Part 2: anatomy


Stenosis of the arteria ilica externa is a rare pathology that often occurs specially in elite cyclists and high level skaters. It is assumed that kinking of this artery during repetitive hip flexion in the typical cycling or skate position provokes this condition. The increase of the cardiac output and systolic blood pressure during intensive cycling or skating could also play a role.

Repair mechanisms may lead to fibrotic alterations of the injured artery. The symptoms are comparable to those of exercise ischemia, the patient complaining of a fatigued, dull  sensation in the leg , especially when performing  at high intensities.  Change in ankle-arm blood pressure ratio after a maximal bicycle or skating exercise test in the typical position is indicative of this pathologic state. Pulse-volume registration of the lower extremities is the most important diagnostic tool. In recent years also diagnostic imaging methods are used for a better diagnosis. MRI, ECHO en Scan.

Until now surgical intervention has been the only effective therapy, although the long term results as well as possible complications have yet to be observed.


Red vessels propose the arterial system (oxygenated) and blue vessels the venous system (deoxygenated).

The aorta coming out of the heart is situated in front of the spine. At the level of the pelvis crest at the level of the belly button it divides into the right and left common iliac arteries. Both iliac arteries divide into an internal iliac artery, which provide the pelvis and the psoas muscle of blood, and an external iliac artery, which runs to the leg below the inguinal ligament of Poupart. In 1984 Walder and co-workers were the first who published about two top cyclists with a narrowing of the external iliac artery. Anatomic pathology examination showed in both cases a fibrosis of the vascular intima, called endofibrosis by them.

Chevalier and colleagues (1986) found in two patients impairment of the entire inner wall of the femoral artery, occurring narrowing of the lumen of the blood vessel for 80 percent. In five other cyclists operated by them there was only a partial destruction of the vascular wall, localized in the greater curvature of the arterial bend. Microscopic examination revealed a hyperplasia of the intima   which also affected the subendothelial layer. The endothelium itself was not affected. In two patients with relatively small stenosis were found many myofibroblasts in the intima. The authors suggest that a reinforcement of the muscular arterial wall in the initial phase of this condition could explain this, after which the affected area by persistent mechanical stress is known  as secondary  fibrotic degeneration which is to be conceived as the formation of scar tissue.

In 23 operated cyclists Rousselet and colleagues (1990) saw during surgery that the artery iliaca externa was lengthened and consequently showed an abnormal loop in flexion or bending of the hip. Although the blood vessel there looked normal to the eye, one could feel a smooth bulge in the middle part. Its length was two to six centimeters. In the majority of cases, it was not put on the entire circumference of the vessel. The degree of vascular occlusion varied greatly between patients. Microscopic examination of the removed vascular narrowing sections showed a thickening of the intima by abundant connective tissue. This thickening was similar to fibrodysplasia of the intima, which is normally only seen above the fiftieth year of life. The endothelium and the outer wall of the blood vessel did not appear to be affected.


Various authors suggested several mechanisms to explain the occurrence of this particular disease in healthy, intensively trained cyclists. The most important factor is the anatomy of the iliac artery in combination to the specific posture mentioned while cycling or skating and the cycling and skating movement which is always accompanied by the bending (flexion) of the hip. Both external iliac arteries are partly well fixed. The internal iliac artery and the artery that supplies the psoas muscle of blood, fixes the external iliac artery in the initial stage. A second point of fixation of the artery is at the level of the groin below the inguinal ligament.

Over the intermediate range, the external iliac artery has no clear fixation points  and the blood vessel runs slightly winding. Due to the constantly repeated extreme flexion of the hip while cycling or skating caused by an attempt to achieve good aerodynamic position, these fixation points come closer together. This creates a distinct kink in the course of the artery. This twisting is more pronounced as the iliac artery is very long.

While pedaling with his increasingly repetitive flexion of the hip artery is always bent. This phenomenon is similar to the kinking of a garden hose to stop the water jet. The forces which are thereby constantly exerted on the vessel wall – especially on the large curvature-, cause local abnormalities arising in the vessel wall. With persistent mechanical stress cause the repair mechanisms ultimately to a fibrotic thickening of the arterial wall (see Figure 1). During heavy efforts like bicycle time trial, climbing or sprinting, blood flow to the legs ‘the pinch’ can literally come and the athlete will experience symptoms.

Figure 1. Schematic overview of the pathogenesis of the narrowing of the femoral artery (1), the feeding artery of the musculus psoas (2) the outer curvatures of the external iliac artery experience the greatest mechanical stress, which fibrotic changes in the vascular genesis. From Chevalier et al., 1986.

Even though so far no indications have been found, that existing anatomical abnormalities of the artery before the cycling career, that may possibly play a role. In view of the low incidence of this condition as well as the difficulty of detection of pre-existent anomalies, this question will have little or no practical significance. In addition, systemic factors, while cycling, could play an important role. The blood pressure can rise significantly during exercise. A systolic blood pressure above 240 mm Hg is not uncommon. This can lead to both a broadening, as well as to an extension of the blood vessel. And thus the blood vessel is more susceptible to kinking and damage. It is known that a long-lasting increase in the cardiac output can cause endo fibrosis of elastic arteries. Whether this will also happen for muscular vessels, such as the arteria iliaca externa, is not known. In addition, local factors, such as changes in the blood flow speed, and local turbulences may be of importance.