The influence of anabolic steroids on physiologic processes and exercise


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Anabolic-androgenic steroids (AAS) abuse is often associated with a wide spectrum of adverse effects. These drugs are frequently abused by adolescents and athletes for aesthetic purposes, as well as for improvement of their endurance and performance[1]

Anabolic-androgenic steroids (AAS) are a group of synthetic compounds that mimic the effects of testosterone in the body[2]. AAS abuse can have profound effects on the cardiovascular system, hepatic function, and adrenal and renal function [3]. As its name refers, AAS has two major effects: androgenic and anabolic. Androgenic effects increase secondary masculine sexual characteristics whereas anabolic effects increase protein synthesis [3]. The latter effect is why many individuals abuse AAS, with the intent of increasing lean muscle mass.
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  • Androgens have various side effects. Complications include:
    • Cardiac hypertrophy
    • Decreased serum HDL cholesterol
    • Hypogonadism after discontinuation of exogenous androgens
    • Neuropsychiatric concerns

Many studies show an association between the non-medical use of androgens and increases in risky and criminal behavior among the androgen intake abusers. In a survey of 10 000 to 15 000 college students, use of androgens correlated highly with drinking and driving, cigarette smoking, illicit drug use, and alcohol abuse.

Cardiovascular Effects

Long-term use of supra-physiological doses of AAS has been associated with the development of pathological changes in the cardiovascular system. AAS users are at an increased risk of myocardial infarction, cardiomyopathy, sudden death, cardiovascular morbidity, and mortality when compared to non-users [6].

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AAS abuse in body builders has been linked with:

  • myocardial infarction
  • cardiomyopathy
  • sudden death
  • elevated blood pressure and increased risk of thrombosis[7][8]
  • lower amount of heart rate variability (HRV) than non-users, putting them at an increased risk of autonomic cardiovascular dysfunction and ventricular arrhythmia [9].
  • atrial fibrillation (AF) [10] - This may be due to inter- and intra-atrial electromechanical delay.
  • decreased vagal and parasympathetic activity in the heart[9][11]. Reduced parasympathetic activity in the heart slows the recovery of the heart rate post exercise.[9] However, the exact mechanism of how AAS abuse contributes to atrial electromechanical delay is poorly understood[12]
  • left ventricular dysfunction. A 2007 study published by the British Journal of Sports Medicine used Doppler myocardial and strain imaging analysis and found that chronic AAS abuse produced a much lower early diastolic peak velocity at the levels of the lateral wall of the left ventricle and the interventricular septum [13]
  • Hypertension
  • ventricular remodeling, and
  • myocardial ischemia [14].

The normal adaptive mechanisms of the heart in response to exercise are negatively affected by both exogenous and endogenous steroids, leading to cellular alterations that are similar to those exhibited with heart failure and cardiomyopathy[14]. These effects persist long after use has been discontinued and have significant impact on subsequent morbidity and mortality[14].

Muscular Effects

AAS utilize three physiological mechanisms on the muscular system to produce its effects.

  • At the cellular level, AAS increases protein synthesis via gene transcription after binding to androgenic receptors [15].
  • AAS disallows glucocorticoids from binding to their receptors. This is important because glucocorticoids produce catabolic effects by depressing protein synthesis [15].
  • AAS psychologically impacts users by producing euphoria, encouraging users to work harder during workouts[15]. In turn, AAS use may lead to rhabdomyolysis by promoting over exertion[16][17][18][19][20]

Athletes use AAS to improve performance as AAS cause muscle hypertrophy and protein synthesis [especially when combined with resistance exercise][21].

  • Stanozolol significantly increased type I muscle fiber size[22], hypothetically hypertrophy of type I fibers allows athletes to exercise longer, in turn causing type II fiber hypertrophy[22].
  • Steroids have not been shown to increase creatine concentrations in the muscle[23].
  • Injection of 600 mg of testosterone in adult males who did not exercise resulted in a greater increase in strength and fat free mass than in individuals who incorporated resistance training but only took a placebo[23].
  • AAS increases exercise capacity, muscle endurance, and running endurance in rats. A 2001 study measured total amount of weight lifted, the total number of sets, 10 Repetition Max (RM), and the number of complete sets at 10RM[21]. Rats in the steroid group performed 47%, 12%, 22%, and 81% better in these areas respectively[21]. The study found that AAS treatment before a single bout of exhaustive weight-lifting exercise enhances the fatigue resistance in involved muscles and increases protein synthesis[21].
  • AAS treatment in combination with exercise delays fatigue during sub-maximal exercise, possibly due to AAS induced muscle fiber transformations[24].
  • AAS can promote muscular development and strength in older populations. AAS use may benefit those recovering from hip surgery[25]. A randomized controlled study of 274 elderly men with frailty concluded that administering testosterone may improve quality of life by improving strength, physical function, and body composition.[26]  AAS may increase quadriceps strength following total knee athroplasty (TKA) but there were no changes in outcomes related to activities of daily living such as hamstring strength, sit-to-stand test, or walking speed.[27] The evidence to support AAS use following TKA is insignificant, but there are some implications that AAS use may benefit those following surgery.[27]

Correlations between AAS use and upper extremity tendon rupture exist.

  • Out of 88 AAS users in one study, 17% had confirmed triceps or biceps tendon ruptures, compared to none of the non AAS users[28] . No significant difference was found between the two groups concerning lower extremity tendon ruptures[28] . The mechanism of AAS-associated tendon rupture is not well understood. One hypothesis is that AAS use combined with intense exercise may cause structural tendon damage. Most evidence supporting this hypothesis comes from animal studie [28]. One study found ultra-structural changes in tendons of mice treated with AAS[29], but strong evidence of structural changes in human tendons has not been demonstrated[28]. A case-control study compared collagen ultra-structure, metabolism, and mechanical properties of patella tendons in 24 individuals assigned to three groups: resistance-trained AAS users (RTS), resistance-trained non-AAS users (RT), and a control group that neither used AAS nor resistance-trained (CTRL). Higher patellar stiffness and tensile modulus was found in the RTS group, but there was no significant difference in mechanical and material properties of the tendons between the RTS and RT groups[30]. A competing hypothesis suggests that AAS use causes hypertrophy in the muscle without causing corresponding changes in the tendon tissue. Sudden or maximal stress can cause tendon injury[28]. Lastly, a study on retired National Football League (NFL) players found an association between AAS use and an increased likelihood of musculoskeletal injury, specifically ligamentous injuries [31].

Neurological Effects

AAS use is associated with both positive and negative psychological effects. AAS abuse and dependence is a potential problem among AAS users, especially those using it for performance or aesthetic purposes.

AAS may increase beta-endorphin levels, decrease cortisol levels, and increase ACTH levels, which may lead to an increase in positive associations with exercise[32].  The increase in endorphin levels and exercise reinforcement may contribute to AAS dependence and abuse[32].

AAS dependence is characterized by increases in AAS cycles, higher doses, and increases in psychological disorders, such as increased aggression[33]. Depression and suicide can be caused by off-cycles of AAS or withdrawal from AAS use.  The risk for depression and suicide may be caused by the decrease in endorphin levels and changes in the reward systems of the brain. AAS can cause or exacerbate anxiety disorders, schizophrenia, and eating disorders[33].  The psychopathology of AAS is theorized to be caused by direct or indirect changes in the central nervous system, including changes to intracellular receptors and neurotransmitter receptors. These changes may influence hormone and neurotransmitter levels, such as serotonin or GABA, and lead to changes in depression, anger, or stress[33]. AAS use may contribute to motivation and positive experiences with exercise, but it can lead to negative effects that are long-lasting and decreases in motivation to exercise.

Deterrence and Patient Education

The potential adverse cardiovascular effects from long-term anabolic steroid use are significant, and health care providers need to bring awareness among patients and implement protocols to help detect patients at risk.[5]


  1. Bertozzi G, Sessa F, Albano GD, Sani G, Maglietta F, Roshan MH, Volti GL, Bernardini R, Avola R, Pomara C, Salerno M. The role of anabolic androgenic steroids in disruption of the physiological function in discrete areas of the central nervous system. Molecular neurobiology. 2018 Jul 1;55(7):5548-56. Available from: (last accessed 20.12.2019)
  2. National Institute on Drug Abuse. Anabolic Steroids. (accessed November 10, 2015)
  3. 3.0 3.1 Modlinski R, Fields KB. The effect of anabolic steroids on the gastrointestinal system, kidneys, and adrenal glands. Current Sports Medicine Reports. 2006;5(2):104-9.
  4. BBC Earth lab What happens when you take steroids Available from: (last accessed 20.12.2019)
  5. 5.0 5.1 AlShareef S, Marwaha R. Anabolic Steroid Use Disorder. InStatPearls [Internet] 2019 Feb 5. StatPearls Publishing. Available from: (last accessed 20.12.2019)
  6. Achar S, Rostamian A, Narayan SM. Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm. The American journal of cardiology. 2010;106(6):893-901.
  7. Kuipers H, Wijnen JA, Hartgens F, Willems SM.Influence of anabolic steroids on body composition, blood pressure, lipid profile and liver functions in body builders. Int J Sports Med 1991;12(4):413-8.
  8. Laroche GP. Steroid anabolic drugs and arterial complications in an athlete-a case history. Angiology 1990;41(11):964-9.
  9. 9.0 9.1 9.2 Maior A, Carvalho A, Marques-Neto S, Menezes P, Soares P, Nascimento J. Cardiac autonomic dysfunction in anabolic steroid users. Scandinavian journal of Medicine and Science in Sports. 2013;23(5):548-55.
  10. Lau DH, Stiles MK, John B, Young GD, Sanders P. Atrial fibrillation and anabolic steroid abuse. International journal of cardiology. 2007;117(2):e86-e7.
  11. Hedman A, Hartikainen J, Tahvanainen K, Hakumäki M. The high frequency component of heart rate variability reflects cardiac parasympathetic modulation rather than parasympathetic ‘tone’. Acta Physiologica Scandinavica. 1995;155(3):267-73.
  12. Akçakoyun M, Alizade E, Gündoğdu R, Bulut M, Tabakcı MM, Açar G, et al. Long-term anabolic androgenic steroid use is associated with increased atrial electromechanical delay in male bodybuilders. Biomed Res Int. 2014;2014:8.
  13. D’Andrea A, Caso P, Salerno G, Scarafile R, De Corato G, Mita C, et al. Left ventricular early myocardial dysfunction after chronic misuse of anabolic androgenic steroids: a Doppler myocardial and strain imaging analysis. British journal of sports medicine. 2007;41(3):149-55.
  14. 14.0 14.1 14.2 Sullivan M, Martinez C, Gennis P, Gallagher E. The cardiac toxicity of anabolic steroids. Prog Cardiovasc Dis 1998;41(1). doi:10.1016/S0033-0620(98)80019-4
  15. 15.0 15.1 15.2 Haupt HA, Rovere GD. Anabolic steroids: a review of the literature. Am J Sport Med 1984;12:469-84
  16. Farkash U., Shabshin N., Pritsch M. Rhabdomyolysis of the Deltoid Muscle in a Bodybuilder Using Anabolic-Androgenic Steroids: A Case Report. Journal of Athletic Training. 2009; 44(1): 98–100.
  17. Adamson R, Rambaran C, D'Cruz D. Anabolic steroid-induced rhabdomyolysis. British Journal of Hospital Medicine (2005). 2005;66(6):362.
  18. Braseth N, Allison Jr E, Gough J. Exertional rhabdomyolysis in a body builder abusing anabolic androgenic steroids. European Journal of Emergency Medicine. 2001;8(2):155-7.
  19. Daniels JM, van Westerloo DJ, de Hon OM, Frissen PH. Rhabdomyolysis in a bodybuilder using steroids. [Abstract]. Nederlands tijdschrift voor geneeskunde. 2006;150(19):1077-80.
  20. Hughes M., Ahmed S. Anabolic androgenic steroid induced necrotising myopathy. Rheumatology International. 2001; 31(7): 915-917.
  21. 21.0 21.1 21.2 21.3 Tamaki T, Uchiyama S, Uchiyama Y, Akatsuka A, Roy RR, Edgerton VR. Anabolic steroids increase exercise tolerance. American Journal of Physiology-Endocrinology And Metabolism. 2001;280(6):E973-E81.
  22. 22.0 22.1 Hosegood JL, Franks AJ. Response of human skeletal muscle to the anabolic steroid stanozolol. BMJ. 1988;297(6655):1028-9.
  23. 23.0 23.1 Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, et al. The Effects of supraphysiologic doses of testosterone on muscle size and strength in normal men.Abridged version: NEJM 1996;335:1–7.Full version: (accessed 28 Oct 2015).
  24. Van Zyl CG, Noakes TD, Lambert MI. Anabolic-androgenic steroid increases running endurance in rats. Med Sci Sport Exer, 1995;27(10):1385-9.
  25. Farooqi V, Van Den Berg M, Cameron I. Anabolic steroids for rehabilitation after hip fracture in older people. The Cochran Collaboration. 2013:
  26. Srinivas-Shankar U, Roberts SA, Connolly MJ, O'Connell MDL, Adams JE, Oldham JA, Wu FCW. Effects of testosterone on muscle strength, physical function, body composition, and quality of life in intermediate-frail and frail elderly men: A randomized, double-blind, placebo-controlled study. J Clin Endocrinol Metab 2010;95(2):639-50.
  27. 27.0 27.1 Metcalfe D., Watts E., Masters JP., Smith N. Anabolic steroids in patients undergoing total knee arthroplasty. BMJ Open. 2011; 2(5): Doi: 10.1136/bmjopen-2012-001435
  28. 28.0 28.1 28.2 28.3 28.4 Kanayama G, DeLuca J, Meehan WP, Hudson JI, Isaacs S, Baggish A, et al. Ruptured Tendons in Anabolic-Androgenic Steroid Users. 2015;43(11):2638-44.
  29. Michna H. Tendon injuries induced by exercise and anabolic steroids in experimental mice. Int Orthop 1987;11(2):157-62.
  30. Seynnes OR, Kamandulis S, Kairaitis R, Helland C, Campbell E-L, Brazaitis M, et al. Effect of androgenic-anabolic steroids and heavy strength training on patellar tendon morphological and mechanical properties. J Appl Physiol 2013;115(1):84-9.
  31. Horn S, Gregory P, Guskiewicz KM. 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. Am J Phys Med Rehab 2009;88(3):192-200.
  32. 32.0 32.1 Hildebrandt T, Shope S, Varangis E, Klein D, Pfaff DW, Yehuda R. Exercise reinforcement, stress, and β-endorphins: An initial examination of exercise in anabolic–androgenic steroid dependence. Drug and alcohol dependence. 2014;139:86-92.
  33. 33.0 33.1 33.2 Piacentino D, D Kotzalidis G, del Casale A, Rosaria Aromatario M, Pomara C, Girardi P, et al. Anabolic-androgenic steroid use and psychopathology in athletes. A systematic review. Current Neuropharmacology. 2015;13(1):101-21.