Written by Jose Antonio, Ph.D.
06 April 2007

No, these aren't experiments that are being done on space shuttle missions. Satellite cells are the stem cells of skeletal muscle. Without them, you could kiss recovery and growth goodbye! Yes, they're that important. A study from the University of Minnesota determined whether treatment of bovine (meaning from cows) satellite cell (BSC) cultures with 17beta-estradiol (E(2)) or trenbolone (a synthetic androgen) directly affects proliferation rate or level of mRNA for estrogen receptor (ER)-alpha, androgen receptor and growth factors that have been shown to affect muscle growth (insulin-like growth factor (IGF)-I, IGF binding protein (IGFBP)-3, and myostatin). Did you get all that? Basically, what is it about steroids that "turns on" the biochemical cascade of signals to promote hooooyyyuge muscles?!So, they treated these satellite cells with either estradiol or trenbolone.  They found that trenbelone increased IGF-1 mRNA as well as androgen receptor mRNA. There was no effect on myostatin mRNA levels. Bottom line:  Treatment of bovine satellite cell cultures with trenbolone increased IGF-I mRNA levels and proliferation rate, thus establishing that these steroids have direct anabolic effects on satellite cells.1   

Can I Trust You Doc?    

Dr. Harrison Pope has done some very interesting work (psychology type stuff) on anabolic steroids or androgens. A current study assessed the anabolic-androgenic steroid (AAS) users' trust in the knowledge and advice of physicians. When I first saw this study, I was thinking to myself that the "average" androgen user typically has no trust in the "average" physician primarily because physicians are (for the most part) quite ignorant of the literature in this area. So, let's see what Dr. Pope found. He interviewed steroid users and non-users. Both groups of subjects gave physicians high ratings on knowledge about general health, cigarette smoking, alcohol and conventional illicit drugs, but gave physicians much lower ratings on knowledge about AAS. This was interesting; when rating sources of information on AAS, users scored physicians as no more reliable than their friends, Internet sites, or the person(s) who sold them the steroids (my emphasis).  
Think of that. Four years of college, four years of medical school and several more years of residency, yet, most steroid users think they get just as worthy information from their friends. In fact, 40 percent of users trusted information on AAS from their drug dealers at least as much as information from any physician that they had seen. And 56 percent had never revealed their AAS use to any physician. Bottom line: Users show little trust in physicians' knowledge about AAS and often do not disclose their AAS use to physicians. Of course, this may not be a good thing because it hinders your doctor's ability to treat you as his or her patient. On the other hand, doctors should spend time actually reading the literature and avoid the pseudo-scientific nonsense that all androgen use is lethal or deadly.2  In fact, see the next topic- giving steroids to children- oh my!

Kids on the Juice

    The University of Texas churns out some cool work on some of the best sports medicine science. The latest study looked at long-term administration of oxandrolone on severely burned kids. Oh my God; you mean scientists are giving kids steroids? Aren't steroids deadly? Don't they cause every medical malady from liver failure to violent outbursts to penile shrinkage to countless deaths in the locker room? If you believe that, you truly do have an IQ equal to an avocado.  
 

   So why give anabolic steroids to kids with burns? Severe burns cause exaggerated catabolism of muscle protein as well as inhibit bone deposition; definitely not good. Loss of lean body mass interferes with recovery and rehabilitation. So, this study determined whether oxandrolone administration for one year (holy smoke, Batman, one year!) after the burn reverses muscle and bone catabolism in hypermetabolic pediatric burn patients.

Children with burns over more than 40 percent total body surface area were enrolled into a randomized controlled trial. All patients received similar clinical care. Subjects were studied at discharge (95 percent healed) and at six, nine and 12 months after the burn, after treatment with 0.1 milligrams per kilogram of bodyweight orally, two times per day, or placebo. So if the kid weighed 20 kilograms, he/she would receive two milligrams twice per day.  What did they find? I think you'll find the results fascinating. The groups were similar in age, weight and total body surface area burned. However, lean body mass (which is mostly muscle and bone) was significantly greater with oxandrolone at six, nine and 12 months after the burn. Also, lo and behold, liver transaminases were unaffected, meaning it had no effect on liver function.  Thus, the scientists concluded that "long-term administration of oxandrolone safely improves lean body mass, bone mineral content and bone mineral density in severely burned children."3 Really, the whole point of bringing this study to you is to show that not all androgen use is abuse and that not all androgen use causes harm and in fact, it's a useful clinical tool.  
      

IGF-1: Another Clinical Tool?


    Not only are there legitimate uses of androgens for various wasting disorders, but count IGF-1 in there, as well. For example, an improvement in fatigue resistance has been observed in diaphragm muscles of mdx (muscular dystrophy) mice following insulin-like growth factor-I (IGF-I) administration. In this study, they looked at the effect of the IGF-I administration (one milligram per kilogram bodyweight daily subcutaneously for eight weeks) on structural, metabolic and functional properties of extensor digitorum longus (EDL) and soleus muscles of mdx mice. They tested the hypothesis that IGF-I treatment would improve function in these muscles. Guess what? IGF-1 was good for the dystrophic muscles. The treated muscles were more resistant to fatigue during repeated maximal contractions than muscles from untreated mice; they found that the treated muscles had higher levels of aerobic enzymes (succinate dehydrogenase activity).4

Brain Food


Creatine is not only a muscle builder, it's pretty damn good for your noggin, too. In fact, prophylactic creatine supplementation protects the brain neuroprotective area after transient cerebral ischemia (deficient blood supply to the brain). Scientists hypothesize that additional protection by creatine may be related to "prevention of calcium overload, prevention of mitochondrial permeability transition pore opening and direct antioxidant effects."7 Couple this with previous work showing that creatine decreases brain trauma, I would think anyone who participates in sports that have a potential for brain injury (e.g. fighting sports, football and arguing with a pissed off woman with a frying pan in her hand) should supplement with creatine!


 References
1.    Kamanga-Sollo, E., et al., IGF-I mRNA levels in bovine satellite cell cultures: Effects of fusion and anabolic steroid treatment. J Cell Physiol, 2004. 201(2): p. 181-9.
2.    Pope, H.G., et al., Anabolic steroid users' attitudes towards physicians. Addiction, 2004. 99(9): p. 1189-94.
3.    Murphy, K.D., et al., Effects of long-term oxandrolone administration in severely burned children. Surgery, 2004. 136(2): p. 219-24.
4.    Gregorevic, P., D.R. Plant, and G.S. Lynch, Administration of insulin-like growth factor-I improves fatigue resistance of skeletal muscles from dystrophic mdx mice. Muscle Nerve, 2004. 30(3): p. 295-304.
5.    Harman, S.M. and M.R. Blackman, Use of growth hormone for prevention or treatment of effects of aging. J Gerontol A Biol Sci Med Sci, 2004. 59(7): p. 652-8.
6.    Bolster, D.R., L.S. Jefferson, and S.R. Kimball, Regulation of protein synthesis associated with skeletal muscle hypertrophy by insulin-, amino acid- and exercise-induced signalling. Proc Nutr Soc, 2004. 63(2): p. 351-6.
7.    Adcock, K.H., et al., Neuroprotection of creatine supplementation in neonatal rats with transient cerebral hypoxia-ischemia. Dev Neurosci, 2002. 24(5): p. 382-8.

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