The Shape of Strength: How muscle architecture drives muscle function and malfunction

Speaker: Caroline Princé, Physiotherapist, Hôpital de La Tour, Meyrin, Switzerland. PhD student, Université Savoie ­Mont-Blanc, France
Congress: Sport & Exercise Medicine Switzerland and Swiss Sport Physiotherapy Association joint conference: “Structure & Function”, Lausanne, October 30^th and 31^st 2025

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Introduction

The relationship between muscle structure and function represents a fundamental principle in musculoskeletal rehabilitation, yet injury-induced alterations to this relationship and our capacity to restore it through training remain incompletely understood. This article synthesizes current evidence on muscle structure-function interactions, injury-related disruptions, and rehabilitation strategies, with particular emphasis on hamstring musculature, drawing from research presented by Caroline Prince, sports physiotherapist and PhD researcher from Geneva.

Part 1: The Structure-function paradigm

Morphological Determinants of Force Production

Muscle force-generating capacity is primarily determined by physical size and architectural arrangement. Strong correlations exist between muscle cross-sectional area (CSA) and maximum voluntary torque, establishing morphology as a quantifiable predictor of strength capacity.
This structure-function relationship extends beyond laboratory isometric testing to sport-specific performance. Athletes with larger hamstring muscle volumes demonstrate superior sprint mechanical properties and performance outcomes. However, muscle size represents only one component of a more complex biomechanical system.

Force Transmission Structures

Effective force transmission requires consideration of passive structures within the muscle-tendon unit, including the free tendon and aponeurosis. Free tendon size demonstrates correlation with muscle function, whereas aponeurosis dimensions show inconsistent relationships with isometric or dynamic strength. This discrepancy likely reflects the aponeurosis’s complex loading environment—receiving tension along longitudinal and multiple oblique axes—combined with substantial inter-individual variation in aponeurotic morphology and architecture.

Part 2: Injury-induced structural and functional alterations

Persistent Structural Deficits

Muscle injuries produce measurable CSA deficits (atrophy) persisting up to six months post-injury, with normalization typically occurring around one year, though deficits may extend beyond this timeframe. Critically, 85% of football players return to sport with residual biceps femoris long head (BFlh) atrophy, representing substantial structural compromise at the point of sport re-entry.

Structure-Function Dissociation

Despite persistent structural deficits, functional strength assessments typically normalize at return-to-play, creating an apparent paradox. This dissociation is explained by compensatory hypertrophy of the biceps femoris short head (BFsh), where agonist muscle adaptation masks ongoing BFlh atrophy during conventional strength testing.

Clinical implications: Current return-to-play strength criteria remain valid but may require methodological refinement. Standard clinical assessment tools cannot isolate BFlh-specific strength deficits, potentially clearing athletes with unresolved structural and functional compromise in the primary injured muscle.

Force-Length Relationship Alterations

Isokinetic assessment reveals that peak torque angle—the muscle length at which maximal force is generated—shifts toward shorter muscle lengths following injury. This phenomenon is hypothesized to reflect reduced sarcomere number in series, producing decreased fascicle length. This architectural alteration represents an established risk factor for recurrent muscle injury, as the muscle achieves peak force production at shorter lengths, potentially limiting functional capacity during activities requiring force generation at longer muscle lengths.

Aponeurosis Structural Changes

Muscle injury may reduce aponeurosis dimensions. Finite element modeling demonstrates that reduced aponeurotic surface area increases strain magnitude in muscle fibers attaching to the aponeurosis. This mechanical consequence suggests that aponeurotic structural deficits may predispose to strain concentration and reinjury risk, particularly during eccentric loading phases.

Part 3: Rehabilitation-induced structural ­adaptations

Exercise-Specific Hypertrophy Responses

The capacity for rehabilitation to modify muscle structure is both exercise-dependent and region-dependent. Comparative analysis of Nordic hamstring curls versus hip extension exercises over 10 weeks of intensive training reveals:
– BFlh: Nordic hamstring exercise produces minimal CSA improvement, while hip extension demonstrates superior hypertrophic response.
– Semitendinosus: Demonstrates differential adaptation patterns compared to BFlh with the same exercises.
– Clinical principle: Muscle CSA enhancement is neither straightforward nor uniform. Hypertrophic adaptations are muscle-specific and exercise-specific, requiring targeted prescription based on individual muscle involvement.

Fascicle Length Adaptations: Regional Heterogeneity

Three weeks of Nordic hamstring training increases hamstring strength while producing non-uniform microstructural adaptations. Fascicle lengthening occurs predominantly in the distal BFlh, with minimal adaptation centrally. This represents a significant concern, as most BFlh injuries occur at the proximal musculotendinous junction—precisely the region showing least adaptation.

Mechanisms of Non-Uniform Adaptation

Electromyographic analysis explains exercise-specific and region-specific adaptations:
– Inter-muscle differences: Semitendinosus demonstrates higher EMG activity during Nordic exercises than BFlh, explaining differential hypertrophic responses between muscles.
– Intra-muscle differences: Within BFlh, electrical activity is higher distally, correlating with the observed distal-predominant structural adaptations.
– Technical execution: Maximal hamstring activation during Nordic exercises requires maintenance of tension through terminal ranges. Inability to control terminal position limits hamstring activation and subsequent adaptive stimulus.

Lengthened-State Training for Aponeurosis Hypertrophy

Eccentric exercise performed at increased muscle lengths produces both muscle hypertrophy and specific BFlh targeting. Critically, lengthened-state training may increase aponeurosis size—a key consideration given the injury-related aponeurotic atrophy and its biomechanical consequences. Lengthening state during eccentric loading appears to be a critical variable for optimizing both muscular and aponeurotic structural adaptations.

Clinical integration and future directions

Return-to-Play Considerations

The documented structure-function dissociation at return-to-sport—with 85% of athletes demonstrating residual atrophy despite normalized strength testing—challenges current clearance paradigms. While strength assessment remains essential, clinicians should recognize that:
1. Conventional testing may mask muscle-specific deficits through compensatory adaptations.
2. Structural deficits persist beyond functional normalization.
3. Altered force-length relationships and aponeurotic changes may elevate reinjury risk despite satisfactory strength scores.

Rehabilitation Programming Principles

Evidence-based structural optimization requires:
– Exercise specificity: Different exercises produce distinct regional and muscular adaptations; prescription must target identified structural deficits in specific muscles and regions.
– Lengthened-state emphasis: Eccentric training at increased muscle lengths appears critical for both fascicle lengthening and aponeurotic hypertrophy.
– Technical execution: Maintaining tension through full range, particularly terminal ranges, is essential for optimal adaptive stimulus.
– Realistic expectations: Clinicians should maintain appropriate humility regarding rehabilitation’s capacity to fully restore pre-injury structure within typical return-to-sport timeframes.

Conclusion

Muscle structure and function demonstrate complex, bidirectional relationships that injury disrupts in both immediate and persistent ways. While rehabilitation can promote structural and functional healing, adaptations are highly specific to exercise selection, muscle region, and technical execution. The documented persistence of structural deficits despite functional normalization at return-to-sport suggests current rehabilitation durations or methodologies may be insufficient for complete structural restoration. Integration of biomechanical and physiological principles into rehabilitation design offers potential to better restore structure-function relationships, though clinicians must recognize the limitations and timescales of structural adaptation when making return-to-sport decisions.

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