean body mass and percent body fat. Significant changes in some treatment means of three peak torque output tests were insufficient to identify any consistent treatment alterations. Since protein and caloric intake was sufficient to elicit anabolic effects from the steroid treatments and weight-training program, the lack of significant results could not be attributed to dietary considerations. Subjects reported subjective feelings of increased strength after administration of anabolic agents, which may partially account for their widespread use. In conclusion, anabolic steroids did not substantially change body composition or the objective power measurements used in this study.

Adult↗
PubMed1993

Effects of sex steroids on hepatic and lipoprotein lipase activity and mRNA in the rat.

In humans, sex steroids have been implicated in the regulation of hepatic and lipoprotein lipase activity. Therefore, the effects of orchidectomy and subsequent androgen or estrogen administration on hepatic lipase (HL) and adipose tissue and heart lipoprotein lipase (LPL) were examined. Relative to intact controls, orchidectomy of male rats resulted in no significant change in HL activity and mRNA, or in heart and adipose tissue LPL activity and mRNA levels. Subsequently, a subcutaneous silastic tubing, delivering either testosterone, dihydrotestosterone, nandrolone, or 17 beta-estradiol, was implanted for 5 weeks. All substitution treatments had a tendency to reduce HL activity and to induce HL mRNA levels. This effect was, however, only significant for testosterone which resulted in a decrease in HL activity (238 +/- 15 vs. 328 +/- 31 mU/g tissue; p vs. control < 0.05) and an increase in HL mRNA (166 +/- 11 vs. 100 RAU; p vs. control < 0.01). No significant effects of androgens on LPL expression either in heart or adipose tissue were observed. Adipose tissue LPL activity (20 +/- vs. 35 +/- 4 mU/g; p vs. control < 0.05) and mRNA (28 +/- 4 vs. 100 RAU; p vs. control < 0.001) levels, but not heart LPL, however, were diminished substantially after 17 alpha-estradiol treatment. In conclusion, rat HL is influenced by testosterone, while adipose tissue, but not heart LPL, is reduced after estrogen administration.

Adipose Tissue↗
PubMedDate not supplied

Anabolic steroids support postoperative gut/liver amino acid metabolism.

The effects of an anabolic steroid (nandrolone decanoate, 5 mg/kg) on postoperative splanchnic fuel metabolism were studied in order to gain further understanding of the regulation of the altered gut/liver amino acid metabolism that occurs following catabolic illness. In addition to studying glutamine and alanine, which together transport 60% of whole blood amino acid nitrogen, we determined the fluxes of glutamate and glucose across the gastrointestinal tract and liver in 12 postoperative dogs. Substrate exchange (flux) was calculated by multiplying bloodflow by the arterial-venous concentration difference for each substrate. Arterial glutamine, glutamate, and alanine were significantly increased in dogs receiving the anabolic steroid (AS) compared to control animals (p less than 0.05). Intestinal bloodflow was unchanged, but gut glutamine uptake doubled in dogs receiving steroids (1.4 +/- 0.3 mumol/kg/min in controls vs 2.8 +/- 0.7 in AS, p less than 0.05). Simultaneously, gut alanine release was augmented by 100% in dogs receiving steroids (p less than 0.05). Control dogs demonstrated net glutamate release by the gut, while dogs treated with the anabolic steroid demonstrated glutamate balance (p less than 0.05). Liver bloodflow remained unchanged in AS dogs, but hepatic alanine uptake nearly tripled (p less than 0.01) and hepatic glucose production increased by 60% (p less than 0.05). Anabolic steroids appear to support postoperative splanchnic fuel metabolism by increasing blood amino acid levels, enhancing gut/liver amino acid uptake and processing, and augmenting hepatic gluconeogenesis.

Alanine↗
PubMedDate not supplied

Morphologic and histologic abnormalities in female and male rats treated with anabolic steroids.

A two-part study was performed to determine the effects of high doses of anabolic steroids on weight, appetite, and organ histology. Initially, 30 white Wistar rats, 15 males and 15 females, were treated weekly with either 0.52 cc of physiologic saline or nandrolone decanoate. After 6 weeks, female treated and control rats had comparable weight gains, but male treated rats were significantly lighter than controls. Rats were sacrificed and organs dissected for histologic preparation. Treated male livers had less lipid than control males. The uteri of treated females displayed abnormal vacuolization, stromal edema, and peliosis. In Part II, 12 male rats, 6 treated and 6 control, were given the drug or saline in a manner identical to that in Part I. Treated rats had lower weights from Weeks 1 through 6 and ate less than controls. Upon sacrifice, treated rats' kidneys were heavier, and testes and liver were lighter compared to controls. Roentgenographic studies of tibias from Parts I and II showed no significant differences in tibial length or height of growth plate between treated and control groups. In summary, when anabolic steroid use is studied in the rat model, numerous pathological and anatomical changes occur.

Anabolic Agents↗
PubMedDate not supplied

Anabolic-androgenic steroid administration causes hypertrophy of immobilized and nonimmobilized skeletal muscle in a sedentary rabbit model.

Although the use of anabolic agents in athletics has generated extensive publicity and controversy, the potential therapeutic benefits of these drugs have not been fully investigated. This randomized, blinded experimental study investigated whether short-term administration of an anabolic-androgenic steroid can limit immobilization-induced muscle atrophy in a rabbit model. We casted one hindlimb each in 48 New Zealand White rabbits and randomly assigned the rabbits to two groups. The treated group received weekly intramuscular injections of the anabolic-androgenic steroid, nandrolone decanoate (15 mg/kg). Immobilization significantly decreased muscle weights in both the treated rabbits and controls. Compared with controls, the body weights of the treated rabbits increased significantly at 2, 4, and 8 weeks. At 4 and 8 weeks, wet weights, dry weights, and contractile forces were significantly greater in both the casted and noncasted tibialis anterior muscle-tendon units of the treated group. Dry weights and casted contractile forces of the extensor digitorum longus muscle unit at 4 weeks and all measures at 8 weeks were greater in the treated rabbits than in controls. These results are contrary to previously accepted views that anabolic-androgenic steroid use leads to muscle hypertrophy only in conjunction with strength training. This study adds to the growing evidence that anabolic-androgenic steroids can produce significant skeletal muscle hypertrophy in sedentary populations.

Anabolic Agents↗
PubMed1996

Hormonal treatment in advanced non-small cell lung cancer: fact or fiction?

In patients with advanced non-small cell lung cancer, cachexia is an important cause of morbidity and mortality. The pathogenic mechanism of this finding, usually referred to as "cancer anorexia and cachexia syndrome" (CACS), is complex and far from completely understood, but a disturbed equilibrium between possible food intake and metabolic needs seems to be fundamental. The literature data on the treatment options in advanced non-small cell lung cancer (NSCLC) with cachexia are reviewed. Based on the clinical studies on cancer cachexia, some recommendations for the therapeutic approach of this disorder in patients with advanced NSCLC can be given. Metoclopramide is easily administered, can alleviate gastric disturbances, but probably does not correct the catabolic spiral of CACS. There are not enough data to advise the use of parenteral nutritional support, hydrazine, cyproheptadine, tetrahydrocannabinol or nandrolone decanoate. Corticosteroids are useful in additional analgesia and fast palliation of very weak and debilitated patients in the final episode of their disease. Recent data in non-small cell lung cancer patients are in favour of the use of high-dose progestagens to improve both appetite and weight.

Cachexia↗
PubMed1984

Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin.

It is unclear whether anabolic steroids act on skeletal muscle via the androgen receptor (AR) in this tissue, or whether there is a separate anabolic receptor. When several anabolic steroids were tested as competitors for the binding of [3H]methyltrienolone (MT; 17 beta-hydroxy-17 alpha-methyl-4,9,11-estratrien-3-one) to the AR in rat and rabbit skeletal muscle and rat prostate, respectively, MT itself was the most efficient competitor. 1 alpha-Methyl-5 alpha-dihydrotestosterone (1 alpha-methyl-DHT; mesterolone) bound most avidly to sex hormone-binding globulin (SHBG) [relative binding affinity (RBA) about 4 times that of DHT]. Some anabolic-androgenic steroids bound strongly to the AR in skeletal muscle and prostate [ RBAs relative to that of MT: MT greater than 19-nortestosterone ( NorT ; nandrolone) greater than methenolone (17 beta-hydroxy-1-methyl-5 alpha-androst-1-en-3-one) greater than testosterone (T) greater than 1 alpha-methyl-DHT]. In other cases, AR binding was weak (RBA values less than 0.05): stanozolol (17 alpha-methyl-5 alpha- androstano [3,2-c]pyrazol-17 beta-ol), methanedienone (17 beta-hydroxy-17 alpha-methyl-1,4-androstadien-3-one), and fluoxymesterolone (9 alpha-fluoro-11 beta-hydroxy-17 alpha-methyl-T). Other compounds had RBAs too low to be determined (e.g. oxymetholone (17 beta-hydroxy-2-hydroxymethylene-17 alpha-methyl-5 alpha-androstan-3-one) and ethylestrenol (17 alpha-ethyl-4- estren -17 beta-ol). The competition pattern was similar in muscle and prostate, except for a higher RBA of DHT in the prostate. The low RBA of DHT in muscle was probably due to the previously reported rapid reduction of its 3-keto function to metabolites, which did not bind to the AR [5 alpha-androstane-3 alpha, 17 beta-diol and its 3 beta-isomer (3 alpha- and 3 beta-adiol, respectively)]. Some anabolic-androgenic steroids (only a few synthetic) bound to SHBG (1 alpha-methyl-DHT much greater than DHT greater than T greater than 3 beta-adiol greater than 3 alpha-adiol = 17 alpha-methyl-T greater than methenolone greater than methanedienone greater than stanozolol). The ratio of the RBA in rat muscle to that in the prostate (an estimate of the myotrophic potency of the compounds) was close to unity, varying only between about 0.4 and 1.7 in most cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Androgens↗
PubMed1998

HIV wasting syndrome: treatment update.

OBJECTIVE: To review the pathophysiology and treatment of HIV wasting syndrome. DATA SOURCES AND STUDY SELECTION: MEDLINE searches (January 1987-September 1997) of the English-language medical literature were conducted. Bibliographies were also selected during a manual review. DATA SYNTHESIS: HIV-related weight loss, often referred to as HIV wasting syndrome, is a common manifestation of advanced HIV infection. Wasting in HIV involves the preferential loss of lean body mass with a paradoxical preservation of body fat. The etiology of wasting appears to be the result of many factors, which may include decreased caloric intake, malabsorption, alterations in energy expenditure and metabolism, cytokine effects, and endocrine dysfunction. Pharmacologic treatment options include appetite stimulants (e.g., dronabinol, megestrol acetate), cytokine inhibitors (e.g., thalidomide, cyproheptadine, ketotifen, pentoxifylline, fish oil, N-acetylcysteine), and anabolic agents (e.g., testosterone, nandrolone, oxandrolone, recombinant human growth hormone). CONCLUSIONS: Wasting associated with HIV has a high morbidity and mortality rate if not adequately managed. Therapeutic strategies include appetite stimulants, cytokine inhibitors, and growth-promoting agents. Selection of the appropriate agent(s) depends on the underlying cause for weight loss, adverse effects, and cost of therapy.

HIV Infections↗
PubMed1980

Changes in the cytoplasmic androgen receptor of rat ventral prostate after administration of androgens, antiandrogens and anabolic steroids.

The effect of the administration of androgens (testosterone and dihydrotestosterone(, antiandrogens (progesterone and cyproterone acetate) and anabolic steroids (Bolandiol, Nandrolone, Furazabol and Methenolone) on depletion and replenishment of the androgen receptor in the cytosol of ventral prostate from castrated rats was examined using 3H-R1881 as the ligand. Administration of androgens lead to a rapid fall in the level of the receptor and the receptor in the cytosol was replenished in the period following treatment. Length of the period of receptor depletion was dependent on the dose of androgen administered. Administration of antiandrogens did not cause any depletion of the receptor and concomitant administration of testosterone induced a pattern similar to that of the depletion observed following administration of testosterone alone. Effect of pretreatment of animals with ethidium bromide, an intercalating dye which has been shown to prevent the in vitro nuclear binding of steroid hormone-receptor complexes, on the depletion of receptor induced by testosterone administration was also insignificant. Anabolic steroids depleted the receptor but the degree of depletion was relatively low. The rate of inhibition of in vitro 3H-R1881 binding by these anabolic steroids was not correlated to the rate of in vivo depletion of the receptor. The significance of these observations is discussed.

Anabolic Agents↗
PubMed2001

Anorexia in end-stage renal disease: pathophysiology and treatment.

Anorexia is a frequent complication of uraemic syndrome, which contributes to malnutrition in dialysis patients. Uraemic anorexia has been associated with many factors. This paper reviews the current knowledge about mechanisms responsible for uraemic anorexia, the treatments and new drugs used to control the loss of appetite. Traditionally, anorexia in dialysis patients has been considered as a sign of uraemic toxicity, therefore, two hypotheses have been proposed, the 'middle molecule' and 'peak-concentration' hypotheses, both of which are still unproved. Recently, our group proposed the tryptophan-serotonin hypothesis, which is based on a disorder in the amino acid profile acquired in the uraemic status. This is characterised by low concentrations of large neutral and branched chain amino acids (LNAA/BCAA) in the cerebrospinal fluid. This situation permits a high level of tryptophan transport across the blood-brain barrier, causing an increase in the synthesis of serotonin (responsible for appetite inhibition). There are two main treatment targets for anorexia in dialysis patients. The first is to decrease the free plasma tryptophan concentration and transport across the blood brain barrier to the cerebrospinal fluid, thus decreasing the intracerebral serotonin levels. Nutritional formulae enriched with LNAA and BCAA have this effect. Secondly, plasma levels of cytokines with cachectin effect (TNF-alpha), should be decreased. This also induces a decrease in LNAA and BCAA levels. In this group are megestrol acetate, anti-TNF-alpha antibodies, thalidomide, pentoxifyilline, n-3 fatty acids and possibly nandrolone decanoate. Additionally, other targets should be explored including antagonists of cholecystokinin (a potent anorexigen retained by renal failure), analogues of neuropeptide Y (the most potent orexigen), cannabinoids, cyproheptadine, hydrazine sulfate. In conclusion, uraemic anorexia is a complex complication associated with malnutrition, high morbidity and mortality. The pharmacological treatment should address key points in the pathogenesis of uraemic anorexia, reducing intra-cerebral concentration of serotonin with LNAA/BCAA oral diet formulae and the plasma levels of pro-inflammatory molecules. Others forms of treatment should also be explored.

Anorexia↗
PubMed2005

Disappearance of a virilizing adrenal tumor following therapy with cyproterone acetate.

A 57-year-old woman presented with an apparently obvious diagnosis of iatrogenic virilization. At the age of 51, she began a 4-year treatment with prednisone or cyclosporine, which are known to promote hair growth, for Behçet disease. At the age of 56, osteoporosis was overtreated with the anabolic steroid nandrolone. Insignificant inhibition by dexamethasone of the extremely high serum concentrations of testosterone and less high concentrations of weak androgens prompted us to search for a virilizing tumor. Computed tomography showed a 2.3 x 1.5 cm nodule in the right adrenal gland. As the patient refused surgery, virilization was treated with the antiandrogen cyproterone acetate (CPA), but for only 4 months because clinical and hormone abnormalities reversed and the tumor was no longer visible. The patient remains symptom-free. This first report of a curative effect of CPA on a purely virilizing adrenal tumor opens new avenues in the management of such tumors.

Adrenal Gland Neoplasms↗
PubMed1996

Corticosteroid-induced bone loss. Prevention and management.

Osteoporosis is one of the most serious adverse effects experienced by patients receiving long term corticosteroid therapy. Bone loss occurs soon after corticosteroid therapy is initiated and results from a complex mechanism involving osteoblastic suppression and increased bone resorption. There are a number of factors that may increase the risk of corticosteroid-induced osteoporosis [smoking, excessive alcohol (ethanol) consumption, amenorrhoea, relative immobilisation, chronic obstructive pulmonary disease, inflammatory bowel disease, hypogonadism in men, organ transplantation]. The initial assessment of patients about to start taking corticosteroids should include measurement of spinal bone density, urinary calcium level and plasma calcifediol (25-hydroxycholecalciferol) level; serum testosterone levels should also be measured when hypogonadism is suspected. Many different drugs have been used to prevent osteoporosis in patients receiving long-term corticosteroid therapy, including thiazide diuretics, cholecalciferol (vitamin D) metabolites, bisphosphonates, calcitonin, fluoride, estrogens, anabolic steroids and progesterone. At present, however, published studies have failed to demonstrate a reduction in the rate of fracture using different preventive pharmacological therapies in patients being treated with corticosteroids on a continuous basis. Among the drugs studied, bisphosphonates (pamidronic acid and etidronic acid) and calcitonin appear to be effective in increasing bone density. Cholecalciferol preparations have been reported to be effective in some, but not all, studies. Limited data have shown positive results with thiazide diuretics, estrogen, progesterone and nandrolone. When treating patients with corticosteroids, the lowest effective dose should be used, with topical corticosteroids used whenever possible. Auranofin may be considered in patients with corticosteroid-dependent asthma. Patients should take as much physical activity as possible, maintain an adequate daily intake of calcium (1000 mg/day0 and cholecalciferol (400 to 800 U/day), stop smoking and avoid excessive alcohol intake. It is important to detect and treat hypogonadism in men, if present, and to replace gonadal hormones in postmenopausal women or amenorrhoeic premenopausal women, and to detect and correct cholecalciferol deficiency. A thiazide diuretic should be considered if hypercalciuria is present (urinary calcium excretion in excess of 4 mg/kg/day). High-risk patients and those with established osteoporosis should be treated with bisphosphonates (cyclical etidronic acid or intravenous pamidronic acid), nasal calcitonin, or calcifediol or calcitriol. Patients receiving cholecalciferol preparations should be carefully monitored for hypercalciuria and hypecalcaemia.

Adrenal Cortex Hormones↗
PubMed2000

[Standards, Options and Recommendations (SOR) for the use of appetite stimulants in oncology. Work group. Federation of the French Cancer Centres (FNCLCC)].

CONTEXT: The "Standards, Options and Recommendations" (SOR) project, started in 1993, is a collaboration between the Federation of the French Cancer Centres (FNCLCC), the 20 French Cancer Centres and specialists from French Public Universities, General Hospitals and Private Clinics. The main objective is the development of clinical practice guidelines to improve the quality of health care and outcome for cancer patients. The methodology is based on literature review and critical appraisal by a multidisciplinary group of experts, with feedback from specialists in cancer care delivery. OBJECTIVES: To develop clinical practice guidelines according to the definitions of the Standards, Options and Recommendations project for the use of appetite stimulants in oncology. METHODS: Data were identified by searching Medline and the personal reference lists of members of the expert groups. Once the guidelines were defined, the document was submitted for review to 55 independent reviewers, and to the medical committees of the 20 French Cancer Centres. RESULTS: The main recommendations for the use of appetite stimulants in oncology are: 1) Corticosteroids and the synthetic progestogens (megestrol acetate and medroxyprogesterone acetate) are appetite stimulants. 2) They can be useful in managing anorexia and weight loss in cancer patients, especially in the palliative setting, despite the potential side-effects of these agents. 3) The most effective way of using these drugs is not known. Inclusion in clinical trials is recommended. 4) Cyproheptadine, metoclopramide, nandrolone and pentoxif line should not be used outside prospective clinical trials. 5) Hydrazine sulfate should not be used.

Adrenal Cortex Hormones↗
PubMed2002

Hair analysis of seven bodybuilders for anabolic steroids, ephedrine, and clenbuterol.

Several bodybuilders, all winners of international competitions, were arrested for trafficking of a number of doping agents including anabolic steroids, ephedrine, beta-adrenergics, human chorionic gonadotropin, antidepressants, and diuretics. In accordance with the recent French law against doping, the judge asked to test seven bodybuilders to identify doping practices. Hair and urine specimens were collected for analysis. After decontamination, a 100 mg hair strand was pulverized in a ball mill, hydrolyzed, extracted, and derivatized to be tested by GC/MS for anabolic steroids, beta-adrenergic compounds, ephedrine, and other doping agents. Urine was analyzed for anabolic steroids and metabolites, beta-adrenergic compounds, ephedrine, and human chorionic gonadotropin, in addition to a broad spectrum screening with GC/MS. The following compounds were detected in urine: ephedrine (29 and 36 ng/mL, n = 2), clenbuterol (0.2 to 0.3 ng/mL, n = 3), norandrosterone (4.7 to 100.7 ng/mL, n = 7), norethiocholanolone (0.9 to 161.8 ng/mL, n = 6), stanozolol (1 to 25.8 ng/mL, n = 4), methenolone (2.5 to 29.7 ng/mL, n = 4), testosterone (3 to 59.6 ng/mL, n = 7), epitestosterone (1 to 20.4 ng/mL, n = 7) and ratio testosterone/epitestosterone >6 for four subjects (18.5 to 59.6). The following drugs were detected in hair: ephedrine (0.67 and 10.70 ng/mg, n = 2), salbutamol (15 to 31 pg/mg, n = 3), clenbuterol (15 to 122 pg/mg, n = 6), nandrolone (1 to 7.5 pg/mg, n = 3), stanozolol (2 to 84 pg/mg, n = 4), methenolone (17 and 34 ng/ml, n = 2), testosterone enanthate (0.6 to 18.8 ng/mg, n = 5), and testosterone cypionate (3.3 to 4.8 ng/mg, n = 2). These results document the doping practice and demonstrate repetitive exposure to anabolic compounds and confirm the value of hair analysis as a complement to urinalysis in the control of doping practice.

Adult↗
PubMed2002

Successful DNA typing of a urine sample in a doping control case using human mitochondrial DNA analysis.

In a doping control case, a urine sample was tested positive for nandrolon. We were asked by the athlete to perform DNA investigations on the questioned urine sample and compare these to a fresh blood sample taken from the athlete in order to detect or rule out manipulation and/or switching of the samples. The urine sample had been collected nine months prior to the investigation and had been stored at 4 degrees C. In a first approach, nuclear DNA systems were investigated that failed with the exception of the Amelogenin system. Due to the high copy number of mitochondrial DNA molecules and the robustness of the mitochondrial genome, we investigated the HVR I and HVR II regions of mitochondrial DNA and obtained reproducible and clear sequencing results for both the blood and the urine samples. Due to the identical sequences, it could not be excluded that the blood sample and the urine sample were from the same individual or an individual having the same maternal lineage.

DNA, Mitochondrial↗
PubMed2004

Contamination of supplements: an interview with professor Ron Maughan by Louise M. Burke.

This issue of IJSNEM features two articles related to supplement use by athletes. In one (Morrison et al. 2004), people who undertake regular exercise in a gym were found to report the use of a wide variety of supplements. The other paper (Goel et al. 2004) dealt with one of the issues that a sub-group of athletes need to consider before deciding to take supplements - the risk of a positive drug test if the product contains substances banned by the anti-doping codes under which their sport is conducted. This issue received much publicity earlier in the year when top tennis player Greg Rusedski tested positive for the steroid nandrolone as the result of inadvertent intake via a contaminated supplement. In this article, Professor Ron Maughan, Chair of Sports Nutrition at Loughborough University in the United Kingdom, advisor to the British Olympic team, and co-editor of IJSNEM, provides his insight on this important topic.

Dietary Supplements↗
PubMed2000

A novel pharmacological approach of musculoskeletal losses associated with simulated microgravity.

Exposure to microgravity (weightlessness) is known to cause rapid bone and muscle losses. We have used the hind limb-suspended (HLS) rat model to simulate microgravity-induced musculoskeletal losses in order to assess resulting hormonal changes and to develop a novel pharmacological countermeasure. Previously, we demonstrated significant decreases in circulatory hormonal levels [serum thyroxin, 1,25(OH)2 vitamin D (p<0.05), and serum testosterone (p<0.001)] in HLS rats. Both thyroxin and 1,25(OH)2 vitamin D levels returned to normal soon after removal from HLS, while testosterone levels matched normal levels only after a further 3-4 weeks. However, even by day 42, bone mineral density (BMD) remained significantly lower, although serum hormones were back to normal. Because serum testosterone levels become undetectable in HLS rats, we hypothesized that the replacement of testosterone during HLS could prevent musculoskeletal losses. Based on these data, an intervention study was carried out to assess the efficacy of testosterone and synthetic anabolic steroid, nandrolone decanoate (ND), in prevention of weightlessness-induced musculoskeletal losses. HLS rats (control) had a significant reduction of muscle volume (42.9 -/+ 3.0, versus 56 -/+ 1.8 in ground control rats; p<0.01). Both testosterone and ND treatments prevented this muscle loss (51.5 -/+ 2 cm(3) and 51.6 -/+ 1.2, respectively; a 63% improvement, p<0.05). Similarly, BMD of the placebo-treated HLS rats was significantly lower than that of ground control rats (0.416 -/+ 0.011 versus 0.354 -/+0.014, p<0.05), and testosterone and ND prevented this bone loss (0.404 -/+ 0.013 versus. 0.409 -/+ 0.011, respectively). These data suggest that both testosterone and ND therapy can minimize the musculoskeletal losses associated with exposure to simulated weightlessness. Experiments using the combination of bisphosphonate and testosterone demonstrated complete protection of both muscle and bone in these HLS rats. Therefore, considering that: 1) testosterone is anabolic to osteoblasts and muscle cells and also decreases the rate of bone turnover, 2) serum testosterone levels are markedly suppressed in simulated weightlessness, and 3) testosterone replacement therapy prevented musculoskeletal losses in HLS rats, we propose that the musculoskeletal losses observed in this animal model (i.e., simulated microgravity) are related to their testosterone deficiency. Since serum sex hormones levels are markedly reduced in this model of simulated microgravity, androgen replacement with a bisphosphonate seems to be a rational counter.

Journal Article↗
PubMed2005

[Management of male sterility in patients taking anabolic steroids].

OBJECTIVES/METHODS: To review the incidence of male infertility secondary to intake of anabolic products and our experience and outcomes with treatment. There is a variety of such substances (testosterone, nandrolone, stanozolol, etc.) in their intake may be unique or combinations, both orally or parenterally. Comparisons between patients and case series are difficult because of the hiding of this practice and various consumption practices and doses employed. RESULTS/CONCLUSIONS: Most of the patients recover normal spermatogenesis does by stopping intake of anabolic substances. The period of time until recovery is 6.35 months. Patients not recovering after six months were given tamoxifen 20 mg/24-hour, if having a normal or inhibited hypothalamus-hypophysis axis. Duration of abuse, doses, and anarchical consumption maderesponse to treatment with antiestrogen drugs or gonadotropins unpredictable in patients not responding to conservative treatment.

Adult↗