Calf muscle strain is one of the most common muscle injuries in high-performance athletes and contributes to substantial player downtime because of its high mean time to return to sport and occurrence during critical periods in the competitive season1-3. Published reports on lower-body muscle strain have provided frequent updates on the rehabilitation of high-profile muscle groups, such as the hamstring muscles, and improvements to calf strain management are seldom discussed despite the prevalence of these injuries in competitive sports. In this article, we discuss the diagnosis, treatment, outcomes, risk factors, and prevention of calf muscle strain in athletes.
First described in 1883, calf strain is also known as “tennis leg” due to its frequent occurrence in that sport4-7. Although the seasonal injury incidence, defined as the number of injuries per team per season, is notable in tennis8-10 (0.3 to 0.8), calf strains are not unique to tennis and have since been reported in numerous other professional and collegiate sports such as American football11,12 (seasonal injury incidence, 2.1 to 2.3), Australian football13,14 (1.8 to 2.9), basketball (1.2)15, and soccer (1.3 to 2.3)16-20 (Table I). Calf injury is most prevalent among athletes 22 to 28 years of age, more frequently affects men, and presents as a recurrent injury in approximately 19% to 31% of cases3,13,16,19-24. Rehabilitation is generally conservative, with a recovery period that ranges from immediate return to play to multiple months of missed practice or playing time2,3,12,13,19.
TABLE I -
Incidence of Calf Strains in Professional and Collegiate Sports*
||Seasonal Injury Incidence†
||Injuries per 1,000 Match Hours
| Mack11 (2020)
||Athletes from 32 National Football League teams
||4 seasons (2015 to 2019)
| Werner12 (2017)
||Retrospective case series
||Athletes from 1 National Football League team
||12 seasons (2003 to 2015)
| Green13 (2020)
||Athletes from 16 Australian Football League clubs
||4 seasons (2014 to 2017)
| Orchard14 (2013)
||4,492 athletes from the Australian Football League
||20 seasons (1992 to 2012)
| McKay15 (2001)
||190 elite and recreational Australian basketball athletes
||2 seasons (1991 to 1992)
| Nilstad16 (2014)
||173 athletes from 12 elite Norwegian soccer clubs
||1 season (2009)
| Hägglund17 (2013)
||1,401 athletes from 26 elite European soccer clubs across 10 countries
||9 seasons (2001 to 2010)
| Bengtsson18 (2013)
||621 athletes from 27 elite European soccer clubs across 10 countries
||11 seasons (2001 to 2012)
| Ekstrand19 (2011)
||2,299 athletes from 51 elite European soccer clubs
||8 seasons (2001 to 2009)
| Faude20 (2006)
||143 athletes from 12 German national league soccer teams
||1 season (2003 to 2004)
| Dakic8 (2018)
||52 athletes from the Australian Open
||1 season (2015)
| Colberg9 (2015)
||58 athletes from 4 collegiate tennis teams
| Winge10 (1989)
||89 athletes from 13 elite Danish tennis teams
||1 season (1984)
*NA = not available.
†Seasonal injury incidence is defined as the number of calf strain injuries per team per season.
‡This sport is referred to as “football” in most countries outside the United States.
The risk of injury to the individual triceps surae muscles appears to be somewhat sport-dependent. For example, isolated gastrocnemius strain is the predominant calf strain injury in American football, whereas isolated soleus strain is more common in Australian football (Table II)12,13,22. Moreover, gastrocnemius strain is associated with high-intensity running, acceleration, and deceleration activities, whereas soleus strain is more likely to occur during steady-state running activities13. Differences between muscles with respect to biomechanical function or muscle fiber profiles may contribute to this observation13. The gastrocnemius, which flexes the leg at the knee and plantar flexes the foot at the ankle, is dense in fast-twitch muscle fibers adapted for rapid contraction1,5,7,25. The soleus, which contributes to plantar flexion, is dense in slow-twitch muscle fibers adapted for postural control1,2,26,27.
TABLE II -
Incidence of Gastrocnemius, Soleus, and Plantaris Strains in Professional Sports*
| Werner12 (2017)
||Retrospective case series
||Athletes from 1 National Football League team for 12 seasons
| Green13 (2020)
||Athletes from 16 Australian Football League clubs for 4 seasons
| Waterworth22 (2017)
||Retrospective case series
||63 athletes from the Australian Football League for 5 seasons
*NA = not available.
†Other includes disruptions to the tibialis posterior, peroneus longus, or Achilles tendon, as well as concomitant tissue disruption for which a primary tissue injury was not specified.
The classic pathogenesis of a gastrocnemius tear involves knee extension with sudden ballistic foot movement from dorsiflexion to plantar flexion1,6,7,28,29. When the gastrocnemius is maximally stretched, the immediate contraction of the tensioned muscle can abruptly rupture the medial head of the gastrocnemius at the myotendinous junction7,28. The medial head of the gastrocnemius is more prone to injury than the lateral head, possibly because the medial head contributes more to muscle activity23. Imaging studies have attributed a 2:1 ratio of tears to the medial head compared with the lateral head of the gastrocnemius30,31.
Soleus strain is an overuse condition from repetitive, passive dorsiflexion of the foot with the knee bent23,29. In runners, this posture is observed while running uphill23,29. Because the mechanism for soleus rupture is associated with overuse, a soleus injury is subacute, with a gradual and cumulative effect, although acute strain can manifest in fatigued athletes23,32.
Although relatively rare, an isolated rupture of the plantaris muscle can occur at the proximal muscle belly or the midportion of the-plantaris tendon5,29. The pathogenesis is similar to that of a gastrocnemius tear and involves knee extension with ballistic foot plantar flexion23. Athletes with isolated lesions can retain a full range of motion without reduction in strength29. However, a plantaris injury is more often diagnosed concomitant with traumatic knee injury, such as lesions of the anterior cruciate ligament or the posterolateral corner5.
An acute strain of the gastrocnemius can present with an audible pop at the onset of the injury, followed by dull to severe pain and swelling in the posterior lower limb within 24 hours1,6,28. The pain can be latent at the time of the injury, manifesting only after the athlete tries to stand, walk, or plantar flex the foot28,33. Individuals are often unable to perform a heel raise on the affected side because of compromised plantar flexion6. Palpation may identify tenderness at the muscle insertion into the Achilles tendon or, in more severe cases, a subcutaneous defect in the medial gastrocnemius from muscle retraction1,6,7,23,28. In addition, mild to severe ecchymosis can appear at the rupture site23,28.
In contrast to gastrocnemius strains, soleus strains are typically subacute and present with muscle tension and tightness, gradual pain development over the course of days to weeks, and mild swelling and disability1. Palpation may identify tenderness deep within the lateral calf and distal to the gastrocnemius muscle bellies1,23. Soleus muscle contraction can be evaluated with the knee in maximal flexion, in which case the soleus becomes the primary contributor to plantar flexion. Imaging is recommended to identify potential concomitant ruptures of both the gastrocnemius and the soleus1,27.
An isolated plantaris strain is rare and can be clinically indistinguishable from a gastrocnemius strain, requiring imaging for a definitive diagnosis1. Plantaris rupture can present with an audible pop at the onset of the injury, and athletes with isolated lesions may retain a full range of motion without reduction in strength23,29. More often, plantaris strain is concomitant with traumatic lesions of the knee, such as those involving the anterior cruciate ligament or posterolateral corner5.
Within the triceps surae, ruptures are possible in the medial or lateral gastrocnemius, soleus, or plantaris muscles, and concomitant injuries of the gastrocnemius and soleus occur in 17% of cases1,27. Moreover, defects in the triceps surae can present with symptoms similar to those of thrombophlebitis, posterior compartment syndrome, popliteal artery entrapment syndrome, a torn Achilles tendon, or a ruptured Baker’s cyst6,7,28. Tenderness in the medial gastrocnemius belly can be normal and is common even in uninjured athletes34. Posterior leg pain can also be referred from defects in other muscles, such as the popliteus, peroneus longus, and other deep posterior compartment or lateral compartment muscles. Physical examination and imaging are useful to confirm the differential diagnosis and inform the best treatment strategy.
Palpation, strength testing, and passive flexion and extension of the knee and ankle joints are effective methods to identify areas of tenderness, tightness, swelling, and, in more severe cases, subcutaneous gaps or masses1,6,7,23,28. Tenderness in the medial gastrocnemius belly or the musculotendinous junction indicates gastrocnemius strain, the most common calf injury, and tenderness distal and lateral to the gastrocnemius implicates the soleus1,23. A palpable defect indicates a possible muscle retraction with complete fiber disruption. Palpable contractions that are spasmodic and involuntary indicate muscle cramps35.
As previously mentioned, athletes with gastrocnemius defects are often unable to perform a heel raise on the affected side because of compromised plantar flexion6. Muscle contraction can be evaluated with the knee in maximal extension, which isolates the contribution of the gastrocnemius to plantar flexion1. Conversely, the soleus can be evaluated with the knee bent from 90° to maximal flexion, which makes it the primary contributor to plantar flexion1. Thus, close attention to knee posture can improve the accuracy of strength tests and inform the diagnosis.
Achilles tendon pathology is also a concern for clinicians. Achilles tendon rupture is best evaluated with the Simmonds triad, which includes the Simmonds-Thompson calf squeeze test, the Matles angle-of-declination test, and palpation for tendon defects near the insertion into the calcaneus1,36. A comparative study showed that positive results on at least 2 of the 3 tests provided confirmation of Achilles tendon rupture in all cases, which indicates high sensitivity for the Simmonds triad36.
Although the diagnosis of calf strain is often based on clinical findings, imaging is valuable to confirm the location of the strain and the grade of the injury1,7. This information guides the choice and duration of rehabilitation and influences return-to-play considerations, which may have financial and strategic consequences for professional teams1,6. Musculoskeletal ultrasound and magnetic resonance imaging (MRI) are appropriate imaging modalities in the context of calf strain injury and have the additional benefit of detecting intramuscular fluid collection, which is associated with delayed return to play1,6,7,12,28.
MRI is an accurate and reliable method for examining muscle fiber integrity and continuity. It can differentiate gastrocnemius strain from other soft-tissue injuries, such as soleus strain or Achilles tendon pathology, and can evaluate the integrity of surrounding connective tissue2,7,28,32. Connective tissue defects are often associated with longer rehabilitation time than muscle tears alone, and studies have identified additional MRI characteristics as indicators for return to play, making MRI useful for the continual evaluation of recovery for professional athletes2,12,13,22,28,32. Moreover, fluid-sensitive MRI can reveal edema, hemorrhage, and hematoma7.
Ultrasound is often considered for its affordability, accessibility, and convenience1,7,29,37,38. Although no direct comparison of ultrasound and MRI diagnostic accuracy is available for calf strain, a comparison of the imaging modalities in the evaluation of hamstring strain found no significant difference39. Ultrasound can provide a differential diagnosis for partial-thickness and full-thickness calf strains and is useful for evaluating edema, hemorrhage, hematoma, and thrombophlebitis7,28. Doppler ultrasound can readily detect deep vein thrombosis, which is sometimes concomitant with gastrocnemius strain7,28. Ultrasound is particularly convenient for its short imaging time, dynamic visualization, and easy comparison with the contralateral, uninjured leg38. However, there are no guidelines that define specific ultrasound characteristics as indications for return to play in professional sports.
Calf strain is graded on the basis of physical and imaging parameters (Table III). A grade-I (mild) strain is associated with micro-tears in muscle fibers that cause mild pain or soreness but minimal reduction in strength and range of motion1. A grade-II (moderate) strain corresponds to a partial muscle tear that causes appreciable reduction in strength and range of motion. Athletes with partial tears are sometimes unable to walk and often have pain and swelling from edema or hemorrhage1. A grade-III (severe) strain signifies complete rupture, which presents with severe pain and disability, loss of muscle function, and extensive edema and hemorrhage1.
TABLE III -
Grades of Injury in Calf Strains and Recovery Times1,2,42
||Tenderness or swelling with no reduction in strength or range of motion
||Edema or fluid adjacent to intact muscle fiber
||0 to 2 weeks
||Mild pain, tenderness, and swelling; minimal reduction in strength and range of motion
||Micro-tears with <10% muscle fiber disruption
||1 to 4 weeks
||Moderate pain, tenderness, and swelling; reduction in strength and range of motion
||Partial tear with 10% to 50% muscle fiber disruption
||2 to 5 weeks
||Severe pain and disability with complete loss of muscle function; palpable subcutaneous defect
||Complete tear with >50% muscle fiber disruption
||Conservative or operative
||5 to 10 weeks for conservative treatment or 24 weeks for operative treatment
*Recovery times are sport-dependent.
Nonoperative management is effective for most calf strain injuries. Treatment generally consists of rest, ice, compression, elevation, and nonsteroidal anti-inflammatory drugs (NSAIDs) in the acute phase, followed by appropriate stretches and exercise in the subacute phase1,6,7,23,28. A delayed progression from the acute phase to the subacute phase should trigger reevaluation for intramuscular hematoma or extensive tissue damage40. Operative treatment, although rarely indicated, may be considered in more severe cases with complete grade-III rupture or complications1,6,7,28,41. Another common event in athletes is exercise-induced muscle cramps, which can be alleviated with passive stretches of the calf muscle35. The utility and evidence for blood flow restriction therapy, deep water running, lower-body positive-pressure therapy (LBPPT), platelet-rich plasma, and stem cell therapy are discussed as well.
In the acute phase, treatment is designed to protect the injured tissue by reducing activity, managing pain, and preventing hemorrhage or other complications1,7,23. This is accomplished with rest, ice, compression, elevation, and NSAIDs1,6,7,23,28. In the first 24 to 72 hours, activities should be limited to allow the injured leg to be rested in an elevated position and NSAID use should be carefully managed to prevent bleeding from antiplatelet effects1,6,7. Alternatively, acetaminophen and celecoxib, which do not interfere with platelet function, may be used for pain management1. Cryotherapy, ice packs, compression bandages, and neoprene sleeves may be used to manage symptoms and to facilitate early ambulation1,6,7,23,34. High compression bandages that exert 20 to 30 mm Hg of pressure have been recommended in published reports, and some evidence has suggested that compression bandage use can improve recovery by up to 7 days6,23. Crutches, boots, or heel lifts may be used to protect the injured area and control pain1,7,23. Soft-tissue massage and moist heat application are generally contraindicated in the acute phase as these techniques increase the risk of hemorrhage1,7.
In the subacute phase, the body repairs the soft-tissue damage and forms scar tissue. Treatment is designed to restore mobility, prevent muscle atrophy or contracture, and guide tissue regeneration to optimize functional improvement28. Rehabilitation includes passive and active stretches, soft-tissue techniques, muscle strengthening, and proprioception exercises for 2 weeks, followed by general and sport-specific reconditioning exercises1,6,7,28. Stretching elongates the intramuscular scar tissue in preparation for strengthening exercises, and altering the degree of knee flexion can isolate the gastrocnemius and soleus during stretches1,28. Soft-tissue techniques such as low-level laser therapy, therapeutic ultrasound, electrical stimulation, and friction massage are also appropriate1,7. As range of motion improves and pain subsides, strength training can progressively incorporate isometric, isotonic, and dynamic exercises as tolerated without pain1,7,28,40,42. Finally, general and sport-specific reconditioning helps to restore strength and agility7,28.
The mainstay of treatment is nonoperative. Operative management, although rarely indicated, may be considered in the most severe cases with complete grade-III ruptures, contractures, fibrosis, substantial hematoma, acute compartment syndrome, or myositis ossificans1,6,7,28,40,41. In cases of complete muscle rupture, the inability to stand on the metatarsal heads of the leg with a calf strain has been described as an indication for a surgical procedure41. Cheng et al. published a surgical technique for complete gastrocnemius rupture41. Surgical intervention reconstructs anatomical structures and removes fibrous scar tissue41. Postoperative management includes use of a compression bandage to immobilize the repaired muscle and ambulation with crutches. The patient is non-weight-bearing for the first 4 to 6 weeks and then weight-bearing with progression to physical therapy40. Recovery from the surgical procedure is gradual over the course of 6 months42.
Additional therapies for muscle rehabilitation include blood flow restriction therapy (BFRT), deep water running, LBPPT, and nascent therapies such as platelet-rich plasma, and, to a limited extent, stem cell therapy.
BFRT involves light resistance training with the use of a restriction band proximally on the extremity to occlude venous blood outflow while maintaining arterial blood inflow. Light resistance training exerts mechanical stress on the muscles, and the use of a restriction band induces tissue hypoxia and stimulates anaerobic metabolism43-45. Research has demonstrated that BFRT can increase muscle strength, hypertrophy, and angiogenesis compared with unrestricted light resistance training, but less muscle is recruited compared with unrestricted heavy resistance training43-48. Although the biological mechanism is unknown, in theory, the combination of mechanical and metabolic stress is thought to facilitate cellular signaling pathways that lead to protein synthesis, fast-twitch muscle fiber recruitment, and stimulation of myogenic stem cells43-45. Because heavy resistance training is often contraindicated in the early stages of recovery, BFRT may be useful as a progressive rehabilitation method to promote the regeneration and healing of muscle43,44.
Hydrotherapy techniques such as deep water running can be considered for muscle rehabilitation. Aquatic exercise has been practiced since the Romans first described the use of hydrotherapy to manage orthopaedic conditions49. Hydrotherapy uses the buoyancy, viscosity, and hydrostatic pressure of water to counterbalance gravity and provide resistance and compression50,51. Deep water running is one technique for weight-supported aerobic training, in which the body is partially submerged in water. The upward buoyant force, which is equal to the weight of water that the body displaces, acts in opposition to the downward force of gravity50-53. Thus, submersion up to various body parts offloads body weight: by 40% up to the hip, by 50% up to the waist, by 60% up to the sternum, or by 85% up to the shoulders50-53. The depth of immersion can be controlled using the slope of the pool, flotation equipment, or hydrotherapy treadmills that encapsulate users in aquatic cabins made of glass50. Deep water running has 2 forms: a high-knee style (high-knee deep water running) with stair-stepping movements, and a cross-country style (cross-country deep water running) with kinematics similar to treadmill running51. Both high-knee deep water running and cross-country deep water running have been observed to reduce gastrocnemius activation in comparison with treadmill running54,55. An environment that reduces muscle activation allows for active recovery with a decreased risk of reinjury50,51.
LBPPT has emerged as a popular alternative to hydrotherapy and other weight-supported rehabilitation methods. Lower-body positive-pressure treadmills, such as the AlterG, allow for weight-supported exercise in which users can designate the percentage of their body weight to be borne by the treadmill in addition to adjustments for speed and incline56-58. Users wear neoprene shorts that secure to a positive air pressure chamber of the treadmill. The differential air pressure of the chamber produces a variable force that lifts users, thereby decreasing the impact of gravitational forces and body weight during exercise56. Published reports on LBPPT have associated it with improved muscle functionality and posture in patients with muscular dystrophy and earlier postoperative return to sport in athletes58. Although LBPPT has not been studied in the context of muscle strain, LBPPT has demonstrated a linear reduction of gastrocnemius and soleus muscle activation in healthy individuals in relation to the amount of body weight unloaded during exercise57. The reduction in muscle activation is similar to that achieved with deep water running at a matched stride frequency59. Furthermore, modifications that decrease the treadmill speed and/or incline also lessen gastrocnemius and soleus muscle activation56. For this protective reason, published reports have suggested LBPPT as an option for patients commencing a rehabilitation program and as an alternative to hydrotherapy56,57.
Platelet-rich plasma is an autologous, platelet-rich blood product obtained from the centrifugation of whole blood. Platelets are purported to release growth factors and cytokines that facilitate the regeneration and healing of muscle tissues60-63. Presently, 1 study has examined platelet-rich plasma treatment in the calf muscles. In a retrospective evaluation of patient outcomes, Borrione et al. reported that early ultrasound-guided platelet-rich plasma treatment of grade-II and III gastrocnemius strain reduced pain, discomfort, and recovery time compared with the standard conservative treatment63. However, the patient sample was limited to recreational sport athletes older in age than elite athletes engaged in competitive sports63. Level-I studies investigating platelet-rich plasma application in other muscle groups have shown inconsistent evidence60-62; in the case of the hamstring muscles, A Hamid et al.64 reported that platelet-rich plasma facilitated a faster recovery with a shorter time to return to play, and Reurink et al.65 and Hamilton et al.66 observed no significant differences in the time to return to play or the reinjury rate between platelet-rich plasma and control cohorts. Thus, additional investigation is necessary to elucidate the benefits of platelet-rich plasma for muscle rehabilitation.
The therapeutic implications of stem cell therapy are still preliminary but demonstrate some potential for muscle rehabilitation. Stem cell therapy aims to restore the structural integrity and functionality of skeletal tissue by stimulating muscle fiber development and vascularization67-69. In animal models, stem cell therapy has demonstrated accelerated muscle recovery with improved angiogenesis and reduced scar tissue formation69,70. Stem cell therapy has been investigated in a limited number of clinical trials and primarily for the treatment of muscular dystrophies and incontinence disorders69,71. In these clinical trials, patients who received transplantation or intra-arterial infusion of progenitor cells such as mesenchymal stromal cells, mesoangioblasts, or myoblasts cultured from muscle satellite cells had outcomes that ranged from no difference in muscle histology and/or functionality to improvements in these measures69,71. The differences across published reports are partly attributable to variations in study methodology, small patient samples, and an incomplete understanding of the biological mechanisms stimulated by stem cell therapy. Future research may provide more evidence for the use of stem cell therapy in muscle rehabilitation.
Return to Play
Most calf strains recover well under conservative treatment; the muscle develops a small fibrous scar without pharmacological or surgical interventions28,40. Full recovery is indicated by symptom relief and the return of strength, flexibility, and range of motion comparable with those of the contralateral side1,34. Early diagnosis and treatment of muscle strain can ameliorate the severity and duration of the injury, and limited evidence has suggested that treatment within 48 hours of an injury facilitates earlier return to play1,28,34,40. Although return to play is often mediated by sports-specific considerations, a general benchmark to begin sports reconditioning is ambulation without pain6,7,72. Premature exertion can delay recovery, can cause incomplete healing, and can increase the risk of reinjury1,13.
MRI is useful to evaluate professional return to play2,12,13,22,28,32. Certain imaging characteristics, such as the severity and the site of the injury, are associated with a longer recovery time. Higher grades of tissue injury generally require longer rehabilitation (Table III). Concomitant connective tissue disruption has been associated with longer time to return to play in elite runners and Australian football, soccer, rugby, and hockey athletes with calf strain2,13. Connective tissues such as tendons, aponeuroses, and epimysium are integral to muscle support and function but heal more slowly than muscle when disrupted2,22. Injury location may also play a role in recovery time. Although gastrocnemius and soleus strains have similar recovery times, the location of the tear within the tissue and the presence of aponeurotic disruption may influence overall recovery2,24. Soleus strains in which the musculotendinous junction or tendon are implicated correspond to more missed games22. In addition, ruptures in the central aponeurosis recover more slowly than those in the lateral or medial aponeurosis and myofascial sites24,32,73. In gastrocnemius strains, tears in the anterior aponeurosis and distal myotendinous junction correlate with higher-grade injuries, which require longer rehabilitation2.
Other considerations for return-to-play decisions include the manner and history of the injury. A study of elite Australian football players showed that calf strains from running activities corresponded to longer recovery periods than calf strains from non-running activities, irrespective of the muscle injured13. Running activities such as high-intensity and steady-state running, acceleration, deceleration, or sudden change of direction may be associated with more tissue disruption of the muscle-tendon unit13. Player reinjuries are another concern for sports managers as calf strain is a recurrent injury in approximately 19% to 31% of cases3,21,24. Reinjuries are associated with longer rehabilitation times and often involve older, more experienced players13. Premature return to play increases the risk of reinjury as tissues have not completely healed1,13. However, the degree of tissue damage in reinjuries compared with the index injuries is subject to debate. Studies of hamstring strain have shown greater muscle damage in reinjuries than in index injuries, which may explain the prolonged recovery time in reinjuries74. However, conflicting evidence of similar muscle damage between reinjuries and the index injuries also exists74. An appropriate rehabilitation timeline may consider other contextual factors as well, such as sport-specific demands, player position, seasonality, and athlete psychology24.
Player age and history of a calf strain or other leg injury are the strongest risk factors for calf strain in elite athletes, and player characteristics such as height, weight, sex, and side dominance are unlikely to be associated with calf muscle injury3,13,16,17,19,20,75. A possible explanation is that age-related tissue changes involve progressive declines in skeletal muscle quality and function, the consequences of which include neuromuscular maladaptations that restrict muscle force and rate of contraction3. In some cases, the rehabilitated tissue has suboptimal functionality compared with the contralateral, uninjured side76. Because optimal tissue functionality is protective, this suggests that a previous muscle injury can be a risk factor for a future injury. Prior injuries in the calf, hamstrings, quadriceps, adductors, and knee have been identified as risk factors for a subsequent calf injury3,16. More limited evidence has shown that increased body mass index and preseason activity are risk factors for calf strain3,16.
Studies have indicated that pre-participation stretching improves range of motion and muscle compliancy, which may be protective against muscle strain77. Although stretching promotes muscle performance in elastic movements such as hops or leaps, it is associated with decreased muscle power in predominantly concentric contractions such as steady-state cycling or jogging77,78. For this reason, the benefits of stretching alone are unclear. However, dynamic and sport-specific pre-participation drills may be able to restore stretch-induced performance loss when coupled with a stretching routine appropriately tailored for the player position77. Because the strongest risk factors for calf strain are unmodifiable, the prevention of calf strain is best accomplished with pre-participation stretching and warm-up exercises that increase flexibility and agility in the tissues most at risk for injury34,77.
Calf muscle strain is a common condition. In high-performance athletes, calf strain contributes to missed practice or playing time in many professional and collegiate sports. Timely diagnosis and treatment can improve outcomes and can facilitate earlier return to sport. Although the diagnosis can be made by clinical examination, MRI and ultrasound are both appropriate imaging modalities to confirm calf strain. MRI may additionally be useful in the evaluation of recovery time as return-to-play decisions often have financial and strategic consequences for professional teams. Conservative treatment is effective for most calf strain injuries. Operative management, although rarely indicated, may be appropriate in severe cases with grade-III ruptures or complications. Player age and history of a calf strain or other leg injury are the strongest risk factors for calf strain injury and reinjury. Athletes are encouraged to practice pre-participation stretching and warm-up exercises to maintain flexibility and agility for prevention of calf muscle injury.
Source of Funding
The Conine Family Fund for Joint Preservation provided funding for this study.
1. Bryan Dixon J. Gastrocnemius vs. soleus strain: how to differentiate and deal with calf muscle injuries. Curr Rev Musculoskelet Med. 2009 Jun;2(2):74-7.
2. Prakash A, Entwisle T, Schneider M, Brukner P, Connell D. Connective tissue injury in calf muscle tears and return to play: MRI correlation. Br J Sports Med. 2018 Jul;52(14):929-33.
3. Green B, Pizzari T. Calf muscle strain injuries in sport: a systematic review of risk factors for injury. Br J Sports Med. 2017 Aug;51(16):1189-94.
4. Pacheco RA, Stock H. Tennis leg: mechanism of injury and radiographic presentation. Conn Med. 2013 Aug;77(7):427-30.
5. Delgado GJ, Chung CB, Lektrakul N, Azocar P, Botte MJ, Coria D, Bosch E, Resnick D. Tennis leg: clinical US study of 141 patients and anatomic investigation of four cadavers with MR imaging and US. Radiology. 2002 Jul;224(1):112-9.
6. Kwak HS, Han YM, Lee SY, Kim KN, Chung GH. Diagnosis and follow-up US evaluation of ruptures of the medial head of the gastrocnemius (“tennis leg”). Korean J Radiol. 2006 Jul-Sep;7(3):193-8.
7. Nsitem V. Diagnosis and rehabilitation of gastrocnemius muscle tear: a case report. J Can Chiropr Assoc. 2013 Dec;57(4):327-33.
8. Dakic JG, Smith B, Gosling CM, Perraton LG. Musculoskeletal injury profiles in professional Women’s Tennis Association players. Br J Sports Med. 2018 Jun;52(11):723-9.
9. Colberg RE, Aune KT, Choi AJ, Fleisig GS. Incidence and prevalence of musculoskeletal conditions in collegiate tennis athletes. Medicine & Science in Tennis. 2015;20(3):137-44.
10. Winge S, Jørgensen U, Lassen Nielsen A. Epidemiology of injuries in Danish championship tennis. Int J Sports Med. 1989 Oct;10(5):368-71.
11. Mack CD, Kent RW, Coughlin MJ, Shiue KY, Weiss LJ, Jastifer JR, Wojtys EM, Anderson RB. Incidence of lower extremity injury in the National Football League: 2015 to 2018. Am J Sports Med. 2020 Jul;48(9):2287-94.
12. Werner BC, Belkin NS, Kennelly S, Weiss L, Barnes RP, Potter HG, Warren RF, Rodeo SA. Acute gastrocnemius-soleus complex injuries in National Football League athletes. Orthop J Sports Med. 2017 Jan 11;5(1):2325967116680344.
13. Green B, Lin M, Schache AG, McClelland JA, Semciw AI, Rotstein A, Cook J, Pizzari T. Calf muscle strain injuries in elite Australian Football players: a descriptive epidemiological evaluation. Scand J Med Sci Sports. 2020 Jan;30(1):174-84.
14. Orchard JW, Seward H, Orchard JJ. Results of 2 decades of injury surveillance and public release of data in the Australian Football League. Am J Sports Med. 2013 Apr;41(4):734-41.
15. McKay GD, Goldie PA, Payne WR, Oakes BW, Watson LF. A prospective study of injuries in basketball: a total profile and comparison by gender and standard of competition. J Sci Med Sport. 2001 Jun;4(2):196-211.
16. Nilstad A, Andersen TE, Bahr R, Holme I, Steffen K. Risk factors for lower extremity injuries in elite female soccer players. Am J Sports Med. 2014 Apr;42(4):940-8.
17. Hägglund M, Waldén M, Ekstrand J. Risk factors for lower extremity muscle injury in professional soccer: the UEFA Injury Study. Am J Sports Med. 2013 Feb;41(2):327-35.
18. Bengtsson H, Ekstrand J, Hägglund M. Muscle injury rates in professional football increase with fixture congestion: an 11-year follow-up of the UEFA Champions League injury study. Br J Sports Med. 2013 Aug;47(12):743-7.
19. Ekstrand J, Hägglund M, Waldén M. Epidemiology of muscle injuries in professional football (soccer). Am J Sports Med. 2011 Jun;39(6):1226-32.
20. Faude O, Junge A, Kindermann W, Dvorak J. Risk factors for injuries in elite female soccer players. Br J Sports Med. 2006 Sep;40(9):785-90.
21. Orchard J. Management of muscle and tendon injuries in footballers. Aust Fam Physician. 2003 Jul;32(7):489-93.
22. Waterworth G, Wein S, Gorelik A, Rotstein AH. MRI assessment of calf injuries in Australian Football League players: findings that influence return to play. Skeletal Radiol. 2017 Mar;46(3):343-50.
23. Fields KB, Rigby MD. Muscular calf injuries in runners. Curr Sports Med Rep. 2016 Sep-Oct;15(5):320-4.
24. Green B, Lin M, McClelland JA, Semciw AI, Schache AG, Rotstein AH, Cook J, Pizzari T. Return to play and recurrence after calf muscle strain injuries in elite Australian football players. Am J Sports Med. 2020 Nov;48(13):3306-15.
25. Bencardino JT, Rosenberg ZS, Brown RR, Hassankhani A, Lustrin ES, Beltran J. Traumatic musculotendinous injuries of the knee: diagnosis with MR imaging. Radiographics. 2000 Oct;20(Spec No):S103-20.
26. Miller M, Thompson S. DeLee, Drez and Miller’s Orthopaedic Sports Medicine: Principles and Practice. 5th ed. Elsevier; 2019.
27. Armfield DR, Kim DHM, Towers JD, Bradley JP, Robertson DD. Sports-related muscle injury in the lower extremity. Clin Sports Med. 2006 Oct;25(4):803-42.
28. Hsu D, Chang KV. Gastrocnemius Strain. StatPearls Publishing; 2018. Accessed 2021 Mar 16. http://www.ncbi.nlm.nih.gov/pubmed/30521187
29. Bright JM, Fields KB, Draper R. Ultrasound diagnosis of calf injuries. Sports Health. 2017 Jul/Aug;9(4):352-5.
30. Koulouris G, Ting AYI, Jhamb A, Connell D, Kavanagh EC. Magnetic resonance imaging findings of injuries to the calf muscle complex. Skeletal Radiol. 2007 Oct;36(10):921-7.
31. Counsel P, Comin J, Davenport M, Connell D. Pattern of fascicular involvement in midportion Achilles tendinopathy at ultrasound. Sports Health. 2015 Sep-Oct;7(5):424-8.
32. Pezzotta G, Querques G, Pecorelli A, Nani R, Sironi S. MRI detection of soleus muscle injuries in professional football players. Skeletal Radiol. 2017 Nov;46(11):1513-20.
33. Campbell JT. Posterior calf injury. In: Foot and Ankle Clinics. Vol 14. Elsevier; 2009. p 761-71.
34. Millar AP. Strains of the posterior calf musculature (“tennis leg”). Am J Sports Med. 1979 May-Jun;7(3):172-4.
35. Troyer W, Render A, Jayanthi N. Exercise-associated muscle cramps in the tennis player. Curr Rev Musculoskelet Med. 2020 Oct;13(5):612-21.
36. Singh D. Acute Achilles tendon rupture. BMJ. 2015 Oct 22;351:h4722.
37. Flecca D, Tomei A, Ravazzolo N, Martinelli M, Giovagnorio F. US evaluation and diagnosis of rupture of the medial head of the gastrocnemius (tennis leg). J Ultrasound. 2007 Dec;10(4):194-8.
38. Hayashi D, Hamilton B, Guermazi A, de Villiers R, Crema MD, Roemer FW. Traumatic injuries of thigh and calf muscles in athletes: role and clinical relevance of MR imaging and ultrasound. Insights Imaging. 2012 Dec;3(6):591-601.
39. Connell DA, Schneider-Kolsky ME, Hoving JL, Malara F, Buchbinder R, Koulouris G, Burke F, Bass C. Longitudinal study comparing sonographic and MRI assessments of acute and healing hamstring injuries. AJR Am J Roentgenol. 2004 Oct;183(4):975-84.
40. Järvinen TAH, Järvinen TLN, Kääriäinen M, Kalimo H, Järvinen M. Muscle injuries: biology and treatment. Am J Sports Med. 2005 May;33(5):745-64.
41. Cheng Y, Yang HL, Sun ZY, Ni L, Zhang HT. Surgical treatment of gastrocnemius muscle ruptures. Orthop Surg. 2012 Nov;4(4):253-7.
42. Brukner P, Khan K. Clinical Sports Medicine. 3rd ed. McGraw Hill; 2006.
43. Vopat BG, Vopat LM, Bechtold MM, Hodge KA. Blood flow restriction therapy: where we are and where we are going. J Am Acad Orthop Surg. 2020 Jun 15;28(12):e493-500.
44. Hughes L, Paton B, Rosenblatt B, Gissane C, Patterson SD. Blood flow restriction training in clinical musculoskeletal rehabilitation: a systematic review and meta-analysis. Br J Sports Med. 2017 Jul;51(13):1003-11.
45. Scott BR, Loenneke JP, Slattery KM, Dascombe BJ. Blood flow restricted exercise for athletes: a review of available evidence. J Sci Med Sport. 2016 May;19(5):360-7.
46. Lixandrão ME, Ugrinowitsch C, Berton R, Vechin FC, Conceição MS, Damas F, Libardi CA, Roschel H. Magnitude of muscle strength and mass adaptations between high-load resistance training versus low-load resistance training associated with blood-flow restriction: a systematic review and meta-analysis. Sports Med. 2018 Feb;48(2):361-78.
47. Slysz J, Stultz J, Burr JF. The efficacy of blood flow restricted exercise: a systematic review & meta-analysis. J Sci Med Sport. 2016 Aug;19(8):669-75.
48. Wortman RJ, Brown SM, Savage-Elliott I, Finley ZJ, Mulcahey MK. Blood flow restriction training for athletes: a systematic review. Am J Sports Med. 2021 Jun;49(7):1938-44.
49. Silva MF, Dias JM, Dela Bela LF, Pelegrinelli ARM, Lima TB, Carvalho RGDS, Taglietti M, Batista Júnior JP, Facci LM, McVeigh JG, Cardoso JR. A review on muscle activation behaviour during gait in shallow water and deep-water running and surface electromyography procedures. J Bodyw Mov Ther. 2020 Oct;24(4):432-41.
50. Torres-Ronda L, Del Alcázar XS. The properties of water and their applications for training. J Hum Kinet. 2014 Dec 30;44(1):237-48.
51. Killgore GL. Deep-water running: a practical review of the literature with an emphasis on biomechanics. Phys Sportsmed. 2012 Feb;40(1):116-26.
52. Alberton CL, Cadore EL, Pinto SS, Tartaruga MP, da Silva EM, Kruel LFM. Cardiorespiratory, neuromuscular and kinematic responses to stationary running performed in water and on dry land. Eur J Appl Physiol. 2011 Jun;111(6):1157-66.
53. Becker BE. Aquatic therapy: scientific foundations and clinical rehabilitation applications. PM R. 2009 Sep;1(9):859-72.
54. Masumoto K, Applequist BC, Mercer JA. Muscle activity during different styles of deep water running and comparison to treadmill running at matched stride frequency. Gait Posture. 2013 Apr;37(4):558-63.
55. Masumoto K, Horsch SE, Agnelli C, McClellan J, Mercer JA. Muscle activity during running in water and on dry land: matched physiology. Int J Sports Med. 2014 Jan;35(1):62-8.
56. Whiteley R, Hansen C, Thomson A, Sideris V, Wilson MG. Lower limb EMG activation during reduced gravity running on an incline. Speed matters more than hills irrespective of indicated bodyweight. Gait Posture. 2021 Jan;83:52-9.
57. Kristiansen M, Odderskær N, Kristensen DH. Effect of body weight support on muscle activation during walking on a lower body positive pressure treadmill. J Electromyogr Kinesiol. 2019 Oct;48:9-16.
58. Cooke MB, Nix CM, Greenwood LD, Greenwood MC. No differences between Alter G-trainer and active and passive recovery strategies on isokinetic strength, systemic oxidative stress and perceived muscle soreness after exercise-induced muscle damage. J Strength Cond Res. 2018 Mar;32(3):736-47.
59. Mercer JA, Applequist BC, Masumoto K. Muscle activity during running with different body-weight-support mechanisms: aquatic environment versus body-weight-support treadmill. J Sport Rehabil. 2014 Nov;23(4):300-6.
60. Sheth U, Dwyer T, Smith I, Wasserstein D, Theodoropoulos J, Takhar S, Chahal J. Does platelet-rich plasma lead to earlier return to sport when compared with conservative treatment in acute muscle injuries? A systematic review and meta-analysis. Arthroscopy. 2018 Jan;34(1):281-288.e1.
61. Le ADK, Enweze L, DeBaun MR, Dragoo JL. Current clinical recommendations for use of platelet-rich plasma. Curr Rev Musculoskelet Med. 2018 Dec;11(4):624-34.
62. Hotfiel T, Seil R, Bily W, Bloch W, Gokeler A, Krifter RM, Mayer F, Ueblacker P, Weisskopf L, Engelhardt M. Nonoperative treatment of muscle injuries - recommendations from the GOTS expert meeting. J Exp Orthop. 2018 Jun 22;5(1):24.
63. Borrione P, Fossati C, Pereira MT, Giannini S, Davico M, Minganti C, Pigozzi F. The use of platelet-rich plasma (PRP) in the treatment of gastrocnemius strains: a retrospective observational study. Platelets. 2018 Sep;29(6):596-601.
64. A Hamid MS, Mohamed Ali MR, Yusof A, George J, Lee LPC. Platelet-rich plasma injections for the treatment of hamstring injuries: a randomized controlled trial. Am J Sports Med. 2014 Oct;42(10):2410-8.
65. Reurink G, Goudswaard GJ, Moen MH, Weir A, Verhaar JA, Bierma-Zeinstra SM, Maas M, Tol JL; Dutch Hamstring Injection Therapy (HIT) Study Investigators. Platelet-rich plasma injections in acute muscle injury. N Engl J Med. 2014 Jun 26;370(26):2546-7.
66. Hamilton B, Tol JL, Almusa E, Boukarroum S, Eirale C, Farooq A, Whiteley R, Chalabi H. Platelet-rich plasma does not enhance return to play in hamstring injuries: a randomised controlled trial. Br J Sports Med. 2015 Jul;49(14):943-50.
67. Dunn A, Talovic M, Patel K, Patel A, Marcinczyk M, Garg K. Biomaterial and stem cell-based strategies for skeletal muscle regeneration. J Orthop Res. 2019 Jun;37(6):1246-62.
68. Schmidt M, Schüler SC, Hüttner SS, von Eyss B, von Maltzahn J. Adult stem cells at work: regenerating skeletal muscle. Cell Mol Life Sci. 2019 Jul;76(13):2559-70.
69. Qazi TH, Duda GN, Ort MJ, Perka C, Geissler S, Winkler T. Cell therapy to improve regeneration of skeletal muscle injuries. J Cachexia Sarcopenia Muscle. 2019 Jun;10(3):501-16.
70. Ota S, Uehara K, Nozaki M, Kobayashi T, Terada S, Tobita K, Fu FH, Huard J. Intramuscular transplantation of muscle-derived stem cells accelerates skeletal muscle healing after contusion injury via enhancement of angiogenesis. Am J Sports Med. 2011 Sep;39(9):1912-22.
71. Biressi S, Filareto A, Rando TA. Stem cell therapy for muscular dystrophies. J Clin Invest. 2020 Nov 2;130(11):5652-64.
72. Orchard J, Best TM, Verrall GM. Return to play following muscle strains. Clin J Sport Med. 2005 Nov;15(6):436-41.
73. Pedret C, Rodas G, Balius R, Capdevila L, Bossy M, Vernooij RW, Alomar X. Return to play after soleus muscle injuries. Orthop J Sports Med. 2015 Jul 22;3(7):2325967115595802.
74. Ekstrand J, Krutsch W, Spreco A, van Zoest W, Roberts C, Meyer T, Bengtsson H. Time before return to play for the most common injuries in professional football: a 16-year follow-up of the UEFA Elite Club Injury Study. Br J Sports Med. 2020 Apr;54(7):421-6.
75. Orchard JW. Intrinsic and extrinsic risk factors for muscle strains in Australian football. Am J Sports Med. 2001 May-Jun;29(3):300-3.
76. Opar DA, Serpell BG. Is there a potential relationship between prior hamstring strain injury and increased risk for future anterior cruciate ligament injury? Arch Phys Med Rehabil. 2014 Feb;95(2):401-5.
77. McHugh MP, Cosgrave CH. To stretch or not to stretch: the role of stretching in injury prevention and performance. Scand J Med Sci Sports. 2010 Apr;20(2):169-81.
78. Witvrouw E, Mahieu N, Danneels L, McNair P. Stretching and injury prevention: an obscure relationship. Sports Med. 2004;34(7):443-9.