Triathletes and competitive swimmers may typically employ one of four different strokes: front crawl (freestyle), butterfly, backstroke, and breaststroke. The biomechanics of the four strokes, with respect to the arm action, are quite similar. Each swimming stroke goes through four common phases: reach, catch, pull, (these three are often combined and called the pull-through phase) and the recovery. In simplified terms, the pull-through involves adduction and internal rotation of the shoulder with simultaneous flexion and extension of the elbow. The recovery phase involves abduction and external rotation of the shoulder, also with simultaneous flexion and extension of the elbow. Freestyle, butterfly, and backstroke all rely on the arms for 75 percent of the propulsion forward, while in the breaststroke the legs and arms contribute equally.
Shoulder pain is the most common pain complaint in swimmers. Studies have shown that between 47 and 73 percent of the musculoskeletal problems in swimmers relate to their shoulders. (Stocker, D. Comparison of shoulder injury in collegiate and master's level swimmers. Clinical Journal of Sports Medicine. 1995; 5:4-8./Richardson, A. The shoulder in competitive swimming. The American Journal of Sports Medicine. 1980; 8:159.)
Several factors, such as intensity of training, overwork, impingement, stroke mechanics, shoulder joint laxity, shoulder instability, acromial shape, and hypovascularity, are implicated in what is typically known as "swimmer's shoulder," the term introduced to the clinical literature by Kennedy and Hawkins in 1974. (Kennedy, J. Swimmers shoulder. Physician and Sportsmedicine. 1974; 2:35.) This entity referred to what was thought to be a tendonitis of the rotator cuff, but because inflammation has not been noted histologically or under direct vision (during surgery), the term "tendinopathy" is a more appropriate description of this disorder. (Fowler, P. Swimming. In Reider, B. (ed.), Sports Medicine: The School-Age Athlete. Philadelphia, PA: W.B. Saunders Company, 1996, pp. 471-489.)
In other words, the rotator cuff tendons of swimmers are not inflamed but degenerated, when viewed under a microscope and during surgery. There are no inflammatory cells present, but evidence of degeneration, including a loss of cells, fragmentation, and disorganization of the collagen fibers.
One of the reasons that the rotator cuff tendons in swimmer's shoulders become degenerated is because of a loss of blood supply. Rathbum and MacNab's study in 1970 found a functional relationship between arm position and blood supply to the supraspinatus and biceps tendon. (Rathbun, J. The microvascular pattern of the rotator cuff. Journal of Bone and Joint Surgery. 1970; 52B:544.)
In adduction and neutral rotation the tendons are stretched tightly over the head of the humerus and their blood supply is compromised. In abduction the vessels fill, restoring full circulation. The swimming motion keeps the arm primarily in the adducted position or close to the body, and it has been proposed that this "wringing out" mechanism, or repeated hypovascularity, may contribute to early degenerative changes in the rotator cuff tendons.
The rotator cuff muscles include the supraspinatus, infraspinatus, teres minor, and subscapularis muscles. The rotator cuff acts in synchrony to provide optimal function and movement of the shoulder joint. The rotator cuff also provides the dynamic stability to the glenohumeral joint against subluxation or dislocation tendencies of the humeral head on the glenoid. The supraspinatus muscle acts in concert with the long head of the biceps tendon to provide an important humeral head-depressing action that helps to prevent superior migration of the humeral head during abduction. The supraspinatus helps to steer the humeral head into the glenoid, providing a fulcrum by which the deltoid muscle can elevate the arm.
The subscapularis, an important anterior stabilizer of the shoulder, acts in concert with other important anterior shoulder girdle muscles and the glenohumeral and coracohumeral ligaments. The infraspinatus and teres minor provide most of the posterior stability to the shoulder. Tendinosis or tendon degeneration and ligament laxities go hand in hand. They can make each other worse or be the etiological basis for the other. When a tendon is injured or degenerated, the ligament no longer has dynamic support in the joint. Likewise, if a ligament is degenerated or lax, the joint becomes unstable, meaning that the tendon has no static support. It must now be the static and dynamic stabilizer. Eventually it degenerates.
Loose Ligaments as the Source of Pain
In 1983, Fowler and Webster evaluated 188 competitive swimmers between the ages of 13 and 26 and compared them to a control group of 50 recreational swimmers. (Fowler, P. Shoulder pain in highly competitive swimmers. Orthop. Trans. 1983; 7:170.) Fifty percent of the competitive swimmers had a history of shoulder pain. On physical examination, 55 percent of the competitive swimmers and 52 percent of the recreational swimmers had some degree of posterior laxity in one or both shoulders. Twenty-five percent of the swimmers had a history of tendinopathy and increased posterior laxity. The tendinopathy was always present in the lax shoulder. Zemek and Magee compared glenohumeral laxity in recreational and competitive swimmers and found an increase in glenohumeral and general joint laxity in competitive swimmers. (Zemek, M. Comparison of glenohumeral joint laxity in elite and recreational swimmers. Clinical Journal of Sports Medicine. 1966; 6:40-47.)
A good question to ask is if there is a correlation between shoulder laxity and interfering pain in competitive swimmers? This question was answered by William C. McMaster, M.D., at the University of California at Irvine. Forty senior national and elite swimmers were evaluated for shoulder pain and laxity. The study found a statistically significant correlation between shoulder laxity and the presence of interfering shoulder pain, confirming the hypothesis of the study. The swimmers with shoulder pain also had anterior shoulder laxity. Dr. McMaster noted that "...the glenohumeral capsule ligaments are the prime stabilizers of the shoulder, especially the anteroinferior glenohumeral ligament. A spectrum of joint mobility and laxity is present in the population. Varying degrees of glenohumeral laxity are consistent with normal function. Laxity that allows excessive joint translations, resulting in instability, may be a key factor in causing shoulder pain. Indeed, if glenohumeral instability is the important variable, this would account for the fact that only certain athletes subjected to the same training program and work load suffer interfering shoulder pain. That is, only those athletes who have crossed the threshold from physiologic laxity to instability would be prone to developing symptoms."
He went on to say, "...we believe that the group of athletes who are asymptomatic yet demonstrate significant shoulder range-of-motion capacity are situated at a point along the spectrum of joint laxity that, while excessive compared to the population norm, has not crossed the threshold between excessive laxity and instability." (McMaster, W. A correlation between shoulder laxity and interfering pain in competitive swimmers. American Journal of Sports Medicine. 1998; 26:83-86.)
He is exactly right! Swimmers, by the very nature of the sport of swimming, have loose ligaments in the shoulder compared to the average person. However, in some swimmers these ligaments (especially the glenohumeral ligaments) become extremely lax and the shoulder becomes unstable. The rotator cuff must stabilize the shoulder when this occurs. It was never meant to be a static shoulder stabilizer, so it becomes degenerated. If the condition is not corrected at this point, even worse things can happen such as glenoid labrum tears, impingement syndrome, and eventual surgery!
Remember, swimmers develop a relative increase in the strength of the internal rotator and adductor muscles. In the pathologically lax shoulder, these changes may potentiate the problem by reinforcing abnormal joint mechanics. The laxity condition may be enhanced as a consequence of fatigue of certain muscle groups such as the external rotators (supraspinatus) that, for example, resist anterior joint translation. If the above was not bad enough, because we were just talking about anterior shoulder instability, most competitive swimmers are actually unstable in multiple directions.(McMaster, W. A correlation between shoulder laxity and interfering pain in competitive swimmers. American Journal of Sports Medicine. 1998; 26:83-86.)
The more you read, it becomes clear that many athletes are not playing or swimming optimally. They have loose ligaments. This is why it is vital for athletes to learn about Prolotherapy.
Prolotherapy to the rotator cuff tendon, biceps tendon, articular capsular, glenohumeral ligament, coracohumeral ligament, and glenoid labrum can be tremendously effective at eliminating chronic shoulder pain. It is best for the athlete to come into the office and receive the treatment before multi-directional instability has resulted, because some of the degenerative changes can be permanent in this condition. For the triathlete/swimmer, it is best to get Prolotherapy initially when it is clear that the shoulder pain is not going to go away. Pain present in an area for more than two months definitely needs to be examined by a Prolotherapy doctor, because it is most likely coming from an injured ligament or tendon.