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Critique of the tests to study reciprocal Ia inhibition Different results have been obtained for the flexors and extensors of the wrist At ankle and elbow proven kamagra effervescent 100 mg back pain causes erectile dysfunction, interneurones mediating di- synaptic reciprocal inhibition are probably analo- Unlike what has been observed at elbow and ankle buy 100mg kamagra effervescent otc diabetes and erectile dysfunction relationship, gous to the Ia inhibitory interneurones mediating radial-induced disynaptic group I inhibition of the reciprocal Ia inhibition studied in the cat and the FCR H reflex was not depressed by the tendon jerk monkey(seepp order kamagra effervescent 100mg overnight delivery erectile dysfunction 30 years old. There is between strictly antagonistic muscles operating at was only a transient depression of the inhibition at the same joint trusted 100 mg kamagra effervescent erectile dysfunction vascular disease, (ii) can be evoked by pure Ia volleys, ISIs of 8–10 ms due to refractoriness of ECR Ia affer- and (iii) is depressed by recurrent inhibition. Pharmacological validation Estimate of the central delay Intravenous administration of a cholinergic ago- An essential criterion of reciprocal Ia inhibition is nist (L-acetylcarnitine, L-Ac) specifically increases that it is disynaptic. Triceps-induced reciprocal Ia inhibi- Intensity of the conditioning volley tion of the biceps tendon jerk and disynaptic group I radial-induced inhibition of the FCR H reflex have Reciprocal inhibition induced by stimuli <1 × MT been measured before and after intravenous admin- is often very small, particularly the common pero- istration of L-Ac (Rossi et al. Recip- neal inhibition of soleus, the most frequently inves- rocal inhibition was potently reduced at elbow level, tigated paradigm. It is therefore tempting to use whereastheradial-inducedinhibitionwasnotmodi- stimuli >1 × MT which elicit more profound inhi- fied at wrist level. This should be avoided because: (i) when the activity induced by L-Ac depresses reciprocal inhi- volley is applied to the deep peroneal nerve, there is bition between antagonistic muscles of the elbow, greaterriskofencroachinguponsuperficialperoneal but not between those of the wrist. Selectiveactivationofthedeeppero- the modulation of the ongoing EMG because tem- neal nerve by the conditioning stimulus is therefore poral resolution is then poor; and (iii) the activation required. Thisisusuallypossiblewhentheelectrodes of Renshaw cells by the resulting antidromic motor are placed distal to the head of the fibula and just volley can depress transmission in Ia interneurones. Superimposition of longer-latency inhibition Elbow level A longer-latency inhibition is superimposed on Because the triceps brachii nerve is stimulated close reciprocalIainhibitionofsoleusmotoneurones1ms to other upper limb nerves (and in particular the afteritsonsetduringactivedorsiflexion(Croneetal. There are reasons to believe that it is medi- sors), it is crucial to ensure that the conditioning ated through lumbar propriospinal neurones (see stimulus does not encroach upon these nerves. Discrepancies between the the other hand, since the electrodes stimulating resultsobtainedbydifferentgroupsduringtonicdor- biceps and triceps brachii afferents are located over siflexion of the foot are presumably due in part to the belly of the muscle, it is important to ensure that a confusion between changes in this longer latency increasing the stimulation above 1×MT results in a inhibition and in the early reciprocal Ia inhibition steep increase in the motor response involving the (see p. Necessity for selective activation of the deep peroneal nerve Conflicting results have been reported concerning Organisation and pattern the amount (or even the existence) of reciprocal of connections Ia inhibition of the soleus H reflex at rest in nor- mal subjects (see below). Part of the discrepancy Pattern and strength of reciprocal Ia betweentheresultsobtainedbydifferentgroupsmay inhibition at rest at hinge joints be explained by the potent Ia monosynaptic exci- tatory projections from peroneal muscles to soleus Reciprocal Ia inhibition between flexors motoneurones (see Meunier, Pierrot-Deseilligny & and extensors of the ankle Simonetta, 1993; Chapter 2,p. Stim- ulation of Ia afferents in the superficial peroneal Reciprocal inhibition between ankle flexors and nervemayobscurereciprocalinhibitionfrompretib- extensors can be considered true reciprocal Ia inhi- ial flexors onto soleus. This could explain why Mao bition, because: (i) the muscles are antagonists, et al. Tibialis anterior H reflexes are inhibited from the posterior tibial nerve to a greater Conflicting results have been obtained at rest. In con- tivedifferencebetweenreciprocalinhibitionofankle trast, others have been able to demonstrate recipro- flexorsandextensorsisreminiscentofthesimilardif- cal Ia inhibition consistently (Kots & Zhukov, 1971; ference in the cat hindlimb (see p. As discussed above, the discrepancy and extensors of the elbow maybeattributedinparttomonosynapticexcitation elicited by inadvertent stimulation of Ia afferents in Attheelbow,anotherhingejoint,thethreecriteriafor the superficial peroneal nerve. However, even when truereciprocalinhibitionbetweenflexorsandexten- greatcareistakentopreventtheconditioningstimu- sors have been met: strictly antagonistic muscles; lus from encroaching on the superficial peroneal elicitation by pure Ia volleys. However, at inhibition of the soleus H reflex varies between nor- this joint, the amount of reciprocal inhibition of the mal subjects. In the large population investigated by tendon jerk is similar at its peak in biceps and triceps Crone et al. This population was dominated by Reciprocal Ia inhibition between flexors young students and, as shown in Fig. This correlation could induced inhibition has been described in the PSTHs be due to plasticity in the pathway of reciprocal Ia of single units from hamstrings (Kudina, 1980; inhibition, much as has been described in normal Bayoumi & Ashby, 1989;Fig. Low-threshold anterior motoneurones short-latency inhibition was found only exception- Reciprocal Ia inhibition can be demonstrated con- ally in the PSTHs of quadriceps units after stimu- sistently at rest in those subjects, in whom it is pos- lation of the nerves of the hamstrings (Bayoumi sible to evoke an H reflex in the tibialis anterior & Ashby, 1989). This does not necessarily reflect (Tanaka, 1974; Pierrot-Deseilligny et al. Similarly, posterior flexors, because it is almost impossible to prevent tibial-induced reciprocal Ia inhibition was observed a conditioning stimulus to the sciatic nerve or its Organisation and pattern of connections 211 (a) (b) Femoral on biceps Ia IN Q Bi MN MN -10 0 10 20 30 40 Ia Ia Latency (ms) Femoral (c) Sciatic on quadriceps nerve Sciatic 120 nerve 100 -8 -4 0 4 8 Conditioning-test interval (ms) Fig. Zero indicates the time of the stimulation, and the inhibition occurs at 22 ms (arrow). The arrow indicates the expected time of arrival of the conditioning volley at the segmental level of Q MNs. Any reciprocal inhibition is obscured by facilitation at monosynaptic latency, probably due to the activation of Ia afferents from leg and foot muscles contained in the sciatic nerve. These afferents have monosynaptic excitatory projections to quadriceps motoneurones (cf. Adapted from Bayoumi & Ashby (1989)(b); and Valls-Sole, Hallett & Brasil-Neto (´ 1998)(c), with permission. Data for knee muscles are uncer- by Renshaw cell activation (Aymard et al. In addition, it cannot be taken for and extensors in the forearm appears to be a non- grantedthatthisinhibitionisbetweenstrictlyantag- reciprocalgroupIinhibition,andisdiscussedbelow. The conver- Convergence of group I afferents from several gence described above does not by itself rule out different muscles the possibility that part of the reciprocal inhibition between wrist muscles is reciprocal Ia inhibition. Group I afferents from elbow muscles However, the finding that interneurones medi- Convergence of group I afferents from elbow mus- ating group I reciprocal inhibition of wrist motoneu- cles on interneurones mediating disynaptic recip- rones receive excitation from group I afferents con- rocal inhibition to FCR motoneurones has been tained in other nerves, including the homonymous observed in the PSTHs of single FCR units (Aymard nerve,indicatethatpartofthisinhibitionismediated et al. In this respect, interneurones medi- the triceps brachii nerves, adjusted to be without atingnon-reciprocalgroupIinhibitionaregoodcan- effect by themselves, produced inhibition on com- didates (see Chapter 6,pp. A similar effect Ib afferents to the activation of interneurones medi- was seen consistently when radial and musculo- ating the radial-induced inhibition of the FCR H cutaneous volleys were combined. This indicates reflex is further supported by experiments in which that interneurones mediating radial-induced dis- theelectricalthresholdofECRIaafferentswasraised ynaptic group I inhibition of FCR motoneurones by long-lasting high-frequency vibration applied to receive excitatory input from elbow muscle group I the ECR tendon (Wargon et al. These affer- ents are presumably Ib afferents, given the latency of These afferents also converge onto common the inhibition. Some Ib afferents respond to vibra- interneurones mediating disynaptic reciprocal inhi- tion of relaxed muscles (Chapter 3,pp. The extra suppression on combined stimulation is presumably due to convergence of Other features of the inhibition are consistent median and radial group I volleys onto common with non-reciprocal group I inhibition interneurones. Convergence of group I afferents from different muscles onto interneurones mediating the radial-induced inhibition of the FCR. Zero on the abscissa indicates the expected time of arrival of the volleys at MN level. While separate stimulation of each nerve has little effect (b), inhibition appears on combined stimulation. The dashed vertical line indicates the onset of the peak of homonymous Ia excitation. Note the lack of suppression in the initial bins of the median group I excitation. This phenomenon is analogous to the post- tude of the test reflex is the same as in the control activationdepressionatthesynapseoftheIafibreon situation). In contrast, at wrist level, the amount of the motoneurone (Chapter 2,pp. Accordingly, radial-induced inhibition of the FCR H reflex is not increasing the frequency of stimulation drastically modified when the frequency of the stimulation is decreases the amount of reciprocal Ia inhibition of increased (Lamy et al. Accordingly, it Mutual inhibition may have been appropriate to treat this disynaptic Radial-induced reciprocal inhibition of the FCR H non-reciprocal group I inhibition in Chapter 6 (Ib reflexisdepressedbyaprecedinggroupIvolleytothe pathways).

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Approx- imately one-half of these fractures are related to the verte- bral bodies best buy for kamagra effervescent erectile dysfunction doctor edmonton, with two-thirds being silent and one-third Fracture etiology: factor of risk symptomatic purchase kamagra effervescent without prescription erectile dysfunction doctor houston. Epidemiological studies have demonstrated that multiple vertebral fractures increase morbidity [67 purchase kamagra effervescent no prescription erectile dysfunction protocol download free, Vertebral bodies sustain fractures under two different me- 69] order kamagra effervescent 100 mg online erectile dysfunction treatment new jersey, and the presence and increasing numbers of fractures chanical environments: repetitive loading that fatigues the significantly increase mortality rates [11, 23, 41, 48]. De- cancellous bone and leads to the accumulation of mi- spite the recognition that osteoporotic fractures increase crofractures, or single traumatic events may overload the the risk for additional vertebral fractures as well as hip frac- vertebral body and lead to fracture [58]. To understand the tures, the majority of individuals with these fractures re- etiology of vertebral fracture, information about the loads main undiagnosed and untreated [28, 31, 74]. Radiographic methods have been enhanced and represents the ratio of the load applied to the bone to aid in the diagnosis of osteoporosis. The load 66 necessary to cause a vertebral fracture is determined by the DXA scan can be performed in a lateral or antero- the characteristics related to the vertebral body structure posterior (AP) mode. However, with the presence of osteophytes and scoliosis, the preci- sion decreases and may be artificially elevated, particu- the determinants of bone failure load larly with osteosclerotic facet joints [62]. Above the age of 60, lateral DXA avoids the posterior elements of the the ability of the vertebral body to bear certain loads de- spine, and may address this problem in patients typically pends on both the material properties of the bone and on with evidence of osteoarthritis of the spine. However, the the geometrical distribution of the tissue components overhanging ribs and the superior projection of the iliac which are able to withstand load [39]. Vertebral fractures wing often obscure the L1 and L2, and L4 and L5 verte- occur in cancellous bone, which has a complex microstruc- bral bodies, respectively, leaving one or two vertebral ture. The volume of tissue contained within cancellous bone bodies available for analysis. This may significantly de- is the bone volume fraction, and the mass of the bone crease the precision of the methodology. As a consequence, tissue within a given volume is the apparent density. Since represents the failure load per cross-sectional area is pro- the hip has a greater content of cortical bone, there may be portional to the square of the apparent density [9]. How- a lag time between bone mineral density and recent bone ever, two regions of apparent density can differ substan- loss [63, 76]. Similarly, a comparable lag time may occur tially in ultimate stress as a result of trabecular microar- in demonstrating improved bone stock as a consequence chitecture. The ultimate stress along the superior to infe- of medical interventions. Presently, noninvasive methods of the vertebral height and shape, has been used to evalu- to accurately characterize the trabecular morphology are ate early vertebral deformities. Local changes in collagen matrix includes the instant vertebral assessment (IVA) tech- cross-linking, such as occur in osteogenesis imperfecta, or nique, also termed morphometric X-ray absorptiometry changes in mineral content, such as occur in osteomalacia, (MXA). This allows visualization of both the lateral and are known to affect the material properties. While the al- AP views of the spine from T4 to L4 [37, 26], and is a tered bone material properties can be determined inva- new method for quantifying vertebral deformities. There sively through chemical analysis, they can often be im- is a close correlation with radiographic evaluation of the plied by patient characteristics and clinical laboratory tests. Overall, the strength of the vertebral body is related to the Comparison with standard X-ray has shown a precision bone mass, the macroscopic and microscopic distribution error of approximately 2–3% [3, 27, 86]. Vertebral height of the bone mass and the material properties of the com- measurement is also significantly associated with bone posite bone. The scoliosis and kyphosis angles can be measured for spinal segments, but placing the patient in the prone position can often lead to an underestima- Diagnosis of osteoporosis tion of the true kyphosis. MXA is a relatively Radiographic methods fast, low-radiation technique to identify prevalent verte- bral deformities, particularly moderate to severe deformi- Commonly used in vivo imaging techniques do not cap- ties of the middle thoracic to lumbar spine. Stud- volumetric bone mineral density of trabecular bone [32, ies have reported good correlation between bone mineral 46], but has poor precision due to increasing fat content in density, as measured by DXA, and vertebral body failure the marrow of older patients. There is a higher risk factor of fracture for a sim- nologist-dependent, with high variability depending on the ilar load as the bone density decreases. It has twenty times the radiation studies have demonstrated that low bone mineral density of a DXA scan, and its current use is mainly in the re- is associated with increased fracture rates for the spine [66]. Consequently, raloxifene has been shown to be an ef- fective anti-resorptive agent in the treatment of osteoporo- Laboratory studies used to assess quality and quantity of sis [24]. Post-menopausal use decreases vertebral frac- bone tissue in the spine are centered on bone marrow ab- tures by approximately 40% and increases spinal bone normalities (complete blood count, sedimentation rate, mass [92]. Unfortunately, similar protective effects have serum and urine immunoelectrophoresis); endocrinopathies not been demonstrated in preventing hip fractures [20, (hyperthyroidism, hyperparathyroidism, type I diabetes mel- 24]. However, by stimulating estrogen hormone, serum calcium and serum phosphate) [4, 94]. In light of the tide, pyridinoline peptide, dehydroxypyridinoline peptide, fact that it has no protection against hip fractures, raloxifene or serum c-terminal peptide. These markers identify ele- is not considered a primary treatment for osteoporosis. There are some controversial data suggesting that calcitonin may relieve bone pain through an unknown mechanism. Its current Treatment modalities use is in alleviating painful vertebral fractures as a conse- quence of osteoporosis, and only as a secondary antiresorp- Osteoporosis has been divided into high-turnover and low- tive agent. The most common form is high- controlled, as other agents are much more successful. Bone formation is compromised both oral agents, and zolendronic acid and pamidronate, in low-turnover osteoporosis. These agents have been shown to be have been suggested and developed to address the high- extremely efficacious in high-turnover osteoporosis [43]. Although calcium and vitamin D They increase bone mass at all measurable sites and de- are not considered anti-resorptive agents, approximately crease fracture incidence by 50%, including in the spine half of patients presenting at hospitals with hip fractures and the hip [7, 18, 57]. Reported side effects of oral bis- in the elderly population, primarily by reversing secondary phosphonates include esophagitis and indigestion, but the hyperparathyroidism [19. Intravenous shown to increase bone mass while effecting a decrease of therapies, while not tested specifically for treatment in os- vertebral fracture incidence by approximately 50% [54, teoporosis, appear to be efficacious, and once yearly zole- 60]. Unfortunately, estrogen in combination with proges- dronate (Zometa) infusions appear to be just as effective terone therapy is associated with increased cardiovascular as the oral dose of alendronate regarding bone mass [22]. As a consequence, estrogen is mainly Bisphosphonates decrease bone turnover, and in very used in the early post-menopausal period to treat post- high dosages in canine models have been shown to cause menopausal symptomatology, and then lowered to the least fatigue fractures that are not actively repaired. It is no indicate that patients on alendronate for 10 years have an longer recommended by the US Federal Government for 8. Patients stopping alendronate therapy after agents which have a significant anti-estrogen effect on 5 years retain the decreased fracture risk. However, osteoblasts are preferentially stim- that bisphosphonates remain active for extended periods ulated by SERMs and upregulate the rate of bone forma- once the bone surface has been coated. The half-lives of 68 alendronate and risedronate are at least 10 years and 1. Therapeu- somewhat delayed, the ultimate mechanical strength of the tic medications do not completely eliminate fractures, and repaired bone was unchanged compared to the controls [84]. Overall, bisphosphonates are critical factor in fracture prevention [81, 98]. Fall history extremely effective in the prevention of osteoporotic fragility can be determined through a complete patient interview, fractures.

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In men seminiferous tubules) proven 100mg kamagra effervescent erectile dysfunction freedom book, and suppresses development of female with a genetic trait toward baldness purchase generic kamagra effervescent canada erectile dysfunction even with cialis, large amounts of testos- sexual characteristics order kamagra effervescent impotent rage random encounter. In the absence of testosterone generic 100 mg kamagra effervescent overnight delivery vodka causes erectile dysfunction, the fetus terone cause alopecia (baldness) of the scalp. Testosterone is largely responsible for the Testosterone also provides the stimulus for the descent of the larger, more powerful muscles of men. This normally occurs after the seventh caused by the effects of testosterone on protein metabolism. If the testes do not descend before acids, and build new muscle protein. At the same time, it birth, administration of testosterone or gonadotropic hormone, slows the loss of nitrogen and amino acids formed by the which stimulates testosterone secretion, produces descent in most constant breakdown of body tissues. After pu- Little testosterone is secreted in boys until 11 to 13 years of age. The and remains at a relatively high level until about 50 years of age, height of a male adolescent increases rapidly for a time, then after which it gradually declines. This happens when the car- • the testosterone secreted at puberty acts as a growth hor- tilage at the end of the long bones in the arms and legs becomes mone to produce enlargement of the penis, testes, and scro- bone. The prostate gland, seminal vesicles, seminiferous tubules, and vas deferens Anterior Pituitary Function also increase in size and functional ability. Under the com- High blood levels of testosterone decrease secretion of FSH and bined influence of testosterone and follicle-stimulating LH from the anterior pituitary gland. This, in turn, decreases hormone (FSH) from the anterior pituitary gland, sperm testosterone production. How- ever, the number is also thought to be increasing, and long- Anabolic steroids are synthetic drugs with increased anabolic term effects may be as bad as the effects that occur with use activity and decreased androgenic activity compared with of other illegal drugs. They were developed during attempts to modify for being dangerous to adult athletes, such as bodybuilders testosterone so that its tissue-building and growth-stimulating and football players, they are considered even more dan- effects could be retained while its masculinizing effects could gerous for teens because teens are still growing. In addition to those who take steroids to enhance athletic performance, some males take ABUSE OF ANDROGENIC AND the drugs to produce a more muscular appearance and im- ANABOLIC STEROID DRUGS press females. Steroid abusers usually take massive doses and often take several drugs or combine injectable and oral Androgens and anabolic steroids are widely abused in at- drugs for maximum effects. The large doses produce po- tempts to enhance muscle development, muscle strength, and tentially serious adverse effects in several body tissues: athletic performance. Because of their abuse potential, the • Cardiovascular disorders include hypertension, de- drugs are Schedule III controlled substances. Although non- creased high-density blood lipoproteins (HDL) and prescription sales of the drugs are illegal, they apparently are increased low-density lipoproteins (LDL), all of which easily obtained. Athletes are considered a high-risk group because some • Liver disorders include benign and malignant neo- start taking the drugs in their early teenage years and con- plasms, cholestatic hepatitis and jaundice, and peliosis tinue for years. The number of teens taking anabolic steroids hepatis, a disorder in which blood-filled cysts develop is thought to be small in comparison with the number using in the liver and may lead to hemorrhage or liver failure. CHAPTER 29 ANDROGENS AND ANABOLIC STEROIDS 427 • Central nervous system disorders include aggression, thetic formulation that is less extensively metabo- hostility, combativeness, and dependence characterized lized by the liver and more suitable for oral admin- by preoccupation with drug use, inability to stop taking istration. They have a rapid onset of action and last cases, psychosis may develop. A topical gel (a 10-g dose • Reproductive system disorders include decreased tes- delivers 100 mg) produces normal serum testosterone ticular function (eg, decreased secretion of endogenous levels within 4 hours after application, and absorption testosterone and decreased formation of sperm), testicu- of testosterone into the blood continues for 24 hours. They include amen- Steady-state serum concentrations occur by the sec- orrhea in women. When the gel is discontinued, • Metabolic disorders include atherosclerosis-promoting serum testosterone levels remain in the normal range changes in cholesterol metabolism and retention of flu- for 24 to 48 hours, but decrease to pretreatment lev- ids, with edema and other imbalances. With Testoderm, the serum trolyte retention contribute to the increased weight testosterone concentration reaches a maximum level associated with drug use. Testoderm must be ap- after the drugs are stopped and may be irreversible. Names plied to the scrotum to achieve adequate blood levels; of anabolic steroids include nandrolone (Deca-Durabolin), scrotal skin is much more permeable to testosterone oxandrolone (Oxandrin), oxymetholone (Anadrol-50), and than other skin areas. Androderm is also applied to nonscrotal skin, and testosterone is continuously absorbed for 24 hours, ANDROGENS AND ANABOLIC with normal blood levels achieved during the first day STEROIDS USED AS DRUGS of drug use. Applying the patch at night produces serum testosterone levels similar to those in healthy • When male sex hormones or androgens are given from young men (ie, higher concentrations in the morning exogenous sources for therapeutic purposes, they pro- and lower ones in the evening). These effects include inhibition of endogenous highly bound (98%) to plasma proteins and serum half- sex hormones and sperm formation through negative life varies (eg, 8 days for IM testosterone cypionate, feedback of pituitary luteinizing hormone (LH) and 9 hours for oral fluoxymesterone). About 90% of a dose is • Male sex hormones given to women antagonize or reduce excreted in urine as conjugates of testosterone and its the effects of female sex hormones. It is given orally, has a half-life of 4 to 5 hours, and is lining of the uterus. This characteris- ° Naturally occurring androgens are given by injec- tic limits the clinical usefulness of these drugs in tion because they are metabolized rapidly by the women and children. Some esters of testosterone sexual development may occur if these drugs are given have been modified to slow the rate of metabolism to young children. For example, intramuscu- lar (IM) testosterone cypionate and testosterone enanthate have slow onsets of action and last 2 to Mechanism of Action 4 weeks. As a result, doses as high as 400 mg/day may ported to the nucleus, where it activates ribonucleic and be needed to produce adequate blood levels for full deoxyribonucleic acid production and stimulates cellular syn- replacement therapy. With male sex hormones, the most clear-cut indication for use is to treat androgen deficiency states (eg, hypogonadism, cryptorchidism, impotence, oligospermia) in boys and men. Individual Androgens Hypogonadism may result from hypothalamic-pituitary or testicular dysfunction. In prepubertal boys, administration of Clinical indications, routes, and dosage ranges are listed in the drugs stimulates the development of masculine character- Drugs at a Glance: Androgens. In postpubertal men who become androgen deficient, the hormones re-establish and maintain masculine characteristics and functions. HERBAL OR DIETARY In women, danazol (Danocrine) may be used to prevent or SUPPLEMENTS treat endometriosis or fibrocystic breast disease. Anabolic steroids are more often abused for body-building purposes Androstenedione and DHEA, androgens produced by the than used for therapeutic effects. They are marketed as safe, natural, alter- cancer and some types of anemia as indications for use, an- native androgens for building muscles. These products, which drogens have largely been replaced by newer drugs for these have weak androgenic activity, act mainly as precursors for purposes. In breast cancer, for example, androgens are second- the production of sex hormones. Androstenedione, for exam- line hormonal agents, after anti-estrogens (eg, tamoxifen). In ple, may be converted to testosterone by way of an enzyme anemia associated with renal failure, synthetic erythropoietin found in most body tissues. In one study, young men with normal serum testosterone levels were given Contraindications to Use an androstenedione supplement for 8 weeks. The researchers found little effect on serum testosterone levels or muscle de- Androgens and anabolic steroids are contraindicated during velopment with resistance training.