The neuromechanical adaptations to Achilles tendinosis.

摘要: Human movement is initiated, controlled and executed in a hierarchical system including the nervous system, muscle tendon. If component loop loses its integrity, entire has to adapt that deficiency. Achilles tendon, when degenerated, exhibits lower stiffness. This local mechanical deficit may be compensated for by an alteration of motor commands from CNS. These modulations CNS lead altered activation agonist, synergist antagonist muscles. The present study aimed investigate effect tendon degeneration on properties, neuromechanical behaviour surrounding musculature existence modulation accompanying tendinosis. We hypothesize degenerated will diminished tissue properties protective patterns, as well up-regulated descending drive Strong evidence, reported study, indicates tendinotic tendons are more compliant compared healthy tendons. unilateral involvement affected neuromuscular control involved side but not non-involved side. muscle–tendon unit lowered temporal efficiency, which leads control. then expressed adapted pattern leg. Taken together, findings illustrate co-ordinated multi-level adaptations lesion caused pathology. Key points Achilles tendinosis localized degenerative musculoskeletal disorder develops over long period time human We demonstrate elicited series different levels such interaction, other muscles These results body’s capacity pathology provide physiological basis intervention or prevention strategies. Introduction Successful relies integrity all components system. includes CNS, plans, initiates sends command (Wolpert et al. 2013). executes generates force pull modulates controls bone. Components send feedback signals assist planning (Scott, 2004; Wolpert single this deficiency (Loeb 1999; Scott, 2004). adaptation possible only through tight connection between sensory systems (Fig. 1). Figure 1 Conceptual framework In vivo studies indicate reduced tendinopathic weight-bearing (Arya & Kulig, 2010; Child Kongsgaard 2010). When (i.e. -opathy becomes -osis), higher strain stiffness individuals Among factors, these attributed disorganized collagen bundle architecture, thinner fibres increased water content extracellular matrix (Wang, 2006). Reduced less efficient unit. Force generated transmitted bone efficiently. electromechanical delay (EMD) lag produced, dictates efficiency Stiffness was increase EMD shorten after training (Grosset, Piscione, Lambertz, Perot, 2009). By contrast, prolonged observed slackened positioning foot plantar flexion (Muraoka suggest negatively correlated with A similar relationship would expected tendinosis, consequently prolonging required transmission bone. Conceivably, readily adapts impaired occur at spinal supraspinal levels. Several factors can evoked responses, (1) neural corticospinal pathway; (2) motoneuron excitability; (3) presynaptic inhibition (Aagaard 2002; Upton, McComas, Sica, 1971). It established exercise increases responses. H-reflex V-wave 7 week 14 week programme (Duclay Martin, 2005; Aagaard 2002). neuron excitability attributable level. stimulus also people unintentionally ‘trained’ presence tendon. During functional activity, mechanism prevents already further injury even rupture. been experimental pain induced saline injection into cause EMG activity (Henriksen 2011). Under mechanism, agonist decreased diminish stress acting However, if result degeneration, compensate (Gardiner 1986; Valero-Cuevas, 2005). Taken overall aim characteristics, musculature. that, enhanced. amplitude gastrocnemius’ electrical accompanied contribution flexors. Furthermore, gastrocnemius earlier, signifying modified feedforward