Abstract

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 significantly 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 findings are consistent with animal and tissue culture findings which support an alternate hypothesis: the intensity and duration of load to tendon fibres and cells cause tendinopathy, impingement and shoulder pain.