Sara Lauren K, Gutsch Savannah B, Bement Marie Hoeger, Hunter Sandra K
Harvard Medical School, Cambridge, MA, USA.
Department of Physical Therapy, Marquette University, Milwaukee, WI, USA.
Exerc Sport Mov. 2023 Fall;1(4):1-7. doi: 10.1249/esm.0000000000000017. Epub 2023 Oct 26.
INTRODUCTION/PURPOSE: The purpose of this study was to determine the following in persons with midportion Achilles tendinopathy (AT): 1) maximal strength and power; 2) neural drive during maximal contractions and contractile function during electrically evoked resting contractions; and 3) whether pain, neural drive, and contractile mechanisms contribute to differences in maximal strength.
Twenty-eight volunteers (14 AT, 14 controls) completed isometric, concentric, and eccentric maximal voluntary contractions (MVCs) of the plantar flexors in a Biodex dynamometer. Supramaximal electrical stimulation of the tibial nerve was performed to quantify neural drive and contractile properties of the plantar flexors. Pain sensitivity was quantified as the pressure-pain thresholds of the Achilles tendon, medial gastrocnemius, and upper trapezius.
There were no differences in plantar flexion strength or power between AT and controls (isometric MVC: = 0.95; dynamic MVC: = 0.99; power: = 0.98), nor were there differences in neural drive and contractile function ( = 0.55 and = 0.06, respectively). However, the mechanisms predicting maximal strength differed between groups: neural drive predicted maximal strength in controls ( = 0.02) and contractile function predicted maximal strength in AT ( = 0.001). Although pain did not mediate these relationships (i.e., between maximal strength and its contributing mechanisms), pressure-pain thresholds at the upper trapezius were higher in AT ( = 0.02), despite being similar at the calf ( = 0.24) and Achilles tendon ( = 0.40).
There were no deficits in plantar flexion strength or power in persons with AT, whether evaluated isometrically, concentrically, or eccentrically. However, the mechanisms predicting maximal plantar flexor strength differed between groups, and systemic pain sensitivity was diminished in AT.
引言/目的:本研究旨在确定患有跟腱中段肌腱病(AT)的人群的以下情况:1)最大力量和功率;2)最大收缩时的神经驱动以及电诱发静息收缩时的收缩功能;3)疼痛、神经驱动和收缩机制是否导致最大力量存在差异。
28名志愿者(14名AT患者,14名对照组)在Biodex测力计上完成了跖屈肌的等长、向心和离心最大自主收缩(MVC)。对胫神经进行超强电刺激以量化跖屈肌的神经驱动和收缩特性。疼痛敏感性通过跟腱、腓肠肌内侧头和斜方肌上部的压痛阈值来量化。
AT患者与对照组在跖屈力量或功率方面无差异(等长MVC:P = 0.95;动态MVC:P = 0.99;功率:P = 0.98),神经驱动和收缩功能也无差异(分别为P = 0.55和P = 0.06)。然而,两组之间预测最大力量的机制不同:对照组中神经驱动预测最大力量(P = 0.02),而AT患者中收缩功能预测最大力量(P = 0.001)。尽管疼痛并未介导这些关系(即最大力量与其影响机制之间的关系),但AT患者斜方肌上部的压痛阈值更高(P = 0.02);而小腿(P = 0.24)和跟腱处(P = 0.40)的压痛阈值相似。
无论通过等长、向心还是离心方式评估,AT患者的跖屈力量或功率均无缺陷。然而,两组之间预测最大跖屈力量的机制不同,且AT患者的全身疼痛敏感性降低。