Table of Contents
Shoulder Impingement: Rethinking the Impingement Paradigm
For decades, the medical understanding of swimmer’s shoulder centered on a straightforward mechanical explanation: the repetitive overhead arm movements during swimming caused the rotator cuff tendons to repeatedly collide with the acromion (the bony roof above the shoulder), creating inflammation and pain through mechanical compression—what physicians termed “subacromial impingement syndrome.” This model seemed logical and led to widespread treatment focusing on increasing the space beneath the acromion through rest, anti-inflammatory measures, and sometimes surgical procedures removing portions of the acromion to “decompress” the subacromial space.
However, modern biomechanical research reveals a far more complex reality. The traditional external subacromial impingement model, while still having merit in some contexts, doesn’t fully explain swimmer’s shoulder pathology. Emerging evidence suggests that internal impingement—specifically anterior superior internal impingement (ASII)—plays a far greater role in the etiology of swimmer’s shoulder than previously recognized, and that this mechanism can also account for the intra-articular findings observed in swimmer’s shoulder, namely labral damage and SLAP (superior labrum anterior-posterior) lesions. Additionally, the relationship between glenohumeral laxity, muscle fatigue, scapular dyskinesis, and impingement symptoms creates a multifactorial picture where “impingement” often represents the consequence of underlying neuromuscular dysfunction rather than the primary problem itself.
The anatomical reality challenges simplistic compression models. Studies examining cadaveric shoulders demonstrate that extensive intra-articular contact occurs between the supraspinatus, subscapularis, long head of biceps, and the anterior superior and posterior superior labrum during shoulder flexion and internal rotation—movements essential for elite swimming—and further, that external subacromial impingement of the supraspinatus above 120 degrees of elevation is unlikely given actual anatomical relationships. This finding suggests that what clinicians diagnose as “subacromial impingement” in swimmers often actually represents internal impingement pathology with pain referred to the lateral shoulder region mimicking external impingement presentation.
The practical implications of this revised understanding prove substantial. If swimmer’s shoulder primarily stems from internal impingement driven by muscle fatigue and laxity rather than fixed structural narrowing of the subacromial space, then treatment should emphasize restoring dynamic muscular control and addressing capsular issues rather than simply attempting to increase subacromial space. Research demonstrates that subacromial impingement in competitive swimmers is typically caused by altered kinematics (non-outlet impingement) due to muscle fatigue or laxity rather than inherent structural abnormalities, meaning rehabilitation targeting muscle balance and scapular control should represent first-line treatment. Understanding both external and internal impingement mechanisms, recognizing how scapular dyskinesis contributes to impingement symptoms, implementing evidence-based rehabilitation addressing the true underlying causes, and managing training appropriately proves essential for resolving shoulder pain in competitive swimmers.
Understanding the Types of Shoulder Impingement
External Subacromial Impingement: The Traditional Model
The classical subacromial impingement model proposes that rotator cuff tendons (particularly supraspinatus) and the subacromial bursa compress between the humeral head below and the coracoacromial arch above during arm elevation. Kennedy and Hawkins originally proposed that shoulder pain resulted from repetitive impingement of the avascular zone of the supraspinatus insertion and the intracapsular portion of the bicipital tendon under the coracoacromial arch during the adducted position of the shoulder—what they termed “outlet impingement”.
In swimmers specifically, researchers identified two phases of the stroke cycle where the shoulder theoretically faced most stress and vulnerability to subacromial impingement: initial catch and early pull (representing 15 percent of stroke time), and recovery phase (10 percent of stroke time), meaning as much as 25 percent of the freestyle stroke time was spent in positions creating potential subacromial compression. During recovery phase particularly—when the arm elevates above water with the shoulder in forward flexion and internal rotation—the traditional model proposed that subacromial space narrowing created mechanical compression of rotator cuff tendons.
However, modern understanding recognizes that true “outlet” impingement from fixed structural abnormalities (hooked acromion shape, thickened coracoacromial ligament, bone spurs) occurs relatively rarely in young competitive swimmers. Instead, most swimmer shoulder impingement represents “non-outlet” or “functional” impingement where altered shoulder mechanics rather than fixed anatomy create pathological compression. This altered mechanics typically stems from muscle fatigue, rotator cuff weakness, scapular dyskinesis, or glenohumeral laxity—all potentially modifiable factors through appropriate training and rehabilitation.
Internal Impingement: The Emerging Explanation
Internal impingement describes pathological contact between intra-articular structures—specifically between the posterior-superior or anterior-superior rotator cuff and the glenoid labrum at extremes of shoulder motion. While posterior-superior internal impingement (PSII) receives most attention in throwing athletes, anterior-superior internal impingement (ASII) appears particularly relevant to swimmers based on stroke biomechanics requiring repetitive shoulder flexion with internal rotation.
ASII occurs when the arm positions in combined flexion, adduction, and internal rotation—the exact position swimmers adopt during hand entry phase and early pull-through when the hand enters water and begins engaging for propulsion. In this position, the anterior rotator cuff (particularly subscapularis) and the long head of the biceps compress against the anterior-superior glenoid rim and labrum, creating mechanical impingement of these intra-articular structures. Research investigating anatomical contact patterns demonstrates extensive contact occurring between subscapularis, supraspinatus, long head biceps, and anterior-superior labrum during movements mimicking swimming positions, providing anatomical evidence supporting the ASII mechanism.
The clinical significance of recognizing internal impingement patterns lies in understanding the associated pathology. Internal impingement creates distinctive injury patterns including partial-thickness rotator cuff tears (affecting the articular/undersurface rather than bursal/top surface of tendons), labral fraying or tears at anterior-superior or posterior-superior regions, and biceps tendon pathology from repetitive compression against glenoid rim. These pathological patterns differ from external impingement creating bursal-side rotator cuff damage and subacromial bursal inflammation.
The Laxity-Impingement Connection
The relationship between glenohumeral laxity and impingement represents a critical piece of the swimmer’s shoulder puzzle. Jobe and colleagues first proposed that repetitive forceful overhead activities cause gradual stretching of anteroinferior capsuloligamentous structures from chronic microtrauma, creating increased laxity and instability that subsequently leads to mechanical impingement—the so-called “laxity-impingement cascade”.
Studies examining swimmers’ shoulders document remarkable laxity prevalence. Research found that the humeral head could be translated to the glenoid rim in most patients, with similar degrees of anterior and posterior translations, and inferior laxity (positive sulcus sign) of 1-2 cm was present in 98 percent of examined shoulders—an extraordinarily high prevalence. Generalized laxity was found in 62 percent of swimmers, definitely higher prevalence compared to general populations. This suggests that combination of acquired factors (from repetitive training) and inherent factors (genetic hypermobility) contribute to shoulder laxity in swimmers.
The mechanism connecting laxity to impingement involves humeral head positioning. Normally, rotator cuff muscles maintain the humeral head centered within the glenoid socket during arm movements. However, when anterior capsular laxity permits excessive anterior translation, and when rotator cuff muscles fatigue from high training volumes, the humeral head migrates superiorly and anteriorly during stroke cycles. This abnormal positioning narrows the subacromial space creating external impingement, and also alters intra-articular contact patterns creating internal impingement—both pathological consequences of the same underlying problem: inadequate dynamic control of an inherently lax joint.
The Role of Scapular Dyskinesis
Understanding Scapular Function in Swimming
The scapula provides the foundation for optimal shoulder function through serving as the stable base from which the glenohumeral joint operates. During normal arm elevation, the scapula should rotate upward, posteriorly tilt, and externally rotate in coordinated patterns maintaining optimal positioning of the glenoid relative to the moving humerus. This scapulohumeral rhythm—the coordinated movement between scapula and humerus—proves critical for maintaining adequate subacromial space and proper glenohumeral joint mechanics throughout arm movement arcs.
In swimmers specifically, proper scapular positioning and movement proves essential throughout all stroke phases. During hand entry and early pull-through, scapular protraction (forward movement) and upward rotation maintain optimal glenoid positioning allowing powerful pulling without impingement. During recovery, scapular upward rotation and posterior tilting maintain subacromial space despite arm elevation. Throughout all phases, scapular stability prevents excessive winging or dysrhythmic movement interfering with rotator cuff function.
Scapular Dyskinesis: When the Foundation Fails
Scapular dyskinesis—abnormal scapular positioning or movement patterns—occurs with remarkable frequency in swimmers experiencing shoulder pain. When examining differences between painful and non-painful shoulders in swimmers, researchers found that serratus anterior action dramatically reduces during the middle pull-through phase, with consequent compensatory action of the rhomboids resulting in scapular destabilization. This muscular imbalance creates abnormal scapular kinematics contributing to impingement pathology.
Several scapular dyskinesis patterns commonly affect swimmers:
Excessive scapular protraction and anterior tilting: Weak scapular retractors (rhomboids, middle trapezius) and tight pectoralis minor create excessive forward scapular positioning. This anterior tilt reduces the subacromial space by bringing the acromion closer to the humeral head, creating mechanical impingement particularly during recovery phases when arm elevation peaks.
Inadequate upward rotation: Weak or fatigued serratus anterior and upper trapezius fail to create adequate scapular upward rotation during arm elevation. Since the glenoid sits on the scapula, inadequate scapular rotation means the glenoid doesn’t orient optimally upward following the rising humerus, forcing compensatory glenohumeral motion that narrows subacromial space creating impingement.
Scapular winging: Severe serratus anterior weakness creates visible scapular winging—the medial border and inferior angle lift away from the thoracic wall creating obvious asymmetry. While dramatic winging occurs relatively rarely, subtle serratus anterior dysfunction proves common in swimmers creating less obvious but still functionally significant scapular destabilization.
The clinical presentation of scapular dyskinesis includes shoulder pain during swimming (particularly during specific stroke phases requiring scapular control), visible asymmetry comparing both scapulae during arm movement, palpable or audible clicking/clunking during shoulder motion from abnormal scapulothoracic articulation, and specific patterns of muscular tightness (pectoralis minor) and weakness (serratus anterior, lower trapezius, rhomboids).
The Fatigue Factor
Muscle fatigue represents perhaps the most important contributor to impingement development in swimmers. Similar to serratus anterior patterns, the subscapularis proves susceptible to fatigue because of its continual activity during swimming, with consequent compensatory activity of infraspinatus resulting in unbalanced glenohumeral stabilization. This creates the fatigue-related dyskinesis underlying much swimmer shoulder pathology.
The mechanisms connecting fatigue to impingement involve several pathways. Fatigued rotator cuff muscles lose their capacity to maintain humeral head centering—the humeral head migrates abnormally during stroke cycles when dynamic stabilizers can’t counteract prime mover forces. Fatigued scapular stabilizers allow abnormal scapular positioning and movement creating the dyskinesis patterns described above. Fatigued muscles alter stroke mechanics as swimmers unconsciously compensate for reduced muscular capacity, potentially adopting technique patterns creating excessive shoulder stress. All these fatigue-related changes concentrate during the latter portions of training sessions or competitions when cumulative fatigue peaks—explaining why shoulder pain often worsens progressively throughout workouts.
Clinical Diagnosis: Distinguishing Impingement Types
History and Symptom Patterns
External impingement presentation: Swimmers typically report lateral shoulder pain (over the deltoid region) worsening during specific stroke phases—particularly recovery when arm elevation peaks. Pain begins after certain training durations or distances (initially only during high-volume or high-intensity sessions, progressively occurring earlier with less provocation). The characteristic “painful arc”—pain occurring during mid-ranges of arm elevation (roughly 60-120 degrees) but less pain below or above this range—suggests subacromial compression during the arc where space proves most restricted. Night pain disturbing sleep, particularly when lying on the affected shoulder, commonly accompanies external impingement.
Internal impingement presentation: Swimmers report deep shoulder pain (sometimes described as “inside” the joint rather than superficial) worsening during hand entry and early pull-through phases when the shoulder positions in combined flexion-adduction-internal rotation creating intra-articular compression. Pain quality might differ from external impingement—sometimes described as “catching” or “clicking” suggesting intra-articular mechanical symptoms from labral pathology. Occasionally athletes report posterior shoulder pain if posterior-superior internal impingement affects posterior rotator cuff and labrum.
Scapular dyskinesis presentation: Shoulder pain associates with visible or palpable scapular asymmetry. Athletes sometimes report that their shoulder blade feels “stuck” or moves differently than the opposite side. Pain might localize to periscapular regions (medial scapular border, inferior angle) from muscular strain in overactive compensatory muscles attempting to control abnormal scapular motion. Specific activities requiring scapular control create symptoms even outside swimming—pushups, overhead reaching, or carrying loads.
Physical Examination Tests
External impingement tests:
- Neer impingement test: Passively elevating arm in forward flexion with internal rotation reproduces pain by compressing rotator cuff against acromion
- Hawkins-Kennedy test: Passively internally rotating shoulder with arm at 90 degrees forward flexion recreates subacromial compression
- Painful arc test: Active arm abduction creates pain during mid-ranges (60-120 degrees) but less pain below or above this arc
- Positive findings support external impingement diagnosis though don’t definitively distinguish from internal impingement given overlap in provocative positions
Internal impingement tests:
- Relocation test: With arm positioned in abduction-external rotation (creating posterior impingement), applying posterior force on humeral head relocates it anteriorly relieving impingement pain
- Position-specific provocation: Placing shoulder in combined flexion-adduction-internal rotation (ASII position) or abduction-external rotation (PSII position) reproduces characteristic deep joint pain
- Insufficient research exists validating specific clinical tests for anterior-superior internal impingement patterns relevant to swimmers
Scapular dyskinesis assessment:
- Visual observation: Watching scapular movement during arm elevation reveals asymmetry, winging, or dysrhythmic motion patterns comparing affected to unaffected sides
- Scapular assistance test: Manually assisting proper scapular upward rotation and posterior tilt during arm elevation reduces or eliminates pain, suggesting that scapular dyskinesis contributes to symptoms
- Scapular retraction test: Actively retracting scapula while performing provocative arm movements reduces pain, again supporting scapular contribution to pathology
- Muscle palpation: Excessive upper trapezius activation with inadequate serratus anterior or lower trapezius recruitment during arm movement suggests muscular imbalance**
Rotator cuff strength testing: Resisted external rotation (infraspinatus/teres minor), resisted internal rotation (subscapularis), resisted abduction with arm at side (supraspinatus), and empty-can test (supraspinatus isolation) assess individual muscle function revealing specific weakness patterns guiding rehabilitation focus.
Range of motion assessment: Swimmers typically demonstrate characteristic ROM patterns with excessive external rotation and limited internal rotation compared to non-swimmers—adaptive changes from sport demands. However, severe asymmetry between shoulders or extreme limitations might suggest pathological capsular tightness contributing to impingement. Posterior capsule tightness limiting internal rotation and horizontal adduction proves particularly relevant to internal impingement risk.
Comprehensive Rehabilitation: Addressing the True Causes
Phase One: Acute Pain Management and Load Reduction
Activity modification: Reducing swimming volume represents the critical first step—continuing full training loads while attempting rehabilitation rarely succeeds. Athletes should reduce weekly swimming distance by 30-50 percent initially, emphasizing technique quality over quantity, and potentially temporarily modifying stroke patterns avoiding most provocative positions (perhaps reducing butterfly if recovery phase proves most painful).
Pain control measures: Ice application following training reduces inflammation and provides symptomatic relief. NSAIDs manage acute pain and inflammation during initial phases though shouldn’t be used long-term masking symptoms while continuing pathological loading. Relative rest from swimming sometimes necessary during severe acute phases, though maintaining fitness through lower-body kick work or land-based cardiovascular training prevents complete deconditioning.
Phase Two: Restoring Muscular Balance and Scapular Control
Scapular stabilization exercises: Research demonstrates that combined intervention of scapular stabilization exercises and taping therapy produces significant effects in scapular dyskinesia in amateur swimmers, reducing pain and disability while improving shoulder ROM more effectively than conventional treatment alone. Key exercises include:
- Serratus anterior activation: Push-up plus variations (standard pushups with additional scapular protraction at top position), wall slides maintaining scapular protraction, and prone scapular protraction exercises develop serratus anterior strength critical for scapular upward rotation and stabilization
- Lower trapezius and rhomboid strengthening: Prone scapular retraction exercises (prone Y’s, T’s, I’s), rowing variations emphasizing scapular retraction, and resistance band exercises targeting middle and lower trapezius develop scapular retractor strength. However, exercises should emphasize proper muscle activation patterns—avoid excessive upper trapezius compensation through tactile cueing ensuring lower trapezius and serratus anterior activate before movement initiation
- Dynamic scapular control: Progress from static holds toward dynamic movements, from stable surfaces toward unstable surfaces, and from isolated exercises toward integrated functional movements simulating swimming positions. Use mirrors or video feedback allowing athletes to visualize proper scapular positioning developing kinesthetic awareness
Rotator cuff strengthening: Progressive resistance training develops rotator cuff strength particularly emphasizing external rotators (infraspinatus, teres minor) often weaker relative to internal rotators in swimmers. External rotation exercises should be performed at multiple shoulder positions (arm at side, 90 degrees abduction, overhead) developing comprehensive capacity. Subscapularis strengthening through internal rotation exercises maintains balanced rotator cuff development. Exercises should emphasize proper technique and control rather than heavy resistance, with eccentric phases (slowly lowering resistance) receiving particular attention given rotator cuff’s critical eccentric role during stroke deceleration phases.
Addressing capsular restrictions: Posterior capsule tightness limiting internal rotation and horizontal adduction contributes to both external and internal impingement through altered glenohumeral mechanics. “Sleeper stretch” (lying on affected side, passively internally rotating shoulder) and cross-body adduction stretches target posterior capsule addressing this common impairment in swimmers. However, recognize that swimmers already demonstrate substantial shoulder mobility—flexibility work should target specific restrictions rather than pursuing global increased laxity potentially worsening underlying hypermobility.
Phase Three: Neuromuscular Control and Proprioception
Motor control retraining: Developing proper muscle activation sequencing proves critical—scapular stabilizers should activate before initiating arm movement rather than reacting after movement begins. Therapists use tactile cueing (touching target muscles) ensuring proper activation patterns, progressing toward verbal cueing, eventually achieving automatic proper sequencing without conscious focus. This neuromuscular retraining addresses the fatigue-related dyskinesis underlying much impingement pathology.
Proprioceptive training: Single-arm balance exercises on unstable surfaces, rhythmic stabilization drills (applying random perturbations while athlete maintains position), and closed-kinetic-chain exercises (planks with alternating arm reaches) develop proprioceptive awareness and reactive stabilization capacity supporting dynamic shoulder control during unpredictable swimming forces.
Stroke technique refinement: Working with coaches addressing technical flaws creating excessive shoulder stress proves essential. Video analysis identifies specific problematic positions or movement patterns. Common technical corrections include improving body rotation during freestyle (reducing isolated shoulder elevation requirements), optimizing hand entry angle and position (avoiding extreme internal rotation), maintaining high elbow positioning during pull-through (reducing excessive shoulder elevation), and refining breathing technique (preventing compensatory shoulder hiking during breathing).
Phase Four: Progressive Return to Swimming
- Easy swimming short distances: Begin with 1000-1500m total distance, easy pace, technique focus, frequent rest intervals allowing adequate recovery between repetitions
- Gradual volume increases: Increase distance 10-15 percent weekly monitoring symptoms carefully. Any pain increase signals excessive progression requiring temporary volume reduction
- Equipment reintroduction: Hand paddles dramatically increase shoulder forces—reintroduce gradually with reduced volume initially, avoiding aggressive paddle usage during rehabilitation
- Intensity progression: Only after tolerating volume increases should intensity advance toward competitive paces. Sprint training and intensive intervals create peak shoulder loading requiring full muscular capacity
- Ongoing prevention: Continue scapular stabilization and rotator cuff strengthening exercises throughout career as maintenance preventing recurrence
Prevention Strategies: Keeping Shoulders Healthy
Year-round strength maintenance: Consistent scapular stabilization and rotator cuff strengthening represents most important prevention. Two to three weekly sessions maintaining conditioning prevents fatigue-related dyskinesis and weakness underlying impingement development.
Appropriate training progression: Gradual volume increases respecting adaptation capacity, periodized training with recovery weeks preventing chronic fatigue accumulation, and judicious equipment use (limiting paddle training preventing excessive force application) reduce overload risk.
Technique emphasis: Regular coaching feedback optimizing stroke mechanics potentially reduces pathological loading. Swimmers should develop efficient technique utilizing coordinated body rotation and kinetic chain force generation rather than isolated shoulder strength.
Monitoring for warning signs: Early intervention when mild symptoms first appear prevents progression. Swimmers experiencing shoulder discomfort should immediately reduce volume and implement preventive strategies rather than ignoring symptoms hoping spontaneous resolution.
Swimming as rehabilitation tool: Interestingly, swimming itself—when properly prescribed—can serve as rehabilitation for scapular dyskinesis in appropriate contexts. Case reports document patients with scapular dyskinesis experiencing pain reduction and functional recovery through structured swimming programs emphasizing all four strokes (developing balanced musculature), using flotation devices on legs (increasing upper extremity demands), and progressively increasing training under supervision. This paradox—that competitive swimming causes shoulder problems while therapeutic swimming rehabilitates them—again highlights that volume, intensity, and biomechanics determine whether swimming proves therapeutic or pathological.
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