Value of basal serum cortisol to detect corticosteroid-induced adrenal insufficiency in elite cyclists.

The frequent use of glucocorticoids by athletes necessitates testing for adrenal insufficiency because of the risk of death in cases of associated severe stress (trauma, infection). During the 2001 and 2002 sporting seasons, we assessed the value of measuring baseline serum cortisol concentrations and the frequency of corticosteroid use during compulsory medical tests carried out by the French Cycling Federation on 659 elite cyclists (585 men and 74 women); the risk of adrenal insufficiency is negatively correlated with the basal serum cortisol level. Adrenal insufficiency was suspected in 34 cyclists (5.2%; 22 in 2001 and 12 in 2002) on the basis of below normal cortisol concentrations and in three cyclists (in 2001) because they had received corticosteroid treatment. In 2001, 10 of the 25 cyclists convoked underwent baseline follow-up serum cortisol determinations and 15 underwent dynamic exploration of adrenal function with the short ACTH test. Adrenal function was found to be deficient in four of these cyclists, at the limits of the normal range in four and normal in seven. Based on these results, the FFC sent a questionnaire in 2002 to all the cyclists to assess the use of corticosteroid in this population. This survey revealed that 85 of 538 cyclists (15.8%) had received corticosteroid treatment in the previous 3 months. Moreover, 11 of the 12 cyclists (92%) with low basal serum cortisol concentrations had received corticosteroid therapy. These results show that basal serum cortisol is relevant to detect adrenal insufficiency in sportsmen, in particular in cases of values below the normal range. The high frequency of corticosteroid use among elite cyclists, and in particular road cyclists who are at risk of trauma and infection, justifies screening tests to detect adrenal insufficiency.

Stenotic intimal thickening of the external iliac artery in competition cyclists.

Twenty-three cases of an arterial disease that affects competition cyclists are reported. Patients complained of intermittent acute claudication appearing on one lower limb only at the time of a maximal strain while cycling. Doppler hemodynamic investigation on an ergometric bicycle revealed a collapse of the ankle systolic pressure. Arteriography showed a sinuous lengthening and moderate stenosis of the external iliac artery. Pathologic examination of the artery disclosed a stenotic intimal thickening due to moderately cellular loose connective tissue with a variable distribution of collagen and elastic fibers. The cells in the affected zone were readily labeled with anti-actin and anti-myosin antibodies, and electron microscopy revealed features of synthetic smooth muscle cells. The lesion observed differs from intimal fibrodysplasia and from artherosclerosis. Abnormal local hemodynamic conditions may lead to this type of lesion. Thus, stenotic intimal thickening of the external iliac artery appears to be a new arterial disease defined by clinical, arteriographic, and pathologic features.

Endofibrosis of the external iliac artery in bicycle racers: an unrecognized pathological state.

Since December 1985, we have operated upon seven bicycle racers for endofibrosis of the external iliac artery. In all instances, the athletes had started cycling early in life and were engaged in top level competition by the age of 17. The principal complaint was intermittent claudication of one lower limb at "near-maximal" exercise. Pain could be reproduced by exertional tests on an ergometric bicycle, and in all cases except one, measurement of ankle systolic pressure of that limb compared with the opposite side and brachial pressures showed a marked decrease on the involved side. Arteriography, performed with multiple views and positions, documented a 5 to 6 cm moderately stenotic (less than 40% diameter) segment, associated with arterial lengthening. Surgical treatment consisted of endarterectomy and shortening of the artery. Four patients were able to return to competition. The origin of this pathology is discussed, based on gross and histologic findings. Under certain predisposing anatomic conditions, abnormal hemodynamics, probably due to a high flow arterial state and an aerodynamic position on the bicycle, provoke repeated trauma which eventually produces the lesion. Practically unrecognized until now with only two previous publications on the subject in the literature, this entity is probably not uncommon.