Neuromechanical activation of triceps surae muscle remains altered at 3.5 years following open surgical repair of acute Achilles tendon rupture

跟腱急性断裂开放手术修复后3.5年,腓肠肌的神经机械激活仍然存在改变。

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Abstract

PURPOSE: To assess whether the neuromuscular activation pattern following Achilles tendon rupture and repair may contributes to the observable functional deficits in this severe and increasingly frequent injury. METHODS: In this study, the neuromuscular activation using surface EMG of n = 52 patients was assessed during a battery of functional performance tasks to assess potential alterations of muscular activation and recruitment. We analyzed the injured leg vs. the contralateral healthy leg at a mean of 3.5 years following open surgical repair. The testing battery included isokinetic strength testing, bipedal and single-legged heel-rise testing as well as gait analysis. RESULTS: During isokinetic testing, we observed a higher activation integral for all triceps surae muscles of the injured side during active dorsiflexion, e.g., eccentric loading on the injured leg, while concentric plantarflexion showed no significant difference. Dynamic heel-rise testing showed a higher activation in concentric and eccentric loading for all posterior muscles on the injured side (not significant); while static heel-rise for 10 sec. revealed a significantly higher activation. Further analysis of frequency of fast Fourier-transformed EMG revealed a significantly higher median frequency in the injured leg. Gait analysis revealed a higher pre-activation of the tibialis anterior before ground contact, while medial and lateral gastrocnemius muscles of the injured leg showed a significantly higher activation during push-off phase. CONCLUSIONS: The results of this study provide evidence on the neuromuscular changes 3.5 years following open surgical Achilles tendon repair. These complex neuromuscular changes are manifested to produce the maximum force output whilst protecting the previously injured tendon. The observed alterations may be related to an increased recruitment of type II muscle fibers which could make the muscles prone to fatigue. LEVEL OF EVIDENCE: III.

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