The Influence of Oral Contraceptives on Athletic Performance in Female Athletes


It is now estimated that the prevalence of oral contraceptive use in athletic women matches that of women in the general population. The oral contraceptive pill (OCP) reduces cycle-length variability and provides a consistent 28-day cycle by controlling concentrations of endogenous sex hormones. The OCP is administered in three different forms that differ widely in chemical constitution and concomitant effects on the human body. As fluctuation in sex steroids are believed to be a possible causal factor in performance and exercise capacity, it is imperative to understand the effect of administering the various types of OCP on women. However, the research into oral contraceptives and exercise performance is not consistent. The type of OCP administered (monophasic, biphasic or triphasic), as well as the type and dose of estrogen and progestogen within, will have varying effects on exercise. To date, research in the area of oral contraceptives and exercise capacity is sparse and much has been plagued by poor research design, methodology and small sample size. It is clear from the research to date that more randomised clinical trials are urgently required to assess the array of OCP formulations currently available to women and their concomitant effect on health and exercise capacity. Therefore, the purpose of this article is to critically appraise the literature to date and to provide a current review of the physiological scientific knowledge base in relation to the OCP and exercise performance. In addition, methodological control, design and conduct will be considered with future areas of research highlighted.

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  1. 1.

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  1. 1.

    Bennett K, White S, Crossley K. The oral contraceptive pill: a revolution for sportswomen? Br J Sports Med 1999; 33: 231–8

    Article  Google Scholar 

  2. 2.

    Lebrun CM. Effects of the menstrual cycle and oral contraceptives on sports performance. In: Drinkwater BL, editor. Women in sport. Oxford: Blackwell Science Ltd, 2000: 37–61

    Google Scholar 

  3. 3.

    Akin JW. Contraception. In: Ireland ML, Nattiv A, editors. The female athlete. Philadelphia (PA): Saunders, 2002: 157–64

    Google Scholar 

  4. 4.

    Kuhl H. Comparative pharmacology of newer progestogens. Drugs 1996; 51 (2): 188–215

    PubMed  Article  CAS  Google Scholar 

  5. 5.

    Lebrun CM, Petit MA, McKenzie DC, et al. Decreased maximal aerobic capacity with use of a triphasic oral contraceptive in highly active women: a randomised controlled trial. Br J Sports Med 2003; 37: 315–20

    PubMed  Article  CAS  Google Scholar 

  6. 6.

    Greydanus DE, Loucharnp D. Contraception in the adolescent: preparation for the 1990s. Med Clin North Am 1990; 74: 1205–24

    PubMed  CAS  Google Scholar 

  7. 7.

    Rosenberg MJ, Meyers A, Roy V. Efficacy, cycle control, and side effects of low- and lower-dose oral contraceptives: a randomized trial of 20pg and 35pg oestrogen preparations. Contraception 2000; 60: 321–9

    Article  Google Scholar 

  8. 8.

    Tortora GJ, Grabowski SR. Principles of anatomy and physiology. New York: John Wiley and Sons Inc., 2003

    Google Scholar 

  9. 9.

    Can BR. Uniqueness of oral contraceptive progestins. Contraception, 1998; 58: 523–7

    Google Scholar 

  10. 10.

    Scharnagl H, Petersen G, Nauck M, et al. Double-blind, randonuzed study comparing the effects of two monophasic oral contraceptives containing etlunylestradiol (20μg or 30μg) and levonorgestrel (100μg or 150μg) of lipoprotein metabolism. Contraception 2004; 69: 105–13

    PubMed  Article  CAS  Google Scholar 

  11. 11.

    Phillips A, Demarest K, Hahn DW, et al. Progestational and androgenic receptor binding affinities and in vivo activities of norgestimate and other progestins. Contraception 1990; 41: 399–41

    PubMed  Article  CAS  Google Scholar 

  12. 12.

    Greer JB, Modugno F, Allen GO, et al. Androgenic progestins in oral contraceptives and the risk of epithelial ovarian cancer. Obstet Gynecol 2005; 105: 731–40

    PubMed  Article  CAS  Google Scholar 

  13. 13.

    LaGuardia ED, Shangold G, Fisher A, et al. Efficacy, safety and cycle control of five oral contraceptive regimens containing norgestimate and ethinyl estradiol. Contraception 2003; 67: 431–7

    PubMed  Article  CAS  Google Scholar 

  14. 14.

    Redman LM, Weatherby RP. Measuring performance during the menstrual cycle: a model using oral contraceptives. Med Sci Sports Exerc 2004; 36: 130–6

    PubMed  Article  Google Scholar 

  15. 15.

    Fotherby K. Bioavailability of orally administered sex steroids used in oral contraception and hormone replacement therapy. Contraception 1996; 54: 59–69

    PubMed  Article  CAS  Google Scholar 

  16. 16.

    Constantini NW, Dubnou G, Lebrun CM. The menstrual cycle and performance. Clin Sports Med 2005; 24: 51–82

    Article  Google Scholar 

  17. 17.

    McNeil AW, Mozingo E. Changes in the metabolic cost of standardised work associated with the use of an oral contraceptive. J Sports Med 1981; 21: 238–44

    Google Scholar 

  18. 18.

    Montes A, Lally D, Hale RW. The effects of oral contraceptives on respiration. Fertil Steril 1983; 39 (4): 515–9

    PubMed  CAS  Google Scholar 

  19. 19.

    Notelovitz M, Zauner C, McKenzie L, et al. The effect of low-dose contraceptives on cardiorespiratory function, coagulation, and lipids in exercising young women: a preliminary report. Am J Obstet Gynecol 1987; 156: 591–8

    PubMed  CAS  Google Scholar 

  20. 20.

    Bonen A, Haynes FW, Graham TE. Substrate and hormonal response to exercise in women using oral contraceptives. J Appl Physiol 1991; 70 (5): 1917–27

    PubMed  CAS  Google Scholar 

  21. 21.

    Bemben DA, Boileau RA, Bahr JM, et al. Effects of oral contraceptives on hormonal and metabolic responses during exercise. Med Sci Sports Exerc 1992; 24 (2): 434–41

    Google Scholar 

  22. 22.

    Grucza R, Pekkarinen H, Titov EK, et al. Influence of the menstrual cycle and oral contraceptives on thermoregulatory responses to exercise in young women. Eur J Appl Physiol 1993; 67: 279–85

    Article  CAS  Google Scholar 

  23. 23.

    Sarwar R, Nicols BB, Rutherford OM. Changes in muscle strength, relaxation rate and fatiguability during the human menstrual cycle. J Physiol 1996; 493 (1): 267–72

    PubMed  CAS  Google Scholar 

  24. 24.

    Rogers SM, Baker MA. Thermoregulation during exercise in women who are taking oral contraceptives. Eur J Appl Physiol 1997; 75: 34–8

    Article  CAS  Google Scholar 

  25. 25.

    Thompson HS, Hyatt JP, DeSouza MJ, et al. The effects of oral contraceptives on delayed onset muscle soreness following exercise. Contraception 1997; 56: 59–65

    PubMed  Article  CAS  Google Scholar 

  26. 26.

    Lynch NJ, Nimmo MA. Effects of menstrual cycle phase and oral contraceptive use on intermittent exercise. Eur J Appl Physiol 1998; 78: 565–72

    Article  CAS  Google Scholar 

  27. 27.

    Giacomoni M, Falgairette G. Decreased submaximal oxygen uptake during short duration oral contraceptive use: a randomised cross-over trial in premenopausal women. Ergonomics 2000; 43 (10): 1559–70

    PubMed  Article  CAS  Google Scholar 

  28. 28.

    Coney P, Wasenik K, Langley RGB, et al. Weight change and adverse event incidence with a low-dose contraceptive: two randomised, placebo-controlled trials. Contraception 2001; 63: 297–302

    PubMed  Article  CAS  Google Scholar 

  29. 29.

    Lynch NJ, Ninuno MA. Low dosage monophasic oral contraceptive use and intermittent exercise performance and metabolism in humans. Eur J Appl Physiol 2001; 84: 296–301

    PubMed  Article  CAS  Google Scholar 

  30. 30.

    Casazza GA, Suh SH, Miller BF, et al. Effects of oral contraceptives on peak exercise capacity. J Appl Physiol 2002; 93: 1698–702

    PubMed  CAS  Google Scholar 

  31. 31.

    Tantbirojn P, Taneepanichskul S. Clinical comparative study of oral contraceptives containing 30μg ethinyestradiol/150μg levonorgestrel, and 35μg etlunyestradiol/250μg norgestimate in Thai women. Contraception 2002; 66: 401–5

    PubMed  Article  CAS  Google Scholar 

  32. 32.

    Suh S, Casazza GA, Horning MA, et al. Effects of oral contraceptives on glucose flux and substrate oxidation rates during rest and exercise. J Appl Physiol 2003; 94: 285–94

    PubMed  CAS  Google Scholar 

  33. 33.

    Ruzic L, Matkovic BR, Leko G. Antiandrogens in hormonal contraception limit muscle strength gain in strength training: comparison study. Croat Med J 2003; 44 (1): 65–8

    PubMed  Google Scholar 

  34. 34.

    Elliot KJ, Cable NT, Reilly T. Does oral contraceptive use affect maximum force production in women? Br J Sports Med 2005; 39: 15–9

    Article  Google Scholar 

  35. 35.

    Jacobs KA, Casazza GA, Suh SH, et al. Fatty acid reesterificadon but not oxidation is increased by oral contraceptive use in women. J Appl Physiol 2005; 98: 1720–31

    PubMed  Article  CAS  Google Scholar 

  36. 36.

    Redman LM, Scroop GC, Westlander G, et al. Effect of a synthetic progestin on the exercise status of sedentary young women. J Clin Endocrin Metab 2005; 90 (7): 3830–7

    Article  CAS  Google Scholar 

  37. 37.

    Laidlaw JC, Ruse JL, Gornall AG. The influence of estrogen and progesterone on aldosterone excretion. J Clin Endocrinol Metab 1962; 22: 161–71

    PubMed  Article  CAS  Google Scholar 

  38. 38.

    Gaebelein CJ, Sonny Jr LC. Vascular volume dynamics during ergonacter exercise at different menstrual phases. Eur J Appl Physiol 1982; 50: 1–11

    Article  Google Scholar 

  39. 39.

    Stachenfeld NS, Taylor HS. Effects of oestrogen and progesterone administration on exuacellular fluid. J Appl Physiol 2004; 96: 1011–8

    PubMed  Article  CAS  Google Scholar 

  40. 40.

    Spruce BA, Baylis PH, Hurd J, et al. Variation in osmoreguladon of arginine vasopressin during thehuman menstrual cycle. Clin Endocrinol 1985; 22: 37–42

    Article  CAS  Google Scholar 

  41. 41.

    Houghton BL, Holowatz LA, Mason CT. Influence of progestin bioactivity on cutaneous vascular responses to passive heating. Med Sci Sports Exerc 2005; 37: 45–51

    PubMed  Article  CAS  Google Scholar 

  42. 42.

    Charkoudian N, Johnson JM. Modification of active cutaneous vasordilation by oral contraceptive hormones. J Appl Physiol 1997; 83: 2012–8

    PubMed  CAS  Google Scholar 

  43. 43.

    Salkeld BD, MacAulay JC, Ball RW, et al. Modulation of body temperature, interleukin-6 and leptin by oral conbaceptiveuse. Neuroimmunomodulation 2001; 9: 319–25

    PubMed  Article  CAS  Google Scholar 

  44. 44.

    Kendrick ZV, Ellis GS. Effect of estradiol on tissue glycogen metabolism and lipid availability in exercised male rats. J Appl Physiol 1991; 71: 1694–9

    PubMed  CAS  Google Scholar 

  45. 45.

    Prange-Hansen A, Weeke J. Fasting serum growth hormone levels and growth hormone responses to exercise during normal menstrual cycles and cycles on contraceptives. Scand J Clin Lab Invest 1974; 34: 199–205

    Article  Google Scholar 

  46. 46.

    Diamond MP, Wentz AC, Cherrington AD. Alterations in carbohydrate metabolism as they apply to reproductive endocrinology. Fertil Steril 1988; 50: 387–97

    PubMed  CAS  Google Scholar 

  47. 47.

    Borten A, Haynes FJ, Watson-Wright W, et al. Effects of the menstrual cycle on metabolic responses to exercise. J Appl Physiol 1983; 55: 1506–13

    Google Scholar 

  48. 48.

    Bunt JC. Metabolic actions of estradiol: significance for acute and chronic exercise response. Med Sci Sports Exerc 1990; 22: 286–90

    PubMed  CAS  Google Scholar 

  49. 49.

    Hackney AC. Effects of the menstrual cycle on resting muscle glycogen content [abstract]. Horm Metab Res 1990; 22: 647

    PubMed  Article  CAS  Google Scholar 

  50. 50.

    Ahmed-Sorour H, Bailey CJ. Role of the ovarian hormones in the long term control of glucose homeostasis, glycogen formation and gluconeogensis. Ann Nutr Metab 1981; 25: 208–12

    PubMed  Article  CAS  Google Scholar 

  51. 51.

    Gillespy M, Notelovitz M, Ellington AB, et al. Effect of longterm triphasie oral contraceptive use on glucose tolerance and insulin secretion. Obstet Gynecol 1991; 78: 108–14

    PubMed  CAS  Google Scholar 

  52. 52.

    Gorlsland IF, Crook D, Simpson R, et al. The effects of different formulations of oral contraceptive agents on lipid and carbohydrate metabolism. N Engl J Med 1990; 323 (20): 1375–81

    Article  Google Scholar 

  53. 53.

    Campbell SE, Angus DJ, Febbraio MA. Glucose kinetics and exercise performance during phases of the menstrual cycle: effect of glucose ingestion. Am J Physiol Endocrinol Metab 2001; 281: E817–25

    PubMed  CAS  Google Scholar 

  54. 54.

    Daggett A, Davies B, Boobis L. Physiological and biomechanical responses to exercise following oral contraceptive use [abstract]. Med Sci Sports Exerc 1983; 15: 174

    Google Scholar 

  55. 55.

    Huisveld IA, Hospers JEH, Bemink MJE, et al. The effect of oral contraceptives and exercise on hemostatic and fibrinolytic mechanisms in training women. But J Sports Med 1983; 4: 97–103

    CAS  Google Scholar 

  56. 56.

    Littler WA, Bojorges-Buend R, Banks J. Cardiovascular dynamics in women during the menstrual cycle and oral contraceptive therapy. Thorax 1974; 29: 567–70

    PubMed  Article  CAS  Google Scholar 

  57. 57.

    Willekes C, Hoogland HJ, Keizer HA, et al. Three months of third generation oral contraceptives does not affect artery wall properties. Ultrasound Med Biol 1999; 25: 723–8

    PubMed  Article  CAS  Google Scholar 

  58. 58.

    Lehtovirta P, Kuikka J, Pyorala T. Hemalynamic effects of oral contraceptives during exercise. Int J Gynecol Obstet 1977; 15: 35–7

    CAS  Google Scholar 

  59. 59.

    Walters WAW, Lim YL. Cardiovascular dynamics in women receiving oral contraceptive therapy. Lancet 1969; II: 879–81

    Article  Google Scholar 

  60. 60.

    De Bruyn-Prevost P, Masser C, Sturbois X. Physiological response from 18-25 years women to aerobic and anaerobic physical fitness tests at different periods during the menstrual cycle. J Sports Med 1984; 24: 144–8

    Google Scholar 

  61. 61.

    McArdle WD, Katch FI, Katch VL. Exercise physiology. 5th ed. Champaign (IL): Human Kinetics, 2000

    Google Scholar 

  62. 62.

    Phillips SK, Sanderson AG, Birch K, et al. Changes in maximal voluntary force of human adductor pollicis muscle during the menstrual cycle. J Physiol 1996; 496 (2): 551–7

    PubMed  CAS  Google Scholar 

  63. 63.

    Wirth JC, Lohman TG. The relationship of static muscle funF lion to use of oral contraceptives. Med Sci Sports Exerc 1982; 14 (1): 18–20

    Google Scholar 

  64. 64.

    Petrofsky JS, LeDonne DM Rinehart JS, et al. Isometric strength and endurance during the menstrual cycle. Eur J Appl Physiol 1976; 35: 1–10

    Article  CAS  Google Scholar 

  65. 65.

    Stanczyk FZ. All progestins are not created equal. Steroids 2003; 68: 879–90

    PubMed  Article  CAS  Google Scholar 

  66. 66.

    Savage KJ, Clarkson PM. Oral contraceptive use and exerciseinduced muscle damage and recovery. Contraception 2002; 66: 67–71

    PubMed  Article  CAS  Google Scholar 

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Correspondence to Dr Melonie Burrows.

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Burrows, M., Peters, C.E. The Influence of Oral Contraceptives on Athletic Performance in Female Athletes. Sports Med 37, 557–574 (2007).

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  • Aerobic Capacity
  • Core Body Temperature
  • Levonorgestrel
  • Oral Contraceptive Pill
  • Active Woman