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Testosterone And Estrogen Increase Satellite Cells

April 7th, 2009 · No Comments

Testosterone And Estrogen Increase Satellite Cells
by Robbie Durand

Excess estrogens have been associated with a wide range of negative health consequences in men. Along with a decline in testosterone with age, many men also experience increases in the levels of estrogen. The result is a testosterone/estrogen imbalance that directly causes many of the debilitating health problems associated with normal aging. High levels of estrogen have been implicated as a cause of benign prostatic hypertrophy (BPH), depressed testosterone levels and gynecomastia development. Estrogen sends a signal to the hypothalamus (brain) to shut down production of a hormone known as GnRH. GnRH is a hormone that stimulates leutinizing hormone (LH), which is the signal that tells the testicles to produce testosterone. Therefore, men with elevated estrogen levels will have suppressed testosterone. High estrogen can also promote excessive water and sodium retention, resulting in a bloated, puffy and smooth appearance. The two most common problems of testosterone use are gynecomastia and difficulty in recovering natural testosterone production. Nutritional products like 6-OXO,14 zinc,15 resveratrol,16 and the grapefruit extract17 (naringenin) are all anti-estrogen that may be included to minimize excess estrogen formation. Antiestrogenic drugs such as anastrozole (Arimidex) can effectively prevent gynecomastia and is safe for most individuals; however the use of high amounts of antiestrogens for long periods of time can reduce muscle growth.

Satellite Cells: To Grow Or Not to Grow…That Is The Question!

Satellite cells function to facilitate growth, maintenance and repair of damaged skeletal muscle tissue. These cells are termed satellite cells because they are located on the outer surface of the muscle fiber, they then fuse to the existing muscle fiber, which helps to regenerate the muscle fiber and make them larger. There is a dose-dependent increase in size and number of satellite cells with testosterone administration.1 Differences in satellite cell activation may be the reason why two people can train at the same intensity, yet one person will make huge gains in muscle mass while another will not. In a recent Journal of Applied Physiology, researchers reported that gains in muscle mass in the gym depend on satellite cell activity. Researchers examined the effects of 16 weeks of resistance exercise and placed the subjects in three groups: extreme muscle hypertrophy responders, modest responders and non-responders. They found that the availability of satellite cells in muscle appears to be an important determinant of hypertrophic potential, as shown by a greater population of satellite cells prior to training in an extreme muscle hypertrophy group. Extreme muscle mass responders experienced a remarkable 117 percent expansion of the available satellite cell pool. On the other hand, the number of satellite cells was unaltered in moderate subjects, who also experienced hypertrophy but roughly only 50 percent of the growth seen in the extreme group.2 The bottom line is that the more satellite cells that are activated…the more you grow!

Estrogen Increases IGF-1 And Satellite Cell Activity

Many studies have demonstrated that estrogen has a positive effect on GH and IGF-1 in men. Remember, IGF-1 is a potent activator of satellite cells in muscle. In one study, hypogonadal men were administered testosterone enanthate with and without the addition of tamoxifen. When the estrogen receptor blocker tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both GH and IGF-1 were elevated with the administration of testosterone enanthate alone. Another study reported that the effects of two types of anabolic steroids on GH/IGF-1 levels. In the study, testosterone enanthate and stanozolol (a.k.a. Winstrol— a non-aromatizing steroid) were compared for their effects on stimulating GH release. Testosterone enanthate increased GH levels by 22 percent and IGF-1 levels by 21 percent, whereas oral stanozolol had no effect on GH or IGF-1 levels.11 Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels.13

In a recent Journal of Animal Endocrinology, researchers reported that mRNA IGF in muscle was inhibited by estrogen blockade.5 In bulls, researchers have reported that both estrogen and trenbolone stimulate satellite cells.3 Estrogen can stimulate muscle IGF-1. Additionally, both estradiol/trenbolone implant causes a significant increase in muscle IGF-1 mRNA.4, 5 Other studies also seem to suggest that estrogen is important for muscle growth in animals as well. For example, male rats had their “berries” whacked off and were assigned to different groups: estrogen supplemented with exercise and exercise without estrogen. Seventy-two hours later, exercised animals were killed. Downhill running resulted in significant elevations in satellite cells and neutrophils detected in both type I and type II muscle samples. Interestingly, estrogen supplementation resulted in significantly greater post-exercise elevations in satellite cells detected in both type I and type II muscle samples compared with “no estrogen” rats. The researchers speculated that estrogen enhanced the actions of satellite cells in several ways:

a.) Estrogen increases NO production, which enhances satellite cells activation.7
b.) Estrogen increases serum IGF-1 levels.8
c.) Estrogen has direct actions on satellite cells.4,5

It has also been proven that after exercise, tissue estrogen levels increase in males due to increases in testosterone. Interestingly, aromatase cytochrome P450, the enzyme responsible for estrogen biosynthesis, is increased in muscle in males after exercise.9 Another study in male endurance athletes reported that endurance-trained men had higher estrogen receptors than sedentary men.18 The study reported that estrogen receptors were highly correlated with type I fibers, which were about 30 percent larger in the endurance-trained athletes group. Estrogen receptors were negatively correlated with type II explosive fibers. No studies have examined if estrogen receptors are increased in resistance-trained men.

While aromatase inhibitors minimize estrogenic side effects, it will also block the beneficial properties of estrogen from becoming apparent (namely its effect on cholesterol values). Studies have clearly shown that when an aromatase inhibitor is used in conjunction with a steroid such as testosterone, suppression of HDL (good) cholesterol occurs.10 The key is to minimize the production of estrogen, but not completely shut it off. Shutting off estrogen production completely may reduce muscle mass through inhibition of satellite cell activity.

1. Sinha-Hikim I, Cornford M, Gaytan H, Lee ML, Bhasin S. Effects of testosterone supplementation on skeletal muscle fiber hypertrophy and satellite cells in community-dwelling older men. J Clin Endocrinol Metab, 2006 Aug;91(8):3024-33.
2. Petrella JK, Kim JS, Mayhew DL, Cross JM, Bamman MM. Potent Myofiber Hypertrophy During Resistance Training in Humans is Associated with Satellite Cell-Mediated Myonuclear Addition: A Cluster Analysis. J Appl Physiol.
3. Kamanga-Sollo E, Pampusch MS, Xi G, White ME, Hathaway MR, Dayton WR. IGF-I mRNA levels in bovine satellite cell cultures: effects of fusion and anabolic steroid treatment. J Cell Physiol, 2004;201:181–9.
4. Pampusch MS, Johnson BJ, White ME, Hathaway MR, Dunn JD, Waylan AT, et al. Time course of changes in growth factor mRNA levels in muscle of steroid-implanted and nonimplanted steers. J Anim Sci, 2003;81:2733–40.
5. Kamanga-Sollo E, White ME, Hathaway MR, Chung KY, Johnson BJ, Dayton WR. Roles of IGF-I and the estrogen, androgen and IGF-I receptors in estradiol-17beta- and trenbolone acetate-stimulated proliferation of cultured bovine satellite cells. Domest Anim Endocrinol, 2008.
6. Tiidus PM, Deller M, Liu XL. Oestrogen influence on myogenic satellite cells following downhill running in male rats: a preliminary study. Acta Physiol Scand, 2005 May;184(1):67-72.
7. Prorock, A.J., Hafezi-Moghadam, A., Laubach, V.E., Liao, J.K. & Ley, K. 2003. Vascular protection by estrogen in ischemia-reperfusion injury requires endothelial Nitric Oxide synthase. Am J Physiol Heart Circ Physiol, 284, H133-H140.
8. Hawke TJ and Garry DJ. 2001. Myogenic satellite cells: physiology to molecular biology. J Appl Physiol, 91, 534-551.
9. Aizawa K, Iemitsu M, Otsuki T, Maeda S, Miyauchi T, Mesaki N. Sex differences in steroidogenesis in skeletal muscle following a single bout of exercise in rats. J Appl Physiol, 2008 Jan;104(1):67-74.
10. Hero M, Ankarberg-Lindgren C, Taskinen MR, Dunkel L. Blockade of oestrogen biosynthesis in peripubertal boys: effects on lipid metabolism, insulin sensitivity, and body composition. Eur J Endocrinol, 2006 Sep;155(3):453-60.
11. Fryburg DA, Weltman A, Jahn LA, Weltman JY, Samojlik E, Hintz RL, Veldhuis JD. Short-term modulation of the androgen milieu alters pulsatile, but not exercise- or growth hormone (GH)-releasing hormone-stimulated GH secretion in healthy men: impact of gonadal steroid and GH secretory changes on metabolic outcomes. J Clin Endocrinol Metab, 1997 Nov;82(11):3710-9.
12. Lima L, Arce V, Lois N, Fraga C, Lechuga MJ, Tresguerres JA, Devesa J. Growth hormone (GH) responsiveness to GHRH in normal adults is not affected by short-term gonadal blockade. Acta Endocrinol, (Copenh). 1989 Jan;120(1):31-6.
13. Hobbs CJ, Plymate SR, Rosen CJ, Adler RA. Testosterone administration increases insulin-like growth factor-I levels in normal men. J Clin Endocrinol Metab, 1993 Sep;77(3):776-9.
14. Rohle D, Wilborn C, Taylor L, Mulligan C, Kreider R, Willoughby D. Effects of eight weeks of an alleged aromatase inhibiting nutritional supplement 6-OXO (androst-4-ene-3,6,17-trione) on serum hormone profiles and clinical safety markers in resistance-trained, eugonadal males. J Int Soc Sports Nutr, 2007 Oct 19;4:13.
15. Vyas S, Asmerom Y, De León DD. Resveratrol regulates insulin-like growth factor-II in breast cancer cells. Endocrinology, 2005 Oct;146(10):4224-33.
16. Nichols M. The fight against tamoxifen resistance in breast cancer therapy: a new target in the battle? Mol Interv, 2007 Feb;7(1):13-6. Review.
17. Galluzzo P, Ascenzi P, Bulzomi P, Marino M. The Nutritional Flavanone Naringenin Triggers Antiestrogenic Effects by Regulating Estrogen Receptor {alpha}-Palmitoylation. Endocrinology, 2008 May;149(5):2567-75.
18. Wiik A, Gustafsson T, Esbjörnsson M, Johansson O, Ekman M, Sundberg CJ, Jansson E. Expression of oestrogen receptor alpha and beta is higher in skeletal muscle of highly endurance-trained than of moderately active men. Acta Physiol Scand, 2005 Jun;184(2):105-12.

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