Background/hypothesis: Shoulder pain in elite swimmers is common, and its pathogenesis is uncertain. Hypothesis/study design: The authors used a crosssectional study design to test Jobe's hypothesis that repetitive forceful swimming leads to shoulder laxity, which in turn leads to impingement pain. Methods: Eighty young elite swimmers (13-25 years of age) completed questionnaires on their swimming training, pain and shoulder function. They were given a standardised clinical shoulder examination, and tested for glenohumeral joint laxity using a non-invasive electronic laxometer. 52/80 swimmers also attended for shoulder MRI. Results: 73/80 (91%) swimmers reported shoulder pain. Most (84%) had a positive impingement sign, and 69% of those examined with MRI had supraspinatus tendinopathy. The impingement sign and MRIdetermined supraspinatus tendinopathy correlated strongly (r s =0.49, p<0.00001). Increased tendon thickness correlated with supraspinatus tendinopathy (r s =0.37, p<0.01). Laxity correlated weakly with impingement pain (r s =0.23, p<0.05) and was not associated with supraspinatus tendinopathy (r s =0.14, p=0.32). The number of hours swum/week (r s =0.39, p<0.005) and weekly mileage (r s =0.34, p=0.01) both correlated signifi cantly with supraspinatus tendinopathy. Swimming stroke preference did not. Conclusions: These data indicate: (1) supraspinatus tendinopathy is the major cause of shoulder pain in elite swimmers; (2) this tendinopathy is induced by large amounts of swimming training; and (3) shoulder laxity per se has only a minimal association with shoulder impingement in elite swimmers. These fi ndings are consistent with animal and tissue culture fi ndings which support an alternate hypothesis: the intensity and duration of load to tendon fi bres and cells cause tendinopathy, impingement and shoulder pain.

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