Inverse dynamics in an accelerating lower limb

Mind map of mutiple hypothesis generated for clinical reasoning. Additional possibilities are bone fatigue and achilles tendonosis creating tight calfs.

Refinement of the working hypothesis

All clinical findings (impairments measures) need to be assessed in relationship to the subjective examination (disability measures, past and current history w.r.t mechanism of injury/onset and/or aggravating/easing factors)

Clinical reasoning process used to confirm and negate correlations between the multiple variable

These findings must then be integrated into the neuro-matrix to determine a management plan which encompasses the goals of the client.

The ultimate goal for the musculoskeletal physiotherapist is to integrate the neuro-matrix into a clinically useful management strategy where predictive reasoning enhances the clients confidence in their therapist and in their own decision making processes

Treatment could consist of

Motor control suggests that the 'degrees of freedom' are controlled using a mass spring analogy of oscillations around a point of CNS stability. This stability is based on the balance of muscle tone as well as predicted feedforward movement oscillations.

Plyometrics and eccentric muscle adaptation (Martin Krause 2003)

The eccentric component to this exercise cause more profound changes to the connective tissue of the muscle (broadening and streaming of Z bands). Investigations into eccentric exercise revealed pain 8 hours after initial exercise which was maximal 48 hours later (Newham, Mills, Quigley, Edwards 1983). These investigators found low frequency fatigue 10 minutes after a 20 minute period of stepping (Newham et al 1983). Additionally, they demonstrated progressive increases in IEMG during the exercise in the rectus femoris (160% increase) and vastus medialis (140% increase) in the eccentric contracting leg (Newham et al 1983). Mechanical damage to the sarcoplasmic reticulum resulting in less calcium release for each excitatory action potential was suggested as the cause of the low frequency fatigue (Newham et al 1983).

Muscles undergo fatigue and weakening after several bouts of concentric and eccentric exercise. However, this fatigue and weakness is usually more extreme after eccentric exercise in the untrained individual

However, a number of sites in the myo-fibrillar complex such as reduce binding sensitivity and capacity of Troponin C for calcium, altered troponin-tropomysosin interaction to impaired binding and force generation by actin and myosin have been implicated in impaired force generation (Green 1990). Indeed, in the absence of any association between relaxation rates and Calcium kinetics raises support for the notion of a rate-limiting process controlling the relaxation of fatigued muscles being located in the contractile proteins (Hill et al 2001). During fatigue the relaxation times can be prolonged as much as 50% (Bigland-Ritchie et al 1986) thus resulting in increased force generation during sub-maximal stimulation due to tetanic fusion despite a substantial fall in the maximum tetanic force (Bigland-Ritchie et al 1986).

The initial overall loss of force production seen may be due to Desmin and Titan damage (Lieber & Friden 2002). Desmin acts as an extra-sarcomeric mechanical stabilizer between adjacent Z discs and the attachment to the costomere at the sarcolemma (Lieber, Shah & Fridén 2002). The costomere complex contains Talin, Vinculin & Dystrophin which attach to the trans-sarcolemmal proteins Integrin and Dystrophin associated proteins. These proteins allow the lateral transmission of force from actin to the basal lamina containing type IV collagen which is contiguous with the endomysium (Kovanen 2002). Desmin loss after eccentric exercise can occur within 5 minutes, possible as a result of increased intracellular Calcium leading to Calpain activation and selective hydrolysis of intermediate filament network (Lieber & Fridén 2002).  This may result in the ‘popping of sarcomeres’ of different length may loose their myofilament overlap of actin and myosin (Lieber & Fridén 2002). Hence, reduced force production would be expected. Additionally, the release of matrix metalloproteinase (MMP) which may degrade the extramyocellular type IV collagen (Korskinen, Kovanen, Komulainen et al 1996). However, this effect occurs many days after exercise (Korskinen et al 1996) and could even effect torque production 28 days after exercise (Lieber & Fridén 2002). This has significant implications in exercise training prescription. 

Is muscle injury the result of an imbalance between intra-muscular transverse and longitudinal forces?

Is muscle tightness due to an imbalance between force and velocity and hence the development of power? This highlights the need for specificity with training and rehabilitation.

Force damping and recoil leads to efficient transfer energy which in the case of walking has been related to sinusoidal movement

The concepts of Young's modulus of elesticity and the Hills Model of viscoelasticity should not be confused with the Mass-Spring Concept of motor control and Inverse Dynamics.

The Swedish method of rehabilitation for Achilles Tendinosis has used the concepts of eccentric loading to propogate nutrition to the muscles, encourage lengthening of the actin-myosin resting position as well as improve viscoelasticity through enhanced collagen turnover. Thereby, a mechanical input is transduced to a cellular response.

The science behind a 12 week eccentric training for Achilles Tendinosis are an increase in collagen synthesis (Langberg et al 207) and reduced neovascularization (Ohberg et al 2004) leading to reduced capillary engorgement and improved venous return (Knobloch et al 2007). These latter authors demonstrated a 45% improvement in capillary blood flow and reduced pain on a VAS after a 12 week eccentric training progam. Furthermore, Webborn (2008) suggested that clinical improvements were also related to nerve blood flow issues coined "neoneurovascularization".

Knobloch K et al (2007) Eccentric training decreases paratendon capillary blood flow and preserves paratendon oxygen saturation in chronic Achilles tendinopathy. Journal Orthopeadic Sports Physical Therapy, 37, 5, 269-276

Langberg H et al (2007) Eccentric rehabilitation exercises increases peritendinous type I collagen synthesis in humans with Achilles tendinosis. Scandinavian Journal Medicine Science Sports, 17, 3, 298-299.

Webborn ADJ (2008) Novel approaches to tendonopathy. Disability Rehabilitation, 1-6.

See links to

Achilles Tendinosis (Pdf)

Foot Biomechanics and the effects of orthotics

Metabolic - Nutritional considerations

Muscle energy techniques

Last update : 14 February 2009