Is it possible AAS make us more likely to become injured?

[Kratos]

Self-reported anabolic-androgenic steroids use and musculoskeletal injuries: findings from the center for the study of retired athletes health survey of retired NFL players.
Horn S, Gregory P, Guskiewicz KM.

Department of Physical Medicine and Rehabilitation, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

OBJECTIVE: The relationship between musculoskeletal injuries and anabolic-androgenic steroids is not well understood. The purpose of our study was to investigate the association between self-reported anabolic-androgenic steroids use and the prevalence of musculoskeletal injuries in a unique group of retired professional football players. DESIGN: A general health questionnaire was completed by 2552 retired professional football players. Survey data were collected between May 2001 and April 2003. Results of self-reported musculoskeletal injuries were compared with the use of anabolic-androgenic steroids using frequency distributions and chi2 analyses. RESULTS: Of the retired players, 9.1% reported using anabolic-androgenic steroids during their professional career. A total of 16.3% of all offensive line and 14.8% of all defensive line players reported using anabolic-androgenic steroids. Self-reported anabolic-androgenic steroids use was significantly associated (P < 0.05) with the following self-reported, medically diagnosed, joint and cartilaginous injuries in comparison with the nonanabolic-androgenic steroids users: disc herniations, knee ligamentous/meniscal injury, elbow injuries, neck stinger/burner, spine injury, and foot/toe/ankle injuries. There was no association between anabolic-androgenic steroids use and reported muscle/tendon injuries. CONCLUSIONS: Our findings demonstrate that an association may exist between anabolic-androgenic steroids use and the prevalence of reported musculoskeletal injury sustained during a professional football career, particularly ligamentous/joint-related injuries. There may also be an associated predisposition to selected types of injuries in anabolic-androgenic steroids users.

[Swifto]

Self-reported anabolic-androgenic steroids use and musculoskeletal injuries: findings from the center for the study of retired athletes health survey of retired NFL players.
Horn S, Gregory P, Guskiewicz KM.

Department of Physical Medicine and Rehabilitation, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.

OBJECTIVE: The relationship between musculoskeletal injuries and anabolic-androgenic steroids is not well understood. The purpose of our study was to investigate the association between self-reported anabolic-androgenic steroids use and the prevalence of musculoskeletal injuries in a unique group of retired professional football players. DESIGN: A general health questionnaire was completed by 2552 retired professional football players. Survey data were collected between May 2001 and April 2003. Results of self-reported musculoskeletal injuries were compared with the use of anabolic-androgenic steroids using frequency distributions and chi2 analyses. RESULTS: Of the retired players, 9.1% reported using anabolic-androgenic steroids during their professional career. A total of 16.3% of all offensive line and 14.8% of all defensive line players reported using anabolic-androgenic steroids. Self-reported anabolic-androgenic steroids use was significantly associated (P < 0.05) with the following self-reported, medically diagnosed, joint and cartilaginous injuries in comparison with the nonanabolic-androgenic steroids users: disc herniations, knee ligamentous/meniscal injury, elbow injuries, neck stinger/burner, spine injury, and foot/toe/ankle injuries. There was no association between anabolic-androgenic steroids use and reported muscle/tendon injuries. CONCLUSIONS: Our findings demonstrate that an association may exist between anabolic-androgenic steroids use and the prevalence of reported musculoskeletal injury sustained during a professional football career, particularly ligamentous/joint-related injuries. There may also be an associated predisposition to selected types of injuries in anabolic-androgenic steroids users.

This is interesting.

What are you thoughts on some AS being able to perhaps aid in repair of joints/tendons?

[Kratos]

This is interesting.

What are you thoughts on some AS being able to perhaps aid in repair of joints/tendons?

No doubt about it, anavar has been notorious in baseball for getting players off the bench quicker. It's very difficult for the AAS community to figure out which injuries will benifit and the best ways to help in healing. When you're a hammer eveything looks like a nail, and AAS users are quick to jump on deca for example to help heal an injury that it might actually be hurting. Doctors who work with the athletes aren't giving out indications or protocols.

[Swifto]

The study is certainly interesting but how much of these "injuries" can be blamed on athletes lifting more too quick due to an increase in LBM and not joint/tendon strength.

[Kratos]

The study is certainly interesting but how much of these "injuries" can be blamed on athletes lifting more too quick due to an increase in LBM and not joint/tendon strength.

I think we'd have to biopsy their tendons after injury to see if their failure was consistant with steroid use to know for sure.

But we do know some steroids such as winstrol are not good for tendons. Estrogen increases turnover of tendons. There are a lot of smoking guns but no dead body on the issue. Basically the issue needs a lot more research to confirm or deny anything. Just thought it was interesting.

[Swifto]

Clin Exp Pharmacol Physiol. 2008 Jul;35(7):852-8.

LinksAnabolic agents for improving muscle regeneration and function after injury.

Lynch GS, Schertzer JD, Ryall JG.

Basic and Clinical Myology Laboratory, Department of Physiology, The University of Melbourne, Parkville, Victoria, Australia. [email protected]

1. In the present review, we describe how muscles can be injured by external factors, internal factors or during the performance of some actions during sports. In addition, we describe the injury to a muscle that occurs when its blood supply is interrupted, an occurrence common in clinical settings. An overview of muscle regeneration is presented, as well as a discussion of some of the potential complications that can compromise successful muscle repair and lead to impaired function and permanent disability. 2. Improving muscle regeneration is important for hastening muscle repair and restoring muscle function and the present review describes ways in which this can be achieved. We describe recent advances in tissue engineering that offer considerable promise for treating muscle damage, but highlight the fact that these techniques require rigorous evaluation before they can become mainstream clinical treatments. 3. Growth-promoting agents are purported to increase the size of existing and newly regenerating muscle fibres and, therefore, could be used to improve muscle function if administered at appropriate times during the repair process. The present review provides an update on the efficacy of some growth-promoting agents, including anabolic steroids, insulin-like growth factor-I (IGF-I) and beta(2)-adrenoceptor agonists, to improve muscle function after injury. Although these approaches have clinical merit, a better understanding of the androgenic, IGF-I and b-adrenoceptor signalling pathways in skeletal muscle is important if we are to devise safe and effective therapies to enhance muscle regeneration and function after injury.





Skeletal muscles can be injured by external factors, such as contusion, laceration or crush1–3 from road trauma, workplace accidents or collisions on the sports field, or by internal factors, such as strains (e.g. a hamstrings muscle tear when running or kicking4–6), during surgery involving muscle laceration, during reconstructive or transplantation surgery (when muscles are excised by surgeons and transferred from one part of the body to another to provide supporting structures and help restore some level of function).7,8 These transplantation procedures involve an unavoidable disruption (or interruption) to the muscle's normal blood supply (called 'ischaemia'). Subsequent return of the blood supply (reperfusion) is problematic in that a severe secondary injury can ensue, mediated by production of damaging free radicals when blood flow is restored.9–12 The same process occurs after revascularization of an amputated limb, compartment syndromes associated with vascular injury and following excessive tourniquet application.13 Muscle injuries, such as crush, ischaemia–reperfusion and contraction-mediated damage, involve injury to the muscle's support structures (including blood and nerve supply), such that functional repair is compromised.14,15 All these events can severely impair muscle structure and function, mobility and quality of life. Skeletal muscle injury is a significant health issue that costs billions in health care every year in most developed nations.

The cellular and molecular mechanisms of muscle regeneration after injury and degeneration have been described extensively.16–20 Unfortunately, all evidence indicates that once muscles are damaged, the muscle repair/regeneration process is not always complete and can often be slow or complicated by fibrotic infiltration and scarring. Incomplete and slow repair can result in disability or handicap. Thus, developing therapeutic approaches to enhance the regeneration process and hasten restoration of muscle function is critical for improving the long-term physical outcome of patients and athletes suffering muscle injuries, as well as to prevent or minimize functional disability after surgery.5,21

Muscle injury and repair involves a complex balance between local muscle fibre repair, regeneration and scar tissue formation.22 A variety of methods have been examined for the purpose of hastening muscle regenerative processes in order to restore muscle function, by either enhancing muscle fibre growth and regeneration and/or promoting vascularity and nerve repair. Anti-inflammatory medications, corticosteroids, surgical methods and exercise protocols have been studied.21,22 Current research efforts are exploring closer interactions between developmental biology and tissue engineering in order to enhance existing tissue or develop new tissues to replace those that are damaged irreparably.23,24 Regenerative medicine and tissue engineering provide novel therapeutic approaches to restore muscle structure and function to damaged skeletal muscles after injury or disease.25–28 These approaches include the use of stem cells (including skeletal muscle-derived stem cells), bioinductive factors and bioscaffolds to facilitate the release of cells or biological growth factors to repair and/or regenerate skeletal muscle.28–31 Although offering considerable promise for the treatment of muscle damage, realistically it will take many years before these emerging techniques are perfected and become mainstream clinical treatments.

To evaluate the current status of all the different approaches for treating muscle injury is beyond the scope of the present brief review. Instead, we have focused attention on therapies that have purported anabolic or growth-promoting effects on skeletal muscle. The basic rationale is that growth-promoting agents can hasten muscle regeneration by increasing the size of existing and newly regenerating muscle fibres, thereby improving muscle function. Muscle growth-promoting agents include (but are not limited to) growth hormone, testosterone-derived or testosterone-like hormones, such as anabolic steroids, insulin-like growth factor (IGF)-I and â2-adrenoceptor agonists. We will provide a brief overview of the current state of knowledge regarding the efficacy of some of these growth-promoting agents (anabolic steroids, IGF-I and â2-adrenoceptor agonists) to improve muscle function after injury.



ANABOLIC STEROIDS


Androgenic-anabolic steroids are synthetic derivatives of the male hormone testosterone that are capable of exerting strong effects on the human body that can benefit athletic performance.32 Testosterone-replacement therapy has been used effectively to counteract loss of lean body mass in hypogonadal men,33,34 in older men with normal or low serum testosterone35,36 and HIV-infected men with low serum testosterone.37 Similarly, muscle growth has been achieved in eugonadal states after supraphysiological administration to young, healthy men,38,39 as well as HIV-infected men with normal testosterone levels.40 Although some studies have demonstrated enhanced muscle strength following testosterone administration,41 others have reported no effect of androgen therapy on muscle function despite increases in muscle size.42 Although anabolic steroids have been used for the treatment of HIV-related wasting and other wasting conditions for many years, many questions remain unanswered, including those regarding appropriate and safe doses for long-term administration and the associated potential risks or side-effects.43,44

There have been numerous studies that have investigated the effects of anabolic steroids on skeletal muscles that are simultaneously responding to other stimuli, such as functional overload,45 hindlimb suspension in rats46 or heavy resistance training in humans.47 However, few studies have examined the effect of anabolic steroids on skeletal muscle regeneration per se. One of the most important investigative techniques used in studying this process is to follow muscle fibre degeneration and the subsequent spontaneous fibre regeneration after an intramuscular injection of a myotoxin, such as snake venoms (e.g. notexin or cardiotoxin) or local anaesthetics (e.g. bupivacaine hydrochloride).48 Ferry et al.49 examined whether treating rats with nandrolone deconoate improved regeneration of fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus muscles after myotoxic injury caused by direct intramuscular injection of notexin. Nandrolone increased the mass of regenerating soleus muscles and decreased the relative amount of fast myosin heavy chain protein, but anabolic steroid treatment had no effect on regenerating EDL muscles.49 In a follow-up study, the authors found that anabolic steroid treatment had no significant effect on the functional properties of regenerating EDL or soleus muscles 21 days after notexin injury.50 Beiner et al.51 examined whether nandrolone deconoate could enhance the function of regenerating rat skeletal muscles following contusion injury. They found that 7 days after injury, anabolic steroid treatment had no beneficial effect on the force-producing capacity of gastrocnemius muscles in situ, but by 14 days after injury muscles from treated rats had improved twitch (but not tetanic) forces. Although interesting, this does not represent a definitive improvement in muscle strength because, in vivo, all muscle actions result from graded tetanic (not twitch) contractions. However, the authors concluded that anabolic steroids could help the functional recovery of injured muscles and therefore '. . . may have an ethical clinical application to aid healing in severe muscle contusion injury and their use in the treatment of muscle injuries warrants further research'.51

In a recent preliminary study, tibialis anterior (TA) muscles from castrated male mice were injured by intramuscular injection of the myotoxic agent bupivacaine and then treated with nandrolone decanoate to determine whether muscle regeneration could be enhanced.52 Anabolic steroid treatment increased the incidence of small diameter fibres (as a proportion of the total number of fibres) 14 days after bupivacaine injury by 65% compared with injured muscles from untreated mice. At 28 days after injury, there was no effect of treatment on the number of these smaller diameter fibres, but the incidence of large fibres (as a proportion of the total number of fibres) was twofold greater in muscles from treated compared with untreated mice. It should be noted that the variable size of the regenerating muscle fibres could also indicate that bupivacaine injured some fibres but spared others. We have shown previously that the extent of muscle fibre injury in mice following an intramuscular injection of bupivacaine is significantly less than that after an intramuscular injection of a more powerful myotoxin, such as notexin.48 Regardless, the study showed that anabolic steroid treatment could improve myofibre growth during the later stages of muscle regeneration.52

Another preliminary study examined the effect of two doses of nandrolone deconoate on regeneration and satellite cells in mouse skeletal muscles following an intramuscular injection of venom from the jararacucu snake (Bothrops jararacussu) of South America.53 At a dose of 6 mg/kg, the anabolic steroid increased the number of myotubes 3 and 7 days after venom injection and the number of muscle fibres with normal morphology after 21 days. Muscle satellite cell proliferation at 7 and 21 days was also increased in mice that received this dose of nandrolone deconoate. However, regeneration was not improved in injured muscles of mice treated with a lower dose of 2 mg/kg nandrolone deconoate. Thus, the higher dose (6 mg/kg) of the anabolic steroid was required in mice in order to produce a beneficial effect on muscle regeneration after severe myotoxic damage.53

Another important issue is whether anabolic steroids may have clinical application in treating the symptoms of skeletal muscle diseases, especially where muscle repair mechanisms are defective and recurring episodes of fibre injury and inefficient and incomplete regeneration are a critical aspect of the pathophysiology, such as in Duchenne muscular dystrophy (DMD). In a study on dystrophic mdx mice, an animal model of DMD that also exhibits ongoing injury and regeneration in the limb muscles throughout the lifespan, treatment with anabolic steroids did not have a beneficial effect.54 In fact, anabolic steroid treatment aggravated the dystrophic pathology in the EDL and soleus muscles, as evidenced by elevated creatine kinase activity and a doubling of the number of centrally nucleated muscle fibres (an index of accumulated injury and repair). Interestingly, the size of some fibre populations actually decreased in mdx mice after anabolic steroid treatment.54



INSULIN-LIKE GROWTH FACTOR-I


Regardless of the initial cause of muscle injury, effective fibre regeneration is dependent on the timed induction of myogenic regulatory factors and growth factors, including IGF-I.3,20,55 Insulin-like growth factor-I activates both myoblast proliferation and subsequent differentiation, crucial processes for successful muscle repair and regeneration.56 The importance of IGF-I in muscle regeneration has been demonstrated in transgenic mice, where muscle-specific overexpression of IGF-I maintained regenerative capacity in aged mice57 and reduced the skeletal muscle pathology in dystrophic mdx mice.58,59 Exogenous administration of recombinant human IGF-I (rhIGF-I) increased the rate of functional recovery after myotoxic injury60 and improved the dystrophic pathology in mdx mice.61–63 Clearly, administration of IGF-I and other growth factors has the potential to accelerate healing processes and other tissues after trauma, but their use in sports medicine is restricted because of the potential for abuse as performance-enhancing agents.64

Although rhIGF-I administration and transgenic IGF-I overexpression have beneficial effects on skeletal muscle, their mechanism of action differs considerably. Transgenic IGF-I overexpression in mice produced muscle hypertrophy,58 whereas rhIGF-I administration to mice did not.61–63 We have speculated that these differential effects may be attributed to different interactions with IGF-binding proteins (IGFBPs) following systemic delivery of IGF-I to mice compared with muscle-specific overexpression of IGF-I in transgenic mice. Although the effects of rhIGF-I administration and IGF-I overexpression on skeletal muscle regeneration have been well characterized, the role of IGFBPs in skeletal muscle regeneration remains poorly understood. Recently, we examined whether inhibiting IGF-I interactions with IGFBPs influenced muscle regeneration after myotoxic injury using the aptamer NBI-31772, which binds all six IGFBPs with high affinity and releases 'free' endogenous IGF-I. Continual release of NBI-31772 into the circulation of mice via a mini-osmotic pump increased the rate of functional recovery in mouse tibialis anterior muscles after notexin-mediated damage.65 These results support the notion that abrogating IGFBP interactions with systemic IGF-I has therapeutic potential for enhancing muscle repair after muscle injury.



â2-ADRENOCEPTOR AGONISTS


Although â2-adrenoceptor agonists are traditionally prescribed for alleviating bronchospasm in the treatment of asthma because of their bronchodilatory effects on smooth muscle, some â2-adrenoceptor agonists actually have potent anabolic effects on skeletal muscle, especially when administered systemically and at higher doses.66–68 These muscle hypertrophic effects of â2-adrenoceptor agonists, combined with their known lipolytic actions, have proved desirable for those working in the livestock industry trying to improve meat quality and yield.69,70 Not surprisingly, â2-adrenoceptor agonists have also been used and abused by many athletes involved in competitive bodybuilding, strength- and power-related sports and sports such as wrestling, where athletes need to 'make weight' in order to compete in specific weight classes.71,72 However, because of their anabolic effects on skeletal muscle, â2-adrenoceptor agonists have significant clinical potential, particularly for muscle wasting disorders, including the muscular dystrophies.72

Skeletal muscle contains a significant proportion of â-adrenoceptors, mostly of the â2 subtype, with approximately 7–10%â1-adrenoceptors present and a sparse population of á-adrenoceptors, usually in higher proportions in slow-twitch muscles.69,70,73,74 Slow-twitch muscles have also been shown to have a greater density of â-adrenoceptors than fast-twitch muscles.70 Because â-adrenoceptors exist in the heart as well as in skeletal muscle, any approach involving the systemic administration of exogenous â-adrenoceptor agonists must take into account potential effects on tissues other than skeletal muscle, particularly the heart. Synthetic â2-adrenoceptor agonists promote skeletal muscle hypertrophy via activation of cAMP-dependent mechanisms that increase protein synthesis and inhibit protein degradation pathways.72,75 Recently, phosphatidylinositol 3-kinase (PI3-K)–Akt signalling, which is known to be implicated in skeletal muscle hypertrophy, has been linked to â2-adrenoceptor signalling.76

We and others have also shown that systemic administration of â-adrenoceptor agonists can promote regeneration of injured skeletal muscles, specifically to hasten the functional recovery of rat muscles after myotoxic injury with bupivacaine77 or notexin.48,78 Daily fenoterol administration to rats (1.4 mg/kg per day, i.p.) enhanced the force output of injured/regenerating rat EDL muscles by 19% at 14 days after injury, which was associated with increases in protein content and muscle fibre size.77 Daily clenbuterol treatment of rats (2 mg/kg per day, by oral gavage) increased protein content in regenerating soleus muscles and caused significant transitions from slow to fast fibres.78 More recently, we have studied aspects of â-adrenoceptor signalling during early regeneration of rat EDL and soleus skeletal muscles after bupivacaine injury and found that despite â-adrenoceptor agonist (fenoterol) treatment decreasing â-adrenoceptor density in regenerating rat EDL and soleus muscles, the cAMP response to â-adrenoceptor stimulation, relative to healthy (uninjured) muscles, remained elevated.79

The potential for â-adrenoceptor agonists to improve the size and strength of muscles of human patients affected by neuromuscular diseases where muscle regenerative mechanisms are defective has received relatively limited attention. Preliminary trials using the â2-adrenoceptor agonist Albuterol to treat young boys with facioscapulohumeral dystrophy found that year-long administration of doses of 16 and 32 mg/day had only limited beneficial effects on strength and was associated with some adverse cardiovascular-related events, such as palpitations and, in some cases, muscle tremor.80 Fowler et al.81 administered Albuterol at a lower dose of 8 mg/day for 28 weeks to boys with DMD or Becker muscular dystrophy (BMD) and found modest increases in strength with no side-effects. Albuterol was well tolerated, but elicited only modest improvements in muscle mass and strength. It is our contention that one of the factors currently limiting the application of â2-adrenoceptor agonists for the treatment of DMD and related disorders is that Albuterol is simply not a powerful enough anabolic agent to counteract the severe muscle wasting and to stimulate muscle regenerative mechanisms sufficiently. We have shown unequivocally that newer-generation â2-adrenoceptor agonists, such as formoterol, have powerful skeletal muscle anabolic effects (in mice and rats) even when administered in micromolar doses.67,82 Most importantly, formoterol is more selective for the â2-adrenoceptor and its effects on the heart (comprising predominantly â1-adrenoceptors) are much less than those of older-generation â2-adrenoceptor agonists such as Albuterol or clenbuterol. Blocking stimulation of the â1-adenoceptors is possible with highly selective â1-adrenoceptor antagonists (such as CGP 20712A65) and the importance of blocking â1-adrenoceptors in heart failure to abrogate cardiotoxic â1-adrenoceptor-mediated effects is well known.83,84



CONCLUSIONS: OVERCOMING SAFETY CONCERNS FOR ANABOLIC TREATMENTS FOR MUSCLE INJURY


It is clear that a better understanding of the androgenic, IGF-I and â-adrenoceptor signalling pathways in skeletal muscle is important for devising and optimizing safe therapies to enhance muscle regeneration and function following different types of muscle injury. Although many aspects of these signalling cascades have been described in detail elsewhere,72,75 the complementary interactions between them, especially in relation to the activation of pathways induced by anabolic agents specifically for enhancing muscle functional recovery after injury, has not been described widely (see Fig. 1). The extracellular and intracellular mechanisms of action of the three classes of anabolic agents discussed in the present review, namely anabolic steroids, IGF-I and related therapeutics and â2-adrenoceptor agonists, exhibit significant 'cross-talk' and converge on pathways responsible for protein synthesis. Extracellular cross-talk between these signals includes increased IGF-I levels and modulation of IGFBPs following administration of â2-adrenoceptor agonists85 and increased levels of IGF-I as a consequence of anabolic steroid administration.86,87 Intracellular cross-talk between these signals is extensive and includes activation of PI3-K by the â/ã-subunits of the G-protein complex following andrenoceptor stimulation72,75 and activation of PI3-K and p70S6K by IGF-I and following â-adrenoceptor stimulation.88,89 Details regarding these signalling pathways and their interactions are incomplete and further delineation of novel signalling molecules will yield new therapeutic targets for enhancing skeletal muscle regeneration after injury (Fig. 1).


Fig. 1 Signalling cascades induced by anabolic agents that result in enhanced functional recovery after skeletal muscle injury. The extracellular and intracellular mechanisms of action of anabolic steroids, insulin-like growth factor (IGF)-I related therapeutics and â2-adrenoceptor agonists exhibit significant 'cross-talk' and converge on protein synthetic pathways. Extracellular cross-talk between these signals includes increased IGF-I levels and modulation of IGF-binding proteins (IGFBPs), leading to either increased or decreased levels of specific IGFBPs, following administration of â2-adrenoceptor agonists85 and increased levels of IGF-I due to anabolic steroid administration.86,87 Intracellular cross-talk between these signals is extensive and includes activation of phosphatidylinositol 3-kinase (PI3-K) by the â/ã-subunits of the G-protein complex following andrenoceptor stimulation (for reviews, see Lynch and Ryall72 and Lynch et al.75) and activation of PI3-K and p70S6K by IGF-I and in response to â-adrenoceptor stimulation.88,89 These signalling pathways have not been characterized completely and further delineation of novel signalling molecules will yield new therapeutic targets for enhancing muscle regeneration. á, á-subunit of the G-protein complex; â/ã, â/ã-subunits of the G-protein complex; AR, androgen receptor; CRE: cAMP response element; CREB, cAMP response element-binding protein; IGF-IR: insulin-like growth factor-I receptor; IRS 1/2, insulin receptor substrate 1/2; p70S6K, 70 kDa ribosomal protein S6 kinase; PKA, protein kinase A.

[Normal View ]

For anabolic therapies, concerns regarding potential pharmaceutical toxicity and safety issues are often only related to high doses, so low-dose, short-term treatment strategies are likely to have fewer toxic effects and their clinical merit is worth testing. To this end, extensive preclinical and clinical studies are needed to determine the optimum doses and treatment regimens that will elicit significant improvements in muscle fibre size and strength without causing deleterious side-effects, such as cardiovascular complications or perhaps the formation of tumours if growth factors are administered systemically. Alternatively, intramuscular delivery and the use of emerging tissue engineering technologies that facilitate the timed and controlled release of growth factors, anabolic and/or antifibrotic agents could help minimize potential side-effects while exerting beneficial effects on regenerating muscle fibres to hasten restoration of muscle function

[Kratos]

good post swifto, but the information isn't out there yet for mainstream anabolic therapy...indications, dosage, compounds, duration. I'd say it's better to not self medicate pending more information.

If I had something where the prognosis is not good, like the shoulder injury I had years ago that eventually resulted in surgery. I might run an experiment on myself in the early stages post injury.

[Kratos]

From Sports Illustrated
The Injury Toll: Steroid use may explain a sharp rise in the time players spend on the disabled list. (Special Report)(Brief Article)(Statistical Data Included) Tom Verducci.
Full Text: COPYRIGHT 2002 Time, Inc.

Byline: Tom Verducci

As more baseball players have built overmuscled bodies using the advanced biochemistry of steroids and other drugs, they have been suffering severe--and costly--injuries in ever greater numbers. "We're seeing more and more injuries you used to associate with a violent contact sport like football," says Seattle Mariners manager Lou Piniella, referring to tears of muscles, ligaments and tendons.

Noted sports orthopedist James Andrews, of Birmingham, says he "seldom used to see these muscle-tendon injuries" in baseball. "It was always the sport for the agile athlete with the small frame," he says. "Over the last 10 years, that's changed. You'd have to attribute that--the bulking up and the increased injuries--to steroids and supplements."

According to figures obtained from Major League Baseball, big league players made 467 trips to the disabled list last season, or about 18 per week. Those players stayed on the DL for an average of 59 days, which was 10 days longer than the average stay in 1997--a 20% increase.

Major league teams last year doled out $317 million--or 16% of the game's total payroll--to players physically unable to play. That cost for DL players was a 130% increase from only four years earlier.

"I see so many body changes--one season they're average, the next season they're massive--that [steroid use] is obvious," Andrews says. "More athletes are carrying more muscle than their frames can support, and therefore the trauma is greater. You wouldn't believe the Achilles tendon ruptures, the quadriceps ruptures, the hamstring tears, the massive rotator cuff tears, the tearing of the biceps muscles at the elbow joints. There's just too much mass for the body to handle. And more and more of these injuries are career-threatening.

"The dangers of these drugs--and even the supplements--aren't fully known yet," Andrews continues. "But from an anecdotal perspective, I'm seeing four to five times as many of these injuries as I did just 10 years ago--and I'm seeing them in younger and younger athletes. If the pros are doing it, the college kids aren't far behind, and the high schools and junior highs are right behind them. I try to counsel some of them, but it is a secret box that they find themselves in, and they don't want to talk to me about it."

San Diego Padres general manager Kevin Towers says suspected steroid use and the economic fallout of related injuries have become important factors in how general managers evaluate players. "It matters when you're doing contracts or when you're looking to acquire a player from another team," he says. "It's a factor whether you're going to open discussions on a long-term contract or go year-to-year. It's become a key issue because a lot of small-market clubs can't continue to insure players. The cost of insurance has gone so high that it's more and more difficult to insure these contracts." According to Pro Financial Services president Brian Burns, who specializes in such policies, the cost of player salary insurance has risen more than 200% since 2000.

[tboney]

Great thread! Very interesting! Thanks to both of you!

[dec11]

The study is certainly interesting but how much of these "injuries" can be blamed on athletes lifting more too quick due to an increase in LBM and not joint/tendon strength.

heres an interesting senario for ya swifto, i couldnt do bicep work for 3mths due to what i think was tendon/connective tissue damage in my forearms, basically half way throught the curling phase it was like a knife stabbing and i couldnt complete a rep with 12.5kgs!!! however, 3 wks into a dbol and sust cycle i was curling 22.5kgs dumbells and now 25kgs with zero pain. gear repairing damage?

[dec11]

bump

[tballz]

very interesting