31/01/2026
https://www.facebook.com/photo/?fbid=775882475551625&set=a.123816967424849
Shoulder Impingement Syndrome – A Biomechanical Perspective
Shoulder impingement syndrome is fundamentally a problem of altered biomechanics rather than isolated tissue damage. The shoulder complex relies on precise coordination between the glenohumeral joint, scapulothoracic motion, acromioclavicular joint, and sternoclavicular joint. When this coordination is disrupted, the subacromial space narrows and compressive forces rise, leading to irritation of the rotator cuff tendons and subacromial bursa.
At the glenohumeral joint, normal arm elevation requires the humeral head to remain centered within the glenoid fossa. This centering is achieved by the rotator cuff producing a compressive and inferiorly directed force that counteracts the upward pull of the deltoid. When the rotator cuff—particularly the supraspinatus and infraspinatus—becomes weak or fatigued, the humeral head migrates superiorly during elevation, increasing mechanical contact with the undersurface of the acromion.
The subacromial space is biomechanically narrow even under ideal conditions. During shoulder abduction between approximately 60° and 120°, the space is naturally reduced as the greater tuberosity approaches the acromion. If superior humeral translation occurs, this reduction becomes excessive, resulting in compression of the supraspinatus tendon, long head of the biceps tendon, and subacromial bursa. This explains the classic painful arc seen during mid-range elevation.
Scapular biomechanics play a decisive role in either protecting or provoking impingement. Normal shoulder elevation follows a scapulohumeral rhythm, where glenohumeral motion is coupled with upward rotation, posterior tilt, and external rotation of the scapula. Reduced scapular upward rotation or posterior tilt decreases clearance beneath the acromion, mechanically predisposing the shoulder to impingement even in the absence of structural abnormalities.
The acromioclavicular joint contributes to impingement biomechanics by influencing scapular motion and acromial orientation. Degenerative changes, osteophyte formation, or altered clavicular motion can shift the acromion inferiorly. This structural change further reduces subacromial space, increasing compressive load on soft tissues during arm elevation and overhead activities.
Muscle imbalance is a major driver of faulty mechanics. Overactivity of the upper trapezius combined with weakness of the lower trapezius and serratus anterior alters scapular force couples. Instead of smooth upward rotation and posterior tilt, the scapula elevates excessively, maintaining a downward-facing acromion. This dysfunctional pattern magnifies impingement forces with repetitive use.
From a load perspective, repetitive overhead activities expose the rotator cuff to cyclical compressive and tensile stress. Each elevation cycle subjects the tendons to friction and compression under the acromion. Over time, this leads to tendon degeneration rather than acute inflammation, explaining why impingement often becomes chronic and resistant to rest alone.
In functional tasks such as lifting, throwing, or reaching overhead, energy should flow efficiently from the trunk and scapula to the arm. When proximal control is lost, the shoulder compensates by increasing local muscular demand, amplifying joint compression. This inefficient force transfer accelerates tissue overload and symptom progression.
Shoulder impingement is not simply a space problem—it is a movement and load-management problem. Restoring humeral head control, optimizing scapular mechanics, and rebalancing force couples are essential to reducing subacromial compression and achieving long-term resolution rather than temporary symptom relief.
