EXSS2021 Movement Analysis: Tissue Properties, Loading, and Adaptation

The Stretch-Shortening Cycle (SSC) and Musculotendon Unit (MTU)

Definition of Stretch-Shortening Cycle (SSC): A natural type of muscle action consisting of a combination of eccentric (stretching) and concentric (shortening) muscle actions. Examples include running, jumping, and hopping.
Potentiation of SSC Performance:
- Elastic Recoil: Occurs when active muscles are stretched or passively stretched muscles are suddenly activated. Tension in these muscles increases, leading to the storage of potential elastic strain energy in the series elastic component (SEC) of the muscles and the musculotendon unit. A portion of this stored energy is recovered and used to potentiate (enhance) performance.
- Stretch Reflex Activation: This is instrumental in force and power enhancement during the SSC. It plays a vital role in stiffness regulation. By making the force output more powerful, it contributes to the efficiency of the motor output. Rapid reflex-induced cross-linkage formation may play a substantial role in generating force during the stretch.
- AFT (Achilles Tendon Force) Data: Passive dorsiflexion at a slow stretch ( $0.44\,rad \cdot s^{-1}$ ) causes no reflex EMG response and a linear increase in ATF. Faster or larger stretches ( $1.2\,rad \cdot s^{-1}$ ) trigger a reflex contribution to the ATF, seen as an additional response above the pure passive influence. The time lag between the onset of EMG and the onset of force increase is approximately $10\text{--}12\,ms$ .
Duration of Muscle Stretch: If a muscle stretch is maintained for too long, the stored energy is wasted as heat, leading to a decrease in the elastic recoil of mechanical energy during the SSC.
Work Output and Metabolic Efficiency: Individuals can perform more work with an active stretch prior to a shortening contraction (e.g., jumping higher in a countermovement jump vs. a squat jump). Utilizing the SSC decreases metabolic costs.
The Musculotendon Unit (MTU):
- Composed of muscle fascicles and the tendon.
- The majority of MTU changes involve the stretch and recoil of the tendon.
- Function: This allows muscle fascicles to generate force economically by optimizing contractile conditions according to force-length and force-velocity relationships.
Submaximal Countermovement Jump (CMJ) Example:
- A deep CMJ involves increased knee and hip flexion Range of Motion (ROM) and an increased hip joint moment.
- Ankle ROM remains similar, but the ankle joint moment decreases.
- Plantarflexor EMG remains unchanged, while hip extensor EMG increases. This leads to unfavourably short biarticular muscle lengths and decreased active fascicle length change during ankle plantarflexion.

Mechanical Stiffness and Modeling

Hooke’s Law: Defined by the formula $F = kx$ . The force ( $F$ ) required to deform a material is related to a proportionality constant ( $k$ ) and the distance ( $x$ ) the material is deformed, provided the shape is not permanently changed.
- k: The spring constant describing the stiffness of an ideal spring and mass system.
- Ideal Spring: Assumed to be massless, move in one direction only, and have stiffness independent of time, length, or velocity.
Stiffness Model Requirements: A comprehensive model must account for:
- Tendons, ligaments, muscles, cartilage, and bone.
- Changes in muscle force as a function of contraction velocity.
- Viscosity, muscle reflexes, time delays, and Central Nervous System (CNS) control.
- Characterization of more than one degree of freedom at joints.
- Multiple series and parallel elastic components.
- Control by two or more muscles and bi-articular muscles.
Simplified Models: Often use "quasi-stiffness," where a single value represents the behavior of all components.
Types of Lower Limb Stiffness:
1. Linear Vertical Stiffness: Applicable to linear movements in the vertical plane (e.g., hopping/jumping). $Vertical\,Stiffness = \frac{F_{MAX}}{\Delta Y}$ Where $F_{MAX} = \text{maximum Vertical Ground Reaction Force (vGRF)}$ and $\Delta Y = \text{maximum vertical displacement of the centre of mass}$ .
2. Leg Stiffness: Used when motion is not purely vertical, accounting for horizontal velocity ( $u$ ), contact time ( $t_c$ ), leg length ( $L_0$ ), and peak vGRF. $Leg\,Stiffness = \frac{F_{MAX}}{\Delta L}$ Where $\Delta L = \text{change in vertical leg length} = \Delta y + L_0(1 - \cos(\theta))$ and $\theta = \sin^{-1}(\frac{u t_c}{2 L_0})$ .
3. Angular Joint Stiffness: Describes the role of individual joints in total lower extremity stiffness. $Joint\,Stiffness = \frac{\Delta M}{\Delta \theta}$ Where $\Delta M = \text{change in joint moment}$ and $\Delta \theta = \text{change in joint angle}$ .

Clinical Implications of Stiffness

Stiff Landing Strategy: Associated with an increased risk of patellar tendinopathy. This includes faster rates of landing and faster knee joint flexion velocity (e.g., in drop landings, spike/block jumps with extended knees forced into flexion).
Tendinopathic Tendon Characteristics (Ultrasound Data): Compared to controls, tendinopathic groups show:
- Larger patellar tendon proximal cross-sectional area ( $133 \pm 11\,mm$ vs. $112 \pm 9\,mm$ ).
- Lower stiffness and lower Young's modulus.
- Higher countermovement jump and squat jump heights ( $3.4 \pm 2.2\,cm$ vs. $1.2 \pm 1.5\,cm$ ).
Injury Relationship:
- Increased Stiffness: Leads to decreased extremity excursions, increased peak forces, and increased loading rates. This results in increased shock to the lower limbs and bony injuries.
- Decreased Stiffness: Leads to excessive joint motion and soft tissue injuries. Runners with Achilles tendinopathy show decreased ankle joint stiffness despite no significant difference in joint moment or ROM.
Performance: A specific level of stiffness is required for optimal SSC utilization, and stiffness levels increase with the demands of the activity.

Tendon Anatomy: The Enthesis and the Four Zones

Definition of Enthesis: The junction between a tendon or ligament and the bone. Its primary function is to transfer mechanical tensile loads from the musculotendon complex to the bone and dissipate stress at the bony interface. It acts as a growth plate balancing cartilage formation and destruction.
Types of Enthesis: Fibrous or fibrocartilaginous (e.g., Patellar or Achilles tendon).
The Four Zones of a Fibrocartilage Enthesis:
1. Dense Fibrous Connective Tissue: Tendon/ligament area. Tendons with a greater physiological cross-sectional area need to dissipate narrowing away from the bone; thus, the fibrocartilage enthesis is more localized to distribute stress.
2. Uncalcified Fibrocartilage (UCF): Offers protection from wear and tear. It ensures tendon fibers do not bend, spread out, or compress at the hard tissue interface.
3. Calcified Fibrocartilage (CF): A thin layer providing a steady change in force transmission and acting as a barrier against diffusion from underlying blood vessels in the bone.
4. Subchondral Bone: The transitional area between CF and bone. It is highly irregular and acts as the true site of tissue union, ensuring secure attachment.
The Tidemark: The line separating the UCF (Zone 2) and CF (Zone 3). It marks the outer limits of calcification and the front between the avascular UCF and CF. It reduces the risk of soft tissue damage as insertional angles change with movement.

Tendon Adaptation and Mechanical Properties

Adaptation to Load: Tendons are dynamic. Cells detect mechanical load changes and coordinate a response to alter the extracellular matrix (ECM) composition.
- Compressive Load: Tendons expected to contain fibrocartilage. Higher molecular weight proteoglycans (e.g., aggrecan) and Type II collagen mRNA dominate.
- Tensile Load: Lower molecular weight proteoglycans (e.g., decorin) and Type I collagen mRNA dominate.
Force-Length Relationship (Structural Properties):
- Region I: Crimp angle of collagen fibers decreases; tendon lengthens. Acts as a shock absorber.
- Region II: Linear region; aligned fibers stretch.
- Region III: Some fibers fail in an unpredictable manner.
- Region IV: Complete failure of tendon fibers.
Viscoelastic Properties:
- Stress Relaxation: Constant deformation leads to decreased stress over time.
- Creep: Constant load leads to increased strain over time.
- Hysteresis: Energy loss during repeated cycles of loading and unloading. Approximately $90\text{--}96\%$ of elastic strain energy is recovered per cycle.
- Strain Rate Effect: A higher strain rate results in a stiffer tendon. Stiffness and ultimate stress are also affected by skeletal maturity and ageing.

Tendon Pathology and Ultrasound Tissue Characterization (UTC)

UTC Method: Uses 3D rendering (600 transverse grey-scale images at $0.2\,mm$ intervals) to analyze the whole tendon. It identifies four echotypes.
Continuum Model of Tendon Pathology:
1. Normal Tendon: Optimised load leading to adaptation.
2. Reactive Tendinopathy: Caused by excess load and individual factors.
3. Tendon Dysrepair: Intermediate stage of structural breakdown.
4. Degenerative Tendinopathy: Chronic structural change.
Short-Term Load Response: In AFL players, Achilles tendons showed a decrease in Echotype I and II on Day 2 post-game, returning to baseline by Day 4. History of tendinopathy leads to more Echotype II than controls.
Treatment Response: Tendon structure may improve (UTC echopattern may return to asymptomatic values), but improvements in structure are not always mediated by or associated with clinical symptoms (VISA-A scores).
Maturation in Adolescence: Maturation is a critical time for patellar tendon development. Structural changes have a stronger association with maturation offset (years from Peak Height Velocity) than chronological age.
- Group 1 (Baseline changes): Maturity status ranged from Pre-PHV to Peri-PHV ( $-2.5$ to $0.5$ years from PHV); mean age $14.1 \pm 1.0$ years.
- Group 2 (Changes during study): Maturity status mostly Post-PHV ( $-1.3$ to $2.5$ years from PHV); mean age $15.6 \pm 1.0$ years.

Load Management in Tendinopathy

Clinical Priorities during Adolescence:
1. Consider maturation stage rather than just age.
2. Structural changes developed in adolescence may persist into adulthood; repeated imaging is often unnecessary for diagnosis.
3. Post-maturation treatment should focus on symptoms and functional capacity rather than changing structure.
Management Steps:
1. Remove the cause of reactivity.
2. Reduce high loads to decrease pain.
3. Use isometric loads to reduce pain in early stages (e.g., $3 \times 3 \times 40\,s$ holds).
4. Adapt volume and rest periods.
5. Increase load capacity by improving structural/mechanical properties.
6. Goal: Regain elastic capacity and kinetic chain function for performance.
Example Progression (12 Weeks): Starts with isometrics. If pain remains low (<4/10), increase duration (to $50\,s$ , then $60\,s$ ). Eventually transition to dynamic slow progression ( $4 \times 8 \times 4\,s$ concentric + $4\,s$ eccentric).

Tissue Remodelling and the Effects of Inactivity

Wolff’s Law: States that bones adapt to the forces placed on them. Density, size, and shape are determined by the magnitude and direction of acting forces.
The Modelling Threshold:
- Strain > Threshold: Bone modelling occurs, resulting in a net gain of bone.
- Conservation Mode: No change in bone mass.
- Disuse Mode (Strain < Threshold): Bone remodelling near the marrow results in a net loss of bone.
Remodelling Mechanism: Tissue responds to force changes by increasing the amount and organization of collagen fibers. Increased cross-linking makes tissue stronger but less flexible.
Immobilisation/Inactivity Effects:
- Decreased tensile forces lead to increased collagen turnover (synthesis and degradation).
- Disorganization of fiber orientation and size.
- Decreased failure load, stiffness, water, and glycosaminoglycan content (potentially causing contractures).
- Recovery from inactivity (e.g., in astronauts or bed-ridden patients) can take up to 18 months to fully restore tissue.
Ageing vs. Inactivity: They share similar effects. Tissue becomes weaker and less able to lengthen. Ageing specifically involves decreased collagen turnover, thinner tissue, and increased cross-links which stiffen the material, alongside a loss of water in the ground substance.