Indiscriminate use of the popular term “shin splints” has led to confusion about the true complexities of exercise related leg pain in athletes, which can include medial tibial stress syndrome, chronic exertional compartment syndrome, stress fractures, and tendinopathies.
By Mark F. Reinking, PT, PhD, SCS, ATC
Exercise related leg pain (ERLP), or pain experienced between the knee and ankle and associated with activity, occurs in athletes across sports and ages. Although only limited epidemiological ERLP data are available in athletic populations, the data consistently show it to be a commonly experienced condition with the greatest occurrence in distance running events including cross-country and track. However, there are reported occurrences of ERLP in other sports, including soccer, volleyball, field hockey, basketball, gymnastics, and dance.1
Almost a century ago, Hutchins2 described an ERLP condition in track athletes which he called “spike soreness.” This soreness was related to training while wearing track spikes and was located along the medial leg, causing “lameness of the shin.” Over time, the term “shin splints” has become associated with exercise related leg pain (ERLP). The origin of this term has not been clearly identified, but it has been used by some health care professionals to describe a specific pathoanatomic manifestation of ERLP, for example medial tibial stress syndrome (MTSS) or chronic exertional compartment syndrome (CECS), and by others as a generic descriptive term.
In 1967, Slocum3 wrote that shin splints “designates a symptom complex characterized by pain and discomfort in the lower part of the leg after repetitive overuse in walking and running.” The American Medical Association (AMA) defined shin splints as “pain and discomfort in the leg from repetitive running on hard surface or forcible excessive use of the foot flexors; diagnosis should be limited to musculotendinous inflammations, excluding fatigue fracture or ischemic disorder.”4 Batt5 wrote a comprehensive review of the terms associated with leg pain and concluded that shin splints is a generic term that does not refer to any specific pathology, but rather to the location of pain. Beck6 identified that this conundrum of injury terminology has delayed the advancement of the science in the area of ERLP, and suggested that the “continued use of the term ‘shin splints’ for diagnostic or research purposes is highly inappropriate.”
The generic descriptive term ERLP includes the pathoanatomic conditions of MTSS, CECS, stress fractures, tendinopathies, nerve entrapment syndromes, and vascular syndromes. Of these conditions, MTSS, stress fractures, CECS, and tendinopathies are most common,1 with vascular and nerve conditions relatively uncommon in athletes.7-9 A brief review of these common conditions follows to help clinicians recognize the common and unique clinical presentations of each of the entities.
Medial tibial stress syndrome
MTSS has been described as pain along the posteromedial border of the tibia, typically most pronounced around the intersection of the middle and distal thirds of the bone.6 In the early stages of the condition, pain is typically present early in the exercise session but may diminish during the session and resolves quickly with rest. Examination reveals diffuse pain along the medial tibial border, minimal to no swelling, and no neurological symptoms.10
The anatomical source of medial leg pain in MTSS was first thought to be the tibialis posterior muscle.11 However, anatomic studies12, 13 have provided evidence that the soleus muscle, its fascia, and the deep crural fascia are likely responsible for the posteromedial pain in MTSS. Tension on the distal tibia fascia is a result of contraction of the superficial and deep posterior compartment muscles, and this tension contributes to the development of MTSS.14
Although MTSS has been described as a pathologic condition occurring at the intersection of the fascia and bone, there is accumulating evidence that MTSS involves changes in bone as well. Work by Magnusson et al15 revealed lower tibial bone density in a group of male soccer players with MTSS compared to a group of non-athletic control subjects and a group of athletic control subjects. In a follow-up study,16 these researchers found that the lower bone density returned to normal levels following recovery from pain symptoms. Franklyn et al17 found that a lower tibial section modulus was the best predictor of the development of MTSS in male and female athletes, clearly suggesting that the tibial bone geometry is involved in the development of MTSS. Beck6 described a continuum of “bone stress-failure” with MTSS being the early stage of the continuum and stress fracture being the late stage.
There is very little evidence to support treatment choices for MTSS; most recommended treatments are largely based on anecdotal reports. Certainly early treatment of MTSS symptoms should include rest from the offending activity, cross-training activities, and cryotherapy. Other recommendations include ankle muscle strengthening, stretching, and a progressive return to running but there is little, if any, evidence to support such recommendations.6,10 In a survey of collegiate athletes who were prescribed foot orthotics for MTSS, most reported that the orthotics helped their condition.18 Loudon and Dolphino19 used a prospective cohort design to assess the effectiveness of the combination of off-the-shelf foot orthoses and calf stretching on medial tibial stress syndrome. They found that male subjects responded better than female subjects and that participants with symptoms of shorter duration also responded better to the orthotic-stretching intervention.
Stress fracture of tibia and fibula is the late stage of the bone stress-failure continuum. Bone remodeling is a dynamic process, with the mineral component constantly being remodeled based on the imposed stresses. In the case of a stress fracture, excessive repetitive microtraumatic stress results in bone mineral resorption exceeding deposition. This causes a net loss of bone mineral content, resulting in a fatigue fracture.20 Stress fractures of the tibia are more common than the those of the fibula, consistent with the greater tibial loads during weight bearing activities.21
The typical presentation of stress fracture is gradual onset of bone pain with running and jumping; in the early stage, pain decreases with rest. As time passes and the athlete attempts to maintain his or her activity level, pain occurs during and after exercise and may be present during daily activities.22 The gold standard diagnostic technique for stress fracture is the triple-phase bone scan.22 In this imaging modality, a stress fracture is visualized as intense uptake of radiotracer in a focal site along the bone.
Bennell and Brukner23 reported that the high risk sports for stress fracture include running and ballet. Johnson, Weiss, and Wheeler24 tracked stress fracture injuries at a Division II institution. In the 914 athletes followed over a two-year period, there were 34 stress fractures in 24 athletes. The most common fracture site was the tibia (13 stress fractures, nine in female athletes and four in male athletes). Goldberg and Pecora25 collected stress fracture data in collegiate athletes over a three-year period. The annual incidence was 1.9%, but they identified that 67% of the injuries occurred in freshman athletes, suggesting changes in training volume as a potential etiological factor. Tibial stress fractures were the second most common stress fracture site, with the metatarsals as the most common site.
A preponderance of data show that female athletes are at greater risk for stress fractures than male athletes.20,21,23,26-28 Bennell et al29 reviewed risk factors for stress fracture and concluded that the female athlete triad of menstrual dysfunction, disordered eating with restricted caloric intake, and decreased bone mineral density increase the risk in female athletes.
In a systematic review of prevention and treatment of stress fractures in athletes, Shaffer and Uhl30 reported that although no high level evidence supports any prevention strategies, limited evidence supports the use of shock absorbing insoles for stress fracture prevention. At present, like MTSS, treatment of stress fractures tends to be based on accumulated anecdotal evidence and initially includes rest from the offending activity, weightbearing modification if necessary, and cross-training activities. Return of the athlete to sport involves a graded progression of activity with close monitoring of athlete symptoms.
Chronic exertional compartment syndrome
Chronic exertional compartment syndrome (CECS) is a pathoanatomic condition in the ERLP complex that is particularly challenging from a diagnostic and therapeutic viewpoint. The leg has five compartments (anterior, lateral, superficial posterior, deep posterior, and posterior tibialis) separated by inelastic fascial layers which enclose the ankle and foot musculature.31 During exercise, there is an increase in muscle volume within the associated compartment, increasing compartmental pressure. In normal subjects, the increase in compartment pressure is minimal, but in the case of an athlete with CECS, the compartment pressure elevates with exercise to the point that it interferes with compartmental perfusion. The precise cause of high intracompartmental pressures is not yet known but is thought to involve fascial tightness, tissue swelling, or muscle hypertrophy.31
The onset of CECS is distinct from MTSS or stress fracture as the athlete describes pain that is not present at the beginning of the exercise session but begins at a predictable time following exercise initiation. The pain is characterized as cramping, burning, or tightness, and may or may not subside immediately after exercise. There may be complaints of distal numbness and weakness of muscles controlling the ankle and foot.31 The standard diagnostic test for CECS is the compartmental pressure study. This study involves the use of a pressure measurement device connected to a needle that is inserted into the muscle compartment of interest. A positive test for CECS is elevated intracompartmental pressure with exercise, although resting pressure may be elevated as well. The anterior compartment is the most common site of symptoms.31,32
At present, there is a paucity of evidence to support non-surgical treatment for CECS. Blackman et al33 reported that a combination of massage and stretching increased the amount of dorsiflexion work performed prior to onset of symptoms, but there was no change in the intracompartmental pressures. Athletes with CECS may require compartmental fasciotomy for symptom reduction.31,34
The fourth common pathoanatomic condition causing ERLP is tendinopathy. Common sites of tendon pain in athletes manifesting as leg pain include the Achilles and posterior tibialis tendons. Khan, Cook, Taunton, and Bonar35 proposed that most tendinopathy is a result of tendinosis, or tendon degeneration, rather than tendinitis, an inflammatory tendon condition. These authors base their contention on histologic evidence, which shows a conspicuous absence of inflammatory cells in painful tendon tissue. Tendon pain may also be a result of tenosynovitis (paratenonitis), an inflammation of the tendon sheath.
The athlete with early stage tendinopathy may have pain only after exercise, but as the condition progresses to a chronic nature, the pain occurs during and after exercise and may become constant with all daily activities in late stage tendinopathy.36 The location of the pain along the tendon is variable; in some cases it may be at the insertion site, in other cases it may be in the midsubstance of the tendon or at the muscle-tendon junction. The tendon pain is worsened with resisted testing of the involved muscle.
Interventions for tendon pain also are largely based on anecdotal reports and clinical habits. Such interventions include relative rest, cross-training, stretching, ultrasound, iontophoresis, cryotherapy, counterforce bracing, foot orthotics and non steroidal anti-inflammatory medications. At present, the non-surgical intervention that has been accumulating supportive evidence is the use of eccentric strength training.37-43
Exercise related leg pain risk factors
In a systematic review on the prevention of ERLP,44 the authors concluded there is “little objective evidence to support the widespread use of any existing interventions to prevent shin splints.” One reason for the lack of evidence is that the risk factors for ERLP are not well understood. Over the past 15 years, I have collaborated with colleagues in the study of ERLP risk factors. Our study populations have included collegiate athletes, high school athletes, and community runners. In an early study on MTSS in high school runners, we found excessive foot pronation to be a risk factor for MTSS,45 and this finding was supported in a study of ERLP risk factors in female collegiate athletes.46 However, four other studies of college and high school athletes have not supported this relationship.47-50 We have examined other potential risk factors including age, sex, body mass index, years running, training mileage, race pace in runners, calf muscle length, menstrual function, and history of ERLP. To date, the only consistent risk factor we have identified for ERLP across athletes is a previous episode of ERLP.
In summary, it is evident from this review that in spite of the common occurrence of ERLP in athletes, there is much work to be done to better understand these conditions. The development of effective prevention and treatment strategies requires well developed knowledge of the factors associated with the development of the condition. Another barrier to addressing this problem is the indiscriminate use of terms like “shin splints”, which can unintentionally lead clinicians to not consider the complexity of the pathoanatomic conditions manifested as ERLP. A competent examination that identifies the location, nature, and chronology of symptoms as well as neuromusculoskeletal impairments is essential in the development of appropriate treatment. There is a need for ongoing investigations leading to better understanding of the pathoanatomic conditions and the identification of modifiable and nonmodifiable risk factors leading to these conditions.
Mark F. Reinking, PT, PhD, SCS, ATC, is an associate professor in the department of physical therapy & athletic training at Saint Louis University in St. Louis, MO.
1. Ugalde V, Batt ME. Shin splints: Current theories and treatment.Crit Rev Phys Rehabil Med 2001;13(3):217-253.
2. Hutchins CP. Explanation of spike soreness in runners. Am Phys Ed Rev 1913;18:31-35.
3. Slocum DB. The shin splint syndrome. Medical aspects and differential diagnosis. Am J Surg 1967;114(6):875-881.
4. American Medical Association, Subcommittee on Classification of Sports Injuries. Standard nomenclature of athletic injuries. Chicago: American Medical Association; 1966: 122-126.
5. Batt ME. Shin splints–a review of terminology. Clin J Sports Med 1995;5(1):53-57.
6. Beck BR. Tibial stress injuries. An aetiological review for the purposes of guiding management. Sports Med 1998;26(4):265-279.
7. Bradshaw C. Exercise-related lower leg pain: vascular. Med Sci Sports Exerc 2000;32(3 Suppl):S34-S36.
8. McCrory P. Exercise-related leg pain: neurological perspective. Med Sci Sports Exerc 2000;32(3 Suppl):S11-S14.
9. McCrory P, Bell S, Bradshaw C. Nerve entrapments of the lower leg, ankle and foot in sport. Sports Med 2002;32(6):371-391.
10. Kortebein PM, Kaufman KR, Basford JR, Stuart MJ. Medial tibial stress syndrome. Med Sci Sports Exerc 2000;32(3 Suppl):S27-S33.
11. James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med 1978;6(2):40-50.
12. Beck BR, Osternig LR. Medial tibial stress syndrome. The location of muscles in the leg in relation to symptoms. J Bone Joint Surg Am 1994;76(7):1057-1061.
13. Michael RH, Holder LE. The soleus syndrome. A cause of medial tibial stress (shin splints). Am J Sports Med 1985;13(2):87-94.
14. Bouche RT, Johnson CH. Medial tibial stress syndrome (tibial fasciitis): a proposed pathomechanical model involving fascial traction. J Am Podiatr Med Assoc 2007;97(1):31-36.
15. Magnusson HI, Westlin NE, Nyqvist F, et al. Abnormally decreased regional bone density in athletes with medial tibial stress syndrome. Am J Sports Med 2001;29(6):712-715.
16. Magnusson HI, Ahlborg HG, Karlsson C, et al. Low regional tibial bone density in athletes with medial tibial stress syndrome normalizes after recovery from symptoms. Am J Sports Med 2003;31(4):596-600.
17. Franklyn M, Oakes B, Field B, et al. Section modulus is the optimum geometric predictor for stress fractures and medial tibial stress syndrome in both male and female athletes. Am J Sports Med 2008;36(6):1179-1189.
18. Eickhoff CA, Hossain SA, Slawski DP. Effect of prescribed foot orthoses on medial tibial stress syndrome in collegiate cross-country runners. Clin Kinesiol 2000;54(4):76-80.
19. Loudon JK, Dolphino MR. Use of foot orthoses and calf stretching for individuals with medial tibial stress syndrome. Foot Ankle Spec 2010;3(1):15-20.
20. Arendt EA. Stress fractures and the female athlete. Clin Orthop 2000;372:131-138.
21. Nattiv A. Stress fractures and bone health in track and field athletes. J Sci Med Sport 2000;3(3):268-279.
22. Brukner P. Exercise-related lower leg pain: bone. Med Sci Sports Exerc 2000;32(3 Suppl):S15-S26.
23. Bennell KL, Brukner PD. Epidemiology and site specificity of stress fractures. Clin Sports Med 1997;16(2):179-196.
24. Johnson AW, Weiss CB Jr, Wheeler DL. Stress fractures of the femoral shaft in athletes—more common than expected. A new clinical test. Am J Sports Med 1994;22(2):248-256.
25. Goldberg B, Pecora C. Stress fractures: a risk of increased training in freshmen. The Phys Sportsmed 1994;22(3):68-78.
26. Nattiv A, Armsey TD Jr. Stress injury to bone in the female athlete. Clin Sports Med 1997;16(2):197-224.
27. Nelson BJ, Arciero RA. Stress fractures in the female athlete. Sports Medicine and Arthroscopy Review. 2002;10:83-90.
28. Zeni AI, Street CC, Dempsey RL, Staton M. Stress injury to the bone among women athletes. Phys Med Rehabil Clin N Am 2000;11(4):929-947.
29. Bennell K, Matheson G, Meeuwisse W, Brukner P. Risk factors for stress fractures. Sports Med 1999;28(2):91-122.
30. Shaffer SW, Uhl TL. Preventing and treating lower extremity stress reactions and fractures in adults. J Athl Train 2006;41(4):466-469.
31. Blackman PG. A review of chronic exertional compartment syndrome in the lower leg. Med Sci Sports Exerc 2000;32(3 Suppl):S4-S10.
32. Hutchinson MR, Ireland ML. Chronic exertional compartment syndrome: gauging pressure. Phys Sportsmed 1999;27(5):90-92.
33. Blackman PG, Simmons LR, Crossley KM. Treatment of chronic exertional anterior compartment syndrome with massage: a pilot study. Clin J Sports Med 1998;8(1):14-17.
34. Black KP, Taylor DE. Current concepts in the treatment of common compartment syndromes in athletes. Sports Med 1993;15(6):408-418.
35. Khan KM, Cook JL, Taunton JE, Bonar F. Overuse tendinosis, not tendinitis part 1: a new paradigm for a difficult clinical problem. Phys SportsMed 2000;28(5):38-47.
36. Curwin S, Stanish WD. Tendonitis: Its etiology and treatment. Lexington, MA: DC Heath & Co; 1984.
37. Alfredson H, Pietila T, Jonsson P, Lorentzon R. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. Am J Sports Med 1998;26(3):360-366.
38. Fyfe I, Stanish WD. The use of eccentric training and stretching in the treatment and prevention of tendon injuries. Clin Sports Med 1992;11(3):601-624.
39. Ohberg L, Lorentzon R, Alfredson H. Eccentric training in patients with chronic Achilles tendinosis: normalised tendon structure and decreased thickness at follow up. Br J Sports Med 2004;38(1):8-11.
40. Purdam CR, Jonsson P, Alfredson H, et al. A pilot study of the eccentric decline squat in the management of painful chronic patellar tendinopathy. Br J Sports Med 2004;38(4):395-397.
41. Rees JD, Wilson AM, Wolman RL. Current concepts in the management of tendon disorders. Rheumatology (Oxford) 2006;45(5):508-521.
42. Wilson JJ, Best TM. Common overuse tendon problems: A review and recommendations for treatment. Am Fam Physician 2005;72(5):811-818.
43. Young MA, Cook JL, Purdam CR, et al. Eccentric decline squat protocol offers superior results at 12 months compared with traditional eccentric protocol for patellar tendinopathy in volleyball players. Br J Sports Med 2005;39(2):102-105.
44. Thacker SB, Gilchrist J, Stroup DF, Kimsey CD. The prevention of shin splints in sports: a systematic review of literature. Med Sci Sports Exerc 2002;34(1):32-40.
45. Bennett JE, Reinking MF, Pluemer B, et al. Factors contributing to the development of medial tibial stress syndrome in high school runners. J Orthop Sports Phys Ther 2001;31(9):504-510.
46. Reinking MF. Exercise-related leg pain in female collegiate athletes: the influence of intrinsic and extrinsic factors. Am J Sports Med 2006;34(9):1500-1507.
47. Reinking MF, Austin TM, Hayes AM. Exercise-related leg pain in collegiate cross-country athletes: extrinsic and intrinsic risk factors. J Orthop Sports Phys Ther 2007;37(11):670-678.
48. Reinking MF, Austin TM, Hayes AM. Risk factors for self-reported exercise-related leg pain in high school cross-country athletes. J Athl Train 2010;45(1):51-57.
49. Reinking MF, Hayes AM. Exercise related lower leg pain in collegiate cross country runners. J Orthop Sports Phys Ther 2003;33(2):Abstract PL-10:A49-A50.
50. Reinking MF, Hayes AM. Intrinsic factors associated with exercise-related leg pain in collegiate cross-country runners. Clin J Sport Med 2006;16(1):10-14.