Androgen

Androgen (from Greek andro meaning male), also called androgenic hormone or testoid, is any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of male characteristics in vertebrates by binding to androgen receptors.[1] This includes the activity of the primary male sex organs and development of male secondary sex characteristics. Androgens were first discovered in 1936. Androgens are also the original anabolic steroids and the precursor of all estrogens. The primary and most well-known androgen is testosterone.[2] Dihydrotestosterone (DHT) and androstenedione are less known generally, but are of equal importance in male development.[2] DHT in the embryo life causes differentiation of penis, scrotum and prostate. Later in life DHT contributes to male balding, prostate growth and sebaceous gland activity. Although androgens are described as male sex hormones, both males and females have them to varying degrees, as is also true of estrogens.

Types

Steroidogenesis, showing the relation between several androgens, is at bottom left. Estrone and estradiol, in contrast, are estrogens.

The main subset of androgens, known as adrenal androgens, is composed of 19-carbon steroids synthesized in the zona reticularis, the innermost layer of the adrenal cortex. Adrenal androgens function as weak steroids (though some are precursors), and the subset includes dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and androstenedione.

Besides testosterone, other androgens include:

Functions

Development of the male

Testes formation

During mammalian development, the gonads are at first capable of becoming either ovaries or testes.[4] In humans, starting at about week 4, the gonadal rudiments are present within the intermediate mesoderm adjacent to the developing kidneys. At about week 6, epithelial sex cords develop within the forming testes and incorporate the germ cells as they migrate into the gonads. In males, certain Y chromosome genes, particularly SRY, control development of the male phenotype, including conversion of the early bipotential gonad into testes. In males, the sex cords fully invade the developing gonads.

Androgen production

The mesoderm-derived epithelial cells of the sex cords in developing testes become the Sertoli cells, which will function to support sperm cell formation. A minor population of nonepithelial cells appear between the tubules by week 8 of human fetal development. These are Leydig cells. Soon after they differentiate, Leydig cells begin to produce androgens.

Androgen effects

The androgens function as paracrine hormones required by the Sertoli cells to support sperm production. They are also required for masculinization of the developing male fetus (including penis and scrotum formation). Under the influence of androgens, remnants of the mesonephron, the Wolffian ducts, develop into the epididymis, vas deferens and seminal vesicles. This action of androgens is supported by a hormone from Sertoli cells, Müllerian inhibitory hormone (MIH), which prevents the embryonic Müllerian ducts from developing into fallopian tubes and other female reproductive tract tissues in male embryos. MIH and androgens cooperate to allow for movement of testes into the scrotum.

Early regulation

Before the production of the pituitary hormone luteinizing hormone (LH) by the embryo starting at about weeks 11–12, human chorionic gonadotrophin (hCG) promotes the differentiation of Leydig cells and their production of androgens at week 8. Androgen action in target tissues often involves conversion of testosterone to 5α-dihydrotestosterone (DHT).

Spermatogenesis

During puberty, androgen, LH and follicle stimulating hormone (FSH) production increase and the sex cords hollow out, forming the seminiferous tubules, and the germ cells start to differentiate into sperm. Throughout adulthood, androgens and FSH cooperatively act on Sertoli cells in the testes to support sperm production.[5] Exogenous androgen supplements can be used as a male contraceptive. Elevated androgen levels caused by use of androgen supplements can inhibit production of LH and block production of endogenous androgens by Leydig cells. Without the locally high levels of androgens in testes due to androgen production by Leydig cells, the seminiferous tubules can degenerate, resulting in infertility. For this reason, many transdermal androgen patches are applied to the scrotum.

Inhibition of fat deposition

Males typically have less body fat than females. Recent results indicate androgens inhibit the ability of some fat cells to store lipids by blocking a signal transduction pathway that normally supports adipocyte function.[6] Also, androgens, but not estrogens, increase beta adrenergic receptors while decreasing alpha adrenergic receptors- which results in increased levels of epinephrine/ norepinephrine due to lack of alpha-2 receptor negative feedback and decreased fat accumulation due to epinephrine/ norepinephrine then acting on lipolysis-inducing beta receptors.

Muscle mass

Males typically have more skeletal muscle mass than females. Androgens promote the enlargement of skeletal muscle cells and probably act in a coordinated manner to function by acting on several cell types in skeletal muscle tissue.[7] One cell type conveys hormone signals to generating muscle, the myoblast. Higher androgen levels lead to increased expression of androgen receptor. Fusion of myoblasts generates myotubes, in a process linked to androgen receptor levels.[8]

Brain

Circulating levels of androgens can influence human behavior because some neurons are sensitive to steroid hormones. Androgen levels have been implicated in the regulation of human aggression and libido. Indeed, androgens are capable of altering the structure of the brain in several species, including mice, rats, and primates, producing sex differences.[9]

Numerous reports have shown androgens alone are capable of altering the structure of the brain,[10] but identification of which alterations in neuroanatomy stem from androgens or estrogens is difficult, because of their potential for conversion.

Evidence from neurogenesis (formation of new neurons) studies on male rats has shown that the hippocampus is a useful brain region to examine when determining the effects of androgens on behavior. To examine neurogenesis, wild-type male rats were compared with male rats that had testicular feminization mutation (TMF), a genetic disorder resulting in complete or partial insensitivity to androgens and a lack of external male genitalia.

Neural injections of Bromodeoxyuridine (BrdU) were applied to males of both groups to test for neurogenesis. Analysis showed that testosterone and dihydrotestosterone regulated adult hippocampal neurogenesis (AHN). Adult hippocampal neurogenesis was regulated through the androgen receptor in the wild-type male rats, but not in the TMF male rats. To further test the role of activated androgen receptors on AHN, flutamide, an antiandrogen drug that competes with testosterone and dihydrotestosterone for androgen receptors, and dihydrotestosterone were administered to normal male rats. Dihydrotestosterone increased the number of BrdU cells, while flutamide inhibited these cells.

Moreover, estrogens had no effect. This research demonstrates how androgens can increase AHN.[11]

Researchers also examined how mild exercise affected androgen synthesis which in turn causes AHN activation of N-methyl-D-aspartate (NMDA) receptors.

NMDA induces a calcium flux that allows for synaptic plasticity which is crucial for AHN.

Researchers injected both orchidectomized (ORX) (castrated) and sham castrated male rats with BrdU to determine if the number of new cells was increased. They found that AHN in male rats is increased with mild exercise by boosting synthesis of dihydrotestosterone in the hippocampus.

Again it was noted that AHN was not increase via activation of the estrogen receptors.[12]

Androgen regulation decreases the likelihood of depression in males. In preadolescent male rats, neonatal rats treated with flutamide developed more depression-like symptoms compared to control rats.

Again BrdU was injected into both groups of rats in order to see if cells were multiplying in the living tissue. These results demonstrate how the organization of androgens has a positive effect on preadolescent hippocampal neurogenesis that may be linked with lower depression-like symptoms.[13]

Social isolation has a hindering effect in AHN whereas normal regulation of androgens increases AHN. A study using male rats showed that testosterone may block social isolation, which results in hippocampal neurogenesis reaching homeostasis—regulation that keeps internal conditions stable. A Brdu analysis showed that excess testosterone did not increase this blocking effect against social isolation; that is, the natural circulating levels of androgens cancel out the negative effects of social isolation on AHN.[14]

Effects specific to females

Androgens have potential roles in relaxation of the myometrium via non-genomic, androgen receptor-independent pathways, preventing premature uterine contractions in pregnancy.[15]

Insensitivity to androgen in humans

Reduced ability of an XY-karyotype fetus to respond to androgens can result in one of several conditions, including infertility and several forms of intersex conditions.

Relative potency of natural androgens (%)

Determined by consideration of all biological assay methods (circa 1970). Data from Steroid Biochemistry and Pharmacology by Briggs and Brotherton, Academic Press.

Testosterone 100
5-alpha-dihydrotestosterone (DHT) 90
Androstanediol 60
Androstenedione 20
Dehydroepiandrosterone 10
Androsterone 10

5-alpha-dihydrotestosterone (DHT) was 2.4 times more potent than testosterone at maintaining normal prostate weight and duct lumen mass (this is a measure of epithelial cell function stimulation). Whereas DHT was equally potent as testosterone at preventing prostate cell death after castration.[16]

Androgenic impact of exercise

In cross-sectional analyses, aerobic exercisers have lower basal total and free testosterone compared to the sedentary.[17][18][19][20] Anaerobic exercisers also have lower testosterone compared to the sedentary[17] but a slight increase in basal testosterone with resistance training over time.[21] There is some correlation between testosterone and physical activity in the middle aged and elderly.[22] Acutely, testosterone briefly increases when comparing aerobic, anaerobic and mixed forms of exercise.[23] A study assessed men who were resistance trained, endurance trained, or sedentary in which they either rested, ran or did a resistance session. Androgens increased in response to exercise, particularly resistance, while cortisol only increased with resistance. DHEA increased with resistance exercise and remained elevated during recovery in resistance-trained subjects. After initial post-exercise increase, there was decline in free and total testosterone during resistance recovery, particularly in resistance-trained subjects. Endurance-trained subjects showed less change in hormone levels in response to exercise than resistance-trained subjects.[24] Another study found relative short term effects of aerobic, anaerobic and combined anaerobic-aerobic exercise protocols on hormone levels did not change. The study noted increases in testosterone and cortisol immediately after exercise, which in 2 hours returned to baseline levels.[25]

Aerobic

In trained long term aerobic exercisers, basal levels are unchanged,[26] or decreased.[25][27] Acutely, endurance based aerobic efforts cause testosterone to rise.[28]

A year long, moderate-intensity aerobic exercise program increased DHT and SHBG in sedentary men age 40–75, but had no effect on other androgens. Both DHT and SHBG increased 14% in exercisers at 3 months, and at 12 months they remained 9% above baseline. SHBG is protective against DHT as it binds free androgen.[29] In acute assessment of hormone levels in soccer players before, during and after a game, DHT and testosterone increased during the match, but returned to baseline after 45 minutes rest.[30] Aerobic exercise in Japanese rats done on a rodent treadmill doubled local concentrations of DHT in calf muscles as assessed by protein assay.[31] After intense aerobic effort, high endurance athletes were also found to have lower free testosterone the next day.[32] In prolonged endurance exercise, such as a marathon, levels ultimately decrease.[33] Similarly, DHT drops, while adrenal androgen and cortisol will increase with the stress response.[34]

Anaerobic

Effects of anaerobic exercise also vary with length of time.

It is unknown if anaerobic training changes individual hormone profiles, or if conditioned athletes in studies self-selected because of physiologic predisposition to athletic conditioning.[35] There is variation of response to anaerobic stress depending on exercise intensity, age, gender, length of time studied, and time at which serum indices were drawn. Most studies report that testosterone increases or is unchanged acutely, though some even report it to decrease. Anaerobic exercisers have testosterone levels below sedentary controls in cross sectional analysis. Over months to years, levels are stable to slightly increased.

The ratio of testosterone to cortisol can both increase[36] and decrease[37] during resistance training, depending on intensity of exercise. A study comparing young and old subjects showed acute increases in GH and testosterone for both, although the latter increased less in older men.[38] Testosterone rises in late hours of sleep after anaerobic exercise.[39] Androgen receptor expression increases with acute exercise in correlation to free testosterone.[40] When comparing men and women in the 30, 50 and 70 year age groups, young and middle aged men showed increased testosterone after exercise, with the latter also having increased cortisol. Elderly men showed no change.[41] Other studies have also shown with age there is a downtrend of testosterone[42] and attenuated growth hormone response.[43] Young men have shown no acute change in testosterone with resistance training, with increase in cortisol and growth hormone depending on intensity.[44] One study in young men showed testosterone acutely stable, with increase in GH and IGF-1.[45] Similarly, a study showed testosterone did not increase in young men, women, and pubescent boys unaccustomed to weight training when corrected for plasma volume.[46] Extreme intensity of strength training may trigger the stress response, resulting in lower testosterone levels,[47] an effect accentuated by energy deprivation.[48] A separate study comparing different ages, however, found no difference in acute testosterone and cortisol levels between groups, but attenuated growth hormone response in the elderly.[43] Acutely, other studies have shown testosterone to increase.[49] In a small group of anaerobically trained athletes, stressful training acutely even decreased serum testosterone and its ratio to cortisol and SHBG, with an increase in LH. With subsequent decompensation, testosterone was stable, but cortisol and SHBG decreased.[37] Another case control showed with intense training followed by rest, testosterone dropped and LH increased initially.[50]

Interval and quality of exercise also affect hormonal response. Sessions of moderate to high intensity with multiple sets and short time intervals, during which energy is derived from glycolytic lactate metabolism, appear to be the greatest stimulus for steroid hormone response. Hormonal response in young men varies with the number of sets in the exercise session. However, when the number increased from 4 to 6, anabolic levels stabilized and cortisol continued to rise, suggesting that alterations in anaerobic volume could alter anabolic and catabolic hormonal balance.[44] When sets are performed at maximum repetitions, interval has no influence at a certain intensity range, with no acute hormone response difference between protocols at 10 maximum reps with 2- and 5-minute intervals.[51] There is a higher total testosterone response in hypertrophy protocols compared to those for strength and power, despite equalization of total work load (defined as load x sets x repetitions).[52] There is a 27% greater testosterone response using protocols with simultaneous use of all four limbs. Androgenic response was also noted in protocols using upper and lower limbs separately to a lesser degree.[38]

A number of studies have looked at effects of anaerobic exercise over months to years, showing it to be constant or slightly increased. A small case-control of anaerobic training in young untrained males over six weeks found decline in free testosterone of 17 percent.[53] With men in their 60s, resistive training over 16 weeks did not affect baseline anabolic hormone levels, although GH increased acutely with exercise.[54] A study over 21 weeks in male strength athletes showed basal hormone levels to be constant, despite strength increase.[55] A follow up study looked at a larger group of weight trainers over 24 weeks, with 12 week decompensation. Training caused no change in total testosterone, but there were decreases in free testosterone, progesterone, androstendione, DHEA, cortisol, transcortin, and in the cortisol:CBG ratio, suggesting androgen turnover increased with training intensity, without change in total testosterone.[36] A study looking at young men and resistance training over 48 weeks found increases in baseline serum testosterone from 20 ± 5 to 25 ± 5 nmol/l, and an increase in testosterone:SHBG ratio, LH and FSH.[21]

Combined training

One study showed GH increase with anaerobic effort to be blunted in those who performed aerobic training for 60 minutes prior to strength training. Testosterone levels remained high only at the end of the training session with aerobic training followed by strength training, a phenomenon not seen with weight training done before aerobics.[56] In an 11-week soccer training program focusing on combined vertical jumps, short sprints, and submaximal endurance running, total testosterone increased, but SHBG rose in parallel, maintaining a constant free androgen index.[57]

Miscellaneous

Non-genomic actions

Androgens have also been found to signal through membrane androgen receptors, which are distinct from the classical nuclear androgen receptor.[58][59][60]

See also

References

  1. ↑ Sriram. "Steroids". Medicinal Chemistry. Pearson Education India. p. 437.
  2. 1 2 Carlson, Neil (January 22, 2012). Physiology of Behavior. Reproductive Behavior. 11th edition. Pearson. p. 326. ISBN 0205239390.
  3. ↑ "Androgens". DIAsource.
  4. ↑ Scott F. Gilbert; with a chapter on plant development by Susan R. Singer (2000). Scott F. Gilbert, ed. Developmental Biology (6th ed.). Sunderland, Massachusetts: Sinauer Associates. ISBN 0-87893-243-7.
  5. ↑ Stephen Nussey and Saffron Whitehead (2001). Saffron A. Whitehead and Stephen Nussey, ed. Endocrinology: an integrated approach. Oxford: British Institute of Organ Studies. ISBN 1-85996-252-1.
  6. ↑ Singh R, Artaza JN, Taylor WE, Braga M, Yuan X, Gonzalez-Cadavid NF, Bhasin S (January 2006). "Testosterone inhibits adipogenic differentiation in 3T3-L1 cells: nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors". Endocrinology 147 (1): 141–54. doi:10.1210/en.2004-1649. PMID 16210377.
  7. ↑ Sinha-Hikim I, Taylor WE, Gonzalez-Cadavid NF, Zheng W, Bhasin S (October 2004). "Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment". The Journal of Clinical Endocrinology and Metabolism 89 (10): 5245–55. doi:10.1210/jc.2004-0084. PMID 15472231.
  8. ↑ Vlahopoulos S, Zimmer WE, Jenster G, Belaguli NS, Balk SP, Brinkmann AO, Lanz RB, Zoumpourlis VC, Schwartz RJ (March 2005). "Recruitment of the androgen receptor via serum response factor facilitates expression of a myogenic gene". The Journal of Biological Chemistry 280 (9): 7786–92. doi:10.1074/jbc.M413992200. PMID 15623502.
  9. ↑ Cooke B, Hegstrom CD, Villeneuve LS, Breedlove SM (October 1998). "Sexual differentiation of the vertebrate brain: principles and mechanisms". Frontiers in Neuroendocrinology 19 (4): 323–62. doi:10.1006/frne.1998.0171. PMID 9799588.
  10. ↑ Zuloaga DG, Puts DA, Jordan CL, Breedlove SM (May 2008). "The role of androgen receptors in the masculinization of brain and behavior: what we've learned from the testicular feminization mutation". Hormones and Behavior 53 (5): 613–26. doi:10.1016/j.yhbeh.2008.01.013. PMC 2706155. PMID 18374335.
  11. ↑ Hamson DK, Wainwright SR, Taylor JR, Jones BA, Watson NV, Galea LA (2013). "Androgens increase survival of adult-born neurons in the dentate gyrus by an androgen receptor-dependent mechanism in male rats". Endocrinology 154 (9): 3294–304. doi:10.1210/en.2013-1129. PMID 23782943.
  12. ↑ Okamoto M, Hojo Y, Inoue K, Matsui T, Kawato S, McEwen BS, Soya H (2012). "Mild exercise increases dihydrotestosterone in hippocampus providing evidence for androgenic mediation of neurogenesis". PNAS 109 (32): 13100–13105. doi:10.1073/pnas.1210023109.
  13. ↑ Zhang JM, Tonelli L, Regenold WT, McCarthy MM (2010). "Effects of neonatal flutamide treatment on hippocampal neurogenesis and synaptogenesis correlate with depression-like behaviors in preadolescent male rats". Neuroscience 169 (1): 544–54. doi:10.1016/j.neuroscience.2010.03.029. PMC 3574794. PMID 20399256.
  14. ↑ Spritzer MD, Ibler E, Inglis W, Curtis MG (2011). "Testosterone and social isolation influence adult neurogenesis in the dentate gyrus of male rats". Neuroscience 195: 180–90. doi:10.1016/j.neuroscience.2011.08.034. PMC 3198792. PMID 21875652.
  15. ↑ Makieva S, Saunders PT, Norman JE (2014). "Androgens in pregnancy: roles in parturition". Hum. Reprod. Update 20 (4): 542–59. doi:10.1093/humupd/dmu008. PMC 4063701. PMID 24643344.
  16. ↑ Wright AS, Thomas LN, Douglas RC, Lazier CB, Rittmaster RS (December 1996). "Relative potency of testosterone and dihydrotestosterone in preventing atrophy and apoptosis in the prostate of the castrated rat". J. Clin. Invest. 98 (11): 2558–63. doi:10.1172/JCI119074. PMC 507713. PMID 8958218.
  17. 1 2 Arce JC, De Souza MJ, Pescatello LS, Luciano AA (1993). "Subclinical alterations in hormone and semen profile in athletes". Fertility and Sterility 59 (2): 398–404. PMID 8425638.
  18. ↑ Hackney AC, Sinning WE, Bruot BC (1988). "Reproductive hormonal profiles of endurance-trained and untrained males". Medicine and science in sports and exercise 20 (1): 60–65. doi:10.1249/00005768-198802000-00009. PMID 3343919.
  19. ↑ Wheeler GD, Wall SR, Belcastro AN, Cumming DC (1984). "Reduced serum testosterone and prolactin levels in male distance runners". JAMA: the Journal of the American Medical Association 252 (4): 514–516. doi:10.1001/jama.252.4.514. PMID 6429357.
  20. ↑ Cooper CS, Taaffe DR, Guido D, Packer E, Holloway L, Marcus R (1998). "Relationship of chronic endurance exercise to the somatotropic and sex hormone status of older men". European Journal of Endocrinology / European Federation of Endocrine Societies (Bioscientifica) 138 (5): 517–523. doi:10.1530/eje.0.1380517. PMID 9625362.
  21. 1 2 Häkkinen K, Pakarinen A, Alen M, Kauhanen H, Komi PV (1988). "Neuromuscular and hormonal adaptations in athletes to strength training in two years". Journal of applied physiology (Bethesda, Md. : 1985) 65 (6): 2406–2412. PMID 3215840.
  22. ↑ Muller M, den Tonkelaar I, Thijssen JH, Grobbee DE, van der Schouw YT (2003). "Endogenous sex hormones in men aged 40-80 years". European Journal of Endocrinology / European Federation of Endocrine Societies 149 (6): 583–589. doi:10.1530/eje.0.1490583. PMID 14641001.
  23. ↑ Kraemer WJ, Häkkinen K, Newton RU, McCormick M, Nindl BC, Volek JS, Gotshalk LA, Fleck SJ, Campbell WW, Gordon SE, Farrell PA, Evans WJ (1998). "Acute hormonal responses to heavy resistance exercise in younger and older men". European journal of applied physiology and occupational physiology 77 (3): 206–211. doi:10.1007/s004210050323. PMID 9535580.
  24. ↑ Tremblay MS, Copeland JL, Van Helder W (2004). "Effect of training status and exercise mode on endogenous steroid hormones in men". Journal of Applied Physiology 96 (2): 531–539. doi:10.1152/japplphysiol.00656.2003. PMID 14514704.
  25. 1 2 Hackney AC, Premo MC, McMurray RG (1995). "Influence of aerobic versus anaerobic exercise on the relationship between reproductive hormones in men". Journal of Sports Sciences 13 (4): 305–311. doi:10.1080/02640419508732244. PMID 7474044.
  26. ↑ Fellmann N, Coudert J, Jarrige JF, Bedu M, Denis C, Boucher D, Lacour JR (2008). "Effects of Endurance Training on the Androgenic Response to Exercise in Man". International Journal of Sports Medicine 06 (4): 215–219. doi:10.1055/s-2008-1025843. PMID 4044106.
  27. ↑ Hackney AC, Fahrner CL, Gulledge TP (1998). "Basal reproductive hormonal profiles are altered in endurance trained men". The Journal of sports medicine and physical fitness 38 (2): 138–141. PMID 9763799.
  28. ↑ Jensen J, Oftebro H, Breigan B, Johnsson A, Ohlin K, Meen HD, Strømme SB, Dahl HA (1991). "Comparison of changes in testosterone concentrations after strength and endurance exercise in well trained men". European journal of applied physiology and occupational physiology 63 (6): 467–471. doi:10.1007/bf00868080. PMID 1765061.
  29. ↑ Hawkins VN, Foster-Schubert K, Chubak J, Sorensen B, Ulrich CM, Stancyzk FZ, Plymate S, Stanford J, White E, Potter JD, McTiernan A (2008). "Effect of Exercise on Serum Sex Hormones in Men". Medicine & Science in Sports & Exercise 40 (2): 223–233. doi:10.1249/mss.0b013e31815bbba9. PMC 3040039. PMID 18202581.
  30. ↑ Lupo C, Baldi L, Bonifazi M, Lodi L, Martelli G, Viti A, Carli G (1985). "Androgen levels following a football match". European journal of applied physiology and occupational physiology 54 (5): 494–496. doi:10.1007/bf00422958. PMID 4085477.
  31. ↑ Sato K, Iemitsu M, Aizawa K, Mesaki N, Ajisaka R, Fujita S (2012). "DHEA administration and exercise training improves insulin resistance in obese rats". Nutrition & Metabolism 9: 47. doi:10.1186/1743-7075-9-47. PMC 3433349. PMID 22647230.
  32. ↑ Daly W, Seegers CA, Rubin DA, Dobridge JD, Hackney AC (2004). "Relationship between stress hormones and testosterone with prolonged endurance exercise". European Journal of Applied Physiology 93 (4): 375–380. doi:10.1007/s00421-004-1223-1. PMID 15618989.
  33. ↑ Dressendorfer RH, Wade CE (1991). "Effects of a 15-d race on plasma steroid levels and leg muscle fitness in runners". Medicine and science in sports and exercise 23 (8): 954–958. doi:10.1249/00005768-199108000-00012. PMID 1956271.
  34. ↑ Morville R, Pesquies PC, Guezennec CY, Serrurier BD, Guignard M (1979). "Plasma variations in testicular and adrenal androgens during prolonged physical exercise in man". Annales d'endocrinologie 40 (5): 501–510. PMID 518032.
  35. ↑ Bunt JC (1986). "Hormonal alterations due to exercise". Sports medicine (Auckland, N.Z.) 3 (5): 331–345. doi:10.2165/00007256-198603050-00003. PMID 3529282.
  36. 1 2 Alén M, Pakarinen A, Häkkinen K, Komi PV (1988). "Responses of serum androgenic-anabolic and catabolic hormones to prolonged strength training". International journal of sports medicine 9 (3): 229–233. doi:10.1055/s-2007-1025011. PMID 3410630.
  37. 1 2 Häkkinen K, Pakarinen A, Alén M, Kauhanen H, Komi PV (1987). "Relationships between training volume, physical performance capacity, and serum hormone concentrations during prolonged training in elite weight lifters". International journal of sports medicine. 8 Suppl 1: 61–65. PMID 3108174.
  38. 1 2 Häkkinen K, Pakarinen A, Newton RU, Kraemer WJ (1998). "Acute hormone responses to heavy resistance lower and upper extremity exercise in young versus old men". European journal of applied physiology and occupational physiology 77 (4): 312–319. doi:10.1007/s004210050339. PMID 9562359.
  39. ↑ McMurray RG, Eubank TK, Hackney AC (1995). "Nocturnal hormonal responses to resistance exercise". European journal of applied physiology and occupational physiology 72 (1–2): 121–126. doi:10.1007/bf00964126. PMID 8789582.
  40. ↑ Willoughby DS, Taylor L (2004). "Effects of sequential bouts of resistance exercise on androgen receptor expression". Medicine and science in sports and exercise 36 (9): 1499–1506. doi:10.1249/01.mss.0000139795.83030.d1. PMID 15354030.
  41. ↑ Häkkinen K, Pakarinen A (2007). "Acute Hormonal Responses to Heavy Resistance Exercise in Men and Women at Different Ages". International Journal of Sports Medicine 16 (8): 507–513. doi:10.1055/s-2007-973045. PMID 8776203.
  42. ↑ Baker JR, Bemben MG, Anderson MA, Bemben DA (2006). "Effects of Age on Testosterone Responses to Resistance Exercise and Musculoskeletal Variables in Men". The Journal of Strength and Conditioning Research 20 (4): 874–881. doi:10.1519/R-18885.1. PMID 17194250.
  43. 1 2 Smilios I, Pilianidis T, Karamouzis M, Parlavantzas A, Tokmakidis SP (2007). "Hormonal Responses after a Strength Endurance Resistance Exercise Protocol in Young and Elderly Males". International Journal of Sports Medicine 28 (5): 401–406. doi:10.1055/s-2006-924366. PMID 17024619.
  44. 1 2 Smilios I, Pilianidis T, Karamouzis M, Tokmakidis SP (2003). "Hormonal Responses after Various Resistance Exercise Protocols". Medicine & Science in Sports & Exercise 35 (4): 644–654. doi:10.1249/01.MSS.0000058366.04460.5F. PMID 12673149.
  45. ↑ Pullinen T, Mero A, Huttunen P, Pakarinen A, Komi PV (2002). "Resistance exercise-induced hormonal responses in men, women, and pubescent boys". Medicine and science in sports and exercise 34 (5): 806–813. doi:10.1097/00005768-200205000-00013. PMID 11984299.
  46. ↑ Kraemer RR, Kilgore JL, Kraemer GR, Castracane VD (1992). "Growth hormone, IGF-I, and testosterone responses to resistive exercise". Medicine and science in sports and exercise 24 (12): 1346–1352. doi:10.1249/00005768-199212000-00007. PMID 1470017.
  47. ↑ Raastad T, Glomsheller T, Bjøro T, Hallén J (2001). "Changes in human skeletal muscle contractility and hormone status during 2 weeks of heavy strength training". European Journal of Applied Physiology 84 (1–2): 54–63. doi:10.1007/s004210000328. PMID 11394254.
  48. ↑ Bergendahl M, Aloi JA, Iranmanesh A, Mulligan TM, Veldhuis JD (1998). "Fasting suppresses pulsatile luteinizing hormone (LH) secretion and enhances orderliness of LH release in young but not older men". The Journal of Clinical Endocrinology and Metabolism 83 (6): 1967–1975. doi:10.1210/jc.83.6.1967. PMID 9626127.
  49. ↑ Kraemer WJ, Marchitelli L, Gordon SE, Harman E, Dziados JE, Mello R, Frykman P, McCurry D, Fleck SJ (1990). "Hormonal and growth factor responses to heavy resistance exercise protocols". Journal of applied physiology (Bethesda, Md. : 1985) 69 (4): 1442–1450. PMID 2262468.
  50. ↑ Busso T, Häkkinen K, Pakarinen A, Kauhanen H, Komi PV, Lacour JR (1992). "Hormonal adaptations and modelled responses in elite weightlifters during 6 weeks of training". European journal of applied physiology and occupational physiology 64 (4): 381–386. doi:10.1007/bf00636228. PMID 1592066.
  51. ↑ Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, Häkkinen K (2005). "Short vs. Long Rest Period Between the Sets in Hypertrophic Resistance Training: Influence on Muscle Strength, Size, and Hormonal Adaptations in Trained Men". The Journal of Strength and Conditioning Research 19 (3): 572–582. doi:10.1519/15604.1. PMID 16095405.
  52. ↑ McCaulley GO, McBride JM, Cormie P, Hudson MB, Nuzzo JL, Quindry JC, Travis Triplett N (2008). "Acute hormonal and neuromuscular responses to hypertrophy, strength and power type resistance exercise". European Journal of Applied Physiology 105 (5): 695–704. doi:10.1007/s00421-008-0951-z. PMID 19066934.
  53. ↑ Ara I, Perez-Gomez J, Vicente-Rodriguez G, Chavarren J, Dorado C, Calbet JA (2006). "Serum free testosterone, leptin and soluble leptin receptor changes in a 6-week strength-training programme". The British journal of nutrition 96 (6): 1053–1059. doi:10.1017/bjn20061956. PMID 17181880.
  54. ↑ Nicklas BJ, Ryan AJ, Treuth MM, Harman SM, Blackman MR, Hurley BF, Rogers MA (2007). "Testosterone, Growth Hormone and IGF-I Responses to Acute and Chronic Resistive Exercise in Men Aged 55-70 Years". International Journal of Sports Medicine 16 (7): 445–450. doi:10.1055/s-2007-973035. PMID 8550252.
  55. ↑ Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, Häkkinen K (2003). "Muscle hypertrophy, hormonal adaptations and strength development during strength training in strength-trained and untrained men". European Journal of Applied Physiology 89 (6): 555–563. doi:10.1007/s00421-003-0833-3. PMID 12734759.
  56. ↑ Goto K, Higashiyama M, Ishii N, Takamatsu K (2005). "Prior endurance exercise attenuates growth hormone response to subsequent resistance exercise". European Journal of Applied Physiology 94 (3): 333–338. doi:10.1007/s00421-004-1296-x. PMID 15714290.
  57. ↑ Gorostiaga EM, Izquierdo M, Ruesta M, Iribarren J, González-Badillo JJ, Ibáñez J (2003). "Strength training effects on physical performance and serum hormones in young soccer players". European Journal of Applied Physiology 91 (5–6): 698–707. doi:10.1007/s00421-003-1032-y. PMID 14704801.
  58. ↑ Bennett NC, Gardiner RA, Hooper JD, Johnson DW, Gobe GC (2010). "Molecular cell biology of androgen receptor signalling". Int. J. Biochem. Cell Biol. 42 (6): 813–27. doi:10.1016/j.biocel.2009.11.013. PMID 19931639.
  59. ↑ Wang C, Liu Y, Cao JM (2014). "G protein-coupled receptors: extranuclear mediators for the non-genomic actions of steroids". Int J Mol Sci 15 (9): 15412–25. doi:10.3390/ijms150915412. PMC 4200746. PMID 25257522.
  60. ↑ Lang F, Alevizopoulos K, Stournaras C (2013). "Targeting membrane androgen receptors in tumors". Expert Opin. Ther. Targets 17 (8): 951–63. doi:10.1517/14728222.2013.806491. PMID 23746222.
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