November 2013

Achilles tendon rupture: The influence of gender

11Achilles-iStock1773499v2The literature suggests that women are less likely than men to experience an Achilles tendon rupture. This may be because women are less capable of generating the large eccentric contractions necessary for rupturing the tendon. Estrogen may also play a protective role.

By Joseph L. Laratta, MD, and J. Turner Vosseller, MD

The Achilles tendon, the common tendon of the gastrocnemius and soleus muscles, is the largest and strongest tendon in the human body. The Achilles tendon is also the most commonly ruptured tendon in the body.1 Although the exact mechanism of rupture is not fully understood, generally speaking, two conditions must be present in the tendon for it to rupture: preexisting degeneration and an eccentric contraction of sufficient force for rupture.

The increasing participation of female athletes in sports in the US is largely attributable to the passage of Title IX of the Education Amendments of 1972 that mandated institutional support for women’s programs.2 The increased participation of girls and women in athletic activities has led to increased recognition and diagnosis of sports injuries in women. While some injuries are more common in women than in men, the incidence of Achilles tendon rupture appears to be less common in women.3 Ligamentous injury in the knee of female athletes has been more specifically investigated than injury in the Achilles tendon, allowing a better establishment of demographic and potential precipitating factors.4

As female athletic involvement continues to grow, physicians will be presented with injury patterns in women comparable to those of men in similar sports, though the likelihood of injury and causative factors may be different. A thorough understanding of the anatomy and mechanism of injury is paramount. However, the role of gender differences in neuromuscular control, biomechanics, genetics, and endocrinology are still being determined.

Achilles tendon anatomy and function

The Achilles tendon, not unlike other tendons, is composed of organized type I collagen fibers, which transmit tension from muscle to bone. The Achilles tendon origin begins near the midcalf and is the distal condensation of the soleus muscle with the gastrocnemius muscle, which inserts posteriorly on the calcaneus.5 These two muscles together make the triceps surae muscle–tendon complex, which acts to plantar flex the ankle through the Achilles tendon. The innervation of the Achilles tendon and sheath comes primarily from branches of the sural cutaneous nerve.6 The vascular supply of the tendon is age-dependent, decreasing with age.7 The posterior tibial artery supplies the tendon proximally and distally, whereas the peroneal artery supplies the midsection. Some cadaveric studies suggest a watershed area approximately 2 cm to 6 cm above the Achilles’ insertion, although this has not been supported in vivo.8

Epidemiology of Achilles tendinopathy

The incidence of Achilles rupture is 7 out of 100,000 in the general population and 12 out of 100,000 in competitive athletes.9 Achilles tendon injuries predominantly affect active young people participating in athletic activities that require quick bursts of energy. Many musculoskeletal injuries occur with a greater frequency among women. Indeed, Jones et al have shown women undergoing basic army training sustain more musculoskeletal injuries than their male counterparts, though most of those injuries were overuse injuries.10 With respect to the knee, many studies have demonstrated an increased incidence of ligamentous injures and a correspondingly increased number of surgeries for female athletes compared with male athletes.11-13 However, the incidence of Achilles tendon rupture is lower in women than in men, with a male-to-female ratio ranging between 1.67:1 and 6.90:1.14-18 More recent data suggest the true ratio is likely on the upper end of that spectrum.3

Mechanism of Achilles tendon injury

11Achilles-iStock28037790v2As noted, Achilles tendon rupture requires two things: first, degeneration (or tendinopathy) of the tendon, and second, an eccentric contraction of sufficient force to tear the tendon apart. Tendinopathy is a failed healing response. The healing response is haphazard, with disruption of collagen fibers, increased noncollagenous matrix, and disorganized proliferation of tenocytes.19,20 Jozsa et al first noted a link between Achilles tendon degeneration and rupture.1 Maffuli subsequently expanded on this work and has shown ruptured tendons are clearly more histologically degenerated than both non­ruptured tendons and tendons of people with Achilles tendinosis.21

An eccentric contraction is one in which the muscle contracts while it is lengthening. In essence, the degenerated Achilles tendon is quite literally pulled apart by a strong contraction performed while the tendon is lengthening. Numerous authors have noted the correlation between athletic activity of various types and Achilles tendon injury, with rates of injury associated with athletic activity ranging from 59% to 81%.12,15,16,22 Most recently, Vosseller et al noted that men most commonly rupture their Achilles tendons while playing basketball, while women most commonly experience such rupture playing tennis.16

Maffuli et al suggested patients with degeneration and those without degeneration are really two distinct populations, with those with degeneration having some unclear risk factor or factors predisposing to rupture not present in the other population.23 Furthermore, data show patients with symptomatic Achilles tendinosis are typically older than those who rupture the tendon. Vosseller et al showed the mean age of patients with Achilles ruptures is 43.8 years, while the mean age for those with nonacute pathology (i.e., Achilles tendinosis) was 55.1 years.16 Perhaps those patients who present with painful tendinotic tendons are those who are at risk for rupture but have not yet experienced an eccentric contraction of sufficient force to rupture the tendon.

Genetic considerations in tendon injury

As mentioned, nearly all intrinsic risk factors for injury have a genetic element. A family history of Achilles tendinopathy raises the risk of pathology nearly fivefold.24 Nine studies have investigated an association of specific genes with Achilles tendinopathy, specifically whether specific variants of genes are over- or under-expressed in Achilles tendinopathy. The genes implicated include COL1A1, COL5A1, COL12A1, and COL14A1, respectively encoding type I, V, XII, and XIV collagen proteins. Other genes encoding matrix metalloproteinases (MMPs) and inflammatory signaling molecules (IL-1β, IL-6) are also implicated.25-33

Some studies reveal a link between ABO blood group and chronic Achilles pathology, though it is more likely due to the fact that the genes for blood group are in close proximity on chromosome 9q34 to the COL5A1 gene and other genes involved directly in Achilles biology.34 The COL5A1 gene encodes for the α1 chain of type V collagen that intercalates with type I collagen fibrils and is believed to regulate fibril diameters.35

Specifically, research has shown the CC genotype of the BstUI restriction fragment length polymorphism (RFLP) within the 3′-untranslated region (UTR) of the COL5A1 gene is significantly underrepresented in participants with chronic Achilles tendinopathy.26,27 Posthumus et al showed a predilection for the CC genotype in a population of female, but not male, athletes with anterior cruciate ligament (ACL)  pathology.36 However, it would be premature to attempt to link these findings directly to risk of Achilles rupture in female athletes without further supporting data.

Metabolic considerations in tendon injury

Medical comorbidities can be associated with increased risk of Achilles injury in rabbits and, possibly, in humans. Diabetes is associated with an increased rate of advanced glycation end products (AGEs) that form covalent links within collagen fibers, altering their stability and accelerating degeneration.37,38

Tendon damage in obese individuals is often due to two distinct mechanisms: increased load-bearing tension and systemic dysmetabolism. Adiposity functions as an endocrine organ and releases bioactive peptides such as leptin, adiponectin, and lipocalin that influence mesenchymal cell phenotypes, and therefore may directly modulate tendon structure.39 In the 20th century the prevalence of obesity in the US among adult men has been greater than that among adult women.40 Moreover, overweight men tend to have more visceral fat, which substantially increases the risk of heart disease, metabolic syndrome, and diabetes.41

Biomechanical considerations

The adaptability of a tendon to loading differs across gender with respect to collagen metabolism and mechanical properties of tendon fascicles. It has been shown that well-trained men had larger patellar tendon cross-sectional areas than untrained men, though this difference was not observed in women.42 Thus, tendons in men may adapt to physical loading with increased collagen synthesis and hypertrophy while such phenomena may not be detectable in women.

Magnusson et al further demonstrated that collagen fascicles from men reached higher levels of ultimate stress than those from women, and that the tangent modulus for male fascicles exceeded those of women.38 In addition to intrinsic properties of tendons, different foot-strike patterns during running and jumping may affect Achilles tendon loading, force, and rate of injury. Rearfoot strike (RFS) patterns, in which the heel contacts the ground first, have been demonstrated to decrease peak force and average loading rate on the Achilles tendon compared with nonrearfoot strike patterns.43 Bertelsen et al showed women had an increased tendency to use a RFS pattern, thus experiencing lower force and loading rate, compared with men.44

Sex hormones in tendon injury

It is accepted that sex hormones, such as estrogen and progesterone, have effects on soft tissues through alteration of gene expression. Sex hormones have not been thoroughly studied in Achilles tendons, but have been explored in relation to ACL rupture. ACL rupture incidence is increased during the ovulatory phase of the menstrual cycle, when estrogen levels are most elevated.45 Wojtys et al further noted that oral contraceptive use decreases the injury incidence peak observed during the ovulatory phase.46

Although ligaments differ from tendons in terms of origin and insertion, both share similar mechanical function and a similar hierarchical structure that allows them to be used interchangeably in reconstructive surgery. The basic architecture consists of type I collagen arranged in a cross-linked triple-helix structure forming fibrils further organized into fascicles and further organized into the ligament or tendon proper.

Higher endogenous estrogen levels in women have been associated with lower collagen synthesis rates and, therefore, smaller tendon cross-sectional area.47 Estrogen receptors have been identified on posterior tibial tendon and flexor digitorum longus tenocytes in both male and female patients and in healthy and diseased hosts.48 Thus, sex hormones may influence the structure and function of these tendons and possibly other tendons, such as the Achilles tendon. Recent evidence suggests that estrogen attenuates fibroblast biosynthesis and may decrease collagen density in the tendon, thus decreasing tendon resistance to injury.49

Conversely, however, Bryant et al demonstrated that acute fluctuations in plasma estrogen across the menstrual cycle did not alter the strain behavior of the Achilles tendon.50 Furthermore, Burgess et al showed no difference in the mechanical properties of patellar and medial gastrocnemius tendons with acute fluctuations in either estrogen or progesterone.51,52

Chronic estrogen exposure, however, has been shown to result ultimately in less Achilles tendon strain.46 Moreover, studies on rat skeletal muscle demonstrate the inhibitory effect of female sex hormones on skeletal muscle fiber diameter, which may decrease the ability of the muscle to produce an eccentric load capable of rupturing the tendon.53


Eccentric calf exercises have primarily been the subject of research involving the treatment of midportion Achilles tendinopathy, but may also be beneficial for prevention of injury. Identification of neuromuscular imbalances, particularly highly dominant dominant legs and single-leg stance deficits, is paramount in formulating an effective preventive exercise regimen.54,55

Jumping and landing strategies with respect to unbalanced weightbearing and dangerous maneuvers should be examined closely and addressed with repetitive movements aimed at building muscle memory. Men in general have greater muscle mass and are capable of generating greater force of contraction, and may more easily exceed the maximal tensile strength of the tendon than women. However, because the pathophysiology of injury is similar across gender and the most consistently identifiable risk factor for rupture is participation in athletic activity, both would likely benefit from appropriate preventive exercise programs.

Extrinsic factors can always be modified to decrease the risk of any musculoskeletal injury. Activity modification is likely the most important prevention strategy for Achilles pathology as an eccentric contraction is always required for rupture. Alteration in shoes, orthotic equipment, and playing surface may also be beneficial in preventing injury, though their effectiveness has not been studied adequately.


The literature shows women have a lower risk of Achilles tendon rupture compared to men. Women generally are less capable of generating the large eccentric contractions necessary for rupturing the tendon. Furthermore, estrogen may play a protective role. The risk factors for tendinosis currently are not clear. Further work to shed light on those risk factors may provide greater insight into why these injuries occur less frequently in women.

Joseph L. Laratta, MD, is a resident in the Columbia University Medical Center Orthopaedic Residency training program in New York City. J. Turner Vosseller, MD, is an associate professor of orthopaedic surgery at Columbia University Medical Center.


1. Józsa L, Kvist M, Bálint BJ, et al. The role of recreational sport activity in Achilles tendon rupture. A clinical, pathoanatomical, and sociological study of 292 cases. Am J Sports Med 1989;17(3):338-343.

2. Kaestner R, Xu X. Effects of Title IX and sports participation on girls’ physical activity and weight. Adv Health Econ Health Serv Res 2007;17:79-111.

3. Vosseller JT, Ellis SJ, Levine DS, et al. Achilles tendon rupture in women. Foot Ankle Int 2013;34(1):49-53.

4. Sutton KM, Bullock JM. Anterior cruciate ligament rupture: differences between males and females. J Am Acad Orthop Surg 2013;21(1):41-50.

5. Doral MN, Alam M, Bozkurt M, et al. Functional anatomy of the Achilles tendon. Knee Surg Sports Traumatol Arthrosc 2010;18(5):638-643.

6. Andres KH, von During M, Schmidt RF. Sensory innervation of the Achilles tendon by group II and IV afferent fibers. Anat Embryol 1985;172(2):145-146.

7. Hastad K. Larsson LG, Lindholm A. Clearance of radio sodium after local deposit in the Achilles tendon. Acta Chir Scand 1959;116(3):251-255.

8. Chen TM, Rozen WM, Pan WR, et al. The arterial anatomy of the Achilles tendon: anatomical study and clinical implications. Clin Anat 2009;22(3):377-385.

9. Hess GW. Achilles tendon rupture: a review of etiology, population, anatomy, risk factors, and injury prevention. Foot Ankle Spec 2010;3(1):29-32.

10. Jones BH, Bovee MW, Harris JM, Cowan DN. Intrinsic risk factors for exercise-related injuries among male and female army trainees. Am J Sports Med 1993;21(5):705-710.

11. Arendt E, Dick R. Knee injury patterns among men and women in collegiate basketball and soccer. NCAA data and review of literature. Am J Sports Med 1995;23(6):694-701.

12. Powell JW, Barber-Foss KD. Sex-related injury patterns among selected high school sports. Am J Sports Med 2000;28(3):385-391.

13. Hewett TE. Neuromuscular and hormonal factors associated with knee injuries in female athletes. Strategies for intervention. Sports Med 2000;29(5):313-327.

14. Maffulli N, Waterston SW, Squair J, et al. Changing incidence of Achilles tendon rupture in Scotland: a 15-year study. Clin J Sports Med 1999;9(3):157-160.

15. Nillius SA, Nilsson BE, Westlin NE. The incidence of Achilles tendon rupture. Acta Orthop Scand 1976;47(1):118-121.

16. Nyyssönen T, Lüthje P, Kröger H. The increasing incidence and difference in sex distribution of Achilles tendon rupture in Finland in 1987-1999. Scand J Surg 2008;97(3):272-275.

17. Clayton RA, Court-Brown CM. The epidemiology of musculoskeletal tendinous and ligamentous injuries. Injury 2008;39(12):1338-1344.

18. Suchak AA, Bostick G, Reid D, et al. The incidence of Achilles tendon ruptures in Edmonton, Canada. Foot Ankle Int 2005;26(11):932-936.

19. Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy 1998;14(8):840-843.

20. van Dijk CN, van Sterkenburg MN, Wiegerinck JI, et al. Terminology for Achilles tendon related disorders. Knee Surg Sports Traumatol Arthrosc 2011;19(5):835-841.

21. Tallon C, Maffuli N, Ewen SW. Ruptured Achilles tendons are significantly more degenerated than tendinopathic tendons. Med Sci Sports Exerc 2001;33(12):1983-1990.

22. Levi N. The incidence of Achilles tendon rupture in Copenhagen. Injury 1997;28(4):311-313.

23. Maffulli N, Barass V, Ewen SW. Light microscopic histology of Achilles tendon ruptures: a comparison with unruptured tendons. Am J Sports Med 2000;28(6):857-863.

24. Kraemer R, Wuerfel W, Lorenzen J, et al. Analysis of hereditary and medical risk factors in Achilles tendinopathy and Achilles tendon ruptures: a matched pair analysis. Arch Orthop Trauma Surg 2012;132(6):847-853.

25. Mokone GG, Gajjar M, September Av, et al. The guanine-thymine dinucleotide repeat polymorphism within the tenascin-C gene is associated with Achilles tendon injuries. Am J Sports Medicine 2005;33(7):1016-1021.

26. Mokone GG, Schwellnus MP, Noakes TD, Collins M. The COL5A1 gene and Achilles tendon pathology. Scand J Med Sci Sports 2006;16(1):19-26.

27. September AV, Cook J, Handley CJ, et al. Variants within the COL5A1 genes are associated with Achilles tendinopathy in two populations. Br J Sports Med 2009;43(5):357-365.

28. Posthumus M, September AV, Schwellnus MP, Collins M. Investigation of the Sp1-binding site polymorphism within the COL1A1 gene participants with Achilles tendon injuries and controls. J Sci Med Sport 2009;12(1):184-189.

29. September AV, Posthumus M, van der Merwe L, et al. The COL12A1 and COL14A1 genes and Achilles tendon injuries. Int J Sports Med 2008;29(3):257-263.

30. Raleigh SM, van der Merwe L, Ribbans WJ, et al. Variants within the MMP3 gene are associated with Achilles tendinopathy: possible interaction with the COL5A1 gene. Br J Sports Med 2009;43(7):498-502.

31. Posthumus M, Collins M, Cook J, et al. Components of the transforming growth factor-beta family and the pathogenesis of human Achilles tendon pathology: a genetic association study. Rheumatology 2010;49(11):2090-2097.

32. September AV, Nell EM, O’Connell K, et al. A pathway-based approach investigating the genes encoding interleukin-1β, interleukin-6 and the interleukin-1 receptor antagonist provides new insight into the genetic susceptibility of Achilles tendinopathy. Br J Sports Med 2011;45(13):1040-1047.

33. Nell EM, van der Merwe L, Cook J, et al. The apoptosis pathway and the genetic predisposition to Achilles tendinopathy. J Orthtop Res 2012;30(11):1719-1724.

34. September AV, Schwellnus MP, Collins M. Tendon and ligament injuries: the genetic component. Br J Sports Med 2007;41(4):241-246.

35. Niyibizi C, Kavalkovich K, Yamaji T, et al. Type V collagen is increased during rabbit medial collateral ligament healing. Knee Surg Sports Traumatol Arthrosc 2000;8(5):281-285

36. Posthumus M, September AV, O’Cuinneagain D, et al. The COL5A1 gene is associated with increased risk of anterior cruciate ligament ruptures in female participants. Am J Sports Med. 2009;37(11):2234-2240.

37. Reddy GK. Cross-linking in collagen by nonenzymatic glycation increases the matrix stiffness in rabbit Achilles tendon. Exp Diabesity Res 2004;5(2):143-153.

38. Abate M, Schiavone C, Pelotti P, Salini V. Limited joint mobility in diabetes and ageing: recent advances in pathogenesis and therapy. Int J Immunopathol Pharmacol 2010;23(4):997-1003.

39. Conde J, Gomez R, Bianco G, et al. Expanding the adipokine network in cartilage: identification and regulation of novel factors in human and murine chondrocytes. Ann Rheum Dis 2011;70(3):551-559.

40. Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999-2010. JAMA 2012;307(5):491-497.

41. Matsuzawa Y, Shimomura I, Nakamura T, et al. Pathophysiology and pathogenesis of visceral fat obesity. Obes Res 1995;3 Suppl 2:187S-194S.

42. Magnusson SP, Hansen M, Langberg H, et al. The adaptability of tendon to loading differs in men and women. Int J Exp Pathol 2007;88(4):237-240.

43. Almonroeder T, Willson JD, Kernozek TW. The effect of foot strike pattern on achilles tendon load during running. Ann Biomed Eng. 2013;41(8):1758-1766.

44. Bertelsen ML, Jensen JF, Nielsen MH, e al. Footstrike patterns among novice runners wearing a conventional, neutral running shoe. Gait Posture 2013;38(2):354-356.

45. Wojtys EM, Huston LJ, Lindenfeld TN, et al. Association between the menstrual cycle and anterior cruciate ligament injuries in female athletes. Am J Sports Med 1998;26(5):614-619.

46. Wojtys EM, Huston LJ, Boynton MD, et al. The effect of the menstrual cycle on anterior cruciate ligament injuries in women as determined by hormone levels. Am J Sports Med 2002;30(2):182-188.

47. Miller BF, Hansen M, Olesen JL, et al. Tendon collagen synthesis at rest and after exercise in women. J Appl Physiol 2007;102(2):541-546.

48. Bridgeman JT, Zhang Y, Donahue H, et al. Estrogen receptor expression in posterior tibial tendon dysfunction: a pilot study. Foot Ankle Int 2010;31(12):1081-1084.

49. Lee CY, Liu X, Smith CL, et al. The combined regulation of estrogen and cyclic tension on fibroblast biosynthesis derived from anterior cruciate ligament. Matrix Biol 2004;23(5):323-329.

50. Bryant AL, Clark RA, Bartold S, et al. Effects of estrogen on the mechanical behavior of the human Achilles tendon in vivo. J Appl Physiol 2008;105(4):1035-1043.

51. Burgess KE, Pearson SJ, Onambélé GL. Menstrual cycle variations in oestradiol and progesterone have no impact on in vivo medial gastrocnemius tendon mechanical properties. Clin Biomech 2009;24(6):504-509.

52. Burgess KE, Pearson SJ, Onambélé GL. Patellar tendon properties with fluctuating menstrual cycle hormones. J Strength Cond Res 2010;24(8):2088-2095.

53. Kobori M, Yamamuro T. Effects of gonadectomy and estrogen administration on rat skeletal muscle. Clin Orthop Relat Res 1989;(243):306-311.

54. Filipa A, Byrnes R, Paterno MV, et al. Neuromuscular training improves performance on the star excursion balance test in young female athletes. J Orthop Sports Phys Ther 2010;40(9):551-558.

55. Hewett TE, Stroupe AL, Nance TA, Noyes FR. Plyometric training in female athletes. Decreased impact forces and increased hamstring torques. Am J Sports Med. 1996;24(6):765-773.

Leave a Reply

Your email address will not be published.

This site uses Akismet to reduce spam. Learn how your comment data is processed.