Triathlon Plus article – low back pain in triathletes

TriPlus back pain article page1

TriPlus back pain article page 2

links to page 1 and 2 of a previously published article in Triathlon Plus magazine.


Core stability in horse riders -RDA article

In recent years we have been inundated with advice on “core stability” training, however, there remains confusion as to what qualifies as the core, and how to specifically train these muscles in a useful manner. Riders need sufficient core stability and strength to maintain good posture and trunk stability in the saddle. Reduced flexibility, tight muscles, restricted joints, or simply nervous tension in the rider can all reduce controlled stability by inhibiting the “core muscles” and thus the ability to adapt to the movements of your horse.

It is commonly thought that the core is comprised of the abdominals and lower back muscles (Rectus abdominus, internal and external obliques, and the transverse abdominus). However, when looking at core training and movement patterns we can not be limited to these three muscle groups. For the lower back/pelvis/hip region there are 29 different muscles that each contribute to providing stability to the core, and this area can not be looked at in isolation from the upper body as issues around the pelvis will effect the shoulders and head stability / positioning, and vice versa.

Any low back pain or discomfort which riders suffer from can be attributed to the vast number of muscles that surround and intersect this region, and which may have been overlooked in any core program. If too much emphasis is placed on certain areas such as the anterior musculature (6 pack!) then muscle imbalances can develop leading to pain and injury. It is therefore necessary to emphasise the importance of a comprehensive core development program to cover the whole lumbar/pelvic/hip region.

Prospective Injuries from poor core stability

Lower back pain (lumbar spine and / or sacroiliac joint)

Abdominal strains

Groin strains

Hip flexor / abductor / adductor strains

Pelvic misalignment

Other musculoskeletal injuries due to compensation

Prospective Performance detriments

Poor balance in your seat causing increased tension in your legs and upper body.

Poor postural alignment

Poor transferability of force from lower to upper extremities and vice versa, eg. Changing body position, communication with the horse.

Inability to withstand and balance external forces from the horse

Core stability exercises can be incorporated into both land based training, and when on the horse. With the warmth and rhythmic movements of the horses movements can help relax tight muscles allowing the core muscles to switch on, and once warmed up the rider can practice simple movements such as pelvic tilts and trunk rotations. Instructors should give coaching cues around ensuring the rider is sat as tall as possible, lengthening through the spine, and activating the abdominals and obliques to support the spine.

Land based exercises can be done on the floor, on gym balls, with exercise bands, pilates trainers or IJoyRide trainer. But the exercise program must be tailored to the individual rider by the instructors and physiotherapist.

An often overlooked aspect of core training though, is endurance. Doing 6-10 reps for 3-4 sets will build the strength in the muscles, but to improve the endurance higher repetitions are needed, typically 25-30 repetitions. Holding contractions (isometric) also builds awareness of the correct positioning as well as strength through the tendons and connective tissues.

So in summary- some of the reasons you should look at incorporating specific core stability sessions into your riding, and off the horse training are:

Improved stability and positioning in the saddle

Greater control and communication with your horse

Lower risk of coming off – able to control/stay in the saddle during a spook/unexpected movement

Greater endurance when trotting/cantering

Reduced risk of injury


Degenerative lumbar spondylosis


Spondylosis is part of the normal aging process of the spine. Dixon (1980) refers to the sequence of changes affecting one of more levels of disc degeneration, disc narrowing, osteophyte formation and osteoarthritis of the facet joints. Degeneration is characterized by slow, destructive changes which are not balanced by the regeneration that occurs in younger tissues (Grieve, 1981).


Roland and Van Tulder (1998) found that roughly 40% of patients with advanced disc degeneration on radiography do not have backpain, indicating that symptoms and radiographic changes may be unrelated.


In old age, the range of lumbar movement decreases. Originally this was thought to be due to the thinning of the intervertebral discs, however, it is now thought that only 30% of discs become thinner and in old age most discs increase in volume, become thicker centrally and more convex. Loss of vertebral column height is caused by loss of vertebral body height. The reason for loss of movement is thought to be due to disc stiffness or reduction of the elasticity of the disc (Twomey and Tayler 1983). The histological and biochemical changes include an increase in the total number of collagen fibres, a decreased in water content and a change in the prosteoglycagen ratios. There is also an increase in the “failure fatigue” of collagen in the older cartilage. These changes lead to a decrease in compliance of the disc fibrocartilage therefore making it less capable as acting as an efficient shock absorber. If the disc becomes vascularised, which can occur when the end plates are damaged, disc degeneration is accelerated. Nerve fibres then accompany the blood vessels into the disc and may serve a nocioceptive function.


Aging is accompanied by loss of both trabecular and cortical bone which results in a decrease in bone strength. The rate at which bone loss occurs is influenced by such factors as the menopause, declining calcium absorption, smoking and reduced physical exercise. The height of the vertebral bodies declines in old age, principally due to the reduction of transverse trabeculae which acts as “cross-braces” to the vertical trabeculae. As the trabeculae weaken, the vertebral body becomes less resistant to deformation and injury.


Osteophytes are outgrowths of healthy bone from the vertebrae. Their development is an important defensive mechanism against compressive forces which exceed the capacity fo the bone to resist them. They are composed of more compact, stronger bone, than the rest of the vertebral body. A young person with normal vertebrae may develop osteophytes when the pressure on the vertebral body is excessive, as in heavy manual work. Disc degeneration and the subsequent impaired shock-absorbing capacity of the vertebral column can also lead to their formation, as can pathological processes such as osteoporosis. Quite marked osteophytosis may be present without giving rise to symptoms.


Progressive resorption and thinning of the articular cartilage in the end plates occurs, with replacement by bone, so that over the age of 60 there is often only a thin layer of calcified cartilage separating the disc from the vertebral body. With increasing age, it is likely that there is a decrease in the diffusion of substances though the end plates. Since the cells in the disc are dependent on this route for the supply of nutrients and the removal of waste products, closure of the end plate route leads to nutritional deficiencies and a build up of metabolic products.


The epidemiology of spondylosis increases markedly with age and is uncommon below 45years of age. The normal aging process can be accelerated by increased exposure to mechanical stresses, which then give rise to degenerative changes. Which part of a motion segment is initially affected depends on the particular mechanical stresses or postures to which the spine is subjected and the integrity of the tissues themselves.


With age, there is a progressive decrease in the water-biding capacity of the nucleus of the disc.

Degenerative changes of intervertebral discs were classified in 1966 by Rolander based on their appearance on mid-dagital sections.


Grade 0 – Macroscopically normal / juvenile discs

Grade 1 – Normal adult discs, white in colour, the nucleus bulges.

Grade 2 – Age changes, less distinct boundary between nucleus and annulus, yellowish colour.

Grade 3 – Frank disc dessication, multiple fissures in nucleus and annulus, disc thinning.



The incidence of disc degeneration does increase in old age and the lower two lumbar levels are most affected as these levels are subject to greatest physical stress. Fissuring of the annulus is seen with increasing frequency in old age. The etiology of degerative disc disease includes both genetic and environmental factors. The incidence of disc degeneration in the spine as a whole is highest at the lowest two lumbar levels, particularly in the lumbosacral disc. This is because there is a large amount of movement at this level and the shear forces acting on the disc with the lordotic posture in the standing posture also increase the forces on the disc. Degenerative changes may predominantly affect the disc in some individuals, while in others they affect the facet joints, at least in the initial stages of degeneration.


Secondary chondrosis interverbralis (osteochondrosis intervertebralis) describes parthological changes outside the intervertebral disc and is characterized by changes in the cartilage end plates and sclerosis of the adjacent spongiosa of the vertebral bodies resulting in erosive chondrosis. Bony osteophytes develop in the region of the vertebral bodies (Spondylosis deformans).


As a result of the changes in the intervertebral discs and subsequent decrease in height, there are degenerative changes in the zygopophyseal joints (spondyloarthrosis). The decrease in height of the vertebral column causes a caudal dislocation of the inferior articular process and stresses the capsule of the joints.


Clinical Presentation

Age onset

  • Usually middle aged and older
  • Often heavy manual work
  • Gradual onset



  • Can be confined to lumbar region but may experience symptoms referred to the lower limbs


Diurnal Pattern

  • worse first thing am./ stiffness, eases off fairly quickly
  • activity dependent.




  • Variable, vague, ache, dull
  • Low back pain, unilateral or bilateral lower limbs
  • Often aggravated with walking, standing (extension activities)
  • Often eased by flexion
  • Eased by movement / resting in neutral



Posture – Flattened lumbar lordosis

Rom – Stiff lumbar segments, usually in an articular restriction

  • Extension and side flexions usually worse than flexion

Neuro – Depends on whether nerve roots are involved.



Postural correction / Back care advice / use of heat/ice.

Isometric exercises to strengthen the abdominal and spinal muscles.

Advise re: medication (analgesia, NSAIDS, glucosamine sulphate, amitriptyline)

Address muscle imbalance / stability as appropriate

Address joint restriction as appropriate, spinal mobilization techniques, often starting in the direction opposite to that of pain aggravation. Most effective in the first 6 weeks.

General activity programme / pacing advice.

Weight reduction if appropriate.

Erganomic adjustments if appropriate.



Dependent upon the level and degree of degeneration. Most cases of acute pain begin to settle within 6 weeks.



Adams, M., Bogduk, N., Burton, K., Dolan, P. The biomechanics of backpain. Churchill livingstone.


Andersson, G. (1997) The epidemiology of spinal disorders. The adult spine: principles and practice. Lippincott-Raven. Philadelphia 93-141


Dixon, A. (1980) Diagnosis of low back pain. The lumbar Spine and Backpain. 2nd Ed. Pitman Medical. P135


Fujiwara, A., Lim, T.H., An, H.S., Tanaka, N., Jean, C.H., Adesson, G., Houghton, V.M. (2000) The effect of disc degeneration and facet joint OA on the segmental flexibility of the lumbar spine. Spine. 25(3) 3036-3044


Grieve, G.P. (1988) Clinical features. In: Grieve, G.P., ed. Common Vertebral joint problems, 2nd ed. New York, Churchill Livingston 299-353.


Prescher, A. (1998) Anatomy of the aging spine. European Journal of Radiology. 181-195


Roland, M., Van Tulder. (1998) Should radiologists change the way they report plain radiographs of the spine. Lancet. 352, 229-230


Rolander, S.,D. (1996) Motion of the lumbar spine with special reference to the stability effect of posterior fusion. Orthopaedic Scandinavia.


Twomey, L.T., Taylor, J.R. (1993) Sagital movements of the human intervertebral lumbar column: a quantitative study of the role of the posterior vertebral elements. Archives of physical medicine and rehabilitation. 64, 322-325

Tietzes Syndrome


“A benign, painful, non-suppurative localised swelling of the costosternal, sternoclavicular or costochondral joints, most often involving the area of the 2nd and 3rd ribs.”

n Tietze’s syndrome, the cartilage of the costochondral joint becomes inflamed and swollen, causing pain and tenderness.

Tietze’s syndrome is very similar to another condition called costochondritis, which also causes pain in the costochondral joint. Sometimes, Tietze’s syndrome and costochondritis are thought to be the same, although only Tietze’s syndrome results in both pain and inflammation.



The cause is unknown but may occur following upper respiratory infections and excessive coughing.

The cause of Tietze’s syndrome is not fully understood, although it may be linked to upper respiratory tract infections, such as sinusitis and laryngitis. In some people with Tietze’s syndrome, it is thought that severe coughing may be a cause.

Anyone can develop Tietze’s syndrome, although it is most common among people who are between 20-40 years of age. The condition affects twice as many men as women.

Tietze’s syndrome could be more a part of seronegative disease than has been previously recognized (Aeschlimann A, Kahn MF 1990)


Pathological Process

Relatively unkown, nutritional and vitamin dificiencies have been suggested as well as traumatic pathogenesis including recurrent microtrauma, severe coughing and alterations of the ligamentus structures. There has also been an association reported with respiratory tract infections. Histological descriptions vary from unchanged costal cartilages to increased vascularity and degenerative changes with calcification or loss of ground substance resulting in a fibrillar appearace.


Clinical Presentation


sharp pain at the sternum

Can be gradual or sudden onset

Can also affect the 2nd and 3rd ribs

Aggravated by physical activity, movement, coughing, sneezing, deep breath



Localised tenderness

Localised swelling, normally at the 2nd and 3rd ribs.

Pain may radiate to the arm.


Differential Diagnosis




Rheumatoid disorders


Non-Traumatic conditions affecting the SCJ



Trigger points



USS may aid diagnosis

Chest X-ray to rule out other pathologies

ECG to exclude cardiovascular conditions

CT scan



Blood testing (sedimentation rate or C-reactive protein test) can show signs of inflammation in patients with Tietze syndrome, whereas patients with costochondritis alone typically have normal tests for inflammation.


a combination of X-ray, CT, MRI and nuclear medicine is the best way to diagnose the disease and rule out other disorders. (Guglielmi G et. al. 2009)




Local corticosteroid injection

Intercostal nerve blocks

Resection of the involved cartilage

Ice packs applied to local swelling can sometimes help to reduce pain and inflammation

Local lidocaine analgesic patch (Lidoderm) application can reduce pain.



Pain usually subsides within a few weeks, with some residual swelling persisting.

The course of the condition varies from spontaneous recovery to persistent symptoms over years.




Guglielmi G, Cascavilla A, Scalzo G, Salaffi F, Grassi W. Imaging of sternocostoclavicular joint in spondyloarthropaties and other rheumatic conditions. Clin Exp Rheumatol. 2009 May-Jun;27(3):402-8.


Aeschlimann A, Kahn MF Tietze’s syndrome: a critical review. Clin Exp Rheumatol. 1990 Jul-Aug;8(4):407-12.


Ankle inversion injuries – “sprained ankle”


Most common injury in sports and recreational activities (Renstom and Konradsen 1997)

Accounts for 25% of all sports related injuries Frost and Amendola (1999)

The ligaments around the ankle are the most commonly sprained ligaments in the body (Hertling and Kessler 1996). Yeung et al (1994) reported that of 563 sprained ankles, 73.5% had been sprained more than once. Frost and Amendola (1999) state that even with treatment there is a 50% chance of recurrent instability.

Anatomy, and likely sites of neural pathology.

The talocrural joint is collaterally restrained by the lateral and medial, or deltoid, ligament complexes. The lateral ligament is the most frequently injured. The lateral ligament consists of the anterior talofibular, calcaneofibular, lateral talocalcaneal and posterior talofibular ligaments.

Neural pathology:

Local sites – Common peroneal nerve, sural nerve.

Remote sites – Common peroneal nerve at the head of the fibula, sciatic nerve, at the sciatic bifurcation in the lower part of the thigh where it splits into the common peroneal and posterior tibial nerves. L4-S3 (Sciatic nerve) and preganglionic fibres for the lower limb which arise from T10-L2.


Types of instability:

Mechanical – a deficiency of the stabilising structures around the joint which allows joint movements beyond normal physiological limits (Frost and Amendola 1999). Most commonly at the Talocrural joint, or less commonly, at the subtalar joing, Ishi et al 1996).

Functional – less well understood, but Freeman et al. (1965) describe it as ankles which suffer from recurrent sprains or a tendency to “give way”.


Mechanial – most widely used is the anterior draw test, assessing the amount of anterior translation fo the talus relative to the fibula and tests the integrity of the anterior talofibular ligament. A good predictor of ligament disruption (Renstom and Konradsen 1997). However, Bonstrom (1996) found the anterior draw sign was only consistently positive in the presence of local anaesthesia. Van Dyjk et al. (1996) found that the test was unreliable if performed within 48hrs of the injury, but if performed after the 5th day then it showed a specificity of 74% and a sensitivity of 86%.

Functional – This diagnosis can only be obtained through a subjective assessment, it cannot be demonstrated by any imaging technique (Jerosh and Bischoff 1996).

Muscle weakness has been considered as a cause of instability, however McKnight and Armstrong found no significant difference between injured and non-injured muscle groups. Although Wilkerson et al.(1997) found that, paradoxically, the invertors had the greatest performance deficiency following the lateral ankle sprains.


Proprioception is also widely considered to be a major factor in maintaining joint stability. Research by Freeman et al. Reported in van der Eikoff and Osternig (1998) suggested that injury to ligaments and joint proprioceptors following ankle sprains would decrease the effectiveness of the reflexes associated with joint receptors. Various studies have found that the proprioceptive abilities of sprained ankles were significantly worse than unaffected ankles (Lentell et al. 1995, Konradsen and Magnusson 2000, Lofvenberg et al. 1995).

Because of the passage of the superficial peroneal nerve over the anterolateral aspect of the ankle, the nerve is tensioned and moves distally in the leg with plantarflexion/inversion of the foot and ankle (Shacklock 2005). Some ankle sprains produce damage in this nerve which may account for peroneal neurodynamic tests (Slump and SLR versions) becoming abnormal in some patients with sprained ankles. Plantarflexion/inversion of the ankle is valuable in the sensitization of peroneal involvement in lower limb pain. Damage to the peroneal nerve can occur as high as the common peroneal nerve at the posterior aspect of the knee where haematomas can develop after traction injury caused by the sprain. Compromise can also occur as far distally as the superficial peroneal nerve. Inflammation then develops and the nerve may incur hypersensitivity, reduced mobility and in some cases, reduced conduction. The clinical picture is one of pain with movement, particularly plantarflexion/inversion, tenderness and aching, dysaesthetic symptoms, tenderness and in cases where there is reduced conduction- a loss of sensation. In more recalcitrant cases, severe mechanical allodynia related to central sensitization may be a prominent feature. Loss of muscle power due to paralysis is not nearly as common as the other symptoms, but should be kept in mind.

Testing.Level 1:Straight leg raise with the foot relaxed. At the height of the SLR, if symptoms have not been provoked, the foot is passively moved into plantarflexion/inversion to the onset of symptoms. At this point, to differentiate the neurodynamic mechanisms the limb is lowered by reducing the hip flexion angle a small amount, whilst holding the foot stationary on the leg.Level 2:The same sequence as above, except that the foot is placed in plantarflexion/inversion prior to the SLR. Ensure there is no uncontrolled internal rotation of the hip.Level 3:a) add internal rotation of the hip prior to SLRb) plantarflexion/inversion taken further into range even evoking symptons prior to SLR. Ensure toes are included in the movement.c) As above but add resisted dorsiflexion/eversion to apply force through the mechanical interface (bone and tendon) and innervated tissues.


Webborn (1999) states that restoration of strength, range of motion and proprioceptive awareness are imperative prior to returning to training, and goes on to say that protective bracing may be required in the early stages. Cote et al. (1988) found that cold therapy significantly reduced the oedema in ankle sprains that were post acute. Cryotherapy also has a pain relieving effect by reducing the nerve conductivity (Thompson et al. 1991). van der Eikoff and Osternig (1998) have postulated that the application of external supports stimulate cutaneous receptors which may increase proprioceptive feedback. Karlsson and Andreasson (1992) found that reaction times of the peroneus muscles were shortened when unstable ankles were taped, so therefore they deduced the proprioceptive effect of taping was to restrict the extreems of ankle motion and to help shorten the reaction time of the peroneus muscles. Eilis and Rosenbaum (2001) carried out research into the effects of proprioception exercises for the ankle, they results showed a significant improvement in joint position sense and postural sway as well as significant changes in muscle reaction times. Goldie et al. (1994) found that eight weeks post injury, those who and received no proprioceptive training had significant worse static posture control that those who had received proprioceptive training.

Neural Treatment. Level 1 Proximal sliders. Patient supine, hip at 45degrees, supported by therapist. Knee flexion and plantarflexion/inversion. Level 2 Tensioners. Ipsilateral long sitting position and leaning forwards over the hip at the same time as performing plantarflexion/inversion. Stabilise the knee in extension if required. Level 3 a) Tensioners as above, but add internal rotation of the hip and contralateral side flexion with the slump. b) start with foot plantarflexed/inverted and knee flexed, extend the knee and then add hip flexion, Lx flexion, and Cx flexion, in that order. c) as per 3a but with active dorsiflexion against the therapist and contract-relax releases are performed at the end of range. If the joint is also stiff it is possible to mobilise the joint in conjunction with the neurodynamic techniques. Sural nerve. When there is a history of severe adduction of the calcaneum or dorsiflexion/inversion of the ankle the sural nerve can be affected. This is because the nerve passes around the dorolateral surface of the ankle posterior to the lateral malleolus. The sural nerve may also cause pain in the region of, and coexist with stiffness in the joints that surround, the cuboid bone. Biomechanics are therefore very important aspects of the assessment. Testing: similar to the peroneal nerve, but with dorsiflexion/inversion

Greater Trochanteric Pain Syndrome

Greater Trochanteric Pain Syndrome

The term greater trochanteric pain syndrome is now being commonly substituted for trochanteric bursitis; because the inflammatory etiology of the pain is being refuted by current research, using ultrasonographic, magnetic resonance imaging and histologic evidence.

Subjective Characteristics

  • Bursitis may develop gradually or traumatically.
  • Pain occurring over the side of the hip.
  • Referred pain that travels down the outside.thigh and may continue down to the knee.
  • Pain when sleeping on your side; especially the affected hip.
  • Pain upon getting up from a deep chair or after prolonged sitting (eg. in a car).
  • Pain when climbing stairs.
  • Increased pain when walking, cycling, or standing for long periods of time.

Contributing / Predisposing factors:

The trochanteric bursa may be inflamed by the glutes rubbing over the bursa and causing friction against the greater trochanter.

Can occur with running, walking, or cycling (especially when the saddle is too high).

It can also occur in some people who have a scoliosis, leg length discrepancy, weak hip muscles, osteoarthritis of the hips or lumbar spine, or rheumatoid arthritis.

Trochanteric bursitis can also occur following direct trauma to the side of the hip, such as in a fall.

Physical Examination

The most classic finding is point tenderness over the greater trochanter, which reproduces the presenting symptoms.  Palpation may also reproduce pain that radiates down the lateral thigh.  Swelling of the bursa may be present, but this will be difficult to identify in many patients due to the overlying tissue.  In obese patients it may be difficult to locate the greater trochanter dirrectly, therefore consider using the iliac crest as a landmark and assessing for the trochanter approximately 8 inches (20 cm) below the iliac crest.  Also consider palpating the region while passively circumducting the hip.  Overlying skin changes of ecchymosis with abrasions may occur with recent trauma.  Lateral hip pain can often be elicited by passive external rotation of the hip without provoking such symptoms by internal rotation.  Pain can also be reproduced with flexion of the hip followed by resisted hip abduction.  Groin pain or referred knee pain provoked by passive internal rotation of the hip may indicate hip joint pathology (such as osteoarthritis).  To assess for sciatica or lumbosacral radiculopathy, a detailed neurological examination of both lower limbs is required.


Rest/training adaptations, Anti-inflammatory medication(?), Ice, Injections, Stretching, massage / myofascial release, Muscle balance re-training, Core strength exercises, Correction of biomechanical abnormalities (eg. Orthotics), bike fit adjustment, ensuring appropriate footwear, Surgical treatment- rare (Bursectomy).

Compartment Syndrome

Chronic exertional compartment syndrome (CECS) is defined as a condition in which exertion increases muscle compartment pressure, interfering with tissue circulation and causing ischemia, pain, and even temporary neurological deficits (Blackman 2000).  Terms such as shin splints, march synovitis, anterior tibial pain syndrome, and medial tibial syndrome, have all been used to describe the symptoms of CECS (Rorabeck 1983).

Acute compartment syndrome is “a condition in which increased pressure within a limited space compromises the circulation and function of the tissues within that space”.  Most commonly occurs in the lower leg, but can occur in the thigh, buttock, and foot.

Acute – occurs following trauma to the lower leg, commonly after intramedullary nailing of long bone fractures, after ischaemic re-perfusion injuries, burns or poor positioning during surgery.
Chronic – reversible, activity related increases in intracompartmental pressure.  Also referred to as exercise-induced compartment syndrome (EICS) or exertional compartment syndrome.

Defining the anatomical compartments is essential in understanding the symptoms and treatment of the various CECS in the lower leg.
The concept of four distinct compartments in the lower leg is well-recognised with anterior, lateral, superficial posterior, and deep posterior compartments (Melberg and Styf, 1989).  More recently, a fifth compartment has been described that is in essence a subdivision of the deep posterior compartment, and contains only tibialis posterior.

1.Anterior compartment:  Comprises the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius.  Neurovascular structures include the anterior tibial artery and vein with the deep branch of the common peroneal nerve running along the interosseous membrane deep to the extensor hallucis longus.
2.Lateral compartment: Contains the peroneus longus and brevis with the common peroneal nerve dividing into its superficial and deep branches, the latter continuing into the anterior compartment.
3.Superficial Posterior: The posterior compartments lie surrounded by the deep fascia of the leg with the deep transverse fascia separating the deep from the superficial compartments.  The superficial compartment contains gastrocnemius, plantaris, and soleus.
4.Deep posterior: Contains the flexor digitorum longus, flexor hallucis longus, tibialis posterior, and more proximally popliteus.  Neurovascular structures in the deep compartment include the posterior tibial artery and vein and tibial nerve, entering beneath the arch of soleus proximally then lying on the posterior surface of tibialis posterior and more distally on the posterior tibia.  The fifth compartment is created by a discrete fascial layer over the posterior surface of tibialis posterior, and it is therefore possible that elevation of pressures in the compartment alone may occur (Blackman, 2000).

Pathological Process
The generally accepted pathophysiology of this condition is that raised intracompartmental pressure causes relative ischemia of the involved muscles (Blackman, 2000).
Ateriovenous pressure gradient theory:
Ischaemia begins when local blood flow cannot meet the metabolic demands of the tissue.  As the intracompartmental pressure rises, the intraluminal venous pressures also increase leading to a reduction in the arteriovenous pressure gradient resulting n diminished or absent local perfusion.  This causes a further rise in intersititial tissue pressure with the formation of tissue oedema.  The lymphatic drainage is then increased to protect against the rising interstitial fluid pressure.  Once this has reached its maximum, further increases in the intracompartmental pressure cause deformation and collapse of the lymphatic vessels.  It is only at the late stages that the arterial flow into the compartment is seriously compromised and the continuing flow of blood into the compartment increases swelling and oedema.  Pain may not only occur due to the increases in pressure, but also due to sensory receptor stimulation in the fascia or periosteum, or due to biochemical factors released due to reduced blood flow.
Raised intracompartmental pressure model:

A number of authors use this theory as a basis for fasciotomy, subsequently demonstrating a reduction in intracompartmental pressures post surgery (Puranen and Alavaikko, 1981; Rorabeck et al, 1983).

Other proposed evidence for this concept includes the demonstration of elevated intracompartmental pressures during and after exercise (Puranen and Alavaikko, 1981).

Studies on normal muscle also corroborate this theory.  The findings of these studies include a 20% increase in muscle size due to an increase in blood volume with exercise, and that chronic exercise causes a lasting muscle volume increase due to hypertrophy (Amendola and Rorabeck, 1985).

Ischemia Model:
There is some debate as to whether these increases in pressure result in clinically significant ischemia, and therefore may not be the main pathological factors linked to pain in CECS (Amendola et al. 1990; Trease et al. 2001)

Evidence Supporting:
Those who support the ischemia hypothesis suggest there are three potential mechanisms to explain the development of tissue ischemia:
1.Increased pressure causes arterial spasm and therefore a decrease in arterial inflow (Matsen, 1975)
2.Increased pressure causes obstruction of the microcirculation (Rorabeck and Macnab, 1975)
3.Increased pressure causes arteriolar or venous collapse leading to ischemia (Matsen, 1975; Black et al, 1990; Hutchinson and Ireland, 1994)

Evidence negating:
In a study by Balduini et al.  (1993) on 26 patients with lower leg pain, 24 patients with positive pressure tests failed to demonstrate signs of ischemia.  The two exceptions (17% of patients with CECS) had evidence of ischemia with associated pressure measurements above 160 mm Hg.  They concluded that, below these very high compartment pressures, ischemia was not a significant factor in the development of CECS.
Amendola et al. (1990) also failed to find any evidence of ischemia in patients with compartment syndrome.  They used nuclear blood flow imaging in their study on magnetic resonance imaging (MRI) in CECS and found that none of the patients with positive pressure studies demonstrated “consistent ischemic changes”.
Alternative explanations for the pain associated with CECS may be:
1.Sensory receptor stimulation in the fascia or periosteum due to increased pressure (Balduini et al. 1993)
2.Biochemical factors released due to minimally reduced blood flow (Balduini et al. 1993; Amendola and Rorabeck, 1985)
3.The symptomatic relief after fasciotomy may be due to the mechanical release of tension or biochemical changes, rather than the reversal of ischemia.

Clinical Presentation

Several months to years history of pain induced by exercise and relieved by rest.
Cramping, burning, or aching pain and tightness in the lower leg with exercise (Black et al. 1990), with continual or progressively increasing pain as exercise continues or intensity is increased (Blackman, 2000).  Eventually causing the individual to stop exercising.
Pain should cease or dramatically reduce within minutes of stopping (Balduini, 1993); however, some authors state that it may continue overnight and into the next day, depending on duration and severity of the condition (Martens and Moeyersoons, 1990)
Maybe bilateral.
Neurological symptoms vary depending on which nerve is involved (Blackman, 2000)

Physical signs are absent at rest, and all patients should therefore be examined post exercise, using the aggravating activity wherever possible (Martens and Moeyersoons, 1990).
This usually reveals a tense, firm compartment that may be painful to deep palpation and passive stretch (Blackman, 2000).
There may be tenderness along the tibial border if it is associated with stress fracture of the tibia, or traction periostitis due to chronic tension of the compartment fascia at the attachment to the tibia (Blackman, 2000)
Neurological examination is essential.  This may reveal patterns suggestive of the specific nerve and, therefore, the compartment involved (Black et al. 1990).
Anterior. Weakness of dorsiflexion and paraesthesia in the first web space (deep peroneal nerve).
Lateral: Weakness of dorsiflexion (deep peroneal nerve) and/or eversion (superficial peroneal nerve), and paraesthesia over the anterolateral distal shin and dorsum of the foot (superficial peroneal nerve) and first web space (deep peroneal nerve).
Deep posterior: involves the tibial nerve and may produce dysaesthesias over the medial arch of the foot and/or cramping of the intrinsic foot muscles. (Blackman, 2000).
Muscle hernias over the anterolateral compartments have been reported, especially at the point where the superficial peroneal nerve pierces the deep fasica (Black et al, 1990).  These hernias are thought to be an indicator of elevated intracompartmental pressure (Beith et al. 1980).
Signs of arterial insufficiency such as distal pulse deficits and poor capillary return are rare and occur only with very high intracompartmental pressures (Balduini et al. 1993)

Diagnostic tests
The most useful test to confirm CECS is a compartment pressure study, using a transducer-tipped probe.  A positive diagnosis requires elevated pressures on exercise which must coincide with reproduction of the patients typical pain (Pedowitz et al. 1990).
Many different pressures have been recorded.  However, the most accepted and predictive values are pre- and post- exercise pressures (Pedowitz et al 1990).  Studies on patients without CECS demonstrate a return to within 1mmHg of resting pressure within 3.4-5 min post exercise (Nkele et al. 1988).  Therefore, a delay of between 6 and 30 min in the return of post-exercise pressure to resting pressure levels must occur to demonstrate a positive test (Rorabeck et al. 1988).
Pedowitz et al. (1990) defined the criteria for diagnosis of anterior CECS in the leg as requiring one or more of the following: pre-exercise >15 mm Hg.  1-min post exercise >30 mm Hg, and 5 min post-exercise >20 mm Hg.  These were based upon a comparison with 210 normal muscle compartments tested using the same protocol.
Other investigations may be indicated in order to make any differential diagnosis, eg. X-ray, MRI, bone scintigraphy, and CT.

Differential diagnosis
Differential diagnosis must include periostitis and stress fracture of the tibia or fibula (Hannaford et al, 1988).  Less common possibilities include: tenosynovitis, vascular and neurological entrapment syndromes, ventral nervous system disorders, primary muscular disorders, infection, and tumours (Styf, 1989).

Often occurs bilaterally (Blackman, 2000)
Equal incidence in male and females (Hutchinson and Ireland, 1994; Wiley et al, 1987; Veith et al. 1980)
Anterior CECS tends to be more common than posterior CECS (Veith et al 1980; Amendola and Rorabeck 1985).
Patients are often described as young and physically active, often runners, reporting recurrent exertion-related pain in the affected muscle compartment (Avramovitz and Schepsis 1994).
However, in a study by Edmundsson et al (2007) most cases had a sedentary lifestyle with leg pain even during walking.
Few predisposing factors for CECS have been reported, although a history of trauma has been mentioned (Tubb and Vermillion 2001).


Early diagnosis is essential, if ischemia has occurred due to trauma, then open and extensive fasciotomies with decompression of all the affected compartments is the treatment of choice.
Many statements discussing conservative methods appear to be based on anecdotal information alone; and more scientific data is required to draw any firm conclusions (Blackman, 2000)
In a retrospective analysis (Blackman et al. 1994), rest from exercise, even for a lengthy period, was not found to be associated with any improvement in pain on resumption of activity.
Modification of intrinsic and extrinsic contributing factors is required; which may include modification of footwear, adjusting training programs, massage, orthotics, strengthening and stretching exercises.
Surgical management for CECS is based on the premise that there is a need to decrease intracompartmental pressure (Blackman, 2000).
This is done by releaseing the fascial barrier of the involved compartment, either through fasciotomy or fasiectomy (Black et al. 1990; Rorabeck et al. 1983; Schepsis et al. 1993; Wiley et al, 1987).
Results for CECS surgery are generally good, with reports demonstrating good functional improvement or symptomatic cure in a high proportion of cases (Puranen and Alavaikko, 1981; Rorabeck et al, 1983; Schepsis et al, 1993; Wiley et al, 1987).
Most reports found a better long-term outcome for anterolateral compared with posterior decompression (Puranen and Alavaikko, 1981; Rorabeck et al, 1983; Schepsis et al, 1993; Wiley et al, 1987).
Postoperatively, anterior compartment releases tend to recover faster, in contrast to deep posterior decompressions (Schepsis et al, 1993; Hutchinson and Ireland, 1994).
Crutches are used until weight bearing is comfortable (usually 3-5 days), although some authors prefer to allow the patient to walk immediately postoperatively (Wallensten, 1983)
Early mobilisation of the affected limb as soon as possible is recognised by many authors as important (Black et al, 1990; Rorabeck et al, 1983; Hutchinson and Ireland, 1994) to prevent excessive scarring and adhesions.  Active range of movement exercises at the knee and ankle are recommended and immediately postoperatively by Hutchinson and Ireland (1994).
Transitional activities such as cycling and swimming (after wound healing) are introduced over the following weeks, and running is commenced between 3 and 6 weeks postoperatively. (Blackman 2000)
Return to full activity usually occurs between 6 and 12 weeks (Black et al, 1990; Rorabeck et al, 1983; Schepsis et al 1993)

The end result of an unidentified acute compartment syndrome can be catastrophic and include nerological deficit, muscle necrosis, ischaemic contracture, severe infection, delayed healing of a fracture, loss of the limb, or even death!  Acute compartment syndrome can lead to the ‘crush syndrome’, marked by acute renal failure as a result of the precipitation of myoglobin released from the damaged muscle in the distal convoluted tubules in the kidney.  Acidic hyperkalaemic blood is also released from the damaged muscle, resulting in cardiac arrythmias and further precipitation of myoglobin in the kidneys.  Extensive muscle damage can result in the need to amputate the limb.
The incidences of complications is strongly related to the timing of fasciotomies, and therefore early diagnosis is essential to prevent irreversible damage occurring.  In acute cases fasciotomy performed within 24hrs gives ‘acceptable’ results as long as the compartment pressure does not exceed 40 mmHg.
Chronic vases may return to running at 6 weeks and competitive sport at 3 months following fasciotomy.  Commonly patients will be pain free following surgery but may continue to experience up to a 20% decrease in strength of the affected compartment.  Studies have shown that men have more successful outcomes than women.


Allen, M.J., Barns, M.R. (1986) Exercise pain in the lower leg. The journal of bone and joint surgery 68B, 5. 818-823

Blackman, P.G. (2000) A review of chronic exertional compartment syndrome in the lower leg. Medicine and science in sports and exercise. 32: 2 S4-S10

Edmundsson, D., Toolanen, G., Sojka, P. (2007) Chronic compartment syndrome also affects non-athletic subjects: a prospective study of 63 cases with exercise-induced lower leg pain. Acta Orthopaedica 78(1) 136-142

Edwards, P.H., Wright, M.L., Hartman, J.F. (2003) A practical approach for the differential diagnosis of chronic leg pain in the athlete. American journal of sports medicine. 33, 1241

Elliott, K.G.B., Johnstone, A.J. (2003) Diagnosing acute compartment syndrome. The journal of Bone and Joint surgery 85B, 5, 625-630

Hislop, M., Tierney, P., Murray, P., O’Brien, M., Mahony, N. (2003) Chronic exertional compartment syndrome: The controversial “fifth” compartment of the leg. American journal of sports medicine. 31: 770-776

Klenerman, L (2007) The evolution of the compartment syndrome since 1948 as recorded in the JBJS (B) The journal of bone and joint surgery. 89B, 10, 1280-1282

McQueen, M.M., Gaston, P., Court-Brown, C.M. (2000). Acute compartment syndrome. Who is at risk? The journal of bone and joint surgery. 82B, 200-203

Micheli, L.J., Solomon, R., Dolomon, J., Plasschaert, F.P., Mitchell, R. (1999) Surgical treatment for chronic lower leg compartment syndrome in young female athletes. American journal of sports medicine. 27: 197

Pearse, M.F., Harry, L., Nanchahal, J. (2002) Acute compartment syndrome of the leg. BMJ 325, 557-558

Rorabeck, C.H. (1984) The treatment of compartment syndromes of the leg. The journal of bone and joint surgery. 66B, 1, 93-97

Styf, J., Korner, L., Suurkula, M. (1987) Intramuscular pressure and muscle blood flow during exercise in chronic compartment syndrome. The journal of bone and joint surgery 69B, 2, 301-305

Coming back from injury

Questions are regularly posted on (and other forums) about returning from injury, or dealing with injuries. So these are a few generic tips to help you come back to full training and racing as quickly as possible.

1) Can you still train, but in an altered format? cross-trainer/eliptical training, Aqua-jogging if it’s a running related injury. Can you make some adjustments to your bike set up, such as changing the saddle hight? Swimming- focus on specific drills, eg. balance and kick. Don’t simply stop altogether if you can avoid it.

2) Seek advice EARLY. See you GP or physio as soon as possible. The longer you put it off, the longer the rehab is likely to be, as more and more compensatory issues will develop as your body tries to deal with the injury.

3) Accept and understand the grieving process if it means missing races, or even a whole season. Some good advice on the psychological element of injury rehab on this site

4) Use the time to progress your skills in other areas. Eg. Learn bike maintenance. Do an evening course in sports massage. Get your coaching qualifications and help out at your club.

5) Set goals. Speak with your physio and coach, set out short, medium and long term goals so that you all know where you are at, and where the rehab is going, and how it all fits into the larger picture of returning to racing.

6) If you haven’t got a coach, get one! The majority of injuries in triathlon are caused by training mistakes. Having a coach to bounce idea’s off or guide you more formally will prevent you from overcooking the training and breaking down in the first place. They can also help you gradually re-build your fitness after your lay-off from injury, in a controlled manner.

7) Learn from your mistakes, and ensure you include pre-habilitation exercises in your weekly program to reduce the risk of being out with injuries in the future.